Registered clinical use in ischaemic stroke [1][2]
Semax is registered in Russia for acute ischaemic stroke and TIA, with domestic clinical studies reporting improved neurological recovery when administered in the acute phase.
PrecisePep/Peptide Library/Semax
Neuro-Cognitive & Nootropic
Semax
Met-Glu-His-Phe-Pro-Gly-Pro · ACTH(4-7)-PGP · N-Acetyl Semax Amidate (NASA) · Adamax (analogue)
A Russian ACTH(4-7) analogue stripped of hormonal activity and registered in Russia as a nootropic and stroke medicine — with a large Russian-language clinical literature and almost no Western replication.
00 Overview
Semax occupies an unusual position: it is a registered medicine — just not here. Developed at the Institute of Molecular Genetics in Moscow, it is a synthetic analogue of ACTH(4-7) extended with a Pro-Gly-Pro tail that confers resistance to enzymatic degradation. The ACTH fragment was chosen because it retains the neurotropic and behavioural effects of the parent hormone while having no corticotropic activity — it does not raise cortisol.
In Russia, Semax is registered for ischaemic stroke, transient ischaemic attack, cognitive disorders and optic nerve conditions, and is used clinically. That is a genuine regulatory approval in a genuine jurisdiction with a real clinical literature behind it. It is also a literature that is overwhelmingly Russian-language, frequently published in domestic journals, and thinly replicated by independent Western groups.[1][2]
The mechanistic work is more portable: Semax reliably increases BDNF and its receptor TrkB, and modulates dopaminergic and serotonergic signalling.[3] Variants circulate in the research market — N-Acetyl Semax Amidate (NASA), and "Adamax", a more potent amidated analogue — which are sold as stronger versions and have thinner evidence still.
On the Russian literature
Dismissing this evidence base because it is Russian would be wrong; treating it as equivalent to a Western phase 3 programme would also be wrong. Much of it predates modern trial-reporting standards, sample sizes are often small, and independent replication is limited. Read it as real but weakly corroborated.
// Mechanism of action
BDNF and NGF upregulation. The most consistently reported and best-corroborated mechanism. Semax increases brain-derived neurotrophic factor and its receptor TrkB in the hippocampus and frontal cortex, plus nerve growth factor expression — the neurotrophic substrate for the cognitive and neuroprotective claims.[3]
Dopaminergic and serotonergic modulation. Reported enhancement of dopaminergic transmission and modulation of serotonin systems, consistent with the reported focus and drive effects.
Enkephalin protection. Semax inhibits enkephalin-degrading enzymes, prolonging the action of endogenous opioid peptides. This is the mechanistic basis for reported analgesic and mood-stabilising effects and is a distinctive property of the Semax family.
Melanocortin-related neuroprotection. As an ACTH fragment, Semax retains melanocortin system interaction relevant to neuroprotection and neuroinflammation, without the adrenal axis stimulation of the parent hormone.
Anti-inflammatory and antioxidant effects in ischaemia. Gene-expression work in cerebral ischaemia models reports modulation of inflammatory and immune-related transcription — the basis of the stroke indication.
Route. Intranasal administration is the registered route and exploits direct nose-to-brain transport, bypassing first-pass metabolism and the blood-brain barrier limitations that would otherwise make a heptapeptide a poor CNS drug.
01 Reported benefits
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.
BDNF and TrkB upregulation [3]
Demonstrated increases in BDNF and its receptor in hippocampus and cortex following administration — the most mechanistically solid finding in the Semax literature.
Neuroprotection in cerebral ischaemia models [3][4]
Reduced infarct volume and improved functional recovery in rodent ischaemia models, with associated modulation of inflammatory gene expression.
Effects on attention and memory in clinical studies [1]
Russian clinical work reports improvements in attention, memory and mental performance in cognitive impairment and in healthy subjects under load. Small studies, domestic publication.
No corticotropic activity [3]
The design objective: neurotropic ACTH-fragment effects without adrenal stimulation or cortisol elevation.
Functional connectomic effects demonstrated [5]
Independent work has examined Semax and Selank effects on functional gene-network and connectomic measures, providing a systems-level description of their action.
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.
Clearance of "brain fog" in healthy adults
The dominant use case in the research community, and one the registered indications do not cover. Extrapolated from cognitive-impairment findings to healthy cognition — a leap that fails routinely across the entire nootropic field.
Sustained neuroplasticity from repeated BDNF elevation
If BDNF elevation is real and repeated, durable plasticity changes are plausible. Whether intermittent intranasal dosing produces lasting structural change has not been shown.
Antidepressant effect
BDNF elevation and dopaminergic modulation are both implicated in antidepressant mechanisms. Semax has not been trialled as an antidepressant to Western standards.
ADHD and executive function support
Proposed on the dopaminergic mechanism. No controlled evidence.
Neuroprotection during high cognitive or physical stress
Generalised from the ischaemia and stress-model literature. Speculative in healthy adults.
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.
Sharp increase in focus and mental drive within 30–60 minutes
The characteristic community report — fast onset, several hours of duration, described as clarity and drive rather than stimulation.
Lifting of brain fog
The single most cited reason for use.
Improved verbal fluency and word recall
Frequently reported and unmeasured.
Overstimulation, irritability or anxiety if dosed late
The reason community protocols specify no dosing after early afternoon — reported sleep disruption from evening administration.
Adamax reported as substantially stronger
Community consensus is that the amidated analogue is more potent and longer-acting than plain Semax. Evidence for the analogue specifically is thinner than for the parent.
Tolerance with daily use
Diminishing effect over weeks is commonly reported and is the practical basis for the equal-time-on/off cycling convention.
02 Adverse effects & risks
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.
Favourable safety profile in registered use [1]
Russian clinical use reports a benign profile with local nasal irritation as the main issue. This is registration-supported but reflects the reporting standards of its jurisdiction and era.
No adrenal axis stimulation [3]
Absence of corticotropic activity removes the endocrine liability of the parent hormone.
No Western safety dataset
No FDA or EMA safety review, no independent Western pharmacovigilance, no long-term data in healthy adults.
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.
Effects of chronic BDNF manipulation are unknown
BDNF is not a substance where more is uniformly better — its signalling is regionally specific and context-dependent, and sustained pharmacological elevation in healthy brains has never been characterised.
Interaction with psychiatric medication
Dopaminergic and serotonergic modulation alongside SSRIs, SNRIs, stimulants or antipsychotics is an entirely uncharacterised interaction space.
Masking of an underlying cause of cognitive symptoms
Brain fog has causes — sleep debt, thyroid dysfunction, anaemia, depression, sleep apnoea. A compound that suppresses the symptom removes the prompt to investigate them.
Residual melanocortin activity
Uncharacterised at chronic exposure.
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.
Nasal irritation, burning and running
The most common complaint with intranasal use.
Insomnia if dosed after early afternoon
Consistently reported and the origin of the "never after 2pm" rule that appears in circulating protocols.
Irritability, agitation or emotional blunting
Reported at higher doses or with continuous use without breaks.
Headache
Occasionally reported, generally transient.
Paradoxical fatigue after the effect wears off
Reported by some users at the end of the active window.
03 Dosing ranges
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.
Registered intranasal dosing [1]
The Russian registered product is supplied as 0.1% and 1% intranasal drops with defined dosing for stroke and cognitive indications, typically expressed as drops per nostril at defined intervals.
Route changes which effect you get, not just how much [6]
The most useful study for anyone considering injecting this, and it is not the one the grey market cites. Rats were given Semax intraperitoneally and intranasally across a dose range and tested for both learning, by passive avoidance, and pain sensitivity, by hindpaw compression. Intraperitoneal Semax was both nootropic and analgesic. Intranasal Semax was more effective for learning and had no effect on pain at all — on a different dose-response curve. The authors concluded that different mechanisms and different brain structures mediate the two effects. The routes are therefore not interchangeable in either direction: injecting trades away part of the cognitive effect the compound is taken for, and gains an analgesic effect nobody is asking it for.
Higher doses in acute stroke than in cognitive use [1][2]
The acute neuroprotective indication uses substantially higher daily amounts over a short course than the cognitive indication does.
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.
Intranasal is the evidenced route
Nose-to-brain transport is how the registered product works and how the clinical data was generated. Subcutaneous administration — common in the research community — is a different pharmacokinetic proposition, and the comparative animal work says it is not a neutral swap: intraperitoneal dosing produced analgesia that intranasal dosing did not, and was less effective for learning.
Morning-only dosing
Follows from the reported activating effect and duration of several hours. Practical rather than pharmacological reasoning.
Cycling to avoid tolerance
Equal time on and off is the community convention. No tolerance mechanism has been characterised; the practice is empirical.
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.
500 mcg daily, mornings only
The figure in the Gold Standard protocol: 500 mcg in the morning, never after 2pm, run for one vial (about 20 days) then cycle off for an equal period.
300–600 mcg intranasal, split between nostrils
The general community range for the plain peptide.
Subcutaneous injection at intranasal-equivalent doses
Widely practised, and widely recommended by vendor dosing guides, typically at the same 250—600 mcg figures used intranasally, on the reasoning that injection absorbs more reliably than a spray. The absorption argument is reasonable. The dose transfer is not. No human study has used this route, so the intranasal figures carry no established equivalence — and the animal comparison found the two routes producing different effects at matched doses rather than the same effect more reliably.
Adamax / NASA at reduced doses
The amidated analogues are reported as more potent, so community doses are typically lower — commonly 100–300 mcg. Substitution ratios are guesswork.
Always with Selank
Community convention is that the two are taken together, Semax for drive and Selank for the anxiolytic counterweight.
| Form | Typical dose | Route | Timing |
|---|---|---|---|
| Semax | 300 – 600 mcg | Intranasal | Morning, never after 2pm |
| Semax (Gold Standard) | 500 mcg | Intranasal | Morning |
| N-Acetyl Semax Amidate | 100 – 300 mcg | Intranasal | Morning |
| Adamax | 100 – 300 mcg | Intranasal | Morning |
04 Synergy & interactions
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.
Semax and Selank studied together at systems level [5]
Functional connectomic and gene-network analysis has examined the two peptides in parallel, describing distinct but complementary effects on regulatory networks — the closest thing to combination evidence in this space.
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.
Semax + Selank
The canonical Russian nootropic pairing. The argument is that Semax supplies drive and cognitive activation while Selank supplies GABAergic calm, preventing the overstimulation Semax alone can produce. Mechanistically complementary; not trialled as a fixed combination.
Semax with GH-axis compounds
Community stacks combine nootropic and GH peptides on the general premise of recovery and neuroplasticity during sleep. No interaction data.
Semax with mitochondrial peptides
Proposed on the grounds that neuronal energy availability limits cognitive benefit. Entirely speculative.
Caution with stimulants and psychiatric medication
Layering dopaminergic modulation on top of prescribed stimulants or antidepressants is uncharacterised and the most plausible route to an adverse interaction with this compound.
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.
Semax + Selank, always together
The near-universal community convention, and the pairing specified in the Gold Standard protocol.
Adamax substituted for Semax for a stronger effect
The Gold Standard protocol explicitly offers Adamax as the stronger alternative.
Stacked with caffeine
Frequently reported; also the most common source of the overstimulation complaints.
05 Protocols
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.
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.
Equal time on and off
Given reported tolerance and the absence of any long-term data, matched on/off periods limit total exposure while preserving the reported effect.
Morning-only, intranasal, single dose
The lowest-complexity approach consistent with both the registered route and the reported activation profile.
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.
Gold Standard Protocol — 500 mcg mornings, one vial on / equal time off
500 mcg Semax (or Adamax for a stronger effect) in the morning, never after 2pm, always taken with Selank. One vial is about 20 days; cycle off for the same period.
15-Compound Matrix — neuro-cognitive pillar
Grouped with Selank in the neuro-cognitive and endocrine axis category, introduced after the metabolic and regenerative phases.
05b Condition-specific interest
Semax occupies a position nothing else in this library does: it is a registered prescription medicine in Russia, has been since the 1990s, and has approved indications. That is more than almost any compound here can say — and it is not the same thing as having the evidence a Western regulator would require. Both halves of that sentence matter, and this section is built around holding them together.
No approval, no trial
The evidence problem is structural, not a matter of one weak study. The Semax literature is overwhelmingly Russian-language, much of it published before modern trial reporting standards, frequently non-randomised or open-label, often comparing against "conventional therapy" rather than placebo, and essentially unreplicated outside Russia and neighbouring states. It has not been evaluated in a controlled Western trial. That is a real limitation and it is not a reason to dismiss the compound — it is a reason to be precise about what is and is not known.
Study — registered in Russia, weak by Western standards
Ischaemic stroke — the registered indication
Pathophysiology
After an ischaemic stroke, the infarct core is lost quickly, but the surrounding penumbra is salvageable for a period. Recovery afterwards depends on neuroplasticity, and BDNF is one of the principal mediators of it.
Mechanistic rationale
Semax is registered in Russia for ischaemic stroke, and the clinical work behind that includes studies reporting elevated plasma BDNF alongside improved Barthel index and motor scores in acute hemispheric stroke. The trials are small, several are non-randomised, and comparison is often against conventional therapy rather than placebo — a design that cannot separate drug effect from attention, expectation and the substantial spontaneous recovery that happens after stroke anyway.
Community reports
Not a self-directed use in any responsible sense. Acute stroke is an emergency where thrombolysis and thrombectomy have time windows measured in hours, and anything that delays presentation costs recoverable brain tissue.
Components carrying the argument: ACTH(4–10) analogue — BDNF and neurotrophic signalling
Theorized — registered indication, thin literature
Cognitive impairment and cognitive decline
Pathophysiology
Cognitive decline has many causes. Vascular contribution, neurodegeneration, sleep disorder, depression, medication effects and hearing loss all present similarly and have very different treatments.
Mechanistic rationale
Cognitive impairment is among the registered Russian indications, and BDNF modulation is a coherent mechanism — BDNF is central to synaptic plasticity and is reduced in several conditions involving cognitive decline. The field of cognition drugs is littered with mechanistically attractive compounds that failed in trials, which is the reason for caution rather than enthusiasm here.
Community reports
Widely used as a nootropic, with subjective reports of focus, verbal fluency and mental stamina. Those endpoints are highly placebo-responsive and are assessed by the person taking it, which is close to the least reliable measurement arrangement available.
Components carrying the argument: BDNF, NGF, monoaminergic modulation
Theorized — a real Russian paediatric use, minimal data
ADHD and attention
Pathophysiology
ADHD involves dysregulation of catecholamine signalling in prefrontal and striatal circuits, which is why the stimulants work and why they are first-line.
Mechanistic rationale
Semax has been used in Russian paediatric practice for attention and cognitive problems, and it does have effects on monoaminergic systems. What does not exist is anything resembling the trial evidence behind methylphenidate or lisdexamfetamine, which are among the more effective treatments in psychiatry.
Community reports
Used by adults self-treating attention problems, frequently in place of an assessment. ADHD is diagnosable and treatable, and the treatments have large effect sizes — substituting an unstudied peptide for that is a poor trade.
Components carrying the argument: Monoaminergic and BDNF effects
Theorized — mechanism is real, translation is not
Anxiety, depression and stress
Pathophysiology
Reduced BDNF signalling is one of the more durable findings in depression research, and increasing it is thought to be downstream of what SSRIs do rather than the mechanism they act on directly.
Mechanistic rationale
A compound that raises BDNF is acting on a pathway genuinely implicated in mood disorder. That pathway is also where a long line of failed antidepressant candidates went, and no controlled trial of Semax in depression exists. It is usually combined with Selank on a stimulating-plus-calming rationale that no study has examined.
Community reports
Mood lift is commonly reported, often within days — faster than any antidepressant mechanism plausibly acts, which is informative about what is generating the report.
Components carrying the argument: BDNF; the antidepressant link is inferential
Study — a registered indication nobody discusses
Optic nerve disease
Pathophysiology
Optic neuropathies involve damage to retinal ganglion cell axons, and the neuroprotective and neurotrophic requirements are similar to those in central nervous tissue generally.
Mechanistic rationale
Optic nerve disease is among the Russian registered indications, which is genuinely interesting and almost never mentioned in the community that uses this compound. The retina is central nervous tissue, so a neurotrophic agent has a coherent target there. As with the other indications, the supporting literature is small and local.
Community reports
Essentially absent from grey-market use. Listed because a registered indication is a fact worth knowing, whichever way it cuts.
Components carrying the argument: Neurotrophic and neuroprotective signalling
Theorized — extrapolated from the stroke work
Traumatic brain injury
Pathophysiology
TBI produces a primary mechanical injury followed by a secondary cascade of inflammation, excitotoxicity and impaired perfusion. The secondary phase is what most intervention targets.
Mechanistic rationale
The rationale carries over from the stroke indication and is coherent. No TBI-specific trial supports it, and post-concussion recovery is highly variable and largely spontaneous — which makes individual assessment of any intervention close to worthless.
Community reports
Discussed in combat sports and contact sport communities. The most important intervention after a concussion remains not sustaining another one while the first is healing.
Components carrying the argument: Neurotrophic support, anti-inflammatory effects
Actionable
How to read the Russian literature — and the route it used
Pathophysiology
Not a condition. A method note that applies to everything above.
Mechanistic rationale
Two things get lost when this compound crosses borders. First, the clinical use is intranasal — that is the route the registered product uses and the route the studies used, and the grey market frequently injects it instead — a route with no human data at all, and animal data suggesting it changes which effect you get rather than delivering the same one more reliably. Second, "registered in Russia" and "proven by trial" are different claims, and vendors routinely present the first as if it establishes the second. Registration in one jurisdiction on a local evidence base is a genuine fact about the compound; it is not a substitute for the trial that has not been run.
Community reports
Community sources cite "clinical use since 1994" as though duration of use were the same as demonstrated efficacy. It is not, though it is a reasonable reason to take the compound seriously as a research subject.
Components carrying the argument: A reading instruction, not a mechanism
| Condition | Russian status | Western evidence | The thing to know |
|---|---|---|---|
| Ischaemic stroke | Registered | None | Trials small, often non-randomised |
| Cognitive impairment | Registered | None | A field littered with failed candidates |
| Optic nerve disease | Registered | None | Never discussed by people using it |
| ADHD / attention | Used in practice | None | Stimulants have large effect sizes |
| Depression / anxiety | Off-label | None | Reports arrive faster than any plausible mechanism |
| TBI | Extrapolated | None | Recovery is spontaneous and variable |
| Route | Intranasal | — | The grey market injects it instead |
What actually has evidence for these conditions
For acute stroke: thrombolysis and thrombectomy within their time windows, and stroke-unit care, which independently improves outcomes. Then secondary prevention — antiplatelets, blood pressure control, lipid lowering — and early, intensive, repetitive rehabilitation, which remains the highest-yield recovery-phase intervention by a wide margin. Time is brain.
For cognitive decline: the evidenced list is unfashionable and consistent — treating midlife hypertension, hearing aids for hearing loss, physical activity, sleep, glycaemic control, social and cognitive engagement, not smoking. The FINGER multidomain trial is the best-supported prevention model available. For established Alzheimer disease: cholinesterase inhibitors, memantine, and the anti-amyloid monoclonals with their real but modest effect and non-trivial ARIA risk.
For ADHD: proper assessment first, then stimulants, which have among the largest effect sizes in psychiatry, or atomoxetine and guanfacine where stimulants are unsuitable. Behavioural and organisational strategies alongside.
For depression and anxiety: cognitive behavioural therapy has the strongest evidence of any intervention for anxiety disorders and is comparable to medication in mild to moderate depression. SSRIs and SNRIs, exercise with a genuine effect size, and treatment of alcohol use where present.
06 Handling, reconstitution & storage
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.
Reconstitution
Supplied lyophilised, commonly 5 or 10 mg per vial, or as a pre-made intranasal spray. For intranasal use the reconstituted solution is transferred to a nasal spray bottle — a step that introduces a sterility and dose-accuracy problem the injectable route does not have.
Storage
Lyophilised: refrigerated or frozen. Reconstituted: 2–8 °C. Nasal spray bottles in daily use are a contamination risk and are typically replaced between vials.
Common vial sizes
Commonly 5 mg and 10 mg lyophilised vials; also 0.1% / 1% intranasal solution in registered form.
Stability notes
The Pro-Gly-Pro tail exists specifically to resist enzymatic degradation, making Semax relatively robust compared with the unmodified ACTH fragment.
07 Legal & regulatory status
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Registered medicine in the Russian Federation for ischaemic stroke, TIA, cognitive disorders and optic nerve conditions. Not approved by the FDA, EMA or MHRA and not marketed in Western jurisdictions.
Material sold in the West is research-chemical supply. "Adamax" and N-Acetyl Semax Amidate are analogues with no registration anywhere and a thinner evidence base than the parent compound.
Regulatory update — current as at August 2026
On 23–24 July 2026 the FDA's Pharmacy Compounding Advisory Committee voted to recommend Semax for inclusion on the Section 503A Bulks List (8–5, one abstention). It was one of six peptides recommended — alongside BPC-157, KPV, TB-500, MOTS-c, Semax and Epitalon — out of seven considered.
This followed the FDA's announcement of 15 April 2026 removing twelve peptides from Category 2, the designation for substances judged to raise significant safety concerns. That removal stripped away the basis for enforcement against compounders but did not itself authorise anything, leaving these compounds in a regulatory grey area pending the PCAC review.
A PCAC recommendation is not an approval, and the 503A Bulks List is not a drug approval either. It is also worth knowing that July 2026 was the second round: across two sittings in October and December 2024 the same committee reviewed seven substances — among them ipamorelin, kisspeptin-10, AOD-9604, CJC-1295 and thymosin alpha-1 — and rejected all seven. Two separate things are being conflated in almost every write-up of the 2026 decision:
- The vote is advisory. PCAC recommendations are non-binding. The pathway from here runs: removal from Category 2 (done, April 2026) → PCAC recommendation (done, July 2026) → placement in Category 1 through notice-and-comment rulemaking, which commonly takes eight to twelve months → and the HHS Secretary must sign off on any addition to the list. Nothing is lawfully compoundable on the strength of the vote alone.
- Even a successful listing would not make these approved drugs. Inclusion on the 503A Bulks List permits a licensed compounding pharmacy to use the substance in a compounded preparation for an individual patient with a prescription. It says nothing about the compound being demonstrated safe and effective — no efficacy trial is required, and none of these has one.
- It would not legitimise research-chemical supply. A compounding pathway runs through a licensed pharmacy and a prescriber. Grey-market vials labelled "research use only" are not that, and nothing in this decision changes their status.
Regulatory and trial claims re-checked against primary sources on 20 August 2026. Checked: Russian registration status and trial quality; the intraperitoneal versus intranasal route comparison and the absence of any human injection study. 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.
Anti-doping
Athletes subject to WADA, USADA, UKAD, NCAA or military testing should assume any peptide is prohibited unless they have verified otherwise against the current WADA Prohibited List. Several classes here (growth-hormone secretagogues, TB-4 analogues, metabolic modulators) are explicitly named. Check the current list — it is republished annually.
§ Sources & further reading
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.
- PubMed: Semax — clinical and experimental literature (live query)Database or literature search
- PubMed: Semax in ischaemic stroke and cerebral ischaemia (live query)Database or literature search
- PubMed: Semax, BDNF and TrkB expression (live query)Database or literature search
- Antistress Action of Melanocortin Derivatives Associated with Correction of Gene Expression Patterns in the Hippocampus of Male Rats Following Acute Stress.Pre-clinical / animal study
- Functional Connectomic Approach to Studying Selank and Semax Effects. 2020.Review or meta-analysis
- Manchenko DM, Glazova NY, Levitskaya NG, et al. The Nootropic and Analgesic Effects of Semax Given via Different Routes. Neurosci Behav Physiol. 2012 — intraperitoneal versus intranasal at matched doses.Pre-clinical / animal study
Reminder
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.