Both are registered prescription medicines in Russia and neither has been evaluated by any Western regulator. Semax is a seven amino acid peptide given by nose. Noopept is a peptide-derived small molecule given by mouth, and it is listed as not qualifying as a lawful dietary ingredient, which is the form most people in the US buy it as.

| Attribute | Noopept | Semax |
|---|---|---|
| Is it a peptide | No, a peptide-derived small molecule [1] | Yes, 7 amino acids |
| Route | By mouth | By nose |
| Russian status | Registered prescription medicine [1] | Registered medicine |
| US status | Unapproved new drug [2] | Unapproved, recommended for compounding July 2026 [2] |
| Western trials | None | None |
| Best human trial | 53 patients, no placebo arm [3] | 110 patients, not randomised, no placebo [4] |
Neither has been assessed by the FDA or EMA. One of them has been specifically listed against. See the FDA section below.
Semax is a seven amino acid fragment of ACTH, registered in Russia since 1994 and given as nasal drops. Noopept is a molecule built from two amino acids with chemical groups attached, registered around 2006 and taken as a tablet.

N-phenylacetyl-L-prolylglycine ethyl ester, also called omberacetam or GVS-111. Built from proline and glycine with a phenylacetyl group at one end and an ethyl ester at the other. In plain terms: a small molecule that started from a peptide idea and stopped being a peptide on the way.

A seven amino acid sequence, the ACTH 4-7 fragment with three residues added to slow its breakdown. Developed at the Institute of Molecular Genetics in Moscow. In plain terms: a piece of a stress hormone, modified so it survives long enough to work.
One of these is a peptide and the other is grouped with peptides because of where it came from.
Noopept is N-phenylacetyl-L-prolylglycine ethyl ester: a proline-glycine pair carrying a phenylacetyl group and an ethyl ester, with a molar mass of 318. That makes it a peptide-derived small molecule, not a peptide. [1]
The core is two amino acids. Proline and glycine, joined as they would be in a peptide. It is described almost everywhere as a dipeptide, and that description is doing some work it should not. A phenylacetyl group sits at one end and an ethyl ester at the other. [1] Those are not amino acids and they are not peptide bonds.
It behaves like a small molecule too. Noopept is a prodrug. It is absorbed, then converted in the body to cycloprolylglycine, and that conversion product is what acts. [1] Oral bioavailability of the parent compound is around 10 percent. [1] Peptides are generally destroyed by digestion; Noopept is taken as a tablet and works that way, because it is not a peptide.
It has company. It belongs with several other compounds sold alongside peptides, among them MK-677 and enclomiphene, which are small molecules, and NAD+ and NMN, which are nucleotides. The word peptide in this market often describes a shelf, not a chemical class.
Noopept converts to cycloprolylglycine, modulates AMPA and NMDA receptors, and raises BDNF and NGF. Semax also raises BDNF and acts on the melanocortin system inherited from ACTH. Both mechanisms rest largely on animal work.
A prodrug. After absorption it converts to cycloprolylglycine, a substance the body makes on its own. That conversion product modulates AMPA and NMDA glutamate receptors, upregulates BDNF and NGF, and acts on cholinergic transmission through alpha-7 nicotinic receptors. [1]
The neuroprotective claims rest on animal work showing protection against oxidative stress and amyloid toxicity. [1]
Comes from ACTH. Its sequence is Met-Glu-His-Phe-Pro-Gly-Pro: the 4-7 fragment of adrenocorticotropic hormone with a Pro-Gly-Pro tail added to slow degradation. [4] It keeps the neurotrophic effects of the parent hormone without its corticotropic activity.
One detail runs against the usual description. Semax is reported to act as an antagonist at the MC4 melanocortin receptor, not an agonist. [4] Melanotan II and PT-141 come from the same hormone family and work by activating melanocortin receptors. Semax works in the opposite direction at MC4.
The mechanisms overlap at BDNF, the one most of the marketing rests on. Both stories have the same weakness: they are built from animal and cell work, with human confirmation that is thin for Noopept and difficult to assess for Semax because most of it was published in Russian.
Noopept's compared it against piracetam in 53 patients with no placebo arm, and Semax's studied 110 post-stroke patients without randomisation or a placebo group. [3][4]
Developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, as a modified fragment of ACTH intended to keep the cognitive effects without the hormonal ones.
Registered with the Russian Ministry of Health for cerebrovascular indications. Two intranasal formulations follow: a 0.1 percent solution for cognitive use and a 1 percent solution for acute conditions including ischaemic stroke and optic nerve disease. [4]
Patented in Russia, designed as a cyclic analogue of piracetam and reported to be active at doses roughly a thousandfold lower by weight. [1]
Completes Russian Phase 3 trials and receives registration in Russia for cognitive disorders of cerebrovascular and post-traumatic origin. [1]
Dolotov and colleagues publish in the Journal of Neurochemistry, showing Semax binds specifically in rat basal forebrain and raises BDNF protein. [4]
J Neurochem 2006;97 Suppl 1:82-86Animal study
Bochkarev and colleagues publish an EEG study of Noopept in patients with cognitive disturbances of traumatic and vascular origin. [3]
PMID 19008801Human study
Neznamov and Teleshova compare Noopept against piracetam in 53 patients with mild psycho-organic disorders following stroke or brain injury. Noopept at 20 mg daily against piracetam at 1,200 mg. Both groups improved. Noopept improved more on most measures of cognition and mood, with fewer adverse effects, and MMSE in the Noopept group rose from 26 to 29. [3]
Neurosci Behav Physiol 2009;39(3):311-321Human trial · active comparator
Added to Russia's Vital and Essential Drugs list. [4]
Amelin publishes an open-label study in 60 stroke patients given 20 mg daily for twelve months, against a control group that received no placebo. Cognitive function improved significantly at two months. The paper does not appear to report cognitive measures at twelve months, so whether the benefit held is unknown. [3]
Gusev, Martynov and colleagues study 110 post-stroke patients, mean age 58, given 6,000 micrograms daily intranasally in two ten-day courses separated by a twenty-day interval. Plasma BDNF rose and stayed elevated, and Barthel index and motor scale scores improved over roughly five months against comparator subgroups. It was not randomised, had no placebo group, and came from a single Russian research group. [4]
The FDA's Pharmacy Compounding Advisory Committee recommends Semax for the 503A bulk substances list, alongside BPC-157, KPV, TB-500, MOTS-c and epitalon. FDA staff had recommended against all seven substances under review, and the committee recommended six of them anyway. The recommendation is non-binding and nothing has been added to the list. [2]
Neither has had a Western regulatory review of any kind.
Russian registration is a real process and these are real medicines there. What is missing is reviewable scrutiny, not approval. The trials supporting both were run and published under a different regulatory system, and most of the Semax literature has never been translated. [4] In both best trials people got better. In neither can anyone say how much of that came from the drug rather than from time, rehabilitation, attention and expectation. That is the same limitation twice, and it is the most important thing on this page. Nobody is going to run those trials now: the original Russian patents on Noopept have expired, removing the commercial incentive to fund Western approval, and the same economics apply to Semax. [1]

| Attribute | Noopept | Semax |
|---|---|---|
| Also called | Omberacetam, GVS-111, N-phenylacetyl-L-prolylglycine ethyl ester | Semax, ACTH (4-7) analogue |
| Chemical class | Peptide-derived small molecule [1] | Peptide, 7 amino acids |
| CAS | 157115-85-0 [1] | See compound page |
| Route | Oral | Intranasal |
| Prodrug | Yes, converts to cycloprolylglycine [1] | No |
| Oral bioavailability | About 10 percent [1] | Not applicable |
| Russian status | Prescription medicine since about 2006 [1] | Registered medicine |
| Russian indications | Cognitive disorders of cerebrovascular and post-traumatic origin [1] | Acute ischaemic stroke, post-stroke recovery, cognitive impairment, optic nerve disease [4] |
| Registered since | About 2006 [1] | 1994, Vital Drugs list 2011 [4] |
| Best trial design | Active comparator, no placebo [3] | Not randomised, no placebo [4] |
| US status | Unapproved new drug; listed as not a lawful dietary ingredient [2] | Unapproved |
| Australia | Schedule 4, prescription only [2] | Not equivalent |
| Western trials | None | None |
| Typical dose in trials | 20 mg daily, split [1] | Varies by preparation |
Noopept is oral, is not a peptide, and carries an adverse supplement-status listing. Semax is nasal, is a peptide, and has been registered in Russia since 1994. Neither has been reviewed by any Western regulator, and neither best trial had a control group.
Nobody has run a Western trial of either compound.No Phase 1, Phase 2 or Phase 3 study under FDA or EMA oversight exists for either, and the expired patents mean nobody has a reason to fund one. [1]
Nobody has translated or replicated most of the Semax literature.The trials exist and are cited constantly, and a reader outside Russia cannot assess them. [4]
Nobody has tested either in healthy adults.The Russian indications are cognitive impairment after stroke or head injury. The people buying these are overwhelmingly healthy people wanting sharper thinking. That is a different question in a different population.
Nobody has established dose-response for Noopept in healthy people.The 10 to 30 mg range in circulation was established empirically in a patient population, not derived from a dose-finding study in anyone else. [1]
Real registration data, from a system whose files most readers cannot check.
These come from the Noopept arm, n=31.
Neither is a lawful product in the US in the form people buy.
*Where this page says nothing is established, it means nobody has studied it. It does not mean a compound is safe.
The percentages that circulate for Noopept, roughly 23 percent for blood pressure and 10 percent for irritability, do trace back to this trial. They are 7 of 31 and 3 of 31 from the Noopept arm. [3] The figures are real; the denominator is thirty-one people. What is missing is a placebo arm, and that is the central limitation of the Noopept evidence base. Our guide on reading a certificate of analysis covers what to check before you buy.
The trials studied someone else. They studied people recovering from stroke or brain injury. Neither compound has been tested in healthy adults wanting sharper thinking, and neither best trial had a control group. [3][4]
Route is the clearest practical basis. Noopept is oral and Semax is intranasal, and for most people that settles it before anything else does.
Legal position separates them too. Noopept carries an adverse listing attached to the form most people buy it in, and Semax has no equivalent ruling. [2] On evidence, neither clears the bar.
Neither compound is named on the 2026 Prohibited List.
Both are approved by one regulator, the Russian one, so applying S0 to them is less obvious than it is for a compound approved nowhere.
That is not a question to resolve by reading the list. Anyone competing under a testing body should ask that body directly.
Noopept is an unapproved new drug as defined at 21 USC 321(p)(1). It appears on industry advisory lists of substances that do not qualify as lawful dietary supplement ingredients, because it was developed as a drug in Russia and was not marketed as a supplement or food first. [2] We could not locate a primary FDA document stating this specifically about Noopept; the conclusion is asserted by third-party compliance bodies using the agency's standard drug-preclusion reasoning. Australia lists it as Schedule 4, prescription only. [2]
Semax has no equivalent ruling. In July 2026 the FDA's Pharmacy Compounding Advisory Committee recommended it for the 503A bulk substances list, alongside BPC-157, KPV, TB-500, MOTS-c and epitalon. [2] FDA staff had recommended against all seven substances reviewed, and the committee backed six anyway.
Semax cannot be legally compounded today. The recommendation is non-binding, and nothing changes until the FDA accepts it and completes a proposed rule, a comment period and a final rule. Both are registered medicines in Russia, and approval there carries no legal weight anywhere else.
No. It is N-phenylacetyl-L-prolylglycine ethyl ester, a proline-glycine pair carrying a phenylacetyl group and an ethyl ester. Those additions are not amino acids, the molecule has a molar mass of 318, and it acts as a prodrug that converts to cycloprolylglycine. It is a peptide-derived small molecule.
No, and it works in the opposite direction at one shared receptor. Both come from the melanocortin family. Semax is reported to act as an antagonist at MC4, while Melanotan II and PT-141 work by activating melanocortin receptors. Semax keeps the neurotrophic effects of ACTH without its hormonal ones.
Neither has been compared to the other, and no Western trial of either exists. Noopept has the clearer human record, from a 2009 trial in 53 patients that compared it against piracetam with no placebo arm. Semax has a longer Russian history with literature most readers cannot assess.
Not as a supplement, on the analysis that applies to it. It is an unapproved new drug under 21 USC 321(p)(1) and appears on industry advisory lists of substances that do not qualify as lawful dietary ingredients, because it was developed as a drug rather than marketed as a supplement first. It is not a controlled substance.
No trial has tested any combination, and people do it regularly. They are reported to work partly through the same mechanism, raising BDNF, so overlap is more likely than addition.
Noopept is oral, at 10 to 30 mg daily in circulating protocols, with the 2009 trial using 20 mg split into two doses. Semax is intranasal. Neither dose range was established in healthy adults.
Because nobody has a commercial reason to fund one. Western approval requires toxicology, Phase 1, Phase 2 and Phase 3 work costing hundreds of millions, and the original Russian patents have expired, so there is no exclusivity to recover it against.
They come from a trial, and the trial was small. The figures trace to the Noopept arm of Neznamov and Teleshova 2009: increased blood pressure in 7 of 31 patients, sleep disturbances in 5 of 31, irritability in 3 of 31. Percentages calculated from thirty-one people carry wide uncertainty.
Cognitive disorders following stroke or head injury, in Russia, where it is a registered prescription medicine. Outside Russia it is sold as a nootropic for healthy people wanting sharper memory and focus. That is a different use in a different population and has never been tested.
Unclear from the published record, and the same is true of Semax. Neither compound's best trial had a control group: Noopept's compared it against piracetam in 53 patients with no placebo arm and both groups improved, and Semax's studied 110 post-stroke patients without randomisation or a placebo. Without a control group nobody can say how much of either improvement came from the drug.
Acute ischaemic stroke, post-stroke recovery, cognitive impairment and optic nerve disease, in Russia, where it has been registered since 1994. Two intranasal strengths exist: 0.1 percent for cognitive use and 1 percent for acute conditions.
The trials ran for weeks to months rather than days. Noopept's main trial and the Semax stroke study both measured outcomes over periods of one to five months. No study has established an onset time in healthy people, because no study has been done in healthy people.
No serious adverse effects are reported in the available literature, and the literature is thin. An independent review by the Alzheimer's Drug Discovery Foundation concluded that published well-conducted studies of Semax are lacking, so any safety statement rests on very little.
Not today. In July 2026 the FDA's Pharmacy Compounding Advisory Committee recommended Semax for the 503A bulk substances list alongside five other peptides, going against FDA staff who had opposed all seven under review. The recommendation is non-binding, nothing has been added to the list, and compounding remains unlawful until the agency accepts it and completes rulemaking.
Neither is named on the 2026 Prohibited List. Section S0 covers substances not approved by any regulatory health authority, and both are approved by the Russian regulator, which makes its application less obvious. Ask your own authority instead of reasoning from the list.
What Europe PMC and ClinicalTrials.gov hold for each, on the same rule.
Noopept has 113 records to Semax's 402. 21 original human studies against 78.
Semax: FDA: Nominated but withdrawn; previously category 2 · FDA: Briefing package prepared for the July 24, 2026 session · FDA: Considered at the July 24, 2026 session
The published recordNoopept
Papers and trials about Noopept
29 papers tagged human · 21 not reviews or lab · 3 clinical trial publications
Counted from Europe PMC indexing, not read by a person; a human tag can land on reviews, commentary or lab papers; clinical trial publications is the narrower count.
The published recordSemax
Papers and trials about Semax
105 papers tagged human · 78 not reviews or lab · 26 clinical trial publications
Compare this against the whole library →
Nominated but withdrawn; previously category 2RegulatorsCounted from Europe PMC indexing, not read by a person; a human tag can land on reviews, commentary or lab papers; clinical trial publications is the narrower count.