N-Acetyl Semax Amidate

N-Acetyl Semax Amidate at a Glance

N-Acetyl Semax Amidate is Semax with both ends chemically capped — acetylated at one terminus and amidated at the other — modifications intended to slow enzymatic degradation and extend its action. It is sold as a research chemical, most often as a nasal spray. The important qualifier is that no published study has tested this analogue itself: its reputation is transferred wholesale from the parent peptide, and whether the end-capping changes potency, duration or effect is unestablished.

History & Development

N-Acetyl Semax Amidate is Semax with both ends chemically capped. No study of this molecule has ever been published - everything claimed for it belongs to the parent.

First described	Not established - no published study of the analogue exists
Discovered / synthesised by	Not established in the sources consulted for this section
Institution	Not established in the sources consulted for this section
Origin	Semax (Met-Glu-His-Phe-Pro-Gly-Pro) acetylated at the N-terminus and amidated at the C-terminus
Key patent	Not established in the sources consulted for this section
Assignee	Not established in the sources consulted for this section
Development status	Not a development programme - sold as a research chemical; never studied, never approved

Discovery

Capping a peptide’s ends is standard medicinal chemistry. Peptidases attack free N- and C-termini, so acetylating one end and amidating the other removes the charged groups those enzymes recognise, typically extending half-life and sometimes improving membrane permeability.

Applied to Semax - itself already stabilised by its Pro-Gly-Pro tail - the rationale is more of the same protection. It is a reasonable modification to attempt.

Development & ownership

There is no development programme. This analogue has not been the subject of a published pharmacokinetic study, a receptor-binding study, an animal efficacy study, or any human research. The modification is chemically sensible and entirely untested.

That creates the central error to avoid. Semax has a genuine Russian clinical record, and every claim made for N-Acetyl Semax Amidate borrows it. But capping both termini changes the molecule’s charge distribution, and that can alter receptor affinity, biodistribution and the metabolite profile. A more stable analogue is not automatically a more effective one - it may bind differently, penetrate differently, or produce different fragments.

Semax’s own activity is partly attributed to its degradation products, which makes this especially uncertain: a molecule engineered to resist degradation may produce fewer of the fragments that mattered.

How it reached the market

It reached consumers without ever being studied. NASA is sold as an “improved” or “stabilised” Semax, usually at a premium, on the strength of a parent compound’s evidence and a plausible chemical argument - with nothing measured about the molecule actually in the bottle.

What It's Used For

N-Acetyl Semax Amidate (“NASA”) is a chemically end-capped analogue of Semax, the Russian heptapeptide nootropic Met-Glu-His-Phe-Pro-Gly-Pro built from the ACTH(4-7) fragment of adrenocorticotropic hormone plus a C-terminal Pro-Gly-Pro tail. It adds an N-terminal acetyl group and a C-terminal amide — a standard, legitimate medicinal-chemistry tactic for blunting the exopeptidases that clip a peptide’s ends. The single most important fact here is that the molecule has never been studied. A PubMed search for an amidated Semax derivative returns zero records (semax AND amidat*, July 2026); the entire “acetyl Semax” literature is two in-vitro chemistry papers, neither of which used the amidated compound and neither of which measured a behavioral, cognitive or clinical outcome ^{1,2Reference 1Magrì A et al. · 2016In vitroInfluence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells)View study →Reference 2Shevchenko KV et al. · 2013In vitroStability of Semax acetyl to proteolysis in various biological media — in vitro (no abstract indexed; compound identity unconfirmed)View study →}.

No animal has received this peptide in a published experiment. No human has. Everything else below is parent Semax, whose own evidence is a Russia-only registered drug resting on small, largely open-label, single-country clinical studies layered over a rodent literature dominated by a handful of Moscow laboratories ^{3,4,12Reference 3Gusev EI et al. · 2018Clinical trialThe efficacy of Semax in the treatment of patients at different stages of ischemic stroke — human (open-label clinical study, n=110, intranasal)View study →Reference 4Gusev EI et al. · 2005Clinical trialSemax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency — human (comparative clinical study, n=187)View study →Reference 12Filippenkov IB et al. · 2020AnimalNovel insights into the protective properties of ACTH(4-7)PGP (Semax) peptide at the transcriptome level following cerebral ischaemia — animal (rat, tMCAO)View study →}.

Two things follow, and they cut in opposite directions from the marketing. First, route is load-bearing and the routes diverge: every piece of human Semax evidence was generated intranasally ^{3,6,10Reference 3Gusev EI et al. · 2018Clinical trialThe efficacy of Semax in the treatment of patients at different stages of ischemic stroke — human (open-label clinical study, n=110, intranasal)View study →Reference 6Polunin GS et al. · 2000Clinical trialEvaluation of therapeutic effect of new Russian drug Semax in optic nerve disease — human (clinical study, intranasal)View study →Reference 10Lebedeva IS et al. · 2018Effects of Semax on the default mode network of the brain — human (fMRI, healthy volunteers, intranasal)View study →}, because peptides of this size have negligible oral bioavailability; NASA is sold both as a nasal spray and as a subcutaneous injection, and no study supports the injected route for this molecule or its parent. Second, and more interesting: much of Semax’s in-vivo activity may be carried not by the intact peptide but by its degradation product Pro-Gly-Pro (PGP), which is itself neurotropic ^{21,22Reference 21Shevchenko KV et al. · 2013In vitroProteolysis of simple glyprolines by leucine aminopeptidase and enzymes from nasal slime, brain membranes, and rat blood (studied comparatively to Semax) — in vitroView study →Reference 22Shevchenko KV et al. · 2006AnimalKinetics of Semax penetration into the brain and blood of rats after intranasal administration — animal (rat, PK)View study →}.

NASA is engineered to resist exactly the proteolysis that generates PGP. If the parent’s effect is partly a metabolite effect, then greater stability would not mean “more Semax” — it would mean a different pharmacology. That is reasoning from the parent’s PK, not a finding; nobody has tested it. But it is the reason the vendor claim of a “stronger, longer-lasting Semax” cannot simply be assumed even in principle.

Evidence by IndicationStrength of support · Beta

Support is an experimental score I’m building — a composite weighted by study type (human > animal > in vitro > review) and study volume. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. Note that scores are not driven by raw publication count — most of the parent literature comes from a small cluster of labs, so more papers do not mean more independent evidence.

Read the numbers below with one caveat that overrides all of them: not one row describes N-Acetyl Semax Amidate. These are parent-Semax ceilings, capped hard because the molecule sold under this name has never been administered in a published study. This is “never tested,” not “tested and failed” — with the narrow exception of the in-vitro copper result ^{1Reference 1Magrì A et al. · 2016In vitroInfluence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells)View study →}, which is a genuine negative for the acetylated form.

01Ischemic stroke & cerebral-ischemia recoveryShaky30%Small open-label Russian human studies + replicated rat tMCAO transcriptomics — parent Semax, intranasal, no Western RCT, nothing on this analogue

02Cognition & nootropic useShaky26%Rodent BDNF/NGF work + healthy-volunteer fMRI network changes; no cognition-endpoint RCT — parent

03Optic neuropathy, glaucoma & retinal diseaseShaky24%Several small Russian adjunct studies, effect never isolated from co-therapy — parent, intranasal/electrophoresis

04Stress, mood & anxietyShaky15%Rodent neonatal-isolation model only; no controlled human mood data — parent

05ADHD & attention in childrenShaky10%Traces to a single Medical Hypotheses proposal, not a trial — parent

06Improved stability / potency over SemaxShaky0%The actual selling claim. One un-abstracted stability note ^{2Reference 2Shevchenko KV et al. · 2013In vitroStability of Semax acetyl to proteolysis in various biological media — in vitro (no abstract indexed; compound identity unconfirmed)View study →} and one in-vitro chemistry paper that found a loss of activity ^{1Reference 1Magrì A et al. · 2016In vitroInfluence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells)View study →}. No head-to-head on any outcome.

Mechanisms

No mechanism has been demonstrated for N-Acetyl Semax Amidate. The table below is parent-Semax rodent and in-vitro work, listed because it is what the analogue is assumed to inherit — an assumption nobody has tested. The one row that genuinely concerns an acetylated compound is flagged.

Pharmacokinetics

Nothing is established. There is no measured half-life, bioavailability, brain penetration, distribution or clearance figure for N-Acetyl Semax Amidate, in any species, by any route. What follows is the parent’s PK, which is the only anchor available.

Semax is given intranasally as a 0.1% or 1% aqueous solution ^{6,8Reference 6Polunin GS et al. · 2000Clinical trialEvaluation of therapeutic effect of new Russian drug Semax in optic nerve disease — human (clinical study, intranasal)View study →Reference 8Nazarova GA et al. · 2013Clinical trialPre-formed physical factors and neuroprotective therapy for the rehabilitative treatment of patients with diabetic retinopathy — human (comparative clinical study)View study →}, chosen because peptides of this size are digested rather than absorbed orally and because intranasal dosing exploits partial nose-to-brain transfer. In tritium-labeled rat work, Semax reaches the brain within minutes of intranasal dosing but is degraded rapidly by peptidases, with Pro-Gly-Pro becoming the predominant species in blood and brain ^{22Reference 22Shevchenko KV et al. · 2006AnimalKinetics of Semax penetration into the brain and blood of rats after intranasal administration — animal (rat, PK)View study →} — and the degradation products carry neurotropic activity of their own ^{21Reference 21Shevchenko KV et al. · 2013In vitroProteolysis of simple glyprolines by leucine aminopeptidase and enzymes from nasal slime, brain membranes, and rat blood (studied comparatively to Semax) — in vitroView study →}. The parent peptide’s own plasma half-life is therefore on the order of minutes; the C-terminal Pro-Gly-Pro tail already exists to slow proteolysis ^{21Reference 21Shevchenko KV et al. · 2013In vitroProteolysis of simple glyprolines by leucine aminopeptidase and enzymes from nasal slime, brain membranes, and rat blood (studied comparatively to Semax) — in vitroView study →}.

The analogue’s rationale extends that logic with end-caps at both termini, supported by a single un-abstracted stability report on “Semax acetyl” ^{2Reference 2Shevchenko KV et al. · 2013In vitroStability of Semax acetyl to proteolysis in various biological media — in vitro (no abstract indexed; compound identity unconfirmed)View study →} whose compound identity I could not confirm (see application 6). The load-bearing vendor claim — that end-capping confers oral or sublingual activity — has never been tested and should be treated as false until it is. Any oral product would need to survive gastric and intestinal proteases as well as exopeptidases, which acetylation and amidation do not address. The routes actually sold are intranasal spray and subcutaneous injection; only the first has any parent precedent, and even that precedent is for a different molecule.

Clinical & regulatory status

N-Acetyl Semax Amidate is an unapproved research chemical with no marketing authorization from any regulator anywhere in the world, and no dietary-supplement status. Its parent, Semax, is an approved prescription drug in Russia only (intranasal, developed at Russian Academy of Sciences institutes and included on the state list of Vital and Essential Medicines) — a status that does not extend to a chemically modified analogue, and that has no Western equivalent. Neither compound is FDA-, EMA- or TGA-approved.

Registered-trial activity is nil for both. A ClinicalTrials.gov v2 API query for “semax” returns zero studies (verified July 2026), and there are no registry entries for the analogue; the parent’s human evidence lives entirely in Russian-language clinical literature outside Western registries. Regulators have begun cataloguing Semax-class peptides: a Belgian official-medicines-control-laboratory analysis of two seized preparations identified Selank and Semax, noting explicitly that these peptides have not completed any clinical trials and are freely sold online as lyophilized powder for injection or as nasal sprays ^{26Reference 26Vanhee C et al. · 2020Clinical trialThe occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations — analytical / forensic (Selank and Semax identified; noted as never having completed clinical trials)View study →}. Semax also appears in recent peptide-therapeutics review literature ^{27Reference 27Mavrych V et al. · 2026ReviewTherapeutic peptides in gerontology: mechanisms and applications for healthy aging — review (covers Semax; does not cover this analogue)View study →}; the analogue does not.

Last checked: July 2026.

Sourcing, Route & Legal Status

Regulatory status. NASA is sold “for research use only / not for human consumption” and has no approval anywhere. It is not a scheduled substance in the US, but “not scheduled” is not “approved” — marketing it for human use is unlawful in most Western jurisdictions, and it is not a lawful dietary-supplement ingredient in the US, UK or EU. The parent’s Russian prescription status is sometimes cited by sellers as though it legitimized the analogue; it does not. NASA is not the molecule Russia approved.

How it’s supplied & administered. Typically a lyophilized powder requiring reconstitution (usually with bacteriostatic water), and increasingly as a pre-mixed nasal spray; it is also sold for subcutaneous injection. This route split matters: the parent’s entire clinical record is intranasal, so the injected route has no precedent even by read-across, and the oral/sublingual products some vendors offer rest on an untested assumption that end-capping confers gastrointestinal survival. Lyophilized peptide is stored refrigerated or frozen; reconstituted solution is unstable and short-lived.

Sourcing reality (a safety issue, not a footnote). These products come from unregulated vendors with no manufacturing oversight. Identity, purity, correct sequence, actual peptide content and absence of bacterial endotoxin cannot be assumed. This is not hypothetical for this compound class: when suspicious preparations were seized and analyzed by an official control laboratory, identifying the peptides they contained required dedicated LC-MS/MS method development, and the peptides were being sold both as injection powder and as nasal sprays ^{26Reference 26Vanhee C et al. · 2020Clinical trialThe occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations — analytical / forensic (Selank and Semax identified; noted as never having completed clinical trials)View study →}. Because the modification is invisible without mass spectrometry, material sold as “NASA” cannot be distinguished from ordinary Semax — or from nothing at all — by any check a buyer can perform. Third-party certificates of analysis are the only partial mitigation, and even those can be forged. No vendor is recommended or linked here.

Safety

Nothing has ever been administered — not to a human, an animal, or a cell culture for a toxicity endpoint — so this compound’s safety is unknown in the strongest sense of the word. Parent Semax’s tolerability record does not carry over, because the one in-vitro comparison found acetylation changed the molecule’s behavior.

Safety at a Glance

❔ Toxicity unknown

• No safety data of any kind. No toxicology, no dose-ranging study, no adverse-event record, no pharmacovigilance.
• Not assessed in pregnancy or breastfeeding. No human or animal reproductive data — see the box below.
• Parent tolerability does not transfer. Acetylation changed the molecule’s biological behavior in the only comparison available.
• Interactions untested. The parent’s dopaminergic and serotonergic activity is a theoretical flag around stimulants and serotonergic drugs, not an assessed interaction.
• Route risks are real. Nasal mucosal irritation with repeated dosing; non-sterile reconstitution, endotoxin exposure and dosing error with injected use.

Full Safety & Interactions Detail

Overall posture: unknown, and unknown in the strongest sense. No study has ever administered this molecule to a cell culture for a toxicity endpoint, an animal, or a human. There is no adverse-event record, no dose-ranging study, no toxicology and no pharmacovigilance. Everything below is either parent data (labeled as such and not transferable) or mechanism-and-route reasoning (labeled as such and not a finding).

• Adverse effects. Parent Semax is described in Russian clinical use as generally well tolerated, with occasional mild nasal irritation from intranasal dosing; that record is methodologically weak and largely uncontrolled, and none of it is verified for the analogue. The one in-vitro comparison available found acetylation changed the molecule’s biological behavior ^{1Reference 1Magrì A et al. · 2016In vitroInfluence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells)View study →}, so parent tolerability should not be assumed to carry over in either direction.
• Dose-limiting effect. Not established. No dose-ranging or toxicity study exists.
• Interactions. No controlled interaction studies for the analogue or the parent. A mechanistic caution only: the parent modulates dopaminergic and serotonergic tone, so co-use with stimulants or serotonergic drugs is a theoretical flag, not an assessed interaction.
• Who should avoid it. Anyone unwilling to take an unapproved, never-studied research chemical of unverifiable identity; anyone pregnant, breastfeeding or trying to conceive; children (see application 5 — the pediatric framing rests on a hypothesis paper); anyone who cannot verify product sterility.
• Route-specific risks. Repeated intranasal dosing risks mucosal irritation. For injected use — which has no precedent for this molecule or its parent — non-sterile reconstitution, contaminated product, endotoxin exposure, injection-site reactions and dosing error from self-mixed concentrations are all real.

Scope disclosure (honesty, not a claim):

• Human data? None — not limited, none. No human has received this compound in a published study. The parent’s human data are small, open-label, single-country and intranasal.
• Animal data? None for the analogue. The parent’s rodent literature is deep but concentrated in a few laboratories.
• Interactions assessed? No — for either molecule.
• Pregnancy/lactation assessed? No — not established.
• Long-term safety established? No. Absence of reported harm here reflects the total absence of study, not evidence of safety.

Never imply safety from silence. For this compound, silence is nearly all there is.

Pregnancy & Lactation

? Not established in pregnancy? Not established in lactation

Not assessed and not established. There are no human pregnancy or lactation data and no animal reproductive-toxicity data for the analogue, and none located for the parent in a form that could support use. Treat as contraindicated by default.

Dosage

There is no established dose for N-Acetyl Semax Amidate — not “no Western dose,” but no studied dose at any point in the published record — and none is recommended here. It is not an approved drug or supplement anywhere, and this section is informational only.

No animal or human study has administered this molecule, so there is no dose-finding data, no bioavailability figure and no route validation to anchor a regimen. Figures circulating in vendor copy and nootropic forums (typically intranasal micrograms per application, or subcutaneous doses adapted from parent-Semax intranasal protocols) are community practice, not evidence, and are not reproduced here as a protocol. For context only, and for a different molecule: the Russian ischemic-stroke regimen used intranasal Semax at 6000 µg/day in two 10-day courses ^{3Reference 3Gusev EI et al. · 2018Clinical trialThe efficacy of Semax in the treatment of patients at different stages of ischemic stroke — human (open-label clinical study, n=110, intranasal)View study →} — reported as data, not as a recommendation, and not a basis for dosing an analogue whose potency relative to the parent is unmeasured. The claim that NASA is stronger and therefore needs less is exactly the kind of unverified potency assumption that makes self-dosing it unsafe; the only relevant experiment found an activity loss, not a gain ^{1Reference 1Magrì A et al. · 2016In vitroInfluence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells)View study →}.

References

1. Magrì A, et al. (2016). Influence of the N-terminus acetylation of Semax, a synthetic analog of ACTH(4-10), on copper(II) and zinc(II) coordination and biological properties — in vitro (Ac-Semax vs Semax, SH-SY5Y cells). Journal of Inorganic Biochemistry. https://pubmed.ncbi.nlm.nih.gov/27586814/
2. Shevchenko KV, et al. (2013). Stability of Semax acetyl to proteolysis in various biological media — in vitro (no abstract indexed; compound identity unconfirmed). Doklady Biological Sciences. https://pubmed.ncbi.nlm.nih.gov/23652441/
3. Gusev EI, et al. (2018). The efficacy of Semax in the treatment of patients at different stages of ischemic stroke — human (open-label clinical study, n=110, intranasal). Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. https://pubmed.ncbi.nlm.nih.gov/29798983/
4. Gusev EI, et al. (2005). Semax in prevention of disease progress and development of exacerbations in patients with cerebrovascular insufficiency — human (comparative clinical study, n=187). Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova. https://pubmed.ncbi.nlm.nih.gov/15792140/
5. Shadrina M, et al. (2010). Comparison of the temporary dynamics of NGF and BDNF gene expression in rat hippocampus, frontal cortex, and retina under Semax action — animal (rat). Journal of Molecular Neuroscience. https://pubmed.ncbi.nlm.nih.gov/19662538/
6. Polunin GS, et al. (2000). Evaluation of therapeutic effect of new Russian drug Semax in optic nerve disease — human (clinical study, intranasal). Vestnik Oftalmologii. https://pubmed.ncbi.nlm.nih.gov/10741256/
7. Kurysheva NI, et al. (2001). Semax in the treatment of glaucomatous optic neuropathy in patients with normalized ophthalmic tone — human (comparative study). Vestnik Oftalmologii. https://pubmed.ncbi.nlm.nih.gov/11569188/
8. Nazarova GA, et al. (2013). Pre-formed physical factors and neuroprotective therapy for the rehabilitative treatment of patients with diabetic retinopathy — human (comparative clinical study). Voprosy Kurortologii, Fizioterapii i Lechebnoi Fizicheskoi Kultury. https://pubmed.ncbi.nlm.nih.gov/24437205/
9. Dragon AK, et al. (2022). Results of the application of complex physiotherapeutic neurostimulation in optical neuropathies of various genesis — human (clinical study). Voprosy Kurortologii, Fizioterapii i Lechebnoi Fizicheskoi Kultury. https://pubmed.ncbi.nlm.nih.gov/36083821/
10. Lebedeva IS, et al. (2018). Effects of Semax on the default mode network of the brain — human (fMRI, healthy volunteers, intranasal). Bulletin of Experimental Biology and Medicine. https://pubmed.ncbi.nlm.nih.gov/30225715/
11. Panikratova YR, et al. (2020). Functional connectomic approach to studying Selank and Semax effects — human (fMRI, healthy volunteers). Doklady Biological Sciences. https://pubmed.ncbi.nlm.nih.gov/32342318/
12. Filippenkov IB, et al. (2020). Novel insights into the protective properties of ACTH(4-7)PGP (Semax) peptide at the transcriptome level following cerebral ischaemia — animal (rat, tMCAO). Genes (Basel). https://pubmed.ncbi.nlm.nih.gov/32580520/
13. Filippenkov IB, et al. (2023). Synthetic adrenocorticotropic peptides modulate the expression pattern of immune genes in rat brain following the early post-stroke period — animal (rat). Genes (Basel). https://pubmed.ncbi.nlm.nih.gov/37510287/
14. Filippenkov IB, et al. (2025). Genes associated with action of ACTH-like peptides with neuroprotective potential in rat brain regions with different degrees of ischemic damage — animal (rat). International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/40650034/
15. Stavchansky VV, et al. (2011). The effect of Semax and its C-end peptide PGP on the morphology and proliferative activity of rat brain cells during experimental ischemia — animal (rat). Journal of Molecular Neuroscience. https://pubmed.ncbi.nlm.nih.gov/20617398/
16. Romanova GA, et al. (2012). Comparison of neuroprotective action of antibodies to glutamate and Semax in focal ischemic damage of the rat prefrontal cortex — animal (rat). Patologicheskaia Fiziologiia i Eksperimentalnaia Terapiia. https://pubmed.ncbi.nlm.nih.gov/23072114/
17. Shakova FM, et al. (2021). Protective effects of PGC-1α activators on ischemic stroke in a rat model of photochemically induced thrombosis — animal (rat, intranasal Semax 25 µg/kg). Brain Sciences. https://pubmed.ncbi.nlm.nih.gov/33806692/
18. Radchenko AI, et al. (2025). The potential of the peptide drug Semax and its derivative for correcting pathological impairments in the animal model of Alzheimer’s disease — animal (transgenic mouse; the “derivative” is not identified in the abstract). Acta Naturae. https://pubmed.ncbi.nlm.nih.gov/41479572/
19. Sheludchenko VM, et al. (2026). Effect of a combined physiotherapeutic approach on functional parameters after endovitreal surgery of rhegmatogenous retinal detachment — human (clinical study). Vestnik Oftalmologii. https://pubmed.ncbi.nlm.nih.gov/42366656/
20. Volodina MA, et al. (2012). Correction of long-lasting negative effects of neonatal isolation in white rats using Semax — animal (rat). Acta Naturae. https://pubmed.ncbi.nlm.nih.gov/22708068/
21. Shevchenko KV, et al. (2013). Proteolysis of simple glyprolines by leucine aminopeptidase and enzymes from nasal slime, brain membranes, and rat blood (studied comparatively to Semax) — in vitro. Bioorganicheskaia Khimiia. https://pubmed.ncbi.nlm.nih.gov/24397030/
22. Shevchenko KV, et al. (2006). Kinetics of Semax penetration into the brain and blood of rats after intranasal administration — animal (rat, PK). Bioorganicheskaia Khimiia. https://pubmed.ncbi.nlm.nih.gov/16523722/
23. Tsai SJ. (2007). Semax, an analogue of adrenocorticotropin (4-10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome — hypothesis / proposal, not a trial. Medical Hypotheses. https://pubmed.ncbi.nlm.nih.gov/16996699/
24. Vyunova TV, et al. (2016). Possible role of transthyretin in the biological mechanism of regulatory peptide neuroprotection — review. Molekuliarnaia Genetika, Mikrobiologiia i Virusologiia. https://pubmed.ncbi.nlm.nih.gov/30383932/
25. Liu R, et al. (2025). Semax peptide targets the µ-opioid receptor gene Oprm1 to promote deubiquitination and functional recovery after spinal cord injury in female mice — animal (mouse). British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/40692165/
26. Vanhee C, et al. (2020). The occurrence of putative cognitive enhancing research peptides in seized pharmaceutical preparations — analytical / forensic (Selank and Semax identified; noted as never having completed clinical trials). Drug Testing and Analysis. https://pubmed.ncbi.nlm.nih.gov/31667971/
27. Mavrych V, et al. (2026). Therapeutic peptides in gerontology: mechanisms and applications for healthy aging — review (covers Semax; does not cover this analogue). Frontiers in Aging. https://pubmed.ncbi.nlm.nih.gov/42021992/

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