Research information only. PrecisePep is an educational library. It is not medical advice and is not intended to assist, encourage or enable self-administration. The compounds documented here are research chemicals — most are not approved for human use. Read the full disclaimer.
PrecisePep/Peptide Library/Octreotide
Hormone Suppression & Oncology
Sandostatin® · Sandostatin LAR® · Bynfezia® · Mycapssa® · SMS 201-995
The mirror image of everything else in the growth-hormone section of this library. Eight residues that suppress GH rather than release it — and the drug that made somatostatin clinically usable at all.
Every growth-hormone compound elsewhere in this library is trying to push the axis up. Octreotide exists to push it down, and looking at the two side by side is the fastest way to understand what the GH axis actually is.
Somatostatin is the brake. It is released by the hypothalamus and by cells throughout the gut and pancreas, and it inhibits growth hormone, insulin, glucagon, gastrin, secretin, and most of the rest of the gastroenteropancreatic hormone repertoire. Its problem as a drug is a two-minute half-life. Octreotide is a cyclic eight-residue analogue with D-amino acid substitutions that resist enzymatic degradation, extending that to well over an hour — and unlike native somatostatin, it is selective, hitting SSTR2 strongly rather than suppressing everything indiscriminately.[1]
That gave it two clinical lives. In acromegaly — growth hormone excess from a pituitary adenoma — it suppresses GH and IGF-1 where surgery has not been curative. In neuroendocrine tumours, which frequently overexpress SSTR2, it controls the hormonal syndromes those tumours produce and, in the PROMID and CLARINET trials, slowed tumour progression itself.[2] The same receptor affinity also made somatostatin analogues the targeting mechanism for radionuclide imaging and therapy in these tumours.
Octreotide is a prescription medicine and this page publishes no unsupervised dosing for it. It is here because the conditions index names neuroendocrine tumours and acromegaly, and because it is the most instructive counterweight on the site to the GH secretagogue pages. Acromegaly is what chronically elevated growth hormone actually looks like — and it is treated by a peptide that does the opposite of ipamorelin and CJC-1295.
SSTR2-selective agonism. Five somatostatin receptor subtypes exist. Octreotide binds SSTR2 with high affinity, SSTR5 moderately, and the others weakly. Native somatostatin binds all five — the selectivity is what makes octreotide tolerable as a chronic therapy rather than a blunt shutdown of every secretory axis at once.
Inhibition of hormone release. Receptor activation reduces adenylate cyclase activity and calcium influx in secretory cells, suppressing growth hormone from somatotrophs, and serotonin, gastrin, VIP, insulin and glucagon from gut and pancreatic sources.
Antiproliferative effects. In neuroendocrine tumours, SSTR2 activation additionally engages phosphotyrosine phosphatases and cell-cycle arrest pathways. This is the mechanistic basis for the progression-free survival benefit seen in PROMID and CLARINET, which is distinct from symptom control.[2]
Why gallstones follow. Somatostatin receptor activation inhibits cholecystokinin release and reduces gallbladder contractility. A gallbladder that empties poorly concentrates bile and forms stones. This is not an idiosyncratic reaction — it is the predictable consequence of the drug working.[3]
Why blood glucose moves in both directions. It suppresses insulin and glucagon simultaneously. Which effect dominates depends on the patient, which is why glucose can rise in some people and fall in others on the same drug.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Suppresses growth hormone and normalises IGF-1 in a substantial proportion of patients with acromegaly, used where transsphenoidal surgery has not achieved remission or is not appropriate. Tumour shrinkage occurs in a minority.
Reduces flushing and diarrhoea driven by serotonin and vasoactive peptide secretion from metastatic neuroendocrine tumours — often the difference between a manageable and an intolerable disease burden.
The PROMID and CLARINET trials reported prolonged progression-free survival with somatostatin analogues in midgut and enteropancreatic neuroendocrine tumours — an antitumour effect separate from symptom control.
A labelled indication in a rare and otherwise refractory condition.
The LAR intramuscular depot converts a three-times-daily injection into a monthly one. An oral delayed-release formulation is also approved for maintenance in acromegaly in patients who have responded to injectable therapy.
SSTR2 affinity is what makes somatostatin-analogue-based imaging and peptide receptor radionuclide therapy possible in these tumours — the receptor becomes the address for the radioligand.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Widely used off-label to reduce splanchnic blood flow in acute variceal haemorrhage. Common practice with a supportive but not definitive evidence base; terlipressin is the agent with the stronger position in this setting.
Off-label uses following logically from reduced splanchnic secretion and slowed transit, supported by case series rather than trials.
Insulin suppression is the rationale. Established in toxicology practice, established less firmly in the trial literature.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Patients moving from three daily injections to one monthly depot describe it as the single largest quality-of-life change in their treatment.
Return of flushing or diarrhoea in the days before the next injection is frequently described, and is a recognised reason to shorten the interval or add short-acting rescue doses.
The depot uses a large-bore needle and a viscous suspension; it is consistently reported as uncomfortable.
A drug that suppresses growth hormone, insulin and appetite has no constituency in performance or physique communities. Where it appears in that context it is a misunderstanding.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Common with chronic use and mechanistically inevitable given the effect on gallbladder motility. Frequently asymptomatic; periodic ultrasound surveillance is standard. Cholecystitis and pancreatitis can follow.
Suppression of insulin and glucagon together produces hyperglycaemia in some patients and hypoglycaemia in others. Diabetic patients on insulin or sulfonylureas require dose review at initiation and at every change.
Sinus bradycardia, conduction abnormalities and arrhythmias are labelled effects; dose adjustment of beta-blockers and calcium-channel blockers may be required.
Diarrhoea, abdominal pain, nausea, flatulence and steatorrhoea are common, particularly early. Fat malabsorption can be clinically significant with chronic use.
Suppression of TSH occurs with chronic use; thyroid function monitoring is recommended.
Reported with long-term use and included in monitoring recommendations.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Carcinoid crisis on sudden discontinuation is a recognised concern, particularly around surgery and procedures.
Pancreatic enzyme suppression and fat malabsorption over years have nutritional implications that are managed rather than eliminated.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most-described chronic effect, reflecting fat malabsorption.
Frequently mentioned in patient discussion; some centres remove the gallbladder prophylactically during unrelated abdominal surgery.
Reported particularly by patients who also have diabetes.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Acromegaly typically begins in the region of 50 mcg two or three times daily and is titrated against GH and IGF-1. Carcinoid and VIPoma use higher labelled ranges titrated against symptoms. Exact figures are in the label and are individualised.
Patients are generally established on the immediate-release form first to confirm tolerance and response, then converted to depot with overlapping short-acting cover for the first weeks.
Approved for patients who have responded to and tolerated injectable octreotide or lanreotide, taken on an empty stomach.
IGF-1 and growth hormone are the endpoints. Symptom improvement can precede or lag biochemical control.
| Formulation | Route | Frequency | Typical setting |
|---|---|---|---|
| Immediate-release | Subcutaneous | 2–3 times daily | Initiation, dose-finding, rescue |
| LAR depot | Intramuscular gluteal | Every 4 weeks | Maintenance |
| Oral delayed-release | Oral, empty stomach | Daily | Acromegaly maintenance in responders |
| Monitoring — acromegaly | IGF-1, GH | Periodic | The titration endpoint |
| Monitoring — all | Gallbladder ultrasound | Periodic | Stones are common and often silent |
| Monitoring — all | Glucose, TSH, vitamin B12 | Periodic | Labelled recommendations |
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Reducing the interval or adding short-acting rescue doses is common clinical practice where symptoms return before the next depot.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
A drug titrated against IGF-1, requiring gallbladder ultrasound and glucose monitoring, has no defensible unsupervised protocol.
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Combination with a GH receptor antagonist or a dopamine agonist is established practice where a somatostatin analogue alone does not normalise IGF-1.
Somatostatin receptor affinity is what allows lutetium-177 dotatate to deliver radiation selectively to SSTR2-expressing tumour tissue.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Sermorelin, CJC-1295, ipamorelin and the GH blends all aim to raise growth hormone. Octreotide is prescribed to suppress it. They are not complementary — they are pharmacological opposites, and the fact that a drug exists to reverse chronic GH excess is worth sitting with before pursuing it deliberately.
Slowed transit and reduced splanchnic secretion alter absorption of orally administered medicines; ciclosporin levels in particular require monitoring.
Beta-blockers and non-dihydropyridine calcium-channel blockers may require dose reduction.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Commonly used to manage the steatorrhoea, and frequently mentioned as making chronic therapy tolerable.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Randomised placebo-controlled trials in metastatic neuroendocrine tumours using progression-free survival as the primary endpoint — the trials that established somatostatin analogues as antitumour rather than purely symptomatic therapy.
Transsphenoidal surgery first where feasible; somatostatin analogue for persistent disease; escalation to combination therapy or radiotherapy where IGF-1 remains elevated.
Gallbladder imaging, thyroid function, glucose and vitamin B12 at intervals during chronic therapy.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Short-acting octreotide is used around surgery and interventional procedures to prevent carcinoid crisis. Widely practised; the evidence is observational.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Patients describe treatment as structured around the injection date, with symptom diaries used to argue for shorter intervals.
The approved indications are covered above. This section covers the substantial off-label use, and the reason this drug sits in a library otherwise devoted to raising growth hormone: it is the drug prescribed to reverse the direction everything else here pushes.
Approved for acromegaly, carcinoid syndrome and VIPoma-associated diarrhoea. The uses below are off-label and mostly hospital-based. Chronic use causes gallstones in a substantial proportion of patients — mechanistically, not idiosyncratically — and requires periodic ultrasound, thyroid, glucose and vitamin B12 monitoring.
Pathophysiology
Acromegaly is chronic growth hormone excess. It causes cardiomyopathy, hypertension, sleep apnoea, insulin resistance, arthropathy and increased colorectal neoplasia, and it shortens life.
Mechanistic rationale
Sermorelin, CJC-1295, ipamorelin, tesamorelin and the GH blends all aim to raise growth hormone. Octreotide is prescribed to suppress it. Nobody using a secretagogue is producing acromegaly — the doses and durations are not comparable, and that should be said plainly. But the direction is shared, and knowing that an entire drug class exists to reverse the far end of it is worth having before assuming more GH is straightforwardly better.
Community reports
No physique or longevity constituency, appropriately — a drug that suppresses growth hormone, insulin and appetite has nothing to offer there.
Components carrying the argument: SSTR2 — the brake on the axis
Pathophysiology
Portal hypertension in cirrhosis causes oesophageal varices, and rupture is a medical emergency with substantial mortality.
Mechanistic rationale
Reduced splanchnic blood flow lowers portal pressure, and octreotide is used widely off-label in this setting alongside endoscopic therapy and prophylactic antibiotics. Terlipressin works through a different mechanism — V1 vasoconstriction — and has the stronger position in hepatorenal syndrome specifically.
Community reports
Hospital practice. Antibiotic prophylaxis independently improves survival in this setting and is the part most easily forgotten.
Components carrying the argument: Splanchnic blood flow reduction
Pathophysiology
Each follows from excessive secretion or rapid transit that reduced splanchnic secretion can moderate; in sulphonylurea overdose the problem is inappropriate insulin release.
Mechanistic rationale
These off-label uses follow logically from the pharmacology and are supported by case series rather than trials. Insulin suppression is the rationale in refractory hypoglycaemia, which is established in toxicology practice.
Community reports
Specialist and emergency settings.
Components carrying the argument: Broad secretory inhibition
| Question | Position |
|---|---|
| Direction of effect | Suppresses GH — the opposite of this library |
| Main chronic risk | Gallstones — common, mechanistic, often silent |
| Glucose | Moves both ways — insulin and glucagon both suppressed |
| Variceal bleeding | Widespread off-label use |
| Monitoring | Gallbladder ultrasound, thyroid, glucose, vitamin B12 |
| Grey market | None — nothing to gain |
For acromegaly: transsphenoidal surgery where the adenoma is resectable, somatostatin analogues for persistent disease, pegvisomant or cabergoline added where IGF-1 remains elevated, and radiotherapy in refractory cases — titrated against IGF-1. For neuroendocrine tumours: somatostatin analogues, peptide receptor radionuclide therapy, and specialist oncology management. For variceal bleeding: resuscitation, endoscopic band ligation, vasoactive therapy and prophylactic antibiotics.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
The immediate-release product is a ready-to-use solution in ampoules or multi-dose vials — no reconstitution. The LAR depot is a microsphere suspension reconstituted with the supplied diluent immediately before deep intramuscular injection, by a healthcare professional. This site publishes no reconstitution arithmetic for either.
Immediate-release solution: refrigerated 2–8 °C for long-term storage, with a defined room-temperature period during use; protect from light. LAR depot: refrigerated, and allowed to reach room temperature before preparation. Do not freeze either.
Immediate-release: 50, 100, 500 mcg ampoules and 200, 1000 mcg/mL multi-dose vials. LAR: 10, 20, 30 mg depot kits.
The depot suspension must be prepared immediately before administration and cannot be stored once mixed. The immediate-release solution should be discarded if discoloured or particulate.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
A generic of the LAR depot is now approved. The FDA approved a generic octreotide acetate for injectable suspension — a generic Sandostatin LAR Depot — in December 2025. Immediate-release generics had been available for longer. Octreotide has also appeared on shortage lists, which is worth knowing for a drug where interrupting supply in carcinoid disease risks a crisis.
Approved prescription medicine. Licensed as Sandostatin and Sandostatin LAR for acromegaly, severe diarrhoea and flushing associated with metastatic carcinoid tumours, and profuse watery diarrhoea associated with VIP-secreting tumours. An oral delayed-release formulation (Mycapssa) is approved for acromegaly maintenance.
Used extensively off-label in variceal bleeding, chylothorax, dumping syndrome and refractory hypoglycaemia. Lanreotide is a closely related depot somatostatin analogue with overlapping indications; pasireotide has broader receptor subtype coverage and a correspondingly larger effect on glucose.
No legitimate research-grade supply exists, and there would be little reason to want one — this is a drug for suppressing hormone axes, prescribed and monitored accordingly.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: generic LAR depot approved December 2025; shortage listings. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
Somatostatin analogues are not performance-enhancing and are not targeted as such, but hormone and metabolic modulators are addressed under the WADA Prohibited List. Verify against the current list.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
