N-acetylated derivatives of Semax (parent: MEHFPGP, the Russian Academy ACTH(4–7) analog). Zero published pharmacology on the N-acetyl forms themselves. The one direct chemistry paper (Magrì 2016) shows N-acetylation changes Cu(II)/Zn(II) coordination — so the modified molecule isn't pharmacodynamically identical to parent Semax, but direction never measured.
This guide covers two related but distinct vendor derivatives of Semax:
| Name | Sequence | Modifications vs parent |
|---|---|---|
| Semax (parent) | Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) | Russian Academy ACTH(4–7) analog with PGP cap. Russian-registered nasal solution drug since 1996. |
| N-Acetyl Semax | Ac-MEHFPGP | N-terminal acetylation only. |
| N-Acetyl Semax Amidate (NASA) | Ac-MEHFPGP-NH2 | N-terminal acetylation plus C-terminal amidation. |
Don't confuse with Adamax (Ac-MEHFPGP-AG-NH2), which is N-Acetyl Semax with an additional adamantyl-AG cap copied from the P21 peptidomimetic — a fourth distinct molecule. See the Adamax guide.
The audit-critical asymmetry: parent Semax has substantial Russian and some Western primary literature; N-Acetyl Semax and N-Acetyl Semax Amidate have zero published pharmacology on the named molecules. Direct PubMed searches for "N-acetyl Semax," "Ac-Semax," "Ac-MEHFPGP," and "Semax amidate" return nothing. Every potency claim, BDNF-fold-increase claim, and half-life claim in vendor copy is design-rationale extrapolation from parent Semax.
The one direct chemistry paper is Magrì A et al. J Inorg Biochem 2016 (PMID 27586814), "N-terminus acetylation of Semax: effect on copper and zinc binding," which demonstrates N-acetylation provably alters Cu(II)/Zn(II) coordination chemistry. Translation: the modified molecule isn't pharmacodynamically identical to parent Semax — but in which direction has never been measured. Tomasello 2025 (PMID 40496623) is a follow-on copper-chelation study.
Every mechanism claim below is anchored to the parent Semax literature. None has been measured for N-Acetyl Semax or Semax Amidate as discrete molecules.
Parent Semax pharmacology: indirect BDNF / NGF / TrkB upregulation in rat hippocampus (Dolotov 2006, PMIDs 16996037 and 16635254 binding-site work); mesolimbic dopamine modulation only with stimuli — Eremin 2005 (PMID 16362768) found Semax modulates dopamine and serotonin in the presence of amphetamine but not at baseline (extended in Glazova 2021, PMID 33418449); rat PK characterized in Shevchenko 2006 (PMID 16523722); anti-inflammatory and immune gene expression in focal-ischemia and immune contexts (Dmitrieva 2010 PMID 19633950; Samotrueva 2019 PMID 31028579); ACTH(4–7) framework specifically designed without HPA-axis activation (Vyunova 2017 PMID 27921334 characterizes the SAR); Russian-Academy N-terminal SAR — Glazova 2005 (PMID 16212268) on N-terminal modifications, the closest published work but still not specifically Ac-MEHFPGP; Russian clinical use in acute ischemic stroke and cognitive disorders (Gusev 2001 PMID 11517472; Gusev 2018 PMID 29798983, n=110).
What the modifications are hypothesized to do: N-acetylation reduces aminopeptidase cleavage at the N-terminus (extends plasma residence) — confirmed chemically in Magrì 2016 to alter metal-binding chemistry, mechanism altered but direction unmeasured. C-terminal amidation (Semax Amidate only) reduces carboxypeptidase cleavage. Vendor framing is "stronger and longer-acting Semax." None measured for these molecules specifically.
The Magrì 2016 finding matters: Semax binds copper and zinc at its N-terminus (histidine and methionine residues), and N-acetylation occupies the N-terminus, altering the metal-binding profile. Some Semax mechanism work proposes metal-binding plays a role in CNS effects. So the N-acetyl modification isn't pharmacodynamically silent — it changes something measurable. What that means for clinical effect: nobody has published.
| Claim | Source | What it measured |
|---|---|---|
| Hippocampal BDNF / TrkB upregulation | Dolotov 2006 PMID 16996037, PMID 16635254 | Parent Semax only. |
| Cognitive enhancement / nootropic effects | Gusev 2001 PMID 11517472; Gusev 2018 PMID 29798983 | Parent Semax only. Russian-registered indications. |
| N-terminal SAR (closest direct work) | Glazova 2005 PMID 16212268 | N-terminal modifications of Semax broadly — not specifically Ac-MEHFPGP. |
| N-acetylation alters metal coordination | Magrì 2016 PMID 27586814; Tomasello 2025 PMID 40496623 | Direct evidence on N-Acetyl Semax chemistry. Establishes the modification isn't silent. Clinical direction: not measured. |
| "More potent than parent Semax" | None | Pure design-rationale extrapolation. |
| "Longer half-life" | None | Not measured for N-Acetyl Semax. |
| "BDNF fold-increase X" | None for the derivative | Some sources cite parent-Semax BDNF data and present it as derivative data. |
| Human PK / safety of N-Acetyl Semax | None | No published study. |
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Start Tracking FreeNo published trial of N-Acetyl Semax or Semax Amidate exists. Dosing reflects vendor / community convention extrapolated from parent Semax.
| Parameter | Common Range |
|---|---|
| Dose (intranasal) | 200–600 µg/spray, 1–3 sprays/day; total ~600–1800 µg/day |
| Dose (SC, less common) | 200–500 µg/day |
| Frequency | Daily, morning preferred (avoid late-day to reduce insomnia per parent-Semax convention) |
| Cycle length | 2–6 weeks (community) |
| Route | Intranasal most common; SC less common |
The "longer half-life" framing is sometimes used to justify less-frequent dosing, but no published PK study supports specific intervals for the N-acetyl forms.
For a typical 5 mg lyophilized vial: add 2 mL bacteriostatic water → 2.5 mg/mL (2500 µg/mL). On a U-100 insulin syringe, 1 unit = 25 µg. For a 500 µg intranasal dose, draw 0.2 mL (20 units).
Storage: lyophilized stable at room temperature short-term, refrigerate longer-term. Reconstituted: refrigerate, use within 28 days. Nasal solution: protect from light; refrigerated. Full protocol in the Bacteriostatic Water guide.
Pre-filled with a typical N-Acetyl Semax setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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No published human safety data on N-Acetyl Semax or Semax Amidate.
Parent Semax safety profile (extrapolated): generally well-tolerated in Russian clinical trials at registered doses; insomnia with afternoon/evening dosing (consistent with mild stimulation); some users report increased focus/drive that can cross into irritability at higher doses; nasal irritation with intranasal route; transient headache; no abuse potential or withdrawal pattern reported.
The Magrì 2016 altered Cu/Zn coordination is a chemical change that could propagate to a different effect profile in vivo. Not characterized.
This area has the highest-confusion risk in the gray-market peptide world. Four similar names sit on top of four different molecules.
| Name | Sequence | What it is |
|---|---|---|
| Semax (parent) | Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) | Russian-registered drug. Substantial primary literature. The actual measured-pharmacology molecule. |
| N-Acetyl Semax | Ac-MEHFPGP | N-terminal acetylation. Zero published pharmacology. One chemistry paper (Magrì 2016) shows altered metal binding. |
| N-Acetyl Semax Amidate (NASA) | Ac-MEHFPGP-NH2 | N-terminal acetylation plus C-terminal amidation. Zero published pharmacology. |
| Adamax | Ac-MEHFPGP-AG-NH2 | N-Acetyl Semax + adamantyl-AG cap from P21. Different molecule. Zero PubMed papers on Adamax. |
Other adjacencies: N-Acetyl Selank applies the same modification to a different parent (TKPRPGP, tuftsin analog) — same logic, different mechanism. Selank (parent) is the sister Russian Academy peptide (GABAergic anxiolytic; not a parent of N-Acetyl Semax). Cerebrolysin is a porcine brain extract (different family). P21/P021 is the source of the adamantyl C-cap added to make Adamax (Iqbal-lab Alzheimer's preclinical candidate; no human trial).
Vendor identity confidence: research-chem vendors selling "N-Acetyl Semax" may be supplying Ac-MEHFPGP, Ac-MEHFPGP-NH2, parent Semax mislabeled, or other variants. No industry-standard verification, no monograph, no reference standard. Buyer-beware.
N-Acetyl Semax is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
StackTrax’s preferred partner NextGen Peptides does not currently carry N-Acetyl Semaxin their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
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Start Tracking FreeN-Acetyl Semax is the N-terminally acetylated derivative of Semax, with sequence Ac-MEHFPGP. There is also a related variant called N-Acetyl Semax Amidate (sometimes NASA) with sequence Ac-MEHFPGP-NH2 — N-terminal acetylation plus C-terminal amidation. Parent Semax is Met-Glu-His-Phe-Pro-Gly-Pro, the Russian Academy ACTH(4–7) analog with a PGP cap, registered in Russia as a nasal solution drug since 1996. The N-acetyl forms are not registered separately anywhere. Do not confuse either with Adamax (Ac-MEHFPGP-AG-NH2), which is a fourth distinct molecule adding an adamantyl-AG cap from the P21 peptidomimetic.
Almost none. Direct PubMed searches for "N-acetyl Semax," "Ac-Semax," "Ac-MEHFPGP," and "Semax amidate" return zero records for the named molecules themselves. Every potency claim, BDNF-fold-increase claim, and half-life claim in vendor copy is design-rationale extrapolation from parent Semax. The one direct chemistry paper is Magri A et al. 2016 (PMID 27586814), "N-terminus acetylation of Semax: effect on copper and zinc binding," which demonstrates N-acetylation provably alters Cu(II)/Zn(II) coordination — so the modified molecule is NOT pharmacodynamically identical to parent Semax, but in which direction has never been measured.
Unknown. The hypothesis is that N-acetylation reduces aminopeptidase cleavage at the N-terminus, extending plasma residence — and Magri 2016 confirmed chemically that the modification alters metal-binding chemistry. So the modification is not pharmacodynamically silent. But whether that translates to a stronger or longer-acting effect in vivo has never been measured head-to-head. Glazova 2005 (PMID 16212268) is the closest direct work — N-terminal SAR of Semax broadly — but it is still not specifically Ac-MEHFPGP. The vendor framing of "stronger and longer-acting Semax" is design-rationale extrapolation, not measured fact.
Parent Semax has been characterized as a nootropic and neuroprotective peptide. Mechanism work shows indirect BDNF, NGF, and TrkB upregulation in rat hippocampus (Dolotov 2006, PMIDs 16996037 and 16635254), mesolimbic dopamine modulation only in the presence of stimuli like amphetamine (Eremin 2005, PMID 16362768), and anti-inflammatory gene expression in focal-ischemia models. The ACTH(4–7) framework was specifically designed without HPA-axis activation (Vyunova 2017, PMID 27921334). Russian clinical use has been in acute ischemic stroke and cognitive disorders (Gusev 2001 PMID 11517472; Gusev 2018 PMID 29798983, n=110).
FDA: never approved (parent or derivatives). EMA: not approved. Russia: parent Semax is registered (1996/1997) as a nasal solution but the N-acetyl forms are NOT registered separately. WADA 2026: not on the prohibited list by name, but S0 catch-all may apply. Important caveat: Semax is an ACTH(4–7) fragment, and while the (4–7) fragment was specifically designed without HPA-axis activation, an anti-doping panel ruling could plausibly invoke S2.4 (Corticotrophins). Athletes should consult their governing body.
No published trial of N-Acetyl Semax or Semax Amidate exists. Dosing reflects vendor and community convention extrapolated from parent Semax: 200–600 mcg per spray intranasally, 1–3 sprays per day (total roughly 600–1800 mcg per day). Subcutaneous dosing is less common at 200–500 mcg per day. Cycles are typically 2–6 weeks. Morning dosing is preferred to reduce insomnia risk, consistent with parent-Semax convention. The "longer half-life" framing is sometimes used to justify less-frequent dosing, but no published PK study supports specific intervals for the N-acetyl forms.
No published human safety data on N-Acetyl Semax or Semax Amidate specifically. Parent Semax safety profile (extrapolated): generally well-tolerated at registered doses, with insomnia from afternoon or evening dosing consistent with mild stimulation, some users reporting increased focus/drive that can cross into irritability at higher doses, nasal irritation with intranasal route, transient headache, and no abuse potential or withdrawal pattern reported. The Magri 2016 altered Cu/Zn coordination is a chemical change that COULD propagate to a different in vivo effect profile, but that has not been characterized.
Disclaimer: This guide is for educational and informational purposes only and is not intended as medical advice, diagnosis, or treatment. The compounds discussed are not FDA approved for human use. Always consult a qualified healthcare provider before starting any new supplement or peptide protocol. StackTrax does not sell peptides or supplements directly — purchase links go to third-party vendors. StackTrax is not responsible for the products, quality, or business practices of any third-party vendor. This page contains affiliate links — StackTrax may earn a commission on purchases at no extra cost to you.
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StackTrax guides cover peptides and compounds that are not FDA-approved for the uses discussed. The dosing, reconstitution, and safety information is compiled from published research and community protocols for educational purposes only.
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