By condition

• Semaglutide Study

  Approved. SUSTAIN established the glycaemic effect; SUSTAIN-6 reported reduced major adverse cardiovascular events; FLOW reported renal benefit in type 2 diabetes with chronic kidney disease.

• Tirzepatide Study

  Approved. Dual GIP/GLP-1 agonist; the SURPASS programme produced the largest HbA1c reductions of any injectable in the class, and beat semaglutide 1 mg head-to-head.

• Liraglutide Study

  Approved. The LEAD programme for glycaemia, LEADER for cardiovascular outcomes. Daily dosing makes it easier to titrate and easier to stop than the weekly agents.

• Dulaglutide Study

  Approved. REWIND is notable for enrolling a largely primary-prevention population — most participants had no established cardiovascular disease.

• Exenatide Study

  Approved; the original GLP-1 agonist. Contraindicated below eGFR 30, which is unusual in the class and matters in the population most likely to need it.

• Insulin & analogues Study

  The oldest peptide drug there is, and the one this site explicitly does not publish community dosing for. Dosing errors here are lethal on a timescale of hours.

• Pramlintide Study

  Approved as an adjunct to mealtime insulin. Carries a boxed warning for severe insulin-induced hypoglycaemia and requires prandial insulin to be halved when started.

• Retatrutide Theorized

  Phase 2 reported roughly 2 points of HbA1c reduction. No phase 3 readout, no approved product, no validated titration — in a condition with two approved alternatives carrying outcome data.

• Cagrilintide Theorized

  No standalone diabetes programme. Its evidence in this condition exists only as half of CagriSema.

• CagriSema Study

  REDEFINE-2 studied the fixed combination in type 2 diabetes with obesity. The result belongs to the trialled ratio, co-escalated — not to two vials assembled at home.

• MOTS-c Theorized

  Mitochondrial-derived peptide that improves insulin sensitivity in rodents via AMPK. No human trial in diabetes.

• Humanin Theorized

  Associated with insulin sensitivity in observational and animal work. No human trial in diabetes.

• 5-Amino-1MQ Theorized

  NNMT inhibition improves metabolic parameters in obese mice. No human data of any kind.

• Insulin & analogues Study

  The treatment, and the reason peptide therapeutics exist as a field. Not a supplement, not optional, and not something to adjust on the basis of anything read online. Every other entry on this site is measured against what a peptide looks like when it genuinely replaces a missing signal.

• Pramlintide Study

  The second approved peptide here. Amylin is co-secreted with insulin and is therefore also deficient in type 1 diabetes — pramlintide replaces it, slowing gastric emptying and suppressing glucagon, approved as an adjunct to mealtime insulin. It carries a boxed warning for severe hypoglycaemia, and mealtime insulin must be reduced when it is started.

• Liraglutide Study

  Tested properly, and the answer was no. The ADJUNCT ONE trial randomised 1,398 people with type 1 diabetes to liraglutide or placebo alongside insulin for 52 weeks. HbA1c fell by around half a percentage point and weight fell by up to 4.9 kg — alongside increased symptomatic hypoglycaemia and increased hyperglycaemia with ketosis. The benefits were real and the safety signal is why it is not approved for this indication.

• Semaglutide Theorized

  Used off-label in type 1 diabetes, particularly where obesity coexists, and not approved for it. The ADJUNCT result above is the class evidence, and ketosis risk in someone with no endogenous insulin reserve is a different order of problem than it is in type 2. This is a specialist decision with sick-day rules attached, not a self-directed one.

• Tirzepatide Theorized

  Same position, same caution, less type 1 data.

• Thymosin Alpha-1 Theorized

  Immune enhancement in an autoimmune disease. The direction problem, and the field is moving decisively the other way — see below.

• BPC-157 Anecdotal

  Discussed for the vascular and neuropathic complications. No evidence, and complication prevention is achieved by glycaemic control, blood pressure and lipid management.

• SS-31 Theorized

  Mitochondrial framing applied to diabetic complications. Untested here.

Approved peptide drugs for this condition that are not in this library: Insulin, pramlintide and glucagon are approved peptides. Teplizumab is an antibody, and it delays the disease rather than treating it.

• Semaglutide Study

  Approved at 2.4 mg weekly (Wegovy). SELECT reported cardiovascular event reduction in people with obesity and established cardiovascular disease but without diabetes.

• Tirzepatide Study

  Approved (Zepbound). SURMOUNT produced the largest weight reductions of any approved agent to date.

• Liraglutide Study

  Approved at 3.0 mg daily (Saxenda) on the SCALE programme. Largely displaced by weekly agents on efficacy, not on failure.

• Retatrutide Study

  The largest weight effect demonstrated by any pharmacological agent: 28.3% at 80 weeks and 30.3% at 104 weeks in the TRIUMPH phase 3 programme, with 45.3% of the top-dose arm losing at least 30% of body weight. Not yet approved — a licence application is planned for early 2027 — and the programme did not include a cardiovascular outcome trial.

• Cagrilintide Theorized

  Amylin analogue, investigational, studied as a dose-sparing partner rather than alone.

• Retatrutide + Cagrilintide Anecdotal

  A community stack, not a trialled product. The ratio is vendor-dependent and the combination has never been studied as assembled.

• CagriSema Study

  The one amylin-plus-incretin combination with actual trial data. REDEFINE-1 landed below market expectation, which is itself informative.

• AOD-9604 Theorized

  A growth-hormone fragment marketed on a fat-loss rationale. The human trials that were run did not separate it from placebo on weight.

• Tesofensine Study

  A triple monoamine reuptake inhibitor with genuine phase 2 weight-loss data — and a blood-pressure and heart-rate signal that stalled its development.

• Tesamorelin Study

  Approved specifically for HIV-associated visceral fat, not general obesity. The distinction is the whole point.

• Peptide YY (PYY) Theorized

  A real satiety signal with a failed clinical programme — the intranasal formulation could not separate the effect from nausea.

• SLU-PP-332 Theorized

  An ERR agonist described as an "exercise mimetic" in mice. No human data by any route.

• Liraglutide Study

  The most randomised PCOS evidence of any agent in the class — small, short trials reporting weight, insulin sensitivity and menstrual regularity, often against or alongside metformin. It is also now available as a generic for both its indications, which matters in a condition that needs long-term management.

• Semaglutide Study

  Randomised off-label evidence in PCOS, plus the largest weight effect of the approved weekly agents — and oral semaglutide is now approved for weight management, which removes the injection from the equation.

• Tirzepatide Theorized

  Mechanistically the strongest candidate; PCOS-specific randomised data is thinnest in the class because it is newest. Note the labelled reduction in oral contraceptive effectiveness — backup or non-oral contraception is advised for four weeks after starting and after each dose increase, which matters enormously in a population being told their fertility may return.

• Orforglipron Theorized

  Same receptor, oral, no injection and no cold chain. No PCOS data, and the practical profile suits a chronic condition in a young population.

• MOTS-c Theorized

  AMPK activation and improved insulin sensitivity in animal models — the same pathway metformin works through, with none of metformin’s six decades of evidence.

• Humanin Theorized

  Mitochondrial dysfunction is documented in PCOS granulosa cells and is implicated in oocyte quality, which makes the anti-apoptotic rationale specific rather than generic. It remains cell-level.

• AOD-9604 Theorized

  Discussed on a weight-loss rationale its own human trials did not support, and rejected 0–12 by the PCAC.

• Retatrutide Theorized

  The mechanism transfers from the approved agents and the phase 3 weight data is now substantial. There is still no PCOS trial and no approval.

• Cagrilintide Theorized

  Route to benefit runs entirely through weight, which is a longer path than the incretin case.

• Kisspeptin-10 Theorized

  Genuinely interesting here rather than incidental: PCOS involves disordered GnRH pulse frequency favouring LH over FSH, and kisspeptin sits directly upstream of that pulse generator. Research-setting only, and stimulating an already dysregulated axis is not obviously the right direction.

• KLOW Anecdotal

  Discussed for the inflammatory and skin components rather than the endocrine core. No PCOS data.

• Thymosin Alpha-1 Theorized

  Immunomodulation is the only plausible route to affecting the autoimmune process itself. It has never been studied in Hashimoto's, and shifting immune balance in an active autoimmune condition can go either way.

• BPC-157 Theorized

  Discussed for the gut-autoimmunity axis. Note that coeliac disease and atrophic gastritis genuinely do impair levothyroxine absorption, and both are more common in Hashimoto's.

• Semaglutide Study

  Relevant for the interaction, not the treatment: delayed gastric emptying alters absorption of a narrow-therapeutic-index, fasting-dependent drug. A thyroid drift after starting an incretin is often an absorption change, not a thyroid change.

• Tirzepatide Study

  Same interaction, and the class boxed warning for thyroid C-cell tumours makes the pairing with thyroid disease worth understanding properly rather than dismissing.

• Cagrilintide Theorized

  Slows gastric emptying independently of any incretin — in a stack, two compounds are doing it at once.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH secretagogues alter deiodinase activity and peripheral T4-to-T3 conversion, which can move thyroid labs without any change in thyroid function.

• Epitalon Anecdotal

  Pineal-axis claims are extrapolated toward the thyroid axis in community writing. There is no human thyroid data.

• Thymosin Alpha-1 Theorized

  Immunomodulation is the only plausible route to the autoimmune process itself, which is exactly why it appears here — and the direction problem applies with full force. Every approved use of this compound depends on enhancing immune response. It has never been studied in Hashimoto’s.

• BPC-157 Theorized

  Discussed for the gut-autoimmunity axis. The defensible version is narrower and genuinely useful: coeliac disease and atrophic gastritis are both more common in Hashimoto’s and both impair levothyroxine absorption. Investigating that is worthwhile; this compound is not the way to do it.

• LL-37 Theorized

  Implicated in autoimmunity broadly. As in lupus and psoriasis, that places it on the wrong side of the mechanism.

• KPV Theorized

  Generic anti-inflammatory action. Thyroid autoimmunity is antibody- and T-cell-mediated, not a generic inflammatory state.

• Semaglutide Study

  Relevant for the interaction rather than the disease: delayed gastric emptying alters absorption of a narrow-therapeutic-index, fasting-dependent drug. A thyroid drift after starting an incretin is often an absorption change, not a thyroid change — and the fix is retesting and retitrating rather than assuming the disease progressed.

• Epitalon Anecdotal

  Pineal-axis claims extrapolated toward the thyroid axis in community writing. No human thyroid data.

Approved peptide drugs for this condition that are not in this library: Levothyroxine treats the consequence. No approved therapy anywhere targets the autoimmunity.

• Octreotide Study

  Approved. Suppresses GH and normalises IGF-1 in a substantial proportion of patients where surgery has not achieved remission. Available as a three-times-daily injection, a monthly depot, and an oral delayed-release capsule for maintenance.

• Sermorelin Theorized

  Listed for contrast. Sermorelin, CJC-1295, ipamorelin and the GH blends all aim to raise the hormone that acromegaly is defined by having too much of.

• CJC-1295 (no DAC) Theorized

  The DAC form produces continuous rather than pulsatile GHRH exposure, which is closer to the acromegaly pattern than to the physiological one. That is the whole argument for the no-DAC version.

• Triple GH Blend Anecdotal

  Three secretagogues at once, in an axis whose pathological state is defined by sustained elevation. No trial has studied any three-compound GH stack.

• Desmopressin Study

  Approved replacement therapy for the central form — vasopressin re-engineered to keep the water effect and lose the blood-pressure effect. It does nothing for the nephrogenic form, where the problem is the kidney rather than the hormone.

• Terlipressin Study

  The same hormone family built from the opposite half of its pharmacology — V1 vasoconstriction rather than V2 water retention. Not a diabetes insipidus treatment; listed because the contrast explains what desmopressin was designed to avoid.

• Oxytocin Theorized

  Differs from vasopressin at only two of nine positions and has meaningful antidiuretic cross-activity at higher doses, which is how prolonged oxytocin infusion causes water intoxication.

• Thymosin Alpha-1 Theorized

  No role. Included because “adrenal support” products frequently appear alongside immune-support marketing aimed at the same fatigue complaint.

• NAD⁺ Anecdotal

  Sold squarely into the “adrenal fatigue” market, which is not a diagnosis — see below. Fatigue is a real symptom deserving a real explanation, and this is not one.

• Epitalon Anecdotal

  Endocrine-axis claims by association with the pineal gland. No adrenal data.

• BPC-157 Anecdotal

  Appears in “HPA axis recovery” protocols. No human evidence.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Relevant for a genuine reason: GH replacement can unmask previously compensated adrenal insufficiency by increasing cortisol clearance, which is a documented interaction in hypopituitary patients. Anyone on both axes needs endocrine supervision, and this is one of the better arguments against self-directed GH-axis manipulation in someone with any pituitary history — see pituitary tumours.

• Insulin & analogues Study

  Two connections. Cortisol opposes insulin, so adrenal insufficiency lowers insulin requirements and raises hypoglycaemia risk. And the insulin tolerance test is a reference method for assessing the axis — performed only in specialist settings, for good reason.

• Semaglutide Theorized

  No direct role. Weight loss, reduced appetite and fatigue overlap with adrenal insufficiency symptoms, which is a reason to keep the differential open rather than attributing everything to the drug.

Approved peptide drugs for this condition that are not in this library: Hydrocortisone and fludrocortisone are steroids, not peptides. Synacthen — tetracosactide — is a synthetic ACTH fragment used diagnostically, and is the peptide in this story.

• Tesamorelin Study

  Randomised trials reported reduced visceral adipose tissue and reduced hepatic fat in HIV-associated lipodystrophy — the clearest visceral-fat result of any compound here.

• Semaglutide Study

  Trials in metabolic dysfunction-associated steatohepatitis have reported steatohepatitis resolution; the fibrosis endpoint has been harder to move.

• Tirzepatide Study

  Reported reductions in liver fat in trial sub-studies, alongside the largest weight effect in the class.

• Retatrutide Theorized

  The glucagon arm is directly relevant to hepatic fat, and phase 2a work reported near-normalisation of liver fat at higher doses. The TRIUMPH phase 3 programme measured weight and glycaemia rather than liver endpoints, so this specific claim still rests on phase 2.

• MOTS-c Theorized

  AMPK activation, improved fatty-acid oxidation and reduced hepatic steatosis in mice.

• 5-Amino-1MQ Theorized

  NNMT inhibition reduced fat mass in obese mice. Nothing in humans.

• NAD⁺ Theorized

  NAD+ decline is well documented with age; that repletion by injection changes hepatic or metabolic outcomes in humans is not.

• SLU-PP-332 Theorized

  ERR agonism increased fatty-acid oxidation and reduced adiposity in mice without exercise.

• SS-31 Theorized

  Mitochondrial cardiolipin stabilisation; relevant to the mitochondrial dysfunction component rather than the adiposity.

• Semaglutide Study

  Approved for this, and the trial is worth knowing properly. The FDA approved semaglutide 2.4 mg for MASH with moderate-to-advanced fibrosis (F2–F3) in August 2025, on the ESSENCE phase 3 trial: at 72 weeks, 62.9% achieved steatohepatitis resolution without worsening fibrosis against 34.3% on placebo, and 36.8% achieved at least one stage of fibrosis improvement against 22.4%. This is an accelerated approval on histology — the second part of ESSENCE runs to 240 weeks to test whether it prevents liver-related events, reading out around 2029.

• Tirzepatide Study

  Phase 2 (SYNERGY-NASH) reported high rates of MASH resolution. It is not approved for this indication and the phase 3 liver programme has not delivered a histological verdict yet, which is the difference between it and the entry above.

• Retatrutide Theorized

  The most interesting mechanism in the class for this specific organ. The glucagon receptor arm acts directly on hepatocytes to increase fatty-acid oxidation — which is a liver mechanism rather than a weight-loss mechanism — and phase 2a reported near-normalisation of liver fat at higher doses. The TRIUMPH phase 3 programme measured weight and glycaemia, not liver histology, so this still rests on phase 2.

• Tesamorelin Study

  The one non-incretin here with real liver data. In people with HIV and lipodystrophy, tesamorelin reduced visceral fat and reduced hepatic fat and progression of fibrosis in a randomised trial. That is a specific population with a specific problem, and it does not generalise to metabolic fatty liver in the general population.

• Cagrilintide Theorized

  Amylin analogue; liver effects would follow from weight loss rather than any hepatic mechanism of its own.

• MOTS-c Theorized

  AMPK activation, improved fatty-acid oxidation and reduced hepatic steatosis in mice.

• 5-Amino-1MQ Theorized

  NNMT inhibition reduced fat mass in obese mice. Nothing human.

• SLU-PP-332 Theorized

  ERR agonism increased fatty-acid oxidation in mice without exercise. Nothing human.

• NAD⁺ Theorized

  Preclinical interest in hepatic NAD+ metabolism; no human outcome data.

• SS-31 Theorized

  Mitochondrial dysfunction is part of the pathology. Untested here, and its trial record elsewhere is poor.

• BPC-157 Anecdotal

  Cited for hepatoprotection on the strength of rodent toxic-injury models. Not the same disease, not the same mechanism, and no human data.

• Glutathione Anecdotal

  Marketed for liver detoxification, which is not a description of anything MASLD does. Oral glutathione is largely broken down before absorption.

Approved peptide drugs for this condition that are not in this library: Resmetirom and semaglutide are approved for MASH with fibrosis. Semaglutide is the peptide.

• Octreotide Study

  The opposite drug. A somatostatin analogue prescribed to suppress growth hormone in acromegaly — worth reading alongside everything below it, because acromegaly is what chronically elevated GH actually looks like.

• Sermorelin Study

  GHRH(1–29); historically used as a diagnostic and therapeutic agent in paediatric GH deficiency. The shortest-acting secretagogue here.

• Tesamorelin Study

  A stabilised GHRH analogue with an approved indication — the only GH-axis compound in this library with one.

• CJC-1295 (no DAC) Theorized

  GHRH analogue. The no-DAC form preserves pulsatility; the DAC form does not, which is the whole argument between them.

• Ipamorelin Theorized

  Selective ghrelin receptor agonist; the selectivity claim is that it raises GH without meaningfully raising cortisol or prolactin.

• Ipamorelin + CJC-1295 (no DAC) Anecdotal

  The archetypal community stack: a GHRH plus a ghrelin agonist, on the argument that two pathways amplify a pulse more than one.

• Triple GH Blend Anecdotal

  A third secretagogue added to the above. No trial has studied any three-compound GH stack.

• IGF-1 LR3 Theorized

  Bypasses the GH axis entirely and acts as the downstream effector — which also bypasses every feedback mechanism that limits it.

• PEG-MGF Theorized

  A splice variant of IGF-1 pegylated for half-life. Rodent muscle data; no human trial.

• Teriparatide Study

  The canonical pulsatility result, and it is worth understanding properly. Parathyroid hormone is what dissolves bone — chronic hyperparathyroidism is a classic cause of bone loss. Yet teriparatide, a 34-residue fragment of that same hormone, is an approved anabolic osteoporosis drug with randomised fracture-reduction data. The difference is not the molecule. It is the time profile: continuous elevation favours resorption, a once-daily spike favours formation. That is why it is a daily injection and why an infusion or a depot of the same peptide would do the opposite of what is wanted. The osteosarcoma boxed warning and the two-year lifetime cap were both removed in November 2020 when human cohort data failed to reproduce the rat signal.

• IGF-1 LR3 Theorized

  IGF-1 is genuinely involved in bone formation, and that is where the argument stops. An unregulated IGF-1 analogue designed to evade its binding proteins is not an osteoporosis intervention, and the growth-signalling caution applies with force in the older population that actually has osteoporosis.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH raises IGF-1 and IGF-1 affects bone turnover, which is real. The step from moving turnover markers to reducing fractures is the one that has never been taken here — and it is the only step that counts. Bone density and bone strength are not the same thing, which is the same “mass is not function” problem this site keeps running into.

• GHK-Cu Theorized

  Copper is a cofactor for lysyl oxidase, which cross-links collagen — including bone collagen. In vitro reasoning, and topical delivery does not reach bone.

• Sermorelin Theorized

  Same GH-axis logic as the blend above, weaker output, same missing fracture data.

• Epitalon Anecdotal

  Longevity framing extended to bone by association. No bone data of any kind.

Approved peptide drugs for this condition that are not in this library: Teriparatide, abaloparatide and calcitonin are the peptides. Romosozumab and denosumab are antibodies; bisphosphonates are small molecules.

• Tesamorelin Study

  Approved for this indication on randomised trials showing reduced visceral adipose tissue. Every other use of this compound is off-label extrapolation from this evidence base.

• BPC-157 Theorized

  The most-cited compound in this library for tendon. The underlying work is rodent tendon and ligament transection studies reporting accelerated healing and increased tendon fibroblast outgrowth. No human trial in tendinopathy exists.

• TB-500 Theorized

  Thymosin beta-4 fragment; actin sequestration, cell migration and angiogenesis in animal models of soft-tissue injury.

• Wolverine Stack Anecdotal

  The BPC-157 + TB-500 combination is the single most-used injury stack in the grey market and has never been studied as a combination in anything.

• GLOW Anecdotal

  Adds GHK-Cu on a collagen-remodelling rationale.

• KLOW Anecdotal

  Adds KPV for an anti-inflammatory component on top of the above.

• GHK-Cu Theorized

  Copper peptide with genuine in vitro data on collagen synthesis and matrix remodelling.

• IGF-1 LR3 Theorized

  Local anabolic signalling. Also the compound in this section with the most serious theoretical downside — see the oncology caution.

• PEG-MGF Theorized

  Mechano-growth factor, upregulated by mechanical loading in muscle. Rodent data.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH and IGF-1 have a documented role in connective-tissue turnover; the human evidence for accelerated tendon recovery does not exist.

• BPC-157 Theorized

  Rodent work on cartilage and joint injury. Widely used intra-articularly in the grey market, which is a sterility problem as much as a pharmacology one — a septic joint is a surgical emergency.

• TB-500 Theorized

  Same animal-model basis, extended to joint tissue.

• GHK-Cu Theorized

  Matrix remodelling rationale; in vitro.

• KPV Theorized

  Alpha-MSH fragment with anti-inflammatory activity in animal models.

• KLOW Anecdotal

  Combines the above on the argument that repair and anti-inflammation should be simultaneous.

• ARA-290 Study

  Reached human trials for neuropathic pain rather than joint disease; the tissue-protective erythropoietin-receptor rationale is what draws interest here.

• IGF-1 LR3 Theorized

  Direct anabolic signalling with the systemic exposure that makes it interesting and dangerous in the same breath.

• PEG-MGF Theorized

  Rodent satellite-cell activation data.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH secretagogues raise IGF-1; GH itself increases lean mass in trials while its effect on strength and function is much less convincing.

• Ipamorelin Theorized

  Ghrelin receptor agonism also drives appetite, which is the more plausible route to benefit in a cachectic patient.

• MOTS-c Theorized

  Exercise-mimetic framing from rodent work; improved exercise capacity in aged mice.

• Humanin Theorized

  Mitochondrial peptide associated with healthspan markers.

• SS-31 Study

  Reached human trials in primary mitochondrial myopathy and in Barth syndrome — the mitochondrial-function endpoint, not general muscle mass.

• SLU-PP-332 Theorized

  Increased running capacity in mice without training.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  The reason this entry exists. Growth hormone causes sodium and water retention, and fluid within the confined carpal tunnel compresses the median nerve. Carpal tunnel symptoms, joint swelling and stiffness are the classic dose-limiting effects of GH — documented in GH replacement therapy and characteristic of acromegaly. In someone using a secretagogue, new hand numbness is far more likely to be this than a coincidence, and the response is to reduce or stop rather than to push through. Symptoms typically resolve when the dose comes down.

• Sermorelin Theorized

  Same axis, generally weaker output, same effect at sufficient dose.

• CJC-1295 (no DAC) Theorized

  Same, and the DAC form’s sustained exposure is the profile more likely to produce it.

• Tesamorelin Study

  Approved, and its trial data lists arthralgia, peripheral oedema and paraesthesia among expected effects — which is the same fluid-retention picture in a properly documented setting.

• IGF-1 LR3 Theorized

  Fluid retention and soft tissue effects are described with IGF-1 administration as well.

• BPC-157 Anecdotal

  Widely injected locally for wrist and hand symptoms. If the cause is systemic fluid retention from another compound, treating the wrist is treating the wrong thing — and persistent numbness needs assessing, because prolonged compression causes permanent nerve damage and muscle wasting.

• TB-500 Anecdotal

  Same local-injection pattern, same objection.

Approved peptide drugs for this condition that are not in this library: No drug treatment is approved. Splinting and surgery are the effective interventions, and the peptides here cause the problem rather than treating it.

• Semax + Selank Theorized

  The only entry here whose mechanism is in the right compartment. Both act centrally, on BDNF and on anxiolytic signalling, and the approved fibromyalgia drugs are centrally acting too. Human data is largely Russian-language and methodologically limited.

• Semax Theorized

  Central BDNF modulation; studied in Russia in stroke and cognition, never in fibromyalgia. Relevant to the cognitive complaint patients describe as “fibro fog”, which is real and disabling.

• Selank Theorized

  Anxiolytic. Anxiety and non-restorative sleep are both core to the fibromyalgia burden, and treating them is a legitimate target even without touching pain processing directly.

• DSIP Theorized

  Non-restorative sleep is close to universal in fibromyalgia, which makes sleep architecture a genuine target — and the newest approved drug for this condition works precisely there. DSIP is the wrong tool for the right target: rejected by the PCAC, no identified receptor, and human evidence from the 1970s and 80s that was small and inconsistent.

• BPC-157 Theorized

  Widely discussed, but its evidence base is peripheral tissue repair — the wrong compartment for a central sensitisation disorder. Where it may help is a genuinely comorbid injury, which is a narrower and more defensible claim.

• TB-500 Theorized

  Same objection, more starkly: a tissue-repair agent in a condition defined by the absence of a structural lesion has nothing to act on.

• KLOW Anecdotal

  Community reporting on pain and sleep. No mechanism that reaches central pain processing.

• Wolverine Stack Anecdotal

  Same.

• ARA-290 Theorized

  More interesting than the repair peptides. Small fibre neuropathy is documented in a subset of fibromyalgia patients, and ARA-290 has randomised human trial evidence in small fibre neuropathy of other causes using an objective structural endpoint. That is a specific hypothesis about a subgroup, not a fibromyalgia treatment, and it has not been tested here.

• Semaglutide Theorized

  Weight loss reduces mechanical load and systemic inflammation. No fibromyalgia-specific evidence.

• Thymosin Alpha-1 Theorized

  Immune framing, on the contested premise that fibromyalgia has an immune driver.

Approved peptide drugs for this condition that are not in this library: Pregabalin, duloxetine, milnacipran and TNX-102 SL are the four approved options; none is a peptide.

• BPC-157 Anecdotal

  Probably the single commonest reason people in this space try this compound, and the mechanism does not fit the condition. Its evidence base is tendon and soft tissue repair in rodents. Most low back pain has no identifiable structural lesion to repair — that is not a dismissal, the pain is real, but it means there is frequently no damaged tissue for a repair agent to act on. Where a specific structural problem does exist, it is usually disc or nerve related, and nothing here has been shown to reach or affect either. Note also that imaging findings correlate poorly with pain: disc degeneration, bulges and annular tears are common in people with no pain at all.

• TB-500 Anecdotal

  Same objection, same absent structural target.

• KLOW Anecdotal

  Marketed for back and joint pain. No component reaches the mechanisms that actually drive persistent back pain.

• Wolverine Stack Anecdotal

  Same.

• KPV Theorized

  Anti-inflammatory in rodent models. Persistent low back pain is not principally an inflammatory disease, which is why anti-inflammatories help acutely and stop helping.

• GHK-Cu Theorized

  Collagen remodelling in vitro. Not delivered to spinal structures by any available route.

• Semaglutide Theorized

  Indirect and genuinely supported: excess weight worsens back pain, and weight loss improves it. That is a real mechanism rather than a peptide one.

• Semax Anecdotal

  Occasionally used for the central and mood components of chronic pain. No evidence in back pain.

• SS-31 Theorized

  Disc degeneration involves mitochondrial dysfunction in laboratory work. The intervertebral disc is avascular — the least accessible tissue in the body for a systemically administered compound — which is a delivery problem before it is an efficacy question.

Approved peptide drugs for this condition that are not in this library: No peptide is approved for back pain anywhere. The intervention with the best evidence is exercise, and it is free.

• BPC-157 Anecdotal

  The misattribution risk, and it is specific. Gout presents as a rapidly painful, hot, swollen joint — classically the base of the big toe, but also the knee, ankle or midfoot. In someone who trains, that reads as an injury, and injury is what compounds like this get used for. Gout is diagnosed and cured pharmacologically; an untreated recurrent gout attack destroys the joint over years. Treating it as a training niggle is how people end up with permanent damage from an entirely preventable disease.

• KPV Theorized

  Anti-inflammatory in rodent models. Gout is an intensely inflammatory condition driven by the NLRP3 inflammasome, so the direction is right and the specificity is absent — colchicine, NSAIDs and steroids all do this better and are proven.

• KLOW Anecdotal

  Marketed for joint pain without distinguishing which joint disease. Gout is not osteoarthritis and is not rheumatoid arthritis, and all three are treated completely differently.

• TB-500 Anecdotal

  Repair framing against a crystal-driven inflammatory process.

• Semaglutide Theorized

  Genuinely relevant. Obesity raises urate and gout risk substantially, and weight loss lowers urate. Observational data suggests GLP-1 use is associated with lower gout incidence. Note the caveat that applies to rapid weight loss generally — sharp changes in urate in either direction can precipitate an attack, which is also why starting urate-lowering therapy needs cover.

• NAD⁺ Anecdotal

  Marketed for joint health. Note that high-dose niacin raises urate and can precipitate gout, which is worth distinguishing from NAD+ precursors and worth knowing before combining products.

Approved peptide drugs for this condition that are not in this library: Pegloticase — a pegylated uricase enzyme — is used in severe refractory tophaceous gout. It is an enzyme rather than a peptide drug, and everything else here is a small molecule.

• GHK-Cu Study

  Human topical data in skin — the strongest evidence of any compound in this library for the use it is actually marketed for. Trials support topical application on wrinkles, skin density and wound healing.

• BPC-157 Theorized

  Rodent wound and burn models.

• TB-500 Theorized

  Cell migration and angiogenesis in animal wound models.

• LL-37 Theorized

  Endogenous antimicrobial peptide with a documented role in wound re-epithelialisation — and a pro-inflammatory profile that makes it a poor candidate for indiscriminate use.

• GLOW Anecdotal

  The skin-and-repair blend; GHK-Cu is doing most of the work in the argument.

• KLOW Anecdotal

  Adds KPV.

• Melanotan-2 Anecdotal

  Not a healing compound. Included here because pigmentation change is what people notice, and because it drives naevus darkening — a real dermatological concern.

• Teduglutide Theorized

  Approved for short bowel syndrome, not for IBD. Listed here because it is the proof that a peptide can grow intestinal mucosa — and because that trophic mechanism cuts both ways in an inflamed, dysplasia-prone colon.

• BPC-157 Theorized

  Rodent colitis models report reduced inflammation and mucosal healing. It was derived from a gastric juice protein, so the tissue is at least the right one. No human trial in IBD.

• KPV Theorized

  Alpha-MSH tripeptide with anti-inflammatory activity in rodent colitis, including via oral and targeted delivery.

• LL-37 Theorized

  Cathelicidin has a documented role in mucosal defence; it is also elevated in active inflammation, which complicates the direction of the argument.

• KLOW Anecdotal

  BPC-157 plus KPV is the most-discussed grey-market IBD combination. Neither component has human data.

• Thymosin Alpha-1 Theorized

  Immunomodulation in a condition treated with immunosuppression — pushing immune tone in an unspecified direction is not obviously the goal.

• Glutathione Theorized

  Oxidative stress is elevated in active IBD. Repletion changing the disease course is not established.

Approved peptide drugs for this condition that are not in this library: None for IBD itself — the biologic classes used here are monoclonal antibodies and small molecules rather than peptides. Teduglutide is approved for short bowel syndrome; see that section.

• Teduglutide Study

  Approved. A GLP-2 analogue — the other hormone cut from the same proglucagon precursor as GLP-1, doing something entirely different. It increases villus height and crypt depth, and randomised trials reported reduced weekly parenteral support volume, with a minority achieving complete independence from it.

• BPC-157 Anecdotal

  Heavily discussed for gut repair on the strength of rodent models. Teduglutide is what an approved intestinal trophic peptide actually looks like, and the comparison is instructive: it requires colonoscopy before starting and surveillance thereafter.

• Semaglutide Theorized

  Listed for contrast. GLP-1 slows transit and suppresses appetite — the opposite of what is wanted here. Same precursor gene, opposite clinical use.

Approved peptide drugs for this condition that are not in this library: Somatropin and glutamine have also held indications in this condition in some jurisdictions.

• BPC-157 Theorized

  This is the one condition in the entire library where the compound under discussion was actually tested in it. Under the code PL 14736, BPC-157 completed a randomised placebo-controlled phase 2 trial of enemas in mild-to-moderate ulcerative colitis, presented in abstract form in 2005, after a published phase 1 in healthy volunteers. The full results were never published and no product followed — a pattern that more often reflects a negative result than a positive one. Note the route the developers chose: rectal, delivered to the inflamed mucosa. Not subcutaneous.

• KPV Theorized

  Rodent colitis models report reduced inflammation via NF-κB and MAPK, and the interesting delivery work is oral and colon-targeted — again, local to the mucosa. Frequently paired with BPC-157 in grey-market protocols, by injection, which is neither compound’s studied route.

• LL-37 Theorized

  Cathelicidin has a genuine role in colonic mucosal defence, and reduced expression has been reported in ulcerative colitis — which, unusually for this compound, points the same way as supplementation for once. It remains elevated in other inflamed tissues and is a T-cell autoantigen in psoriasis; the direction is condition-specific rather than favourable in general.

• KLOW Anecdotal

  BPC-157 plus KPV is the most-used grey-market colitis combination. Neither component has published controlled human evidence in ulcerative colitis, and the one trial that exists was of a single component, by a different route, with unpublished results.

• Glutathione Theorized

  Mucosal oxidative stress is elevated in active disease. Repletion altering the course is not established, and the antioxidant caution on that page matters if thiopurines are in use.

• Teduglutide Theorized

  Not indicated, and mechanistically questionable here — a trophic agent increasing crypt proliferation in a colon already under dysplasia surveillance is the wrong direction.

Approved peptide drugs for this condition that are not in this library: The IL-23 inhibitors, anti-TNF and anti-integrin biologics, and the oral S1P modulators and JAK inhibitors. None is a peptide.

• BPC-157 Theorized

  Widely sold on tight-junction and barrier-integrity claims, and heavily discussed in coeliac communities. Read the established section below before this one — the tight-junction mechanism has been tested directly in this condition, by a purpose-built drug, and it did not work.

• KPV Theorized

  Mucosal anti-inflammatory action. Coeliac is antigen-driven rather than generically inflammatory, so suppressing inflammation without removing the trigger addresses the consequence and not the cause.

• LL-37 Theorized

  Altered antimicrobial peptide expression has been described in coeliac mucosa. No therapeutic evidence, and the autoimmune cautions on that page apply.

• Thymosin Alpha-1 Theorized

  Immune modulation in an immune-mediated disease driven by a specific antigen, using a compound whose approved uses depend on enhancing immune response. The direction problem is at its clearest here.

• Teduglutide Theorized

  Mucosal growth in a condition defined by villous atrophy sounds like an obvious match, and it is not indicated. Refractory coeliac disease carries a risk of enteropathy-associated T-cell lymphoma, which makes a trophic agent with a labelled neoplastic-growth warning a poor fit specifically here.

• KLOW Anecdotal

  The general grey-market gut protocol, applied to a condition with a definitive treatment that costs nothing pharmacologically.

Approved peptide drugs for this condition that are not in this library: None. There is no approved pharmacological treatment for coeliac disease anywhere, which is precisely what makes the two failed peptide programmes worth knowing about.

• Linaclotide Study

  Approved for IBS with constipation, and the only compound in this library with randomised human evidence in IBS at all. A 14-residue peptide taken as a capsule, acting on the luminal surface. It improves stool frequency and abdominal pain on a composite endpoint — the pain component runs through a separate mechanism, cyclic GMP acting on submucosal afferent nerves, which is why it outperforms an ordinary laxative.

• BPC-157 Theorized

  The most-used compound for IBS in the grey market, and its human history is more interesting than usually reported — see the IBD and Crohn entries. For IBS specifically there is no controlled evidence, and this is the category with the largest placebo response in the library because every endpoint is subjective and fluctuating.

• KPV Theorized

  Mucosal anti-inflammatory action, with the useful animal work using oral and colon-targeted delivery rather than injection. IBS is not primarily an inflammatory disease, which weakens the rationale relative to IBD.

• KLOW Anecdotal

  The common grey-market gut protocol. Four components, no controlled evidence in IBS, and no way to attribute anything.

• Semaglutide Theorized

  Runs the wrong way for IBS-C. GLP-1 agonism delays gastric emptying and slows transit, which worsens constipation — and constipation is among the most commonly reported effects of this class. Relevant as an interaction rather than a treatment.

• Glutathione Anecdotal

  Marketed for gut health. Its injectable evidence concerns hepatic and dermatological endpoints, not intestinal ones.

Approved peptide drugs for this condition that are not in this library: Plecanatide and tenapanor for IBS-C; rifaximin and eluxadoline for IBS-D — none of them peptides except the guanylate cyclase-C agonists.

• BPC-157 Theorized

  The compound with the most relevant history here, and it is not purely preclinical. It was developed by a Croatian pharmaceutical company under the codes PL-10, PLD-116 and PL 14736, completed a published phase 1 study by rectal administration in healthy volunteers, and completed a randomised placebo-controlled phase 2 trial of enemas in mild-to-moderate ulcerative colitis, presented in abstract form in 2005. The full results were never published and no product followed. That is not proof the trial failed — but unpublished results plus abandoned development is a pattern that more often reflects a negative result than a positive one. Separately, rodent work from the same programme reports healing of colocutaneous fistulas and intestinal anastomoses.

• Teduglutide Study

  Not a Crohn treatment — the treatment for what Crohn surgery leaves behind. Approved for short bowel syndrome with parenteral dependence, and extensive resection for Crohn is one of the commonest routes into that condition. Its trophic mechanism is also the reason it is not used in active Crohn: increased crypt proliferation in an inflamed, dysplasia-prone bowel is not obviously desirable.

• KPV Theorized

  Rodent colitis models report reduced inflammation through NF-κB and MAPK signalling, and the more interesting work used oral and colon-targeted delivery designed to act at the mucosa. Subcutaneous injection for a gut condition delivers it everywhere except the tissue the evidence is about.

• LL-37 Theorized

  Cathelicidin has a real role in mucosal defence, and NOD2 — the strongest genetic association in Crohn — sits in the same innate immune pathway. It is also elevated in active inflammation, which complicates the direction entirely.

• KLOW Anecdotal

  BPC-157 plus KPV is the most-discussed grey-market IBD combination. Neither component has controlled human evidence in Crohn, and the combination has none in anything.

• Thymosin Alpha-1 Theorized

  Immune modulation in a disease treated by immunosuppression, in a compound whose approved uses all depend on enhancing immune response. Anyone on a biologic should treat this as an interaction question for their gastroenterologist.

• Glutathione Theorized

  Oxidative stress is elevated in active disease. Repletion changing the course is not established, and the antioxidant/chemotherapy caution on that page is worth reading if thiopurines or methotrexate are in the picture.

Approved peptide drugs for this condition that are not in this library: The IBD armoury is monoclonal antibodies and small molecules — anti-TNF, anti-integrin, anti-IL-12/23, anti-IL-23 and JAK inhibitors. None is a peptide, and together they are why this disease is now controllable.

• Linaclotide Study

  Approved for IBS with constipation. A 14-residue peptide taken as a capsule that is not absorbed — it activates guanylate cyclase-C on the luminal surface, increasing secretion and reducing visceral pain through a separate effect on afferent nerves.

• BPC-157 Theorized

  Tight-junction and barrier-integrity effects in rodent models.

• KPV Theorized

  Anti-inflammatory at the mucosal level in animal work.

• LL-37 Theorized

  Antimicrobial activity relevant to the microbiome argument.

• KLOW Anecdotal

  The most-used grey-market gut protocol. Entirely community-reported.

• Glutathione Theorized

  Marketed heavily for gut health; the intravenous and injectable evidence is about hepatic and dermatological endpoints, not intestinal ones.

Approved peptide drugs for this condition that are not in this library: Plecanatide (Trulance) — the same receptor target built on uroguanylin rather than the heat-stable enterotoxin scaffold, with the same paediatric contraindication.

• Semaglutide Study

  A predictable consequence rather than a side effect. GLP-1 agonists delay gastric emptying — that is part of how they work — and a stomach that empties slowly refluxes more. Reflux, nausea and vomiting are common early and usually settle with slower titration. Two things not to accept without assessment: new or worsening difficulty swallowing, and food regurgitated hours after eating. Also relevant for anaesthesia — tell the anaesthetist, because retained stomach contents despite fasting is a recognised aspiration risk and guidance on withholding doses before procedures now exists.

• Tirzepatide Study

  Same mechanism, same advice.

• Cagrilintide Theorized

  Amylin analogues slow gastric emptying independently of the incretin effect. In a combination, two components are doing it at once.

• BPC-157 Anecdotal

  Heavily marketed for reflux, gastritis and “gut healing”. The objection is the one set out under gastric and oesophageal cancer: reflux symptoms that respond to something and then return are the classic history of a cancer diagnosed late. Alarm features need endoscopy, not treatment.

• Linaclotide Study

  Approved for constipation-predominant IBS, not for reflux. Included because upper and lower GI symptoms get conflated in self-treatment.

• KPV Theorized

  Anti-inflammatory in models. Reflux is a mechanical and acid problem before it is an inflammatory one.

Approved peptide drugs for this condition that are not in this library: PPIs, H2 blockers and alginates are the treatments; none is a peptide. The peptides on this page cause reflux rather than treating it.

• Semaglutide Theorized

  Two roles that meet here. It treats the metabolic half of the problem — see MASH — and there is now randomised evidence that it reduces drinking, covered under alcohol use disorder. Neither makes it a treatment for established liver disease, and dosing in cirrhosis is a specialist question.

• Tirzepatide Theorized

  Same metabolic rationale, less alcohol-specific data.

• Terlipressin Study

  Approved for hepatorenal syndrome — a complication of advanced liver disease, most often decompensated cirrhosis. A hospital drug, with a boxed warning for respiratory failure.

• Octreotide Study

  Used for acute variceal bleeding by reducing splanchnic blood flow. Again a complication of the cirrhosis, not a treatment for the liver.

• Glutathione Anecdotal

  The single most heavily marketed compound to this population, and the argument is more seductive than most. Hepatic glutathione depletion in alcohol-related liver injury is real biochemistry — and N-acetylcysteine, a glutathione precursor, is genuinely the antidote in paracetamol poisoning, which gives the whole idea a borrowed credibility. None of that establishes intravenous glutathione as a treatment for alcohol-related liver disease, and no trial supports the infusion-clinic version.

• NAD⁺ Anecdotal

  Same channel, same claim structure. Note that alcohol metabolism itself consumes NAD+, which is where the mechanistic story comes from and where it stops.

• BPC-157 Anecdotal

  Promoted for liver support. Rodent models only.

• Thymosin Alpha-1 Theorized

  Immune framing, and relevant only insofar as advanced liver disease causes immune dysfunction and infection risk. Not studied here.

Approved peptide drugs for this condition that are not in this library: No approved drug treats the liver disease itself. Terlipressin and octreotide treat its complications, and both are peptides.

• BPC-157 Theorized

  Rodent studies report protection against NSAID-induced gastric lesions and accelerated ulcer healing. This is the closest the compound comes to a coherent evidence base, and it remains preclinical.

• GHK-Cu Theorized

  Tissue-remodelling rationale extended to mucosa.

• Semax Theorized

  ACTH(4–10) analogue with BDNF-modulating activity; used clinically in Russia in cognitive and cerebrovascular indications. Trials are small and largely unblinded.

• Adamax Theorized

  A Semax-family analogue with an even thinner evidence base — essentially none outside supplier claims.

• Selank Theorized

  Anxiolytic; cognition claims are secondary to the anxiolytic effect.

• Semax + Selank Anecdotal

  A community pairing rather than a formulated product.

• Humanin Theorized

  Neuroprotective against amyloid toxicity in cell models — one of the more genuinely interesting preclinical stories in this library, with nothing human behind it.

• SS-31 Study

  Human trials exist, in mitochondrial disease rather than dementia. Mitochondrial dysfunction is a plausible neurodegeneration mechanism.

• NAD⁺ Theorized

  NAD+ decline with age is documented; that injectable repletion improves cognition is not.

• Epitalon Anecdotal

  Telomerase and pineal claims from a small Russian literature. Extended to cognition by association.

• MOTS-c Theorized

  Metabolic and mitochondrial framing.

• IGF-1 LR3 Theorized

  IGF-1 signalling is implicated in neuronal survival. It is also implicated in cancer, which is the trade-off nobody discussing this raises.

• Semaglutide Study

  EVOKE and EVOKE+ tested this directly in 3,808 people with early Alzheimer disease and found no benefit over placebo at 104 weeks. Together with the negative Exenatide-PD3 trial in Parkinson disease, the incretin neuroprotection hypothesis has now failed at phase 3 twice, in two diseases, despite supportive epidemiology and mechanism in both.

• Semaglutide Study

  The definitive negative result, and it is recent. EVOKE and EVOKE+ tested semaglutide directly in 3,808 people with early Alzheimer’s disease over 104 weeks and found no benefit over placebo. The epidemiology was supportive, the mechanism was plausible, the trial was large and well run, and the answer was no. Anyone still selling the incretin neuroprotection story is selling something that has been tested.

• Insulin & analogues Theorized

  The route is the entire argument here. Brain insulin resistance is a real feature of Alzheimer’s, and injected insulin cannot reach the brain in useful quantity — which is why the trials use the intranasal route to bypass the blood-brain barrier. Results across the SNIFF programme have been mixed and confounded by delivery-device problems, with small positive signals on cognitive and biomarker endpoints and nothing definitive. It is a serious research question. It is also not something anyone should attempt at home: subcutaneous insulin in a person without diabetes causes hypoglycaemia, not cognition.

• Humanin Theorized

  A mitochondrial-derived peptide that is protective against amyloid toxicity in cell models — genuinely one of the more interesting preclinical stories in this library, and it was discovered in an Alzheimer’s brain. There is nothing human behind it.

• Semax Theorized

  ACTH(4–10) analogue with BDNF-modulating activity, used clinically in Russia in cognitive indications. Trials are small and largely unblinded, and none is in Alzheimer’s specifically.

• SS-31 Study

  Mitochondrial dysfunction is a genuine feature of the disease. Elamipretide has human trials — in mitochondrial myopathy and heart failure, not dementia — and missed its primary endpoints in three of them.

• IGF-1 LR3 Theorized

  IGF-1 signalling is implicated in neuronal survival, and also in cancer. The trade-off is never raised by anyone recommending it, and the epidemiology on IGF-1 and dementia risk points in both directions depending on the study.

• NAD⁺ Theorized

  NAD+ decline with age is documented; that injectable repletion improves cognition is not. Marketed heavily to this population and to their families.

• Epitalon Anecdotal

  Telomerase and pineal claims from a small Russian literature, extended to dementia by association.

• MOTS-c Theorized

  Same mitochondrial-derived peptide family as humanin, same absence of human data.

Approved peptide drugs for this condition that are not in this library: Lecanemab and donanemab are monoclonal antibodies against a peptide, not peptide drugs. Cholinesterase inhibitors and memantine are small molecules.

• Desmopressin Study

  The clearest documented hazard here, and it is on its own page. Desmopressin causes water retention, water retention causes hyponatraemia, and hyponatraemia lowers the seizure threshold and can cause seizures outright. This is the mechanism behind its boxed warning, not a theoretical concern. Anyone with epilepsy is the last person who should be experimenting with it.

• Insulin & analogues Study

  Same category of hazard by a different route: hypoglycaemia causes seizures. Insulin in someone without diabetes, or mistimed insulin in someone with it, is a direct seizure risk and one of the reversible causes checked first when someone presents fitting.

• Tesofensine Theorized

  A monoamine reuptake inhibitor. Stimulant and pro-monoaminergic agents are a recognised class concern for seizure threshold, and this one has no epilepsy safety data at all.

• Leuprolide Theorized

  The one entry with a real historical rationale. Catamenial epilepsy — seizures clustering with the menstrual cycle — is a genuine phenomenon, and GnRH analogues were investigated for it decades ago. The evidence never became convincing, the side-effect burden of induced hypo-oestrogenism is substantial, and this is a specialist decision.

• Semax Anecdotal

  Russian-literature neuroprotection claims, occasionally extended to seizure disorders. No controlled evidence, and it is an ACTH fragment — which is interesting given what full-length ACTH does in infantile spasms, and not evidence of anything.

• BPC-157 Anecdotal

  Community claims of neurological benefit. No seizure data in either direction, which means it is untested rather than safe.

• NAD⁺ Anecdotal

  Marketed by infusion clinics for neurological complaints generally. No epilepsy evidence.

Approved peptide drugs for this condition that are not in this library: ACTH for infantile spasms is the peptide. Everything else in routine use is a small molecule, a device, a diet or surgery.

• Thymosin Alpha-1 Theorized

  The direction problem, and MS is a good place to state it plainly: every approved use of this compound depends on enhancing immune response, and MS is treated by suppressing or redirecting it. Several MS disease-modifying therapies work by depleting or sequestering lymphocytes. Anyone on one should treat this as an interaction question for their neurologist.

• SS-31 Theorized

  Mitochondrial dysfunction contributes to axonal degeneration in progressive MS, which is a real mechanistic hypothesis. Its own trial record — three randomised failures in populations with demonstrable mitochondrial pathology — is the reason to hold it lightly.

• BPC-157 Anecdotal

  Discussed for neurological repair on the strength of rodent nerve injury models. Peripheral nerve is not central myelin, and there is no MS evidence.

• Semax Anecdotal

  Used for fatigue and cognitive symptoms, which are genuinely among the most disabling features of MS. No evidence in the condition.

• ARA-290 Theorized

  Tissue-protective erythropoietin-derived signalling, with the neuroprotection rationale that made erythropoietin itself interesting before its trials disappointed.

• LL-37 Theorized

  Implicated in autoimmune mechanisms generally. As in psoriasis and lupus, that makes it part of the problem rather than a candidate solution.

• NAD⁺ Anecdotal

  Marketed to this population for fatigue by infusion clinics, with no controlled evidence in MS.

Approved peptide drugs for this condition that are not in this library: Glatiramer acetate is the peptide. The rest — anti-CD20 antibodies, natalizumab, S1P modulators, cladribine, interferon beta — are not.

• Exenatide Study

  The negative phase 3. Exenatide-PD3 randomised 194 people with Parkinson’s over 96 weeks, double-blind and placebo-controlled, and found no benefit and no slowing of progression — published in The Lancet in February 2025. The authors noted the result was discordant with the earlier laboratory, epidemiological and phase 2 findings.

• Liraglutide Theorized

  Class member without a Parkinson’s trial of its own. Included because the class question is now the interesting one rather than any individual agent.

• Semaglutide Study

  Relevant by analogy rather than directly. Its own neurodegeneration trials — EVOKE and EVOKE+ in Alzheimer’s disease, 3,808 participants — were also negative, which makes two large phase 3 failures of the incretin neuroprotection hypothesis in two different diseases.

• SS-31 Theorized

  Mitochondrial dysfunction is a long-standing hypothesis in Parkinson’s — the MPTP story that first linked complex I inhibition to parkinsonism is one of the cleaner mechanistic narratives in neurology. Elamipretide has not been tested here, and has missed its primary endpoints in three other trials.

• Glutathione Study

  Nigral glutathione depletion is among the earliest identified biochemical changes in Parkinson’s, which made it an obvious target. Intravenous and intranasal glutathione were studied and did not establish clinical benefit — a clean example of a documented tissue deficiency not being correctable by supplying the depleted molecule systemically.

• Semax Theorized

  Neurotrophic framing from the Russian literature. No Parkinson’s trial.

• NAD⁺ Theorized

  NAD+ precursor trials in Parkinson’s have been run and have not delivered a clear answer. The SARM1 axonal degeneration pathway is genuinely serious science, and it is being targeted by SARM1 inhibitors rather than by flooding the system with substrate.

• Humanin Theorized

  Mitochondrial-derived peptide with neuroprotection in cell models. Nothing human.

Approved peptide drugs for this condition that are not in this library: Levodopa and the dopaminergic classes. None is a peptide, and no disease-modifying therapy exists.

• Kisspeptin-10 Theorized

  Not a migraine compound. Included because migraine is strongly sex-hormone-linked, oestrogen withdrawal is a well-documented trigger, and the hypothalamic circuitry involved overlaps with the KNDy biology described in the menopause entry.

• Semax Anecdotal

  Used for headache and cognitive symptoms in the Russian tradition. No migraine evidence.

• BPC-157 Anecdotal

  Appears in headache discussion. No plausible mechanism and no evidence.

• Semaglutide Theorized

  Indirect. Obesity is a risk factor for migraine chronification, and weight loss is associated with improvement in chronic migraine. A metabolic route rather than a neurological one. GLP-1 agonists have also been explored in idiopathic intracranial hypertension, which is a different headache disorder frequently confused with migraine.

• NAD⁺ Anecdotal

  Marketed by infusion clinics for headache. No controlled evidence, and infusion settings produce large placebo effects in pain conditions.

Approved peptide drugs for this condition that are not in this library: The CGRP antibodies and gepants, triptans and lasmiditan. The peptide here is the target, not the drug.

• Semax Theorized

  The indication it is actually used for in Russia, in the acute and subacute ischaemic stroke setting. The trial quality does not meet the standard that would be required for approval elsewhere.

• Selank Theorized

  Post-stroke anxiety and mood rather than neurological recovery.

• BPC-157 Theorized

  Rodent TBI models.

• SS-31 Theorized

  Mitochondrial protection in ischaemia-reperfusion models.

• ARA-290 Theorized

  An erythropoietin-derived peptide designed to keep the tissue-protective effect without the haematopoietic one — the rationale that made erythropoietin itself interesting in stroke before the trials disappointed.

• Humanin Theorized

  Neuroprotection in cell models.

• ARA-290 Study

  The strongest entry in this section: reached randomised human trials in sarcoidosis-associated small-fibre neuropathy and in type 2 diabetes, with reported improvements in corneal nerve fibre measures and symptom scores.

• BPC-157 Theorized

  Rodent nerve injury models.

• TB-500 Theorized

  Animal nerve regeneration work.

• Semax Theorized

  Neurotrophic framing.

• SS-31 Theorized

  Mitochondrial dysfunction is implicated in chemotherapy-induced and diabetic neuropathy.

• MOTS-c Theorized

  Metabolic rationale in the diabetic form.

• Semaglutide Study

  Glycaemic control is the intervention that alters the course of diabetic neuropathy; this is the mechanism by which the incretins are relevant here.

• Selank Theorized

  Tuftsin analogue with anxiolytic activity in animal models and small Russian clinical work, framed as benzodiazepine-like without dependence.

• Semax Theorized

  BDNF modulation; the antidepressant argument runs through the same pathway SSRIs are thought to touch downstream.

• Semax + Selank Anecdotal

  Used together on a stimulating-plus-calming rationale.

• DSIP Theorized

  Sleep architecture, and through it mood. The original human work is from the 1970s and 1980s and is not robust.

• Adamax Anecdotal

  Supplier claims, no literature.

• Epitalon Anecdotal

  Sleep and circadian claims by way of the pineal framing.

• Semaglutide Study

  Relevant in the other direction. Reports of suicidal ideation prompted regulatory review, and the FDA subsequently concluded there was no increased risk and requested removal of the suicidal behaviour and ideation warning from GLP-1 labelling. Disproportionate reporting persists in pharmacovigilance databases, which is what those databases do; the controlled evidence did not support a causal link.

• Exenatide Study

  The positive trial. Extended-release exenatide alongside a 21 mg nicotine patch and counselling produced abstinence of 46.3% against 26.8%, with reduced craving and withdrawal.

• Dulaglutide Study

  The null trial, and the more instructive one. Alongside varenicline and counselling, abstinence was 63% against 65% — no difference — while weight went −4.6 kg against +0.5 kg on placebo. It did not help people quit; it solved the problem that stops many people trying.

• Semaglutide Study

  A large target trial emulation in type 2 diabetes found lower risk of tobacco-dependence encounters against all seven comparator antidiabetic drugs. The investigators stated explicitly that the limitations preclude firm conclusions and that the result should not be read as justifying off-label use.

• Liraglutide Theorized

  Class inference. No smoking cessation trial for this agent.

• Tirzepatide Theorized

  Class inference, with the GIP arm adding nothing known to this question.

• Retatrutide Theorized

  Class inference only, and unapproved for anything.

• Orforglipron Theorized

  Same receptor, oral route. No cessation data, and the newest agent in the class.

Approved peptide drugs for this condition that are not in this library: Varenicline, bupropion, nicotine replacement and cytisinicline are the approved options; none is a peptide.

• Semaglutide Study

  Real randomised data, and it keeps replicating. A 2025 randomised trial in 48 adults with alcohol use disorder found low-dose semaglutide reduced alcohol consumed in a laboratory self-administration task, with medium-to-large effect sizes. A 2026 randomised trial in 108 adults with moderate-to-severe alcohol use disorder and obesity — all receiving cognitive behavioural therapy — found heavy drinking days fell by 41.1 percentage points on semaglutide against 26.4 on placebo over 26 weeks. A separate randomised trial of oral semaglutide reported consistent findings. Keep the tier honest: these are small, short, and not phase 3, and this site has documented repeatedly what happens to promising phase 2 results. But this is randomised, replicated, mechanistically coherent, and moving toward larger trials — which is more than almost anything else in this library can say.

• Tirzepatide Theorized

  Same class rationale, less alcohol-specific trial data. The mechanism is thought to run through mesolimbic reward signalling rather than through the gut.

• Liraglutide Theorized

  Earlier class member, some supportive signals, superseded by the semaglutide trials.

• Kisspeptin-10 Theorized

  No addiction role. Included because alcohol suppresses the reproductive axis, and heavy drinking is a genuine and reversible cause of low testosterone that gets attributed to other things.

• Semax Anecdotal

  Used in the Russian literature and in community practice for withdrawal and craving. No controlled evidence in addiction.

• Selank Anecdotal

  Anxiolytic framing applied to withdrawal-related anxiety. Same absence of evidence, and alcohol withdrawal is not a condition to self-manage — see below.

• NAD⁺ Anecdotal

  Marketed aggressively for addiction recovery by infusion clinics, at high cost, with no controlled evidence. “NAD+ detox” programmes are sold to people at their most vulnerable and least able to evaluate the claim. The absence of evidence here is not a technicality.

• Glutathione Anecdotal

  Same channel, same claim structure, same absence.

Approved peptide drugs for this condition that are not in this library: Naltrexone, acamprosate, buprenorphine and methadone are approved and effective. None is a peptide, and the peptide class here is investigational.

• Semax Theorized

  Used in Russian paediatric practice for attention and cognitive problems, with monoaminergic and BDNF effects that make the rationale coherent. No controlled trial in ADHD, and nothing published outside Russia and neighbouring states.

• Adamax Anecdotal

  Marketed for focus with no published literature under that name at all. Every claim is read across from Semax, which itself has no Western trial evidence.

• Selank Theorized

  Anxiety degrades working memory by consuming attentional capacity, so treating it can improve attention without acting on attention. That is a real mechanism and a different claim from treating ADHD.

• Semax + Selank Anecdotal

  The common community pairing for focus. No study has examined it for anything.

• CJC-1295 (no DAC) Anecdotal

  Appears in nootropic stacking discussion. Nothing connects GH secretagogues to attention.

• Semax Theorized

  BDNF modulation, which is a pathway genuinely implicated in mood disorder and thought to be downstream of what SSRIs do. No controlled trial in depression exists.

• Selank Theorized

  Anxiolytic with reported antiasthenic and mildly activating effects — relevant because anxiety and depression are comorbid far more often than not, and because fatigue is poorly served by sedating agents.

• Semax + Selank Theorized

  The community pairing, on a stimulating-plus-calming rationale. Rapid subjective mood lift is the usual report, and it arrives faster than any BDNF-mediated mechanism plausibly acts.

• Semaglutide Study

  Relevant for safety rather than benefit. Reports of suicidal ideation prompted regulatory review, and the FDA subsequently concluded there was no increased risk and requested removal of the warning from GLP-1 labelling. Weight loss also has genuine effects on mood in both directions.

• DSIP Theorized

  Sleep and mood are bidirectional, and non-restorative sleep is a core depressive symptom. DSIP was rejected by the PCAC and has no identified receptor.

• Epitalon Anecdotal

  Circadian framing extended to mood by association.

• NAD⁺ Anecdotal

  Marketed heavily by infusion clinics for mood and fatigue, with no controlled evidence in depression.

• Oxytocin Study

  The largest and most rigorous trial was negative. SOARS-B randomised 290 children and adolescents with autism to 24 weeks of daily intranasal oxytocin or placebo and — published in the New England Journal of Medicine in 2021 — found no significant difference from placebo on its primary social-withdrawal endpoint or on its secondary social and cognitive measures. Smaller pilots reported benefit, particularly designs pairing infrequent dosing with structured social interaction, and that remains unconfirmed at scale.

• Desmopressin Theorized

  Included for the vasopressin connection rather than as a candidate. The vasopressin system was a serious autism target: balovaptan, a V1a receptor antagonist, failed a phase 3 trial in adults and a phase 2 trial in children, and the adult trial was stopped early when interim analysis showed it was unlikely to succeed.

• Semax Anecdotal

  Used off-label in the Russian tradition for developmental and cognitive indications. No autism trial.

• BPC-157 Anecdotal

  Sold on gut-brain-axis reasoning. There is no controlled evidence in autism for this or any other repair peptide.

• KLOW Anecdotal

  Same gut-axis framing, same absence of evidence.

Approved peptide drugs for this condition that are not in this library: Risperidone and aripiprazole are approved for irritability associated with autism — a specific behavioural target, not the core features.

• Semax Anecdotal

  The specific hazard. Stimulating and antidepressant-like compounds — whether prescribed antidepressants, nootropics, or anything with activating effects — can trigger a manic or hypomanic episode in someone with bipolar disorder, including someone who does not yet know they have it. This is not a theoretical concern; antidepressant-induced mania is well documented, which is why psychiatrists screen for a history of elevated mood before prescribing. Nobody screens before selling a nootropic.

• Selank Anecdotal

  Anxiolytic framing rather than activating, but the same absence of evidence and the same lack of any screening.

• Tesofensine Theorized

  Monoamine reuptake inhibition — pharmacologically the most activating compound in this library, and stimulants and monoaminergic drugs are recognised precipitants of mania.

• NAD⁺ Anecdotal

  Infusion clinics market these preparations for mood and energy. Sleep disruption alone can precipitate an episode, and infusions marketed for energy are aimed at exactly the population most likely to have undiagnosed mood disorder.

• Semaglutide Theorized

  Relevant for the interactions rather than the disease. Lithium has a narrow therapeutic index and is affected by fluid balance and kidney function — vomiting, dehydration or significant weight change can raise levels into toxicity. Anyone on lithium starting an incretin needs monitoring, not assumption. Many psychiatric drugs also cause weight gain, which is why this class is increasingly used in this population and why that should be done with the psychiatric team.

• Insulin & analogues Study

  No direct role. Included because people with bipolar disorder have markedly higher rates of diabetes and cardiovascular disease, partly from medication and partly from the illness — and that physical health gap is a leading cause of the reduced life expectancy in this group.

Approved peptide drugs for this condition that are not in this library: Lithium, anticonvulsants and antipsychotics. None is a peptide, and nothing in this library has been studied in bipolar disorder.

• Oxytocin Theorized

  The most-studied peptide here, and the results are genuinely mixed. Intranasal oxytocin has been trialled for fear extinction, social processing and PTSD prevention after trauma, with some early-administration signals and considerable inconsistency between studies. The same delivery question that dogs every intranasal peptide applies — how much reaches the brain, and whether findings replicate. It is not an established treatment, and the approved use of oxytocin is obstetric, covered under postpartum haemorrhage.

• Selank Anecdotal

  Anxiolytic framing from the Russian literature. No PTSD trials, and the methodological quality of the available work is poor.

• Semax Anecdotal

  Same tradition, same absence.

• DSIP Anecdotal

  Sleep framing, and sleep disturbance and nightmares are among the most distressing features of PTSD. No identified receptor, rejected by the PCAC, and human evidence from the 1970s and 80s that was small and inconsistent — while an effective, cheap, prescribable option for nightmares exists and is described below.

• Semaglutide Theorized

  Indirect. PTSD is associated with substantially increased rates of substance use, obesity and cardiovascular disease, and those are treatable in their own right.

• NAD⁺ Anecdotal

  Marketed for trauma and “nervous system reset” by infusion clinics. No evidence, aimed at a population with high distress and, frequently, limited means.

Approved peptide drugs for this condition that are not in this library: Sertraline and paroxetine are approved for PTSD. The best-evidenced treatments are psychotherapies, and no peptide is approved anywhere.

• Tirzepatide Study

  Approved for this, and it is the first pharmacological treatment obstructive sleep apnoea has ever had. SURMOUNT-OSA tested tirzepatide in adults with moderate-to-severe OSA and obesity and reported a substantial reduction in the apnoea-hypopnoea index — the actual disease measure, not a weight surrogate — in participants both using and not using CPAP. That is the second indication where this compound produced a benefit measured as something other than a number on a scale.

• Semaglutide Theorized

  Not approved for OSA, and the mechanism — reducing the fat load on the upper airway and the chest wall — is the same one. It has no equivalent trial with an apnoea-hypopnoea endpoint, which is exactly the distinction this site exists to make.

• Retatrutide Theorized

  Largest weight effect in the class and the most likely to help by the same route. No OSA endpoint.

• Cagrilintide Theorized

  Same reasoning, weaker weight effect alone.

• DSIP Anecdotal

  Listed as a caution, not a candidate. Anything marketed to deepen sleep is being sold into a condition where the problem is that the airway collapses during sleep. Sedatives and central depressants can worsen obstructive apnoea by reducing upper airway muscle tone and blunting arousal from an obstructive event — and the arousal is what ends the apnoea. Feeling like you slept more deeply is not evidence you breathed.

• Desmopressin Theorized

  Appears in this space because nocturia is a common and under-recognised OSA symptom — apnoea drives natriuretic peptide release and night-time urine production. Treating the nocturia while leaving the apnoea untreated addresses the symptom that wakes you and none of the risk that matters.

• Tesamorelin Theorized

  Visceral fat reduction with a plausible route to airway loading. No OSA data.

• BPC-157 Anecdotal

  No mechanism, no data, appears in general wellness discussion.

Approved peptide drugs for this condition that are not in this library: Tirzepatide is approved for obstructive sleep apnoea with obesity — the only drug approved for the condition anywhere.

• DSIP Theorized

  Delta sleep-inducing peptide — named for the effect it was reported to have in rabbits in 1977. The human work that followed was small and inconsistent, and the compound was rejected for the compounding list.

• Epitalon Anecdotal

  Pineal and melatonin-axis framing.

• Selank Theorized

  Sleep improvement secondary to anxiolysis.

• Ipamorelin + CJC-1295 (no DAC) Anecdotal

  Deeper sleep is among the most consistently reported subjective effects of GH secretagogues — and also among the most placebo-susceptible.

• Thymosin Alpha-1 Study

  The strongest immune entry here: approved in a number of countries as Zadaxin, with human trial use in hepatitis B, hepatitis C and as a vaccine adjuvant, and investigated in sepsis.

• Epitalon Anecdotal

  Pineal peptide from a small Russian literature; telomerase claims are frequently overstated.

• LL-37 Theorized

  Innate antimicrobial peptide, part of the vitamin D–cathelicidin axis.

• KPV Theorized

  Anti-inflammatory rather than immune-stimulating — the opposite direction to most claims in this section.

• Glutathione Theorized

  Antioxidant framing; lymphocyte glutathione does decline with age.

• NAD⁺ Theorized

  Metabolic support of immune-cell function.

• Enfuvirtide Study

  Approved HIV fusion inhibitor — a 36-residue peptide that blocks gp41 from folding into the six-helix bundle that pulls the membranes together. It works; it also requires twice-daily injection and causes injection site reactions in 98% of patients, which is why oral agents displaced it.

• Thymosin Alpha-1 Study

  Randomised trials in chronic hepatitis B, and use in hepatitis C, generally in combination with interferon. Approved in several countries for this use.

• LL-37 Theorized

  Broad antimicrobial activity including some antiviral effects in vitro.

Approved peptide drugs for this condition that are not in this library: Ibalizumab, and the entry inhibitors maraviroc and fostemsavir, target the same entry process at different steps.

• BPC-157 Anecdotal

  Aimed at the wrong disease. The joint claims for this compound come from tendon and soft-tissue repair models. Rheumatoid arthritis is an immune attack, not a repair deficit — a repair agent does not address the driver, and the erosion continues underneath any symptomatic improvement. Intra-articular injection is also a worse idea here than anywhere else on this site, because RA patients are frequently on immunosuppression and a septic joint in that context is more likely and more dangerous.

• TB-500 Anecdotal

  Same objection, same wrong target.

• KLOW Anecdotal

  Marketed for joints without distinguishing which joint disease. KPV at least has an anti-inflammatory rationale; nothing in the blend touches the autoimmune mechanism.

• KPV Theorized

  Generic anti-inflammatory action in rodent models. Suppressing inflammation without modifying the immune process is what corticosteroids do, and they are used in RA precisely as a bridge rather than as a treatment.

• Thymosin Alpha-1 Theorized

  The direction problem at its clearest. Every approved use of this compound depends on enhancing immune response, and RA is treated by suppressing or redirecting it. Anyone on a biologic or a JAK inhibitor should treat this as an interaction question for their rheumatologist rather than an addition.

• ARA-290 Theorized

  The innate repair receptor is genuinely anti-inflammatory and tissue-protective, which makes this the most coherent rationale here. It has no RA evidence, and its developer appears to have wound down.

• LL-37 Theorized

  Cathelicidin is implicated in RA synovial inflammation and in neutrophil extracellular traps, which are a proposed source of citrullinated autoantigens. That makes it part of the disease process rather than a treatment for it — the same pattern as psoriasis and lupus.

• Semaglutide Theorized

  Indirect. Obesity worsens RA disease activity and reduces treatment response, and weight loss improves both. Acts through the metabolic route, not the immune one.

Approved peptide drugs for this condition that are not in this library: Methotrexate, the anti-TNF, IL-6, CTLA4-Ig and anti-CD20 biologics, and the JAK inhibitors. None is a peptide.

• LL-37 Theorized

  Part of the disease mechanism, not a candidate treatment. Cathelicidin complexes with self-DNA released from dying cells and from neutrophil extracellular traps, converting it into a potent stimulus for plasmacytoid dendritic cells through TLR7 and TLR9 — which drives the type I interferon signature that defines this disease. Administering more of a molecule that participates in breaking tolerance to self-DNA, in a disease defined by that failure, is the clearest contraindication by mechanism in this library.

• Thymosin Alpha-1 Theorized

  Immune enhancement in a disease of immune over-activity. The direction problem, again, and lupus is where it matters most — anyone on immunosuppression should treat this as an interaction question for their specialist.

• KPV Theorized

  Anti-inflammatory, which is at least the right direction, and entirely generic against a disease with a specific mechanism.

• GHK-Cu Theorized

  Appears in discussion of cutaneous lupus for skin remodelling. Photosensitivity is central to cutaneous lupus and sun protection is the intervention that matters.

• BPC-157 Anecdotal

  Discussed for joint and gut symptoms. No evidence, and the pro-angiogenic property is not obviously desirable in an inflammatory vasculopathy.

• Epitalon Anecdotal

  Longevity framing applied to an autoimmune disease. No data.

Approved peptide drugs for this condition that are not in this library: Hydroxychloroquine, belimumab, anifrolumab and voclosporin. None is a peptide, and the peptide that was developed for lupus failed phase 3.

• Enfuvirtide Study

  An approved antiretroviral, and a peptide that shows what the delivery problem costs. Enfuvirtide is a 36-residue peptide that blocks HIV entry by binding gp41 and preventing the virus fusing with the cell membrane — a genuinely novel mechanism when it arrived, and it worked. It requires twice-daily subcutaneous injection, and injection site reactions occur in almost everyone who uses it. That is why it has been largely displaced by oral tablets and long-acting injectables that are just as effective and far more tolerable: not because the science failed, but because a peptide that cannot be swallowed loses to a small molecule that can. It survives as a salvage option in multi-drug-resistant infection.

• Thymosin Alpha-1 Theorized

  The immunological framing is obvious and the history is instructive: thymic peptides were investigated in HIV in the era before effective antiretrovirals, and what actually restored immune function was suppressing the virus, not stimulating the immune system. CD4 counts recover when viral replication stops. That is a complete answer to the immune-support argument in this disease.

• Tesamorelin Study

  Approved specifically in this population — for excess visceral abdominal fat in HIV-associated lipodystrophy, which has its own entry. One of very few GH-axis compounds with a real approval and real trial data.

• LL-37 Theorized

  Cathelicidin has antiviral activity in laboratory work, including against HIV in vitro. In vitro antiviral activity is abundant and clinically meaningless without a drug that works in a person.

• Semaglutide Theorized

  Increasingly relevant: people with HIV now live long enough to develop ordinary metabolic disease, and weight gain on modern regimens — particularly integrase inhibitors — is a recognised issue. Check interactions with antiretrovirals rather than assuming, and note that delayed gastric emptying can alter absorption of drugs where consistent levels matter enormously.

• BPC-157 Anecdotal

  No evidence. And a caution that applies to this whole page: nothing here substitutes for antiretroviral therapy, and interruptions in treatment cause resistance and harm.

Approved peptide drugs for this condition that are not in this library: Enfuvirtide is an approved peptide antiretroviral, and tesamorelin is approved for a complication of the disease. The drugs that transformed HIV are small molecules.

• BPC-157 Theorized

  Named because it is among the most frequently injected compounds in this space, and often locally, into or near a joint or tendon. Intra-articular and peri-tendinous injection carries meaningfully higher stakes than subcutaneous: a septic joint is a surgical emergency that destroys cartilage within days. Sterile technique and a sterile product are different problems, and research-grade material addresses neither.

• TB-500 Theorized

  Same pattern of local use, same considerations.

• KLOW Theorized

  Blends multiply the variables — more components, more excipients, more chances that one of them is the problem, and no way to tell which.

• Melanotan-2 Theorized

  Frequently injected daily during loading, often by people with no clinical background, and reconstituted vials are commonly kept far longer than they should be.

• Semaglutide Study

  The contrast worth drawing. Pharmaceutical pens are sterile, single-patient, dose-accurate and manufactured under regulated conditions. Compounded and grey-market versions bypass all four of those, and dosing errors from drawing “units” out of a vial with an insulin syringe have caused documented overdoses severe enough to require hospital treatment.

• Insulin & analogues Study

  The most dangerous thing in this library by a wide margin. Insulin is a peptide, it is available, and it is used non-medically for its anabolic reputation. Hypoglycaemia can cause seizures, brain injury and death, it can develop while asleep, and there is no dose that is reliably safe in someone who does not need it. This is not a cautionary framing; people have died. If someone using insulin becomes confused, sweaty, shaky or drowsy, that is an emergency requiring sugar immediately and an ambulance.

• GHK-Cu Theorized

  Frequently injected intradermally or used in mesotherapy-style protocols. The skin is not a low-risk compartment — it is where mycobacterial and atypical infections from non-sterile injection typically show up, often weeks later.

Approved peptide drugs for this condition that are not in this library: Not applicable. This entry is about the route, not the drug.

• LL-37 Theorized

  The human cathelicidin, with broad-spectrum activity and anti-biofilm effects in vitro. Its systemic use is limited by exactly the pro-inflammatory and cytotoxic properties that make it effective locally.

• KPV Theorized

  Some reported antimicrobial activity alongside its anti-inflammatory profile.

• GHK-Cu Theorized

  Copper has intrinsic antimicrobial properties.

• SS-31 Theorized

  Mitochondrial dysfunction is a leading hypothesis for post-exertional malaise, which makes a cardiolipin-stabilising agent the most mechanistically pointed candidate here. Read its own page first: three randomised trials in populations with genuine, measurable mitochondrial pathology missed their primary endpoints. Expecting more in a condition where mitochondrial dysfunction is hypothesised rather than demonstrated is the opposite of what that record predicts.

• MOTS-c Theorized

  Same mitochondrial rationale, weaker evidence — rodent and human association only.

• Humanin Theorized

  Same family, same rationale, same absence of human intervention data.

• NAD⁺ Anecdotal

  Marketed aggressively to this population by infusion clinics. No controlled evidence in ME/CFS, an unresolved question about whether infused NAD+ enters cells intact at all, and a price point that lands on people who frequently cannot work.

• Thymosin Alpha-1 Theorized

  Immune dysregulation is a serious research hypothesis in ME/CFS, particularly in post-infectious onset. This compound has real approvals elsewhere and pushes immune tone in a direction nobody has established is the right one here.

• LL-37 Theorized

  Viral persistence is another live hypothesis, which is where the antimicrobial framing comes from. No evidence in this condition, and the autoimmune cautions on that page apply.

• Semax Anecdotal

  Used for the cognitive component — the difficulty with concentration and processing that patients describe and that is genuinely disabling. No evidence here.

• BPC-157 Anecdotal

  Widely discussed, entirely on community reporting.

• Glutathione Anecdotal

  Oxidative stress framing, delivered by infusion clinics alongside NAD+. The antioxidant trial record generally is poor.

Approved peptide drugs for this condition that are not in this library: Rintatolimod (Ampligen) holds an approval in Argentina and is not FDA-approved. There is no approved treatment in the US, UK or EU.

• Semaglutide Theorized

  Actually being tested. Semaglutide is one of the interventions in the NIH RECOVER-TLC programme, alongside baricitinib, low-dose naltrexone and stellate ganglion block. That makes it the only compound in this library in a funded long COVID trial — and the trial has not reported, so there is nothing to cite yet beyond the fact that someone is doing this properly.

• Thymosin Alpha-1 Theorized

  Immune dysregulation framing, and it was investigated during acute COVID with mixed results. It did not enter standard care anywhere, which is the informative outcome.

• SS-31 Theorized

  Mitochondrial dysfunction is a leading hypothesis for post-exertional malaise. Its own trial record — three randomised failures in populations with demonstrable mitochondrial pathology — is the reason to hold this lightly.

• MOTS-c Theorized

  Same mitochondrial rationale, rodent evidence.

• NAD⁺ Anecdotal

  Marketed heavily to this population by infusion clinics, with no controlled evidence. See the POTS entry for the saline confound.

• LL-37 Theorized

  Viral persistence is a serious hypothesis and is one of the mechanisms RECOVER is investigating. This compound has no evidence in it, and its autoimmune liabilities are documented on its own page.

• BPC-157 Anecdotal

  Heavily discussed, entirely on community reporting.

• Semax Anecdotal

  Used for the cognitive component, which is real and disabling. No evidence here.

• Glutathione Anecdotal

  Oxidative stress framing, delivered alongside NAD+ by the same clinics.

• IGF-1 LR3 Theorized

  The clearest concern in the library. IGF-1 signalling is associated with proliferation in multiple cancer types, and this analogue was designed to evade the binding proteins that normally restrain it.

• PEG-MGF Theorized

  An IGF-1 splice variant with the same class of concern.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH secretagogues raise IGF-1 systemically. The concern is about the downstream hormone, not the secretagogue itself.

• BPC-157 Theorized

  Pro-angiogenic in the animal models used to argue for it. Angiogenesis is a hallmark of tumour growth; anti-angiogenic drugs are a cancer treatment class.

• TB-500 Theorized

  Promotes cell migration and angiogenesis — the two processes central to metastasis. Thymosin beta-4 expression correlates with metastatic potential in some tumour studies.

• GHK-Cu Theorized

  Presented in the literature as having gene-expression-normalising effects, with in vitro work pointing in both directions.

• Melanotan-2 Theorized

  Darkens existing naevi and can obscure the change in appearance that skin cancer surveillance depends on. Melanoma cases have been reported in users.

• Epitalon Theorized

  Telomerase activation is the specific claim, and telomerase reactivation is a near-universal feature of cancer cells. The Russian literature argues the opposite; neither position is settled.

• Leuprolide Study

  Approved and part of standard care, by the same pulsatility paradox described under prostate cancer. Continuous GnRH-agonist exposure desensitises the pituitary and suppresses ovarian oestrogen production. In the randomised SOFT and TEXT trials, adding ovarian suppression to endocrine therapy in premenopausal women with hormone-receptor-positive disease improved disease-free survival and, on longer follow-up, overall survival — and ovarian suppression with an aromatase inhibitor outperformed ovarian suppression with tamoxifen. Goserelin is the agent used most often in this setting. This induces menopause; it is not something to approach casually.

• IGF-1 LR3 Theorized

  IGF-1 signalling is implicated in breast cancer proliferation and in resistance to endocrine therapy, and this analogue was built to evade the binding proteins that restrain IGF-1. The standing caution at its sharpest.

• PEG-MGF Theorized

  IGF-1 splice variant, same concern.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically. The concern is the downstream hormone.

• Semaglutide Theorized

  Genuinely relevant, and for a reason that is often stated backwards. Obesity raises postmenopausal breast cancer risk because adipose tissue is where oestrogen is produced after the ovaries stop — aromatase in fat converts androgens to oestrogen. Less fat means less oestrogen exposure. Observational data presented in 2026 also reported lower rates of metastatic progression among GLP-1 users, at 10% against 20% — real-world and unrandomised, so treat it as a hypothesis worth testing rather than a result. Weight loss during active treatment is a decision for the oncology team, not a self-directed one.

• Tesamorelin Theorized

  Reduces visceral fat, which looks aligned with the paragraph above — but it does so by raising GH and IGF-1, in a cancer where IGF-1 signalling drives proliferation. The wrong route to the right destination.

• Oxytocin Theorized

  Appears because of lactation, and the honest note is epidemiological rather than pharmacological: breastfeeding is associated with reduced breast cancer risk. That is not an argument for administering oxytocin, which has an approved obstetric role covered under postpartum haemorrhage.

• GHK-Cu Theorized

  Used topically for radiotherapy skin changes. Anything applied to skin inside a radiotherapy field should be cleared with the radiation oncology team, because some topical preparations alter surface dose.

• BPC-157 Theorized

  Pro-angiogenic in the models used to promote it. Also discussed for post-surgical and post-radiotherapy recovery, with no human evidence in either.

• TB-500 Theorized

  Promotes cell migration and angiogenesis — the two processes that define metastasis.

• Epitalon Theorized

  Telomerase activation is the explicit claim, and telomerase reactivation is a near-universal property of cancer cells.

Approved peptide drugs for this condition that are not in this library: Goserelin, leuprolide and triptorelin are approved peptides here, used for ovarian suppression. The targeted agents are antibodies and small molecules.

• Teduglutide Study

  An approved peptide whose licence requires cancer surveillance — which is a category of fact this library should have covered sooner. Teduglutide is a GLP-2 analogue, and GLP-2 is intestinotrophic: making intestinal tissue grow is precisely the therapeutic effect in short bowel syndrome. The label states it has the potential to cause hyperplastic changes including neoplasia, and mandates colonoscopy of the entire colon with polyp removal within six months before starting, a follow-up at one year, and then every five years. Colorectal polyps were found in the trials, and treatment must stop if colorectal cancer is diagnosed. A growth signal strong enough to regrow gut is a growth signal strong enough to worry about.

• BPC-157 Anecdotal

  The most important entry on this page, and the harm is not the one people expect. This compound is promoted for “gut healing” and taken for exactly the symptoms that colorectal cancer presents with: altered bowel habit, bleeding, abdominal pain, unexplained anaemia. The risk is not that it causes cancer — it is that symptomatic improvement, real or placebo, buys the delay that turns a curable cancer into an incurable one. Rectal bleeding attributed to “haemorrhoids that got better on BPC” is how young patients present late. It is also pro-angiogenic, which is a separate and lesser concern. Any change in bowel habit lasting weeks, any rectal bleeding, and any unexplained iron deficiency needs investigating before anything is taken for it.

• Linaclotide Study

  Approved for constipation-predominant IBS, and the same principle applies: constipation of recent onset in an adult over 40, or with bleeding or weight loss, is a red flag requiring investigation before symptomatic treatment. The drug is legitimate; treating an unexamined change in bowel habit is not.

• Semaglutide Theorized

  Obesity is an established colorectal cancer risk factor. A large observational study of over 170,000 people with diabetes and obesity reported modestly reduced rates of fourteen obesity-related cancers among GLP-1 users compared with DPP-4 inhibitor users, with colorectal cancer showing the strongest signal. Unrandomised and confounded by the reasons people are prescribed one drug over another — encouraging, not established.

• Tirzepatide Theorized

  Same reasoning, same limitation, less accumulated data.

• IGF-1 LR3 Theorized

  IGF-1 signalling is associated with colorectal cancer risk in epidemiological work. The standing caution.

• KPV Theorized

  Anti-inflammatory in colitis models, and chronic colonic inflammation is itself a cancer risk — see ulcerative colitis. Suppressing inflammatory symptoms without documenting mucosal healing is the same delayed-diagnosis problem in a different form.

• TB-500 Theorized

  Cell migration and angiogenesis.

Approved peptide drugs for this condition that are not in this library: No peptide treats colorectal cancer. Teduglutide is the peptide that requires screening for it.

• Melanotan-2 Study

  Read this before using it, and read it as the strongest warning on this site. Melanotan-II is a melanocortin agonist that tans by stimulating melanocytes — the cells melanoma arises from. The published literature is not theoretical: eruptive new naevi and darkening of existing moles have been documented within 24 hours of a single subcutaneous dose, dermatoscopic changes in existing naevi are reported, and the British Journal of Dermatology carried a case of melanoma in a user — a woman whose moles enlarged and darkened over three months, with histology confirming melanoma. There are two separate harms and both matter. The first is biological: synthetic α-MSH analogues can drive proliferation of melanocytic cells in predisposed people. The second is diagnostic, and it is the one nobody plans for — melanoma is detected by noticing that a mole has changed, and this compound makes every mole change. It destroys the signal the entire surveillance system depends on. Anyone who has used it should have a full-skin dermatology examination with dermatoscopy, and should say what they used.

• PT-141 Theorized

  Directly relevant, and often missed. Bremelanotide is a melanocortin agonist and is in fact the active metabolite of melanotan-II. It is more selective for MC4R and much shorter-acting, which is why it is an approved drug and melanotan is not — but hyperpigmentation and darkening of naevi have been reported with it, and its label acknowledges focal hyperpigmentation. The selectivity reduces the concern; it does not remove it.

• KPV Theorized

  Also derived from α-MSH — it is the C-terminal tripeptide — and worth distinguishing clearly: it lacks the core melanotropic sequence and is not reported to cause pigmentation or naevus change. Its anti-inflammatory action is the part of α-MSH biology it retains. Same parent molecule, different consequences.

• GHK-Cu Theorized

  Widely used topically. Skin-remodelling claims are not the issue — the issue is that anything applied to a pigmented lesion to “improve” its appearance may make it look better while it is progressing underneath. Cosmetic treatment of a changing pigmented lesion is never appropriate.

• BPC-157 Theorized

  Pro-angiogenic, and melanoma is one of the more angiogenesis-dependent tumours. Also promoted for wound healing over lesions that have not been examined.

• TB-500 Theorized

  Cell migration and angiogenesis. Thymosin beta-4 expression correlates with metastatic potential in some tumour studies, and melanoma is among the malignancies where that work has been done.

• IGF-1 LR3 Theorized

  The standing growth-signalling caution.

• LL-37 Theorized

  Cathelicidin is expressed in skin and is implicated in tumour-promoting inflammation in some models. Direction unclear, evidence absent.

Approved peptide drugs for this condition that are not in this library: Afamelanotide (Scenesse) is an approved melanocortin peptide — for erythropoietic protoporphyria, a rare photosensitivity disorder, under specialist supervision with mandatory skin monitoring. It is not approved for cosmetic tanning anywhere, and the monitoring requirement is the point.

• Semaglutide Theorized

  Two indirect roles. Obesity is a risk factor for several cancers, though the obesity-lung cancer relationship is confounded by smoking. More usefully, the GLP-1 class has randomised evidence for smoking cessation — and smoking cessation is the intervention that matters most in this disease. Observational 2026 data also reported lower metastatic progression in lung cancer among GLP-1 users, 10% against 22%, which is unrandomised and hypothesis-generating only.

• IGF-1 LR3 Theorized

  IGF-1 signalling is implicated in lung cancer proliferation. The standing caution.

• Thymosin Alpha-1 Theorized

  The most defensible immune rationale in this library, and still not enough. It has been studied as an adjunct in lung cancer in some settings, and immune modulation genuinely matters here — checkpoint inhibitors transformed the disease. But “immune stimulation” and “releasing a specific brake on T-cell recognition of tumour” are different things, and only the second one worked.

• LL-37 Theorized

  Expressed in airway epithelium and implicated in tumour-promoting inflammation in some lung models. Direction of effect unresolved.

• GHK-Cu Theorized

  Carried over from the emphysema gene-signature work under COPD. COPD and lung cancer share smoking as a cause and frequently coexist; the connectivity-map work says nothing about malignancy.

• BPC-157 Theorized

  Pro-angiogenic. Also, and more practically: a persistent cough, haemoptysis or unexplained weight loss needs investigating rather than treating.

• SS-31 Theorized

  Mitochondrial framing. Not studied here.

Approved peptide drugs for this condition that are not in this library: No approved peptide drug. The bombesin/GRP receptor is a validated target that never yielded one.

• Semaglutide Study

  The honest state of the evidence, in order. On pancreatic cancer: a 2025 meta-analysis of 62 randomised trials covering more than 66,000 patients found no significant association with GLP-1 use, and large recent cohorts point if anything the other way. On pancreatitis, which is a different question: the picture is genuinely mixed — some cohorts report increased odds of acute pancreatitis with current use, while others report reduced recurrent pancreatitis in people with a prior episode. Acute pancreatitis remains a labelled warning and the practical rule is unchanged: severe persistent abdominal pain radiating to the back means stop and seek assessment. Also unchanged: a history of pancreatitis is a reason for a prescriber to be involved, not a footnote.

• Tirzepatide Study

  Same class question, same labelled pancreatitis warning, shorter record.

• Exenatide Study

  The agent that generated the original pancreatitis signal in post-marketing reports, which is where two decades of this debate started.

• Liraglutide Study

  Longest exposure history in the class and no pancreatic cancer signal has emerged from it.

• Retatrutide Theorized

  Investigational, same class caution inherited.

• IGF-1 LR3 Theorized

  The standing caution. Pancreatic adenocarcinoma is heavily KRAS-driven, and growth factor signalling contributes to its biology.

• Octreotide Study

  Distinguish carefully: somatostatin analogues treat pancreatic neuroendocrine tumours, which are a different disease with a far better prognosis — see neuroendocrine tumours. They are not a treatment for pancreatic adenocarcinoma, and the two are frequently conflated in discussion.

• BPC-157 Theorized

  Pro-angiogenic, and promoted for the vague upper-abdominal and digestive symptoms with which this cancer often presents. The delayed-diagnosis argument applies with more force here, because the window in which this disease is operable is narrow.

Approved peptide drugs for this condition that are not in this library: No approved peptide drug for pancreatic adenocarcinoma. Somatostatin analogues treat the unrelated neuroendocrine tumours of the same organ.

• Semaglutide Theorized

  Relevant through the disease upstream of it. MASH is now a leading cause of hepatocellular carcinoma, and treating the metabolic liver disease is how you prevent the cancer. Observational 2026 data reported less metastatic progression in liver cancer among GLP-1 users, 19% against 28% — unrandomised. The meaningful claim is upstream: less steatohepatitis, less cirrhosis, less cancer. That chain is plausible and not yet demonstrated end to end.

• Tirzepatide Theorized

  Same reasoning via the same route.

• Thymosin Alpha-1 Study

  The most legitimate entry here. It has approvals in some countries as an adjunct in chronic hepatitis B, and chronic hepatitis B is a major cause of this cancer — see chronic viral infection. Note what actually changed the picture though: nucleos(t)ide analogues for hepatitis B and direct-acting antivirals for hepatitis C, neither of which is a peptide.

• Terlipressin Study

  A cirrhosis drug rather than a cancer drug — approved for hepatorenal syndrome, and used for variceal bleeding, both complications of the cirrhosis in which this cancer arises.

• Octreotide Study

  Used for acute variceal bleeding in portal hypertension by reducing splanchnic blood flow. Again a complication of the underlying liver disease, not a treatment for the tumour.

• IGF-1 LR3 Theorized

  The liver is the main site of IGF-1 production and IGF signalling is implicated in hepatocellular carcinoma. The standing caution, in the organ most directly involved.

• BPC-157 Theorized

  Promoted for liver support with no human data. Pro-angiogenic, and hepatocellular carcinoma is a strikingly vascular tumour — which is why several of its treatments are anti-angiogenic.

• Glutathione Anecdotal

  Heavily marketed for liver detoxification by infusion clinics. Hepatic glutathione biology is real; intravenous glutathione as a treatment for liver disease or its prevention is not established.

• NAD⁺ Anecdotal

  Same marketing channel, same absence of evidence.

Approved peptide drugs for this condition that are not in this library: Thymosin alpha-1 has hepatitis B adjunct approvals in some countries. Terlipressin and octreotide are approved peptides for complications of cirrhosis. None treats the tumour.

• Semaglutide Theorized

  The obesity-cancer link is stronger here than anywhere else, and the mechanism is specific rather than vague. Adipose tissue converts androgens to oestrogen through aromatase, so obesity produces continuous unopposed oestrogen exposure of the endometrium — and unopposed oestrogen is what drives endometrial hyperplasia and then cancer. This is the same aromatase biology described under breast cancer. Weight loss reduces that exposure. It is a risk-reduction argument, not a treatment.

• Tirzepatide Theorized

  Same mechanism, larger weight effect, no cancer outcome data.

• Leuprolide Study

  Approved for endometriosis and fibroids rather than for these cancers, and included because GnRH-agonist suppression is sometimes used in fertility-sparing management of low-grade endometrial disease and in some hormone-sensitive gynaecological tumours — always as a specialist decision. Progestin therapy, including the levonorgestrel intrauterine system, is the better-established fertility-sparing option in atypical hyperplasia and early low-grade endometrial cancer.

• Kisspeptin-10 Theorized

  Drives the reproductive axis upstream of GnRH. In a hormone-sensitive gynaecological cancer that is the wrong direction, exactly as it is in prostate cancer.

• Oxytocin Theorized

  No cancer role. Included for the epidemiology that keeps appearing in discussion: parity, breastfeeding and combined oral contraceptive use are all associated with reduced ovarian cancer risk, and the contraceptive effect is substantial and long-lasting.

• IGF-1 LR3 Theorized

  The standing caution. IGF signalling is implicated in endometrial cancer, and the population at risk overlaps heavily with metabolic syndrome.

• BPC-157 Theorized

  Pro-angiogenic. Also promoted for pelvic pain and menstrual symptoms — and postmenopausal bleeding is the cardinal symptom of endometrial cancer and needs investigating, not treating.

• Epitalon Anecdotal

  Pineal and longevity framing extended to reproductive ageing. Telomerase activation claims in a cancer context are the concern.

Approved peptide drugs for this condition that are not in this library: GnRH agonists are approved peptides for benign gynaecological conditions and used selectively here. The treatments that work are surgery, platinum chemotherapy, PARP inhibitors and immunotherapy.

• Semaglutide Study

  The boxed warning, explained properly. Every GLP-1 agonist carries a warning about thyroid C-cell tumours and is contraindicated in anyone with a personal or family history of medullary thyroid carcinoma or MEN2. It came from rodent toxicology: rats and mice developed C-cell hyperplasia and tumours on chronic exposure. The reason it may not translate is specific and mechanistic — human C-cells express substantially fewer GLP-1 receptors than rodent C-cells, and human studies have not shown a meaningful rise in calcitonin, the marker of C-cell activity. Human cohorts and meta-analyses have not found increased rates of the common differentiated thyroid cancers. The contraindication still stands, and the reason to respect it is that MTC is exactly the tumour the rodent data pointed at.

• Tirzepatide Study

  Same class warning, same rodent origin, same contraindication for MTC and MEN2. The reassuring human data on common thyroid cancers is shorter for the newer agents simply because they have been in use for less time.

• Liraglutide Study

  Carries the identical warning; the longest human exposure record in the class, and it has not produced a thyroid cancer signal.

• Dulaglutide Study

  Same class warning.

• Exenatide Study

  Same class warning. Worth noting that the warning is a class property inherited from rodent studies rather than a finding for each individual agent.

• Retatrutide Theorized

  Investigational and carries the same class caution by inheritance. The trial programmes exclude people with a history of MTC or MEN2, which is why no trial will ever answer the question directly.

• IGF-1 LR3 Theorized

  General growth-signalling caution rather than anything thyroid-specific.

• Thymosin Alpha-1 Theorized

  Immune framing. Note that immune checkpoint inhibitors cause thyroid dysfunction frequently, which is a reminder that the thyroid is unusually exposed to immune modulation.

Approved peptide drugs for this condition that are not in this library: Thyrotropin alfa is a recombinant protein used diagnostically. Calcitonin is the peptide tumour marker. The treatments are surgery, radioiodine and kinase inhibitors.

• Leuprolide Study

  An approved cornerstone treatment, and a paradox worth understanding. Leuprolide is a GnRH agonist, and it suppresses testosterone. That sounds backwards until you know that GnRH is normally released in pulses — continuous receptor stimulation desensitises and downregulates the pituitary, shutting the axis down. The same principle as teriparatide, running in the opposite direction: pulses stimulate, continuous exposure suppresses. The clinical consequence is the testosterone flare — an initial surge before suppression sets in, which can cause real deterioration in someone with spinal metastases or urinary obstruction, and is covered with an anti-androgen for the first weeks. This is not a compound to explore recreationally; it induces medical castration.

• Kisspeptin-10 Theorized

  The direction problem, and here it is genuinely serious. Kisspeptin sits upstream of GnRH and drives the axis — it is used experimentally to stimulate the reproductive axis and raise testosterone. In a hormone-sensitive prostate cancer, that is the exact opposite of the therapeutic goal. Anyone on androgen deprivation should treat this as contraindicated by mechanism rather than untested.

• IGF-1 LR3 Theorized

  IGF-1 signalling is associated with prostate cancer risk and progression in epidemiological work, and this analogue was engineered to evade the binding proteins that normally restrain IGF-1. The clearest single concern in this library, applied to one of the diseases where the association is best documented.

• PEG-MGF Theorized

  An IGF-1 splice variant, same class of concern.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH secretagogues raise IGF-1 systemically. The concern is the downstream hormone, not the secretagogue.

• Tesamorelin Theorized

  Tempting for the wrong reason. Androgen deprivation causes visceral fat gain, muscle loss and insulin resistance, so a compound that reduces visceral fat looks well matched — but it works by raising GH and therefore IGF-1, in a cancer where IGF-1 signalling is implicated. Resistance training and the metabolic drugs below achieve the same goal without that trade-off.

• PT-141 Theorized

  Erectile dysfunction after prostatectomy, radiotherapy or androgen deprivation is common, under-discussed and genuinely distressing. Bremelanotide acts centrally rather than on the vasculature, which is a different mechanism from the PDE5 inhibitors — but low libido on androgen deprivation is caused by the absence of testosterone, and no central agent replaces it. Bremelanotide is approved for women with hypoactive sexual desire disorder, not for men, and not in this setting.

• Semaglutide Theorized

  Genuinely relevant to the collateral damage. Androgen deprivation reliably causes weight gain, insulin resistance and increased cardiovascular risk, and metabolic management is part of good survivorship care. Not a cancer treatment.

• BPC-157 Theorized

  Pro-angiogenic in the models used to argue for it, in the presence of a tumour. Also discussed for radiation proctitis and post-surgical recovery, with no human evidence.

• TB-500 Theorized

  Promotes cell migration and angiogenesis — the two processes central to metastasis.

Approved peptide drugs for this condition that are not in this library: Leuprolide, goserelin, triptorelin and degarelix are all approved peptides for this disease. Relugolix is a small molecule; lutetium-177 PSMA is a peptide-targeted radioligand.

• Octreotide Study

  An approved first-line treatment, and one of the two compounds in this library whose primary indication is oncology. A somatostatin analogue that binds somatostatin receptors, which most well-differentiated neuroendocrine tumours express heavily. It does two separate jobs: it controls the hormonal syndrome — the flushing and diarrhoea of carcinoid — and it slows tumour growth, which was shown in a randomised trial rather than assumed. It also stops a carcinoid crisis, which can be precipitated by anaesthesia or by handling the tumour during surgery. Long-acting depot formulations are the practical form.

• Leuprolide Study

  Listed for the structural parallel rather than the indication. Both it and octreotide are modified hypothalamic-pituitary peptides made durable enough to be drugs, and both earn their place in oncology by acting on a receptor the tumour depends on — see prostate cancer.

• SS-31 Theorized

  No role. Included because the naming similarity to somatostatin analogues causes genuine confusion in community discussion — SS-31 is a mitochondrial-targeted peptide with no relationship to somatostatin whatsoever.

• IGF-1 LR3 Theorized

  The growth-signalling caution, in the presence of a tumour that is often indolent and lived with for years.

• BPC-157 Theorized

  Pro-angiogenic, and neuroendocrine tumours are notably vascular. Everolimus and sunitinib — both used here — work partly by restricting exactly the signalling and vascular support that a pro-angiogenic compound would promote.

• TB-500 Theorized

  Cell migration and angiogenesis, same objection.

Approved peptide drugs for this condition that are not in this library: Octreotide and lanreotide are approved peptide drugs here, and lutetium-177 dotatate is an approved peptide-targeted radioligand therapy. This is the strongest peptide oncology story in medicine.

• Epitalon Theorized

  The clearest inversion of a marketing claim on this site. Epitalon is sold on a telomerase activation premise: lengthen telomeres, extend lifespan. Meanwhile the first and only telomerase drug to reach approval — imetelstat, approved in June 2024 for lower-risk myelodysplastic syndromes with transfusion-dependent anaemia — is a telomerase inhibitor, and it works by selectively killing malignant clones, cells that depend on telomerase precisely because they divide without limit. The pharmaceutical read on telomerase in blood cells was that too much of it is the problem. That does not prove epitalon is dangerous. It does show which direction the serious money went.

• ARA-290 Theorized

  Read the erythropoietin history below before considering this in any cancer. ARA-290 is derived from the tissue-protective region of erythropoietin specifically to avoid the erythropoietic effects — which is the right instinct, given what happened when cancer patients were given the full molecule. It has no evidence here.

• Thymosin Alpha-1 Theorized

  The direction problem in its most acute form. Leukaemia is a cancer of the immune system, and patients are frequently both immunosuppressed and immunologically abnormal at the same time. “Boosting immunity” is not a coherent instruction in a disease where the immune cells themselves are the malignant clone. Anyone in treatment should treat every compound here as a question for their haematologist.

• IGF-1 LR3 Theorized

  IGF-1 signalling contributes to proliferation and to chemotherapy resistance in acute leukaemias. The standing caution.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically.

• NAD⁺ Anecdotal

  Marketed to cancer patients for fatigue by infusion clinics. NAD+ metabolism is genuinely active in leukaemic cells, which cuts against the marketing rather than for it, and cancer-related fatigue has better-evidenced management.

• Glutathione Anecdotal

  A specific caution worth stating. High-dose antioxidants during chemotherapy or radiotherapy are theoretically able to interfere with treatments that work partly through oxidative damage. The clinical evidence is inconclusive in both directions — which is exactly why this belongs to the oncology team and not to an infusion clinic.

• BPC-157 Theorized

  Pro-angiogenic, and bone marrow angiogenesis is increased in acute leukaemia and MDS. Also frequently taken for the bruising, fatigue and infections that are how these diseases present.

Approved peptide drugs for this condition that are not in this library: Imetelstat is an approved telomerase inhibitor — an oligonucleotide, not a peptide. Erythropoiesis-stimulating agents are approved glycoproteins carrying a boxed warning in cancer.

• Thymosin Alpha-1 Theorized

  Lymphoma is a malignancy of the exact cells this compound is supposed to modulate, and its whole rationale is thymic T-cell maturation. Stimulating the lineage that has become malignant is not an obviously good idea, and nobody has studied whether it is. Patients are also often immunosuppressed by treatment, making this a haematologist question rather than a supplement decision.

• LL-37 Theorized

  Implicated in lymphoproliferative and autoimmune processes. As in lupus, that puts it on the wrong side of the mechanism.

• IGF-1 LR3 Theorized

  IGF-1 signalling contributes to lymphoma proliferation in laboratory work. The standing caution.

• Epitalon Theorized

  Telomerase activation claims — see the leukaemia entry for what the only approved telomerase drug actually does.

• BPC-157 Anecdotal

  The delay risk, and it is real here. Painless swollen lymph nodes, night sweats, itch and unexplained weight loss are the presentation of lymphoma. They are also the sort of vague, systemic complaint that gets self-treated. A lymph node that has been enlarged for more than a few weeks, especially if painless, hard, or over a centimetre, needs examining — and Hodgkin lymphoma is curable in the large majority of patients when treated, which is exactly what makes delay costly.

• NAD⁺ Anecdotal

  Marketed for fatigue, which is a prominent lymphoma symptom. No evidence, and the fatigue is worth diagnosing.

• Glutathione Anecdotal

  Antioxidant infusions during treatment — see the caution under leukaemia.

• Leuprolide Theorized

  One genuinely relevant use, and it is about fertility rather than cancer. GnRH-agonist ovarian suppression during chemotherapy has been studied for preserving ovarian function, with randomised data in breast cancer and mixed results elsewhere. It does not replace established fertility preservation — egg, embryo or sperm banking before treatment starts — which is the conversation that too often does not happen in time, particularly in young patients with aggressive disease who are treated urgently.

Approved peptide drugs for this condition that are not in this library: No peptide treats lymphoma. The transformative agents are antibodies, antibody-drug conjugates, bispecific engagers and cell therapies.

• Teriparatide Study

  Contraindicated, and this is worth stating plainly because the reasoning looks superficially attractive. Myeloma destroys bone, teriparatide builds bone — so the pairing suggests itself. But teriparatide is contraindicated in skeletal malignancy and bone metastases, and myeloma is a malignancy of the bone marrow with lytic lesions. An anabolic bone agent is exactly what you do not add to a malignant process inside bone. Bone disease in myeloma is treated with bisphosphonates or denosumab — antiresorptives — which is the opposite approach to osteoporosis and for good reason.

• Insulin & analogues Study

  Genuinely relevant, and often unmanaged. Myeloma regimens are built around high-dose dexamethasone, which reliably causes hyperglycaemia — sometimes severe, sometimes newly diagnosed diabetes. Insulin requirements swing with the steroid schedule rather than staying flat, which is a pattern that catches people out.

• IGF-1 LR3 Theorized

  Among the strongest mechanistic concerns in this library. IGF-1 signalling is a well-documented survival and proliferation pathway in myeloma cells specifically, and has been an explicit drug target in the disease. This analogue was engineered to escape the binding proteins that normally restrain IGF-1.

• PEG-MGF Theorized

  IGF-1 splice variant, same pathway.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically.

• ARA-290 Theorized

  Anaemia is near-universal in myeloma — and see the erythropoietin boxed warning under leukaemia before reasoning from that.

• BPC-157 Theorized

  Pro-angiogenic, and bone marrow angiogenesis increases with myeloma progression — thalidomide and its successors, which are backbone myeloma drugs, are anti-angiogenic. Also promoted for the bone pain that is the commonest presenting symptom.

• Desmopressin Theorized

  No role, and a caution: myeloma can cause both kidney impairment and acquired bleeding tendencies, which makes fluid and haemostatic management a specialist matter.

• SS-31 Theorized

  Untested here.

Approved peptide drugs for this condition that are not in this library: Motixafortide is an approved cyclic peptide, used for stem cell mobilisation rather than to treat the cancer. Everything treating the disease itself is a small molecule, antibody or cell therapy.

• Kisspeptin-10 Theorized

  The tumour marker problem, and it has a published case behind it. Beta-hCG is one of the tumour markers for testicular cancer and is not normally detectable in men — which is exactly what makes it useful. Exogenous hCG, widely used post-cycle to restart the testicular axis, produces the same signal. The literature contains a bodybuilder with previously treated seminoma whose routine follow-up hCG came back elevated after he injected hCG; it triggered restaging and could have led to chemotherapy he did not need. Kisspeptin acts higher up the same axis and is used for the same purpose. If you have used hCG or anything acting on this axis, say so before any marker is interpreted. It is the difference between a false alarm and an unnecessary course of chemotherapy — or, worse, a real recurrence dismissed as “probably the hCG”.

• PT-141 Theorized

  Sexual dysfunction after orchidectomy, retroperitoneal lymph node dissection or chemotherapy is common and under-discussed. Bremelanotide acts centrally and is approved for women with hypoactive sexual desire disorder, not for men in this setting. Ejaculatory dysfunction after RPLND is a nerve problem and no drug fixes it, which is why nerve-sparing technique and sperm banking matter beforehand.

• IGF-1 LR3 Theorized

  The standing growth-signalling caution in a young population that is disproportionately exposed to these compounds.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically.

• BPC-157 Anecdotal

  No relevance to the disease, and a delay risk: a painless testicular lump is the classic presentation and it does not hurt, which is precisely why it gets ignored.

• Oxytocin Theorized

  No role in the disease. Included only to note that testicular tumours can secrete hormones — see the gynaecomastia point below — which is a different and more useful hormonal connection than anything in this list.

Approved peptide drugs for this condition that are not in this library: No peptide treats it. hCG — a peptide hormone widely used non-medically — is one of its tumour markers, which is the practical point of this entry.

• IGF-1 LR3 Theorized

  Read this even if you skip everything else on the page. IGF-1 receptor signalling is a validated therapeutic target in sarcoma — not a theory. Multiple pharmaceutical companies developed monoclonal antibodies to block IGF-1R specifically for Ewing sarcoma and rhabdomyosarcoma: figitumumab, ganitumab, cixutumumab, dalotuzumab. They produced objective responses in around 10–14% of patients with relapsed Ewing sarcoma, including occasional durable complete remissions, before resistance developed quickly and the programmes largely wound down. The industry’s considered read on IGF-1R signalling in muscle- and bone-origin tumours was to try to shut it off. This library contains an IGF-1 analogue engineered to evade the binding proteins that normally restrain IGF-1, injected to make muscle grow. That is the same axis, driven hard, in the same tissue — without monitoring, without a diagnosis, and without anybody counting what happens. No human study shows this causes sarcoma. Nobody has looked, and the target validation runs the other way.

• PEG-MGF Theorized

  Mechano growth factor is an IGF-1 splice variant produced by muscle in response to loading, and rhabdomyosarcoma is a tumour of skeletal-muscle lineage. Same argument, same axis, arguably closer to the tissue in question.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically rather than locally, which is a different exposure profile but the same hormone.

• BPC-157 Theorized

  Two distinct concerns. It is pro-angiogenic, and sarcomas are vascular tumours. More practically, it is injected — often locally, into muscle and around tendons, for lumps and injuries that have not been imaged. See the warning below.

• TB-500 Theorized

  Promotes cell migration and angiogenesis. Thymosin beta-4 expression has been correlated with metastatic potential in tumour studies.

• GHK-Cu Theorized

  Promotes fibroblast activity and collagen remodelling in vitro. Fibroblasts are the lineage several soft tissue sarcomas arise from.

• Tesamorelin Theorized

  Raises GH and IGF-1. Approved for HIV lipodystrophy and not studied in any malignancy.

Approved peptide drugs for this condition that are not in this library: No peptide treats sarcoma. Antibodies against the IGF-1 receptor were developed as treatment and reached phase 2 — which is the point.

• BPC-157 Anecdotal

  The most direct delayed-diagnosis risk in this library, more so than the colorectal version. BPC-157 is derived from a gastric juice protein and is marketed explicitly for stomach healing, gastritis, ulcers and reflux. Those are the presenting symptoms of gastric and oesophageal cancer. Dyspepsia that responds to something, then returns, is the classic history of a cancer diagnosed late. The alarm features that need endoscopy rather than treatment: difficulty or pain swallowing, unintentional weight loss, vomiting, iron deficiency anaemia, a palpable mass, and new persistent dyspepsia in anyone over about 55. Acting on those beats anything on this page by an enormous margin.

• KPV Theorized

  Anti-inflammatory in gastrointestinal models, and the same objection applies: suppressing an inflammatory symptom is not the same as knowing what is causing it.

• Semaglutide Theorized

  A real interaction rather than a benefit. GLP-1 agonists delay gastric emptying, which can worsen reflux and cause vomiting — symptoms that overlap with the alarm features above and can therefore both mask them and mimic them. Obesity is separately an established risk factor for oesophageal adenocarcinoma, via reflux and Barrett’s oesophagus, so weight loss reduces risk through that route. New or worsening dysphagia on a GLP-1 is not a side effect to accept without assessment.

• Tirzepatide Theorized

  Same delayed emptying, same reasoning.

• Linaclotide Study

  Approved for constipation-predominant IBS. Upper GI alarm features are not IBS and need investigating first.

• LL-37 Theorized

  Cathelicidin has antimicrobial activity against Helicobacter pylori in laboratory work, which is where the interest comes from. H. pylori eradication is achieved with proven antibiotic regimens and confirmed with a test of cure — an antimicrobial peptide with in vitro activity is not a substitute, and partial treatment of H. pylori is worse than none.

• IGF-1 LR3 Theorized

  The standing caution.

• Octreotide Study

  Used for acute variceal bleeding and in some upper GI bleeding contexts, and for hormone-secreting tumours of the stomach — which are neuroendocrine tumours, a different disease from gastric adenocarcinoma with a much better outlook.

Approved peptide drugs for this condition that are not in this library: No peptide treats these cancers. H. pylori eradication with antibiotics is the intervention that prevents one of them.

• Desmopressin Study

  Listed for a specific hazard. Desmopressin is approved for nocturia and reduces urine production, and nocturia is common, benign and usually treated symptomatically. But urinary symptoms are also how bladder cancer presents, and reducing urine output does not treat a tumour — it can make the frequency more tolerable while the cause goes unexamined. Anyone with visible haematuria, or unexplained microscopic haematuria over 45, needs urological assessment before symptomatic treatment. The hyponatraemia risk on its own page is a separate matter.

• Terlipressin Study

  Vasopressin analogue used in hospital for bleeding and hepatorenal syndrome, not for urological cancer. Included because the vasopressin family keeps appearing in urinary contexts and the distinction is worth keeping clear.

• ARA-290 Theorized

  Relevant for an unusual reason. Kidney cancer classically produces erythropoietin — it is a recognised cause of secondary polycythaemia, so a raised haematocrit can be a presenting sign of a renal tumour. That makes the erythropoietin axis genuinely connected to this disease, though not in a way that suggests a treatment. See the ESA boxed warning under leukaemia.

• IGF-1 LR3 Theorized

  The standing caution.

• BPC-157 Theorized

  Pro-angiogenic — and renal cell carcinoma is among the most angiogenesis-dependent cancers there is, which is why anti-angiogenic drugs are a mainstay of treating it. Also promoted for bladder and kidney “healing” with no human data.

• Semaglutide Theorized

  Obesity is an established risk factor for renal cell carcinoma, so weight reduction plausibly reduces risk. Not a treatment, and no outcome data.

• Glutathione Anecdotal

  Marketed for kidney detoxification, which describes nothing the kidney does. See chronic kidney disease.

Approved peptide drugs for this condition that are not in this library: No peptide treats either. BCG immunotherapy for bladder cancer predates modern immuno-oncology by decades and still works.

• Semax Anecdotal

  The delivery claim, examined where it matters most. Semax is promoted for brain effects on the premise that intranasal administration reaches the central nervous system. Whether it does so in humans at meaningful concentrations is unresolved — and note what the paragraph below establishes: pharmaceutical companies built purpose-designed peptide shuttles to get molecules across the blood-brain barrier, demonstrated ten-fold brain accumulation, and still missed their efficacy endpoints. Nothing here treats a brain tumour, and a compound taken for cognitive symptoms may be treating the first sign of one.

• Epitalon Theorized

  An unusually specific concern rather than a generic one. TERT promoter mutations — which switch telomerase back on — are among the most common genetic alterations in glioblastoma, present in the large majority of cases, and they are used diagnostically to classify these tumours. Epitalon is sold on a telomerase activation premise. Telomerase reactivation is not an incidental feature of this cancer; it is close to a defining one. See also leukaemia, where the only approved telomerase drug is an inhibitor.

• BPC-157 Theorized

  Pro-angiogenic — and glioblastoma is among the most vascular tumours in the body, which is why bevacizumab, an anti-VEGF antibody, is used in it. Promoting angiogenesis is the explicit opposite of one of the few systemic treatments this disease has. Also taken for headaches, which is a presenting symptom.

• IGF-1 LR3 Theorized

  IGF-1 signalling contributes to glioma proliferation and invasion in laboratory work. The standing caution.

• TB-500 Theorized

  Promotes cell migration — and diffuse infiltration into surrounding brain is precisely what makes glioma impossible to fully resect.

• Insulin & analogues Study

  Genuinely relevant. High-dose dexamethasone is used continuously to control peritumoural oedema and reliably causes hyperglycaemia, sometimes severe. As in myeloma, insulin requirements track the steroid dose rather than staying flat.

• SS-31 Theorized

  Mitochondrial framing. Not studied here.

• NAD⁺ Anecdotal

  Marketed to brain tumour patients for fatigue and cognition by infusion clinics. No evidence, and see the antioxidant caution under leukaemia regarding treatments that work through oxidative damage.

• Glutathione Anecdotal

  Same channel, same absence of evidence.

Approved peptide drugs for this condition that are not in this library: No approved peptide drug. Angiopep-2 remains the best-developed peptide shuttle across the blood-brain barrier and did not produce an approved therapy.

• BPC-157 Anecdotal

  The delayed-diagnosis risk, and it is as direct as the gastric one. BPC-157 is promoted for oral and gum healing, mouth ulcers and mucosal repair. A mouth ulcer that has not healed in three weeks is the classic presentation of oral cancer — along with a persistent white or red patch, a lump in the neck, persistent hoarseness beyond three weeks, difficulty or pain swallowing, a loose tooth with no dental cause, and numbness of the lip or tongue. These need examining, not treating. Oral cancer is visible and reachable, which makes late diagnosis particularly avoidable and particularly costly.

• KPV Theorized

  Anti-inflammatory in mucosal models, and oral mucositis during treatment is genuinely one of the worst toxicities in oncology. See the palifermin paragraph below for why a growth or repair signal in this setting is more complicated than it appears.

• GHK-Cu Theorized

  Promoted for mucosal and skin repair, including within radiotherapy fields. Nothing should be applied to skin inside a radiotherapy field without the radiation oncology team’s agreement, because some topical preparations alter surface dose. And the same tissue-growth question applies.

• IGF-1 LR3 Theorized

  The same argument as sarcoma, from the other direction. Head and neck squamous cell carcinoma is driven substantially by EGFR signalling — which is why cetuximab, an antibody that blocks the EGFR receptor, is an established treatment. Growth factor receptor signalling in this tumour is something oncology spends money trying to switch off.

• LL-37 Theorized

  Present in saliva and oral innate defence, and implicated in tumour-promoting inflammation in some models. Direction unresolved, evidence absent.

• Thymosin Alpha-1 Theorized

  Immune framing, in a cancer where immunotherapy genuinely works — but pembrolizumab works by releasing a specific brake on T-cell recognition of tumour, which is not what generic immune stimulation does.

• Semaglutide Theorized

  Two opposite considerations, and both matter. Alcohol is a major risk factor for these cancers, and there is growing evidence that GLP-1 agonists reduce alcohol consumption — alongside the smoking cessation data, that is a plausible prevention route. But during or after treatment it inverts: these patients frequently cannot eat, and malnutrition and weight loss are among the strongest predictors of a bad outcome. An appetite-suppressing drug in someone with treatment-related dysphagia is actively harmful.

• Tirzepatide Theorized

  Same reasoning both ways.

Approved peptide drugs for this condition that are not in this library: Palifermin is an approved protein for oral mucositis — in haematological malignancy, notably not in this one. Cetuximab blocks a growth factor receptor. The vaccine that prevents much of this disease is an HPV vaccine.

• IGF-1 LR3 Theorized

  This is the mechanism, and it is worth reading slowly. Mineralised bone matrix is where the body stores growth factors — TGF-beta and IGF-1 among them. When osteoclasts resorb bone they release those stored factors locally. Tumour cells in bone respond by secreting signals that recruit and activate more osteoclasts, which resorb more bone, which releases more growth factor. This is called the vicious cycle, and it is the accepted model of how bone metastasis works. The skeleton is the largest reservoir of stored IGF-1 in the body, and the entire pathology here is that reservoir feeding a tumour. It is also why bisphosphonates and denosumab help in bone metastasis without killing a single cancer cell — they work by closing the tap. Introducing an engineered IGF-1 analogue built to evade its binding proteins is the exact opposite intervention.

• Teriparatide Study

  Explicitly contraindicated, and this is the clearest contraindication in the library. Teriparatide is contraindicated in patients with bone metastases or skeletal malignancy. The reasoning follows directly from the paragraph above: an anabolic bone agent stimulates the exact bone remodelling that drives the cycle. Note how completely this inverts osteoporosis, where building bone is the goal — in malignant bone disease the objective is to suppress turnover, not stimulate it. Same skeleton, opposite strategy, and getting it the wrong way round is dangerous.

• PEG-MGF Theorized

  IGF-1 splice variant, same reservoir, same cycle.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Raises IGF-1 systemically.

• BPC-157 Anecdotal

  The delayed-diagnosis risk here has a specific and dangerous shape. This compound is promoted for bone and injury healing, and taken for exactly the sort of unexplained bone pain that bone metastasis causes. A pathological fracture is a bone that broke under a load it should have tolerated — a fracture from a minor tweak, a lift that should not have caused it, or no trauma at all. In this readership that will look like an ordinary training injury, and treating it as one is how a metastasis goes unrecognised. Bone pain that is worse at night, worse at rest, or progressive rather than mechanical is not a training injury pattern.

• TB-500 Anecdotal

  Same repair marketing, same objection, plus cell migration and angiogenesis.

• Leuprolide Study

  Approved and genuinely central in prostate cancer, which is the commonest cause of bone metastasis in men — with the caveat that androgen deprivation itself causes bone loss, so bone protection runs alongside it rather than being optional. The testosterone flare at the start of GnRH-agonist treatment matters most in exactly this population, because a surge in someone with spinal deposits can precipitate cord compression.

• ARA-290 Theorized

  Marrow infiltration causes anaemia. Read the erythropoietin boxed warning under leukaemia before reasoning from that.

• Semaglutide Theorized

  No role in the disease, and a caution: unintentional weight loss in someone with cancer is a prognostic marker, and an appetite-suppressing drug in that setting works against nutritional goals.

Approved peptide drugs for this condition that are not in this library: Denosumab is an antibody; bisphosphonates and radium-223 are not peptides. The approved peptide relevant here is leuprolide, treating the primary disease. Teriparatide is contraindicated.

• Thymosin Alpha-1 Theorized

  The most coherent rationale on this page, and still not a reason to use it. Most HPV infections are cleared by the immune system, and persistence — not infection — is what causes cancer; immunosuppressed people, including those with HIV, have far higher rates of both cervical and anal cancer. So cell-mediated immunity genuinely is the determining factor. That is an argument for treating immunosuppression where it exists and for vaccinating, not for an unstudied immune stimulant. There is no evidence it affects HPV clearance.

• LL-37 Theorized

  Antimicrobial peptide with activity in mucosal defence, and implicated both in viral clearance and in tumour-promoting inflammation depending on the model. No human evidence in HPV disease.

• KPV Theorized

  Generic anti-inflammatory action. Cervical inflammation is not the mechanism here — viral oncoprotein-driven cell cycle disruption is.

• GHK-Cu Theorized

  Appears in cosmetic and intimate-wellness marketing. Nothing should be applied to a lesion that has not been examined, and cosmetic treatment of visible anogenital lesions is how diagnosis gets delayed.

• BPC-157 Anecdotal

  The delayed-diagnosis pattern again. Bleeding after sex, between periods or after the menopause; persistent discharge; and pelvic pain are cervical cancer symptoms. Anal bleeding, pain, a lump or a non-healing ulcer are anal cancer symptoms — and they are routinely attributed to haemorrhoids or fissures, by patients and clinicians alike. That misattribution is the commonest reason anal cancer is diagnosed late. Anything taken for those symptoms without an examination first buys delay.

• Oxytocin Theorized

  No role. Included only to note the epidemiology that surrounds this area: long-term combined oral contraceptive use is associated with a modest increase in cervical cancer risk, which declines after stopping, and is substantially outweighed by its protective effect against ovarian and endometrial cancer.

Approved peptide drugs for this condition that are not in this library: No peptide is involved. The intervention that prevents these cancers is a vaccine — the second on this site, alongside hepatitis B and liver cancer.

• Octreotide Study

  Approved for GH-secreting adenomas, covered in full under acromegaly. A somatostatin analogue that suppresses GH secretion where surgery has not achieved remission — available as short-acting injection, monthly depot and an oral delayed-release capsule.

• Desmopressin Study

  Approved, and directly downstream of pituitary surgery. Transsphenoidal surgery and larger tumours can both damage the posterior pituitary or the stalk, causing arginine vasopressin deficiency — the inability to concentrate urine, with enormous urine volumes and unquenchable thirst. Desmopressin replaces the missing hormone and it is genuinely transformative. Post-operative sodium disturbance can swing in both directions in the days after surgery, which is why this is managed by an endocrine team rather than adjusted independently.

• Sermorelin Theorized

  The point of this entry for most readers. GH secretagogues drive an axis that a pituitary adenoma may already be disrupting. Anyone using them has a plausible-sounding explanation ready for exactly the symptoms a pituitary tumour causes — fatigue, low libido, headaches, mood and body-composition change — and a reason to attribute abnormal pituitary bloodwork to their compounds. See the prolactin paragraph below.

• CJC-1295 (no DAC) Theorized

  Same axis, and the DAC form produces sustained rather than pulsatile GHRH exposure — see acromegaly for why that direction matters.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Same.

• Kisspeptin-10 Theorized

  Acts upstream on the gonadotroph axis. In someone with an undiagnosed pituitary lesion, manipulating that axis adds a variable to an already confusing hormonal picture.

• Oxytocin Theorized

  A posterior pituitary hormone, included for anatomy rather than treatment. Posterior pituitary function is what surgery threatens and what desmopressin replaces.

• Tesamorelin Theorized

  GHRH analogue, same axis, approved for HIV lipodystrophy rather than anything pituitary.

• Epitalon Anecdotal

  Marketed with pineal-axis claims that are frequently muddled with pituitary function in community writing. The pineal and the pituitary are different glands doing different things, and neither claim has human data.

Approved peptide drugs for this condition that are not in this library: Octreotide, lanreotide and pasireotide are approved peptides for functioning pituitary adenomas, and desmopressin replaces what surgery can destroy. Cabergoline — the most effective of the lot — is a small molecule.

• Thymosin Alpha-1 Theorized

  This is where the compound comes from. Thymosin alpha-1 was isolated from thymosin fraction 5, a partially purified extract of bovine thymus, in work dating to the 1960s and 70s. It is a fragment of the signalling chemistry of the organ that educates T cells. So a tumour of the thymus is the closest thing in oncology to a disease of its tissue of origin — and the honest position is that nobody has studied whether administering a thymic peptide to someone with a thymic tumour, or with the immune syndromes it causes, is helpful, harmful or irrelevant. Given that thymoma produces both excessive autoimmunity and defective antibody production simultaneously, it is not even obvious which direction “help” would point in.

• TB-500 Theorized

  Same extract, same organ. Thymosin beta-4 was the other sequenced constituent to come out of thymosin fraction 5. Two of the most widely used compounds in this library trace to a single calf thymus preparation, which is a fact more people using them should know. Its own concerns — cell migration and angiogenesis — apply here as everywhere in oncology.

• LL-37 Theorized

  Implicated in autoimmune mechanisms. Thymoma is already generating autoimmunity without assistance.

• KPV Theorized

  Generic anti-inflammatory action against a specific and unusual immunological lesion.

• IGF-1 LR3 Theorized

  The standing caution.

Approved peptide drugs for this condition that are not in this library: No approved peptide. The peptides named after this organ came out of an extract of it and treat nothing about its tumours.

• Tesofensine Theorized

  The specific hazard on this page. Phaeochromocytoma secretes adrenaline and noradrenaline, and the classic presentation is episodic headache, sweating, palpitations and hypertension — which is also what a stimulant does, and therefore what an undiagnosed case looks like when the person is already taking one. Tesofensine is a triple monoamine reuptake inhibitor. Sympathomimetic drugs can precipitate a hypertensive crisis in phaeochromocytoma, and the symptoms being attributed to the compound is precisely how the tumour stays undiagnosed. Severe episodic hypertension with headache and sweating is not a side effect to titrate around.

• IGF-1 LR3 Theorized

  Unusually specific here rather than generic. Adrenocortical carcinoma characteristically overexpresses IGF-2, and the IGF axis is prominent enough in this tumour that IGF-1 receptor inhibitors were taken into clinical trials for it. This is another case, like sarcoma, where the pharmaceutical read on IGF signalling in the tumour was to try to block it.

• Octreotide Study

  Relevant through targeting rather than hormone control — see below. Somatostatin receptor expression is what makes peptide-receptor radionuclide therapy possible in metastatic paraganglioma.

• Insulin & analogues Study

  Two connections. Mitotane and adrenal insufficiency change glucocorticoid status and therefore glucose handling. And IGF-2-secreting tumours can cause non-islet-cell tumour hypoglycaemia — IGF-2 in excess acts on the insulin receptor, producing low blood sugar with suppressed insulin, which is a diagnostic clue worth knowing exists.

• BPC-157 Theorized

  Pro-angiogenic, no data, and taken for the vague fatigue and abdominal symptoms these tumours can cause.

• SS-31 Theorized

  Mitochondrial framing. Note that hereditary paraganglioma is frequently caused by mutations in succinate dehydrogenase — a mitochondrial enzyme complex — which makes this the rare case where a mitochondrial mechanism is genuinely central to the tumour. That is a reason for genetic testing, not for a mitochondrial peptide.

Approved peptide drugs for this condition that are not in this library: Lutetium-177 DOTATATE is an approved peptide-targeted radioligand used here. Iobenguane is a catecholamine analogue, not a peptide.

• Melanotan-2 Theorized

  The honest answer to a question this site should expect. Uveal melanoma arises from melanocytes in the eye — the same cell lineage as skin melanoma, and melanocortin receptors are present there. But uveal melanoma is a different disease from cutaneous melanoma: it has a distinct genetic profile, ultraviolet exposure is not its dominant cause, and it spreads characteristically to the liver. There are no case reports linking melanotan to uveal melanoma, and it would be dishonest to imply otherwise. The documented harms are cutaneous and are set out under melanoma. What is fair to say is that this compound stimulates the lineage from which both arise, and that a regular eye examination is worthwhile regardless.

• PT-141 Theorized

  Melanocortin agonist and a melanotan-II metabolite. Same lineage argument, more receptor selectivity, no ocular evidence.

• GHK-Cu Theorized

  Used topically on the face, and a caution: a persistent, bleeding, crusting or non-healing lesion — particularly on the head, neck or a sun-exposed area — should be examined rather than treated cosmetically. Merkel cell carcinoma in particular can look deceptively unremarkable.

• KPV Theorized

  Alpha-MSH fragment without melanotropic potency — see the distinction drawn under melanoma.

• IGF-1 LR3 Theorized

  The standing caution.

Approved peptide drugs for this condition that are not in this library: Tebentafusp is an engineered T-cell receptor fusion protein, not a peptide drug — but its target is a peptide, which is the point.

• Semaglutide Study

  A real labelled effect, and the honest version of what it does and does not mean. GLP-1 agonists increase the risk of gallbladder disease — gallstones and cholecystitis — through delayed gallbladder emptying and, separately, through rapid weight loss, which independently promotes stone formation. That is on the label. Gallstones and chronic gallbladder inflammation are in turn the dominant risk factor for gallbladder cancer. Do not over-read this: gallbladder cancer is rare, the interval from stones to cancer is measured in decades, and no study shows GLP-1 agonists cause it. The practical point is smaller and more useful — right upper abdominal pain on a GLP-1 needs assessing rather than assuming, because gallbladder disease is a known effect and not merely nausea.

• Tirzepatide Study

  Same class effect, same reasoning, and greater weight loss means the weight-related component is at least as relevant.

• Retatrutide Theorized

  Investigational, larger weight effects still, same expected class issue.

• Octreotide Study

  Worth knowing as a mirror image. Somatostatin analogues also cause gallstones, and for the same mechanistic reason — reduced gallbladder motility. Two entirely different peptide classes converging on the same complication through the same mechanism is a useful reminder that gallbladder emptying is under peptide hormone control, principally by cholecystokinin.

• BPC-157 Anecdotal

  Marketed for liver and digestive support. Painless jaundice — yellowing of the eyes or skin without pain — is the presentation of biliary obstruction and is a red flag, not a detox target. Pale stools, dark urine and itching accompany it. This needs imaging the same week.

• IGF-1 LR3 Theorized

  The standing caution.

• Glutathione Anecdotal

  Liver and gallbladder “flush” and detoxification marketing is heavy in this area and describes nothing physiological. See liver cancer.

Approved peptide drugs for this condition that are not in this library: No peptide treats these. Two peptide classes in this library — incretins and somatostatin analogues — both promote the gallstone disease that precedes one of them.

• Thymosin Alpha-1 Theorized

  Immune framing, in a cancer where immunotherapy genuinely works — checkpoint inhibition improved survival here. As elsewhere, releasing a specific brake on T-cell recognition is not the same as generic immune stimulation, and there is no evidence for the latter.

• BPC-157 Anecdotal

  Promoted for lung and chest symptoms. Breathlessness with a pleural effusion, or persistent chest wall pain, in anyone with a history of asbestos exposure needs investigating.

• IGF-1 LR3 Theorized

  The standing caution.

• SS-31 Theorized

  Untested.

• LL-37 Theorized

  Implicated in chronic inflammatory processes in the pleura. No evidence.

Approved peptide drugs for this condition that are not in this library: None. Asbestos control is the intervention that works, and it works before the disease rather than after.

• IGF-1 LR3 Theorized

  The standing caution, in a situation where the tumour biology is by definition not fully characterised — which makes any growth-signalling exposure a less quantifiable risk rather than a smaller one.

• BPC-157 Anecdotal

  Widely reached for. No evidence in any malignancy.

• Thymosin Alpha-1 Theorized

  Immune framing. Immunotherapy has a genuine role here where the molecular features support it — which is a specific decision made on tissue testing, not a general immune intervention.

• NAD⁺ Anecdotal

  Marketed hard to people in exactly this position. No evidence, real cost.

• Glutathione Anecdotal

  Same channel, same absence of evidence, and see the antioxidant caution under leukaemia.

• Epitalon Anecdotal

  Telomerase activation claims in an active malignancy.

Approved peptide drugs for this condition that are not in this library: Not applicable. Treatment follows the molecular profile and the clinical pattern.

• Leuprolide Study

  Androgen deprivation — the backbone of systemic treatment in hormone-sensitive advanced prostate cancer. A GnRH agonist that suppresses the axis by overstimulating it, after an initial testosterone flare that can be dangerous in metastatic bone disease.

• Octreotide Study

  Controls the hormonal syndromes of neuroendocrine tumours and, in PROMID and CLARINET, slowed tumour progression itself. Its receptor affinity is also what makes peptide receptor radionuclide therapy possible.

• Ipamorelin Theorized

  Ghrelin receptor agonism drives appetite; the ghrelin agonist anamorelin has been through cachexia trials and improved weight without clearly improving function or survival.

• ARA-290 Theorized

  Chemotherapy-induced peripheral neuropathy is the natural extension of its small-fibre neuropathy trials.

• KPV Theorized

  Oral mucositis, on an anti-inflammatory rationale.

• BPC-157 Anecdotal

  Discussed for mucositis and gut toxicity — with the angiogenesis caution above applying in full.

• Glutathione Theorized

  Studied for platinum-induced neuropathy with inconsistent results, and with a live concern that antioxidants may blunt the efficacy of some chemotherapies.

• SS-31 Theorized

  Mitochondrial protection framing.

Approved peptide drugs for this condition that are not in this library: Goserelin and triptorelin (GnRH agonists), degarelix and relugolix (antagonists, no flare), lanreotide (depot somatostatin analogue) and lutetium-177 dotatate (peptide receptor radionuclide therapy). Leuprolide and octreotide are now in this library.

• PT-141 Study

  Approved as bremelanotide (Vyleesi) for hypoactive sexual desire disorder in premenopausal women, on randomised trials. Acts centrally at melanocortin receptors. The most legitimate compound in this section by a distance.

• Melanotan-2 Theorized

  The unselective predecessor — erectile and libido effects were the observed side effect that led to PT-141 being developed as a separate drug. Carries the pigmentation, nausea and naevus concerns that PT-141 does not.

• Kisspeptin-10 Study

  Human research studies at Imperial College reported effects on sexual and attraction-related brain processing, in a research setting rather than a therapeutic one.

• Semaglutide Theorized

  Indirect: weight loss improves erectile function and testosterone in men with obesity, which is a real effect through an unglamorous route.

• Tesofensine Theorized

  Monoamine effects on libido are reported in both directions.

• Oxytocin Anecdotal

  A large consumer market in intranasal oxytocin rests on trust and intimacy claims. The most rigorous trial in the wider literature — 24 weeks in autism — found no difference from placebo, and only a small, poorly characterised fraction of a nasal dose reaches the brain.

• Leuprolide Study

  The same axis, driven the other way. Continuous GnRH exposure downregulates the pituitary receptor and shuts the axis down — used for prostate cancer, endometriosis, fibroids and central precocious puberty. Short-acting antagonists from the same family (cetrorelix, ganirelix) are standard in assisted reproduction.

• Kisspeptin-10 Study

  The most physiologically interesting entry: kisspeptin is upstream of GnRH and is the switch that starts puberty. Human research use includes triggering oocyte maturation in IVF with a lower risk of ovarian hyperstimulation than the standard trigger.

• Liraglutide Study

  Restores ovulation in PCOS through weight and insulin sensitivity. See the PCOS entry for the contraception consequence.

• Semaglutide Study

  Same, with the same pregnancy contraindication.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH has a permissive role in reproductive function; the community use is not for fertility.

• PT-141 Study

  Desire rather than fertility.

Approved peptide drugs for this condition that are not in this library: Cetrorelix and ganirelix — short-acting GnRH antagonists that prevent a premature LH surge in assisted reproduction. hCG and selective oestrogen receptor modulators where fertility is the goal.

• Kisspeptin-10 Theorized

  Drives the reproductive axis upstream of GnRH, raising LH and therefore testosterone — and testosterone aromatises to oestradiol. Anything that raises testosterone raises oestradiol too, which is the mechanism behind most compound-associated gynaecomastia and behind the entire post-cycle aromatase-inhibitor culture.

• Insulin & analogues Study

  No direct role. Relevant because obesity increases aromatase activity in adipose tissue, converting androgens to oestrogen — the same mechanism described under breast cancer and endometrial cancer. Much of what is called gynaecomastia in higher-body-fat men is partly or wholly fat rather than gland.

• Semaglutide Theorized

  Weight loss reduces aromatase activity and can improve the fatty component. It will not remove established glandular tissue, which is a fibrous structure that does not respond to weight loss — a distinction worth understanding before spending a year trying.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH-axis compounds do not directly cause gynaecomastia. Listed because they are commonly stacked with the compounds that do, which muddies attribution.

• PT-141 Theorized

  No causal role. Included because sexual dysfunction and gynaecomastia arriving together is a pattern that points at the endocrine causes below rather than at either symptom alone.

• IGF-1 LR3 Theorized

  No direct role. The standing caution applies as it does to breast tissue generally.

Approved peptide drugs for this condition that are not in this library: No approved drug treatment; tamoxifen is used off-label in early disease and surgery is definitive. The peptides relevant here are the ones that raise testosterone and therefore oestradiol.

• Oxytocin Study

  The exception that proves the rule, and it is nothing like the community use. Oxytocin is genuinely central to obstetric care — inducing and augmenting labour, and preventing and treating postpartum haemorrhage, where it saves lives. It is given intravenously by titrated infusion, in hospital, with continuous fetal monitoring, because excessive uterine stimulation can cause fetal distress and uterine rupture. Intranasal oxytocin bought for mood or bonding is a completely different proposition, and using anything that stimulates the uterus outside that setting is dangerous.

• Semaglutide Study

  Stop before conceiving, and plan the timing. GLP-1 agonists are not recommended in pregnancy — animal reproductive toxicity, no adequate human data, and the additional problem that the substantial weight loss and reduced intake they cause are not what a pregnancy needs. Manufacturers advise discontinuing in advance of a planned pregnancy, with the interval depending on the agent’s half-life; semaglutide’s is long, so the advised gap is measured in weeks to months. Fertility frequently improves with weight loss — including in PCOS — so unplanned pregnancy on these drugs is a real and recurring scenario. If you could become pregnant, use reliable contraception and discuss stopping before trying.

• Tirzepatide Study

  Same, plus a specific interaction that catches people out. Tirzepatide can reduce the effectiveness of oral contraceptives through delayed gastric emptying, and the guidance is to switch to a non-oral method or add a barrier method for four weeks after starting and after each dose increase. That is on the label and it is widely unknown.

• Leuprolide Study

  Used in fertility treatment protocols under specialist control, and otherwise contraindicated in pregnancy. Not a compound to encounter outside that setting.

• Kisspeptin-10 Theorized

  Central to reproductive physiology and studied in fertility research, including as a trigger in IVF protocols. That is a research and specialist context, not a self-directed one.

• Melanotan-2 Theorized

  Specifically inadvisable. Pregnancy already causes hyperpigmentation — melasma, linea nigra, darkening of naevi — through hormonal effects on melanocytes. Adding a melanocortin agonist compounds that, and the surveillance problem becomes worse at exactly the time when changing moles most need honest interpretation.

• IGF-1 LR3 Theorized

  Growth factor signalling during fetal development, with no safety data of any kind. The absence of studies is not reassurance.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  No pregnancy safety data. The GH axis changes substantially in pregnancy on its own, driven by placental hormones.

• BPC-157 Anecdotal

  No human pregnancy data. Widely used by people who may become pregnant without the question being raised.

Approved peptide drugs for this condition that are not in this library: Oxytocin is an approved and essential obstetric peptide, used in hospital. Nothing else in this library has established safety in pregnancy or lactation.

• Oxytocin Study

  A first-line uterotonic for prevention and treatment of postpartum haemorrhage, and approved for medically indicated induction and augmentation of labour. Carries a boxed warning stating it is not indicated for elective induction. The heat-stable analogue carbetocin extends the same benefit to settings without a reliable cold chain.

• Desmopressin Study

  Not a uterotonic. Relevant because it raises factor VIII and von Willebrand factor several-fold and is used haemostatically in mild haemophilia A and von Willebrand disease type 1 — conditions that complicate obstetric bleeding.

• Terlipressin Theorized

  Can induce uterine contractions and can cause fetal harm. It appears here as a contraindication rather than as a treatment.

Approved peptide drugs for this condition that are not in this library: Carbetocin (heat-stable oxytocin analogue). Ergometrine and carboprost are not peptides but are part of the same treatment sequence.

• Kisspeptin-10 Study

  The most important entry here, and not for the reason people expect. Kisspeptin is co-expressed with neurokinin B and dynorphin in hypothalamic KNDy neurons, which respond to oestrogen withdrawal and project to the thermoregulatory centre — the circuit that produces hot flushes. That biology produced two approved drugs, and they work by blocking the neighbouring neurokinin-3 receptor rather than by giving anyone kisspeptin.

• Teriparatide Study

  Approved for postmenopausal osteoporosis at high fracture risk, with randomised fracture-reduction data. Bone loss accelerates sharply after menopause, and this is the anabolic peptide that addresses it.

• Semaglutide Study

  The menopausal shift toward visceral fat is real and metabolically consequential. The incretin class has the largest pharmacological effect on it, with cardiovascular outcome data — though nothing in the class has been trialled specifically in a menopausal population for that indication.

• Tirzepatide Study

  Same argument, larger weight effect. Note the labelled reduction in oral contraceptive effectiveness, which matters in perimenopause where contraception is still required.

• GHK-Cu Study

  Skin thickness, collagen density and elasticity fall measurably after menopause. Topical GHK-Cu has human evidence for those endpoints — applied to skin, which is how it was studied.

• Ipamorelin + CJC-1295 (no DAC) Anecdotal

  Marketed for menopausal body composition and energy. GH secretagogues have no menopause-specific evidence, and the lean-mass-versus-function problem applies here as everywhere.

• DSIP Anecdotal

  Discussed for menopausal sleep disruption, which is a real and disabling symptom. DSIP was rejected by the PCAC and has no identified receptor.

• Epitalon Anecdotal

  Longevity framing extended to menopause by association. No data.

Approved peptide drugs for this condition that are not in this library: Fezolinetant and elinzanetant (neurokinin receptor antagonists) for vasomotor symptoms — small molecules, not peptides, but a direct product of kisspeptin/KNDy neuron biology.

• Leuprolide Study

  Approved for preoperative treatment of anaemia associated with uterine fibroids. Continuous GnRH agonism shuts the axis down, reducing fibroid volume and correcting anaemia before surgery — sometimes allowing a less invasive operation. Use is time-limited because sustained hypo-oestrogenism causes bone loss, which is what add-back therapy exists to counter.

• Kisspeptin-10 Theorized

  Upstream of the same axis, and pointing the wrong way — kisspeptin switches the axis on. Included so the direction is not confused.

• Semaglutide Theorized

  Adipose tissue is a peripheral source of oestrogen through aromatisation, so weight reduction lowers circulating oestrogen and is associated with fibroid risk in observational data. That is an indirect and unstudied route, not a treatment.

Approved peptide drugs for this condition that are not in this library: Elagolix and relugolix combination products (oral GnRH antagonists with add-back), and linzagolix — the drug class that has changed fibroid management.

• Leuprolide Study

  Approved for endometriosis. Continuous GnRH agonism suppresses ovarian oestrogen production, and randomised evidence supports reduction in pelvic pain. Used with hormonal add-back beyond about six months, because sustained hypo-oestrogenism causes bone loss — which is the limitation the newer oral antagonists were designed around.

• Semaglutide Anecdotal

  An international survey reported that a majority of respondents using a GLP-1 noted improvement in at least one endometriosis symptom and a third reported complete resolution of at least one. Read what that is: a self-selected, self-reported survey with no control group and no blinding, in a condition with fluctuating symptoms and a large placebo response. It is structured anecdote. It is also interesting enough to warrant a trial, and no trial has been run.

• Tirzepatide Anecdotal

  Appeared in the same survey. Same caveat, and the same absence of controlled data.

• Kisspeptin-10 Theorized

  Upstream of the axis and pointing the wrong way — kisspeptin switches the reproductive axis on, and endometriosis treatment works by switching it off. Included so the direction is not confused.

• BPC-157 Anecdotal

  Discussed for adhesions and post-surgical recovery. No evidence in endometriosis, and a pro-angiogenic agent in a condition where lesion neovascularisation is part of the pathology is not an obviously neutral choice.

• TB-500 Anecdotal

  Same adhesion rationale, same absence of evidence, and the same angiogenesis question.

• KPV Theorized

  Endometriosis has a genuine inflammatory component, and a generic anti-inflammatory is a generic answer to it. No endometriosis data.

Approved peptide drugs for this condition that are not in this library: Elagolix, relugolix combination and linzagolix — oral GnRH antagonists with add-back, the drug class that changed endometriosis management.

• Desmopressin Study

  Approved for nocturia due to nocturnal polyuria and for primary nocturnal enuresis — a V2-selective vasopressin analogue that concentrates urine. Carries a boxed warning for hyponatraemia on the nocturia formulations, and fluid restriction around dosing is part of the treatment rather than advice attached to it.

• BPC-157 Theorized

  Urothelial protection in rodent models; the community use is for the epithelial-barrier rationale.

• KPV Theorized

  Anti-inflammatory.

• ARA-290 Theorized

  The neuropathic component of chronic pelvic pain.

• LL-37 Theorized

  Relevant to recurrent urinary tract infection rather than interstitial cystitis, and elevated cathelicidin is part of the inflammatory picture rather than a treatment for it.

• Semaglutide Study

  SUSTAIN-6 in diabetes and SELECT in obesity without diabetes both reported reduced major adverse cardiovascular events. STEP-HFpEF reported symptom and function improvement in heart failure with preserved ejection fraction and obesity.

• Liraglutide Study

  LEADER reported reduced cardiovascular death.

• Dulaglutide Study

  REWIND, notable for a largely primary-prevention population.

• Tirzepatide Study

  SUMMIT reported benefit in HFpEF with obesity. SURPASS-CVOT ran against dulaglutide rather than placebo and demonstrated non-inferiority on three-point MACE rather than superiority, with improvements in renal function and all-cause mortality. SURMOUNT-MMO, the morbidity and mortality trial in obesity without diabetes, is not expected until 2027.

• SS-31 Study

  Human trials in heart failure and in mitochondrial myopathy; the cardiolipin-stabilisation rationale is aimed directly at cardiac mitochondrial dysfunction.

• MOTS-c Theorized

  Metabolic and mitochondrial framing; animal data only.

• BPC-157 Theorized

  Rodent cardioprotection studies.

• ARA-290 Theorized

  Tissue protection in ischaemia-reperfusion models.

• Tesofensine Theorized

  Listed for the opposite reason — the blood-pressure and heart-rate increase is why its development stalled.

• Melanotan-2 Theorized

  Melanocortin agonism can raise blood pressure.

• Retatrutide Theorized

  Dose-dependent heart-rate increases were visible in phase 2, and no cardiovascular outcome trial has reported.

Approved peptide drugs for this condition that are not in this library: Nesiritide (recombinant B-type natriuretic peptide). Terlipressin is now in this library — see chronic kidney disease.

• Semaglutide Study

  Lowers blood pressure modestly and reliably, largely through weight loss — a few millimetres of mercury, which is a real effect and not a treatment for hypertension. The class has separate cardiovascular outcome benefit that does not depend on the blood pressure change.

• Tirzepatide Study

  Same, with larger weight loss and correspondingly larger blood pressure reduction.

• Tesofensine Theorized

  The opposite direction, and it matters. Monoamine reuptake inhibition raises heart rate and blood pressure — that is a predictable pharmacological consequence, not an idiosyncratic side effect. Anyone with uncontrolled hypertension is the wrong person for a sympathomimetic weight-loss agent. See adrenal tumours for the rarer hazard.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  Fluid retention is the GH-axis effect people underestimate. Growth hormone causes sodium and water retention through the renal tubule, which is why oedema, joint stiffness and carpal tunnel symptoms are the classic dose-limiting effects. Fluid retention raises blood pressure. Acromegaly — the pathological far end of this axis — causes hypertension in a large proportion of patients.

• Tesamorelin Theorized

  Same axis, same fluid effect, approved indication elsewhere.

• Desmopressin Study

  Causes water retention by design, which is the mechanism behind its hyponatraemia risk. In someone with hypertension or heart failure that is a meaningful consideration rather than a footnote.

• Terlipressin Study

  A vasoconstrictor used in hospital. Listed to keep the vasopressin family straight: this one raises blood pressure deliberately.

• BPC-157 Theorized

  Rodent work reports blood-pressure-modulating effects in both directions depending on model. No human data, and nothing here justifies substituting it for treatment that prevents strokes.

• NAD⁺ Anecdotal

  Marketed for vascular health. No controlled evidence on blood pressure or outcomes.

Approved peptide drugs for this condition that are not in this library: Sacubitril inhibits the enzyme that degrades natriuretic peptides — the peptides are endogenous. Everything else is a small molecule or an siRNA.

• Semaglutide Study

  Improves lipids modestly, mostly via weight loss — lower triglycerides, small LDL reduction. The class has cardiovascular outcome benefit, but it is not a lipid drug and does not replace one.

• Tirzepatide Study

  Larger weight effect, larger triglyceride reduction. Same caveat.

• 5-Amino-1MQ Theorized

  NNMT inhibition with metabolic claims in rodents. No human lipid data.

• SLU-PP-332 Theorized

  Exercise-mimetic framing from rodent work. No human data of any kind.

• MOTS-c Theorized

  Metabolic framing, association studies in humans, no intervention outcome data.

• Tesamorelin Study

  Genuinely relevant: it reduces visceral adipose tissue and lowers triglycerides in HIV-associated lipodystrophy, which is an approved indication. It also modestly raises glucose.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH affects lipolysis and lipid profiles, in ways that are dose- and context-dependent and have never been tied to cardiovascular outcomes.

• NAD⁺ Anecdotal

  Distinguish carefully: niacin — nicotinic acid, a different molecule — raises HDL substantially and was tested in two large outcome trials, AIM-HIGH and HPS2-THRIVE, which showed no benefit and meaningful harm. That is one of the cleanest demonstrations that raising HDL is not the same as helping, and it is worth knowing before reasoning from any NAD-family compound to cardiovascular benefit.

Approved peptide drugs for this condition that are not in this library: PCSK9 inhibitors are antibodies; inclisiran and the Lp(a) agents are nucleic acid therapeutics. No peptide drug treats dyslipidaemia.

• IGF-1 LR3 Theorized

  No direct thrombotic mechanism established. Included because it sits in stacks alongside the compounds that do matter here.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  GH-axis fluid shifts do not raise haematocrit the way androgens do. The concern on this page is androgenic, not somatotropic.

• ARA-290 Theorized

  Directly relevant by design. ARA-290 was engineered from erythropoietin specifically to keep tissue protection without stimulating red cell production — because erythropoietin’s haematopoietic effect is what caused thrombotic harm when erythropoiesis-stimulating agents were pushed to higher haemoglobin targets. That history is set out under leukaemia, and it is the whole reason this compound exists in the form it does.

• Desmopressin Study

  The opposite direction and an approved use: it improves haemostasis in bleeding disorders and in uraemic platelet dysfunction — see chronic kidney disease. Relevant here for keeping the two directions distinct.

• Semaglutide Theorized

  Weight loss reduces venous thromboembolism risk over time. Also relevant acutely: any period of immobility, including after surgery, raises risk, and rapid weight loss is a reason people have surgery.

• BPC-157 Theorized

  Pro-angiogenic in animal models. No established effect on coagulation, and no human data either way.

• Melanotan-2 Anecdotal

  No coagulation mechanism. Listed because it is commonly stacked with androgens, and the androgens are the issue.

Approved peptide drugs for this condition that are not in this library: Anticoagulants are small molecules; erythropoiesis-stimulating agents are glycoproteins. Desmopressin is the approved peptide here, and it works in the opposite direction.

• Semaglutide Study

  Indirect but real. Obesity and sleep apnoea are both major drivers of atrial fibrillation, and weight loss reduces the burden of atrial fibrillation and improves the success of rhythm control — shown in dedicated weight-management trials. That makes this one of the better-supported indirect roles for the class.

• Tirzepatide Study

  Separately approved for obstructive sleep apnoea, which is the other major modifiable driver.

• Tesofensine Theorized

  Sympathomimetic. Raising catecholaminergic tone is a recognised trigger for atrial fibrillation, as are stimulants generally.

• Ipamorelin + CJC-1295 (no DAC) Theorized

  No direct arrhythmic mechanism. The relevance is via fluid retention and blood pressure, and via acromegaly, where sustained GH excess causes cardiomyopathy and arrhythmia.

• NAD⁺ Anecdotal

  Marketed for heart health. Note that infusion clinics deliver these preparations quickly enough to cause palpitations, which are then attributed to the compound working.

• BPC-157 Theorized

  No cardiac evidence. Palpitations are a symptom to investigate, not to self-treat.

Approved peptide drugs for this condition that are not in this library: No peptide is involved. Anticoagulants, rate and rhythm drugs and ablation are the treatments.

• Semaglutide Study

  Randomised evidence, and it is good. STEP-HFpEF randomised 529 people with heart failure with preserved ejection fraction and obesity to semaglutide 2.4 mg or placebo for 52 weeks. Symptom and physical-limitation scores improved by 16.6 points against 8.7 on placebo, weight fell 13.3%, C-reactive protein fell 43.5%, and NT-proBNP — the natriuretic peptide used to diagnose and stage the condition — fell too. Obesity-related HFpEF is a phenotype where this class is now genuinely part of the answer.

• Tirzepatide Study

  The SUMMIT trial tested tirzepatide in HFpEF with obesity and reported reduced risk of worsening heart failure events alongside improved symptom scores. Same phenotype, same direction, consistent picture.

• SS-31 Study

  Tested here, and it missed. Mitochondrial dysfunction in failing myocardium is one of the better-supported rationales for elamipretide anywhere, and it was taken into human heart failure trials on that basis. It did not deliver on its primary endpoints — which, with the mitochondrial myopathy results, makes this a compound with a genuinely serious mechanism and a consistently disappointing trial record.

• MOTS-c Theorized

  Mitochondrial-derived peptide with cardioprotective signalling in rodents. Nothing human.

• Humanin Theorized

  Same family, cardioprotective in cell and animal models, no human intervention data.

• BPC-157 Anecdotal

  Community cardiac-repair claims extrapolated from rodent soft-tissue models. Its pro-angiogenic action is not obviously desirable in a condition managed partly with anti-remodelling drugs, and nobody promoting it has studied that question.

• IGF-1 LR3 Theorized

  Induces cardiomyocyte hypertrophy. Note carefully that pathological cardiac hypertrophy is a mechanism of heart failure, not a treatment for it — this is the mass-is-not-function problem in the organ where it matters most.

• NAD⁺ Anecdotal

  Myocardial NAD+ depletion is documented in failing hearts. That infused NAD+ corrects it or changes outcomes is not.

• GHK-Cu Anecdotal

  Remodelling claims from dermal and wound models. Cardiac remodelling is a different process and largely an undesirable one.

Approved peptide drugs for this condition that are not in this library: Sacubitril/valsartan works on the natriuretic peptide system without being a peptide. Nesiritide was the peptide, and it did not survive its outcomes trial.

• Desmopressin Study

  The one compound in this library with a randomised result in POTS — and the reason it is not used routinely is on its own page. In a randomised crossover study of 30 patients, a single 0.2 mg oral dose significantly reduced standing heart rate (101.9 against 109.2 beats per minute) and improved symptoms. The mechanism is straightforward: POTS involves relative hypovolaemia, and desmopressin causes water retention. The investigators concluded the safety profile would need examining before routine use — which is the hyponatraemia risk that carries a boxed warning on the nocturia formulations. An acute single-dose result is not a treatment.

• Terlipressin Theorized

  Same hormone family, opposite receptor emphasis — V1 vasoconstriction rather than V2 water retention. Listed because the vasopressin system is genuinely relevant to orthostatic physiology, not because this hospital intravenous drug has any place here.

• SS-31 Theorized

  Where POTS accompanies ME/CFS, the mitochondrial hypothesis is imported wholesale. Its own trial record argues against expecting much.

• MOTS-c Theorized

  Same imported rationale, weaker evidence.

• NAD⁺ Anecdotal

  Marketed to this population by infusion clinics. Worth noting the confound: an intravenous infusion delivers a litre of saline, and volume expansion is an established POTS treatment in its own right. Someone feeling better after an NAD+ drip may be responding to the fluid, which is available far more cheaply and without the rest of it.

• Thymosin Alpha-1 Theorized

  Autoimmune and post-infectious mechanisms are live hypotheses in POTS, including autoantibodies against adrenergic receptors. Pushing immune tone in an unspecified direction is not obviously the answer to that.

• BPC-157 Anecdotal

  Discussed in dysautonomia communities. No evidence.

Approved peptide drugs for this condition that are not in this library: None. No drug is approved for POTS in the US, UK or EU — everything used is off-label.

• Semaglutide Study

  Genuine renal outcome data, which almost nothing here has. The FLOW trial reported reduced risk of kidney disease progression and of kidney and cardiovascular death in people with type 2 diabetes and chronic kidney disease. That is a hard-outcome renal trial, not a surrogate, and it is why this class now appears in kidney guidelines rather than only in diabetes ones.

• Exenatide Study

  Listed for the contraindication rather than the benefit. Unlike the rest of the class it is renally cleared to a degree that matters, and it is not recommended below an eGFR of 30. Assuming class-wide safety is exactly the error this entry exists to prevent.

• Insulin & analogues Study

  The most under-appreciated interaction in this section. Insulin is cleared by the kidney, so as kidney function falls insulin requirements fall with it and hypoglycaemia risk rises. Someone whose control was stable for years can start having hypos without changing anything they do. The dose needs revisiting as eGFR declines, and this is a well-recognised clinical trap.

• Desmopressin Study

  An established use most people do not know about. Uraemia causes platelet dysfunction and a bleeding tendency, and desmopressin improves haemostasis in that setting by releasing von Willebrand factor — used around procedures in people with advanced kidney disease. Note the mirror image of its risk: the same water retention that makes it useful for nocturia is more dangerous in kidney disease, where the ability to excrete a water load is already impaired.

• Terlipressin Study

  Approved in September 2022 as the first US treatment for hepatorenal syndrome — kidney failure in a structurally normal kidney, driven by splanchnic vasodilation elsewhere. A hospital drug with a boxed warning for serious or fatal respiratory failure.

• ARA-290 Theorized

  The most mechanistically interesting entry here. It is derived from the region of erythropoietin responsible for tissue protection rather than red cell production — a deliberate attempt to keep erythropoietin’s protective effects without the thrombotic and cardiovascular risks that made high-dose ESAs harmful in kidney disease. That is a serious idea. It has no renal trial, and its developer appears to have wound down.

• SS-31 Study

  Reached human trials on a mitochondrial-protection rationale, including in renal contexts. Its record across three randomised trials in other indications is of missed primary endpoints.

• Teriparatide Theorized

  Relevant to CKD mineral and bone disorder, and a caution rather than a suggestion: bone disease in advanced kidney disease is not simply osteoporosis, adynamic bone disease is common, and PTH-analogue therapy in that setting is a specialist decision requiring bone-turnover assessment.

• BPC-157 Theorized

  Rodent nephroprotection in toxic-injury models. No human data.

• MOTS-c Theorized

  Metabolic framing, no renal outcome data.

• Glutathione Anecdotal

  Marketed for kidney detoxification, which is not a description of anything the kidney does or of anything chronic kidney disease is.

Approved peptide drugs for this condition that are not in this library: Etelcalcetide is an approved peptide for a CKD complication. Erythropoiesis-stimulating agents are glycoproteins. The drugs that slow progression — SGLT2 inhibitors, ACE inhibitors, finerenone — are small molecules.

• Semaglutide Theorized

  The one entry here with a coherent rationale. Obesity-associated asthma is a recognised phenotype — typically neutrophilic rather than eosinophilic, poorly responsive to inhaled corticosteroids, and it improves with weight loss. Observational work suggests GLP-1 agonists reduce exacerbations in people with obesity and asthma. That is a metabolic route to a respiratory benefit, and it is not an asthma drug.

• Tirzepatide Theorized

  Same phenotype, same reasoning, larger weight effect. It is separately approved for obstructive sleep apnoea, which frequently coexists with asthma and worsens control when untreated.

• Thymosin Alpha-1 Theorized

  A more interesting direction problem than usual. Allergic asthma is Th2-driven and this compound promotes Th1 responses, so the direction is arguably favourable here — unlike in lupus or rheumatoid arthritis. It has never been tested in asthma, and “plausible direction” is where this library draws the line between interesting and useful.

• LL-37 Theorized

  Cathelicidin has a genuine role in airway innate defence and is also elevated in chronic airway inflammation, so the direction of the argument is unclear. It is also a mast cell activator, which is not what anyone wants in an airway that already over-reacts.

• KPV Theorized

  Alpha-MSH fragment with anti-inflammatory action in rodent models, including some airway work. Generic anti-inflammatory action is not the same as controlling type 2 airway inflammation, which is what the drugs below do specifically.

• GHK-Cu Theorized

  Carried over from the emphysema gene-signature work described under COPD. Airway remodelling in asthma is a different process from alveolar destruction, and there is nothing in asthma.

• BPC-157 Anecdotal

  No mechanism in the airway, no data, and it appears in general wellness discussion.

Approved peptide drugs for this condition that are not in this library: The asthma biologics are monoclonal antibodies against cytokines and IgE, not peptide drugs. Inhaled corticosteroids and bronchodilators are small molecules.

• GHK-Cu Theorized

  A 2012 study identified 127 genes associated with emphysema severity and used a connectivity-map search to find compounds predicted to reverse that signature. GHK came out of it, and the prediction held up in vitro: COPD-patient lung fibroblasts that had lost the ability to contract and remodel collagen regained it at 10 nM. A real result in the relevant human cells — and several long steps from treating a person.

• SS-31 Theorized

  Mitochondrial dysfunction in airway and muscle tissue is one component of the COPD picture. No respiratory trial.

• Thymosin Alpha-1 Theorized

  Immunomodulation framing, in a disease driven by exacerbations that are frequently infective. No COPD evidence.

• LL-37 Theorized

  Cathelicidin has a real role in airway innate defence, and is also elevated in chronic airway inflammation — which complicates the direction of the argument.

• IGF-1 LR3 Theorized

  Expected to make acne worse, not better. IGF-1 drives sebocyte lipogenesis and amplifies androgen signalling in the sebaceous gland — it is a substantial part of why high-glycaemic and dairy-heavy diets are associated with acne, and why skin changes feature in acromegaly. Raising IGF-1 systemically is acting on acne pathogenesis from the wrong end.

• Ipamorelin + CJC-1295 (no DAC) Anecdotal

  GH secretagogues raise IGF-1, which is the same mechanism one step upstream. Acne appearing or worsening on a GH protocol is commonly reported and is exactly what the biology predicts.

• Melanotan-2 Theorized

  Melanocortin receptors sit on sebocytes: MC5R is expressed specifically in differentiating, lipid-laden sebaceous cells and drives sebum production, and MC1/MC5 antagonists reduce sebaceous differentiation. Non-selective melanocortin agonism would therefore be expected to increase sebum. A small report of an alpha-MSH analogue benefiting acne exists, so the direction is not fully settled — but the sebotropic mechanism is established.

• KPV Theorized

  The anti-inflammatory C-terminal fragment of alpha-MSH, truncated to remove the melanocortin receptor activity above. Topical anti-inflammatory action is the rationale; there is no acne trial.

• GHK-Cu Theorized

  Relevant to post-inflammatory scarring and remodelling rather than to active acne. Topical, where the evidence is.

• LL-37 Theorized

  Cathelicidin is part of the inflammatory response to C. acnes in the follicle. Elevated rather than deficient here, which makes administering more of it a poor idea — see the rosacea and psoriasis entries for the same pattern.

• Semaglutide Theorized

  Indirect and plausible: hyperinsulinaemia raises free androgens and IGF-1 bioactivity, so improving insulin sensitivity should reduce that drive. Relevant mainly where acne accompanies PCOS or insulin resistance. No acne trial.

• LL-37 Theorized

  This is the entry that matters, and it runs opposite to every other LL-37 claim in this library. Cathelicidin and beta-defensin expression is significantly decreased in atopic dermatitis lesions compared with psoriasis, and that deficiency is thought to account for the characteristic susceptibility to Staphylococcus aureus colonisation and infection. So atopic dermatitis is the one skin condition where the antimicrobial peptide is genuinely missing — which makes it the only place a cathelicidin argument is even facing the right way. It has still never been tested, and the compound is a T-cell autoantigen in psoriasis, so this is a narrow window rather than an endorsement.

• KPV Theorized

  Alpha-MSH fragments have well-described anti-inflammatory activity in skin, and topical application to inflamed skin is the version that makes pharmacological sense. Preclinical only.

• GHK-Cu Theorized

  Barrier and matrix effects; the human evidence is cosmetic rather than in dermatitis.

• Thymosin Alpha-1 Theorized

  Immune modulation in a Th2-driven condition, in a compound whose approved uses all involve enhancing immune response. The direction question applies here as in every autoimmune and immune-mediated entry.

• BPC-157 Anecdotal

  Sold on gut-barrier and gut-skin-axis reasoning. No evidence in atopic dermatitis.

• GLOW Anecdotal

  Marketed for skin generally. Nothing in it has been studied in dermatitis, and injecting a copper peptide for a barrier problem is not the route the evidence uses.

Approved peptide drugs for this condition that are not in this library: Dupilumab, tralokinumab and lebrikizumab are monoclonal antibodies rather than peptides, but they are the drugs that changed this condition.

• LL-37 Theorized

  A specific reason to avoid it, not a reason to try it. LL-37 is overexpressed in psoriatic lesions, where it does two distinct things: it complexes with self-DNA from dying cells and converts it into a potent stimulus for plasmacytoid dendritic cells through TLR7 and TLR9, driving type I interferon and breaking tolerance to self-DNA — and it acts as a T-cell autoantigen in its own right, presented by HLA-C*06:02. Anyone with psoriasis or a family history has a specific reason to avoid administering more of it.

• Thymosin Alpha-1 Theorized

  An immune-enhancing agent in a disease treated by suppressing the IL-23/IL-17 axis. The direction is wrong, and anyone on a biologic should treat this as an interaction question for their dermatologist.

• KPV Theorized

  Anti-inflammatory, which is at least the right direction. Generic rather than psoriasis-specific, and untested.

• GHK-Cu Theorized

  Matrix remodelling. No psoriasis evidence, and the barrier problem here is secondary to the immune one.

• Semaglutide Theorized

  Indirect but genuine: obesity worsens psoriasis severity and reduces response to systemic treatment, and weight loss has been associated with improvement. That is a real relationship acting through the metabolic route rather than a skin-directed one.

• Epitalon Anecdotal

  Appears in longevity-adjacent skin claims. No data.

Approved peptide drugs for this condition that are not in this library: The anti-TNF, anti-IL-17 and anti-IL-23 biologics are monoclonal antibodies; apremilast and deucravacitinib are small molecules. None is a peptide, and together they are the reason this condition is now controllable.

• LL-37 Theorized

  This is the mechanism of the disease, not a candidate treatment — and here the case is tighter than in psoriasis or lupus. In rosacea-affected skin the protease kallikrein 5 is elevated, and KLK5 is the enzyme that cleaves the inactive precursor hCAP18 into active LL-37. The result is raised LL-37 and abnormal LL-37 fragments in lesional skin, and those peptides directly drive the vascular changes and inflammatory cell recruitment that are rosacea. In animal work, LL-37 injected into skin produces rosacea-like lesions — and it fails to do so in mast-cell-deficient mice, which is how mast cells were established as essential to the mechanism. Several existing rosacea treatments are thought to work partly by reducing this pathway. Administering LL-37 to someone with rosacea is giving them more of the molecule the disease is made of.

• KPV Theorized

  Anti-inflammatory alpha-MSH fragment, and the direction is at least correct. No rosacea evidence, and the approved topicals below are specific and effective.

• GHK-Cu Theorized

  Widely used in facial skincare, including by people with rosacea who do not know they have it. Rosacea-prone skin has an impaired barrier and reacts badly to a great many actives, and the practical harm is usually irritation rather than anything mechanistic — stinging and burning from products is one of the most common complaints in this condition.

• Melanotan-2 Theorized

  Flushing is a well-recognised effect of melanocortin agonists, and flushing is the cardinal feature of rosacea. Whether that provokes the condition is unstudied; that it will confuse the picture is not in doubt.

• PT-141 Theorized

  Same family, and facial flushing is among its commonest reported effects.

• BPC-157 Anecdotal

  Promoted for skin healing. No mechanism reaching the vascular and innate-immune processes at work here.

• Semaglutide Theorized

  No direct role. Worth knowing that rapid facial fat loss changes facial appearance and can make underlying redness and vessels more visible — which is a different problem from developing rosacea.

Approved peptide drugs for this condition that are not in this library: Ivermectin, metronidazole, azelaic acid, brimonidine and doxycycline are the approved treatments. None is a peptide — and the peptide in this library is on the disease side of the equation.

• Melanotan-2 Theorized

  The honest position, and it cuts both ways. Melanocortin agonists stimulate melanocytes, and vitiligo is a disease of melanocyte loss — so unlike almost every other use, the mechanism is at least pointed at the problem. But the melanocytes in a vitiligo patch have been destroyed, and stimulating what is not there does nothing. Repigmentation depends on melanocytes migrating in from hair follicles and lesional borders, which is why the treatments below combine stimulation with immune suppression and light. The predictable result of using melanotan with vitiligo is that unaffected skin darkens while the patches do not — increasing the contrast and making the condition look worse. The melanoma surveillance harms apply regardless.

• PT-141 Theorized

  Melanocortin agonist and a melanotan-II metabolite. Focal hyperpigmentation is a recognised effect; it is not a vitiligo treatment.

• KPV Theorized

  An alpha-MSH fragment without melanotropic potency — so it lacks the one property that would be relevant here. Its anti-inflammatory action is at least aimed at the right side of an autoimmune disease, and there is no evidence.

• Thymosin Alpha-1 Theorized

  Immune stimulation in an autoimmune disease driven by CD8 T cells attacking melanocytes. The direction problem, and here it is unambiguous.

• GHK-Cu Theorized

  Skin-remodelling claims. No effect on pigmentation or on the autoimmune process.

• LL-37 Theorized

  Implicated in autoimmunity broadly, as in rosacea, psoriasis and lupus.

Approved peptide drugs for this condition that are not in this library: Topical ruxolitinib is the approved repigmentation treatment. Afamelanotide is an approved melanocortin peptide — for a different condition — studied here only as an adjunct to phototherapy.

• LL-37 Theorized

  A direct mast cell activator, which is how it produces the skin inflammation described under rosacea — LL-37 fails to generate those lesions in mast-cell-deficient animals. In a condition defined by inappropriate mast cell degranulation, that is the wrong molecule to add.

• KPV Theorized

  Anti-inflammatory alpha-MSH fragment; alpha-MSH has documented effects on mast cells and cutaneous inflammation, so the direction is defensible. No human urticaria evidence, and antihistamines are cheap, safe and effective.

• KLOW Theorized

  Blends are worth naming here for a practical reason: if you react to a multi-component product, you cannot tell which component you reacted to, which makes future avoidance guesswork.

• BPC-157 Theorized

  Injection site reactions are common with many injectables and are usually local irritation rather than allergy. The distinction that matters is local versus systemic — a weal at the site is one thing; hives elsewhere on the body, lip or tongue swelling, or wheeze is another entirely, and means stop and seek help. See injection safety.

• Melanotan-2 Theorized

  Flushing and localised reactions are commonly reported and commonly dismissed. Persistent or spreading reactions deserve more attention than they usually get.

• Semaglutide Theorized

  Injection site reactions occur and are usually mild. Genuine hypersensitivity to any injectable is possible and is a reason to stop and take advice rather than push through.

Approved peptide drugs for this condition that are not in this library: Antihistamines and omalizumab, an antibody. No peptide treats urticaria — and LL-37 activates the cell that causes it.

• BPC-157 Anecdotal

  Reached for because the lesions look like wounds that will not heal. They are not failing to heal — they are being continuously regenerated by an immune process, which is why repair-focused approaches do not work and why immunological treatment does. Injecting into or near actively inflamed, frequently colonised lesions is also a poor idea.

• LL-37 Theorized

  Cathelicidin is dysregulated in hidradenitis lesional skin, which places it alongside rosacea and psoriasis as a condition where this peptide is part of the pathology.

• KPV Theorized

  Anti-inflammatory in models. The direction is right; the effective treatments target specific cytokines rather than inflammation generally.

• Semaglutide Theorized

  Genuinely relevant, though not a treatment. Obesity and smoking are the two strongest modifiable factors in hidradenitis, and weight loss reduces severity and friction in the affected skin folds. Observational reports suggest improvement in people started on GLP-1 agonists for other reasons. Unrandomised, and worth pursuing alongside proper treatment rather than instead of it.

• GHK-Cu Theorized

  Scarring and tunnel formation are prominent, which is where the interest comes from. Established tunnels are structural and are addressed surgically, not by topical remodelling.

• Thymosin Alpha-1 Theorized

  Immune stimulation in an inflammatory skin disease treated with immune suppression. The direction problem.

Approved peptide drugs for this condition that are not in this library: Adalimumab, secukinumab and bimekizumab are approved biologics — antibodies, not peptides. No peptide drug treats it.

• LL-37 Theorized

  Present in airway secretions and part of innate defence, and also a mast cell activator. As in urticaria, that is the wrong direction in an allergic condition.

• KPV Theorized

  Anti-inflammatory in models, including some mucosal work. No human allergic rhinitis evidence, and the approved treatments are cheap and highly effective.

• Thymosin Alpha-1 Theorized

  Allergic disease is a Th2-skewed condition and this compound promotes Th1 responses, so the direction is arguably favourable — the same argument set out under asthma. It has never been tested, and “plausible direction” is not evidence.

• Semaglutide Theorized

  No role. Included because untreated rhinitis worsens asthma control and sleep-disordered breathing, both of which this class does affect.

• BPC-157 Anecdotal

  No mechanism, no evidence, and nasal symptoms lasting more than a few weeks on one side only need examining rather than treating.

Approved peptide drugs for this condition that are not in this library: Intranasal corticosteroids, antihistamines and allergen immunotherapy. Omalizumab is an antibody. No peptide is involved.

• GHK-Cu Theorized

  Reported to stimulate dermal papilla cell proliferation, with some 5-alpha reductase inhibitory activity in vitro. Small studies and mechanism only. Copper peptides are a large commercial hair-care category, which is a reason for more scepticism about the claims rather than less.

• IGF-1 LR3 Theorized

  IGF-1 signalling is genuinely involved in the follicular growth phase. Using an unregulated systemic IGF-1 analogue for hair is a poor trade against the oncology caution.

• GLOW Anecdotal

  Discussed for skin and hair together on the strength of its GHK-Cu content — the component whose evidence is topical.

• Melanotan-2 Anecdotal

  Affects hair and skin pigmentation, not hair density. Included because the two get conflated.

• Thymosin Alpha-1 Theorized

  Raised in the context of alopecia areata, which is an autoimmune condition and a different disease from androgenetic alopecia. No evidence in either.