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N-Acetyl Semax Amidate

NA-Semax Amidate · N-Acetyl Semax Amidate

Animal replicated

Research chemicalSemax Analog Nootropic Peptide ACTH Fragment Analog

RouteNasalGray-market only

Evidence grade: Animal replicated

Effect demonstrated in multiple animal studies; human data sparse or extrapolated. Grades summarize evidence quality, not whether a compound is appropriate, legal, or risk-free.

At a glance

What it is: NA-Semax Amidate — Dual-Modified Semax Analog — Community Research Chemical — Zero Human Trials for This Form — Semax Analog, Nootropic Peptide, ACTH Fragment Analog.
Why people use it: Used primarily for cognitive support.

If you only read one thing

N-Acetyl Semax Amidate is a compound built on layered extrapolations: (1) Semax's pharmacology extrapolated from ACTH(4-7) chemistry; (2) NA Semax Amidate's effects extrapolated from Semax's evidence base; (3) the potency enhancement extrapolated from general peptide chemistry principles about N-acetylation and amidation. Each layer is pharmacologically coherent. None of the layers constitutes a human clinical trial for this specific compound. The community uses it widely, reports consistent cognitive enhancement effects, and has developed a coherent dosing protocol. The evidence grade for the compound-specific claims is E (community consensus) layered on D (modification chemistry) layered on B (Semax underlying evidence). Understanding which layer each claim rests on is the chapter's essential contribution.

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Route / form

Same compound, route-specific context. Switch forms instead of opening separate pages.

Evidence fit

Route-specific

Use the route notes below to match form, goal, and evidence quality.

Route caveat

Protocol not standardized

No route-matched protocol rows were parsed for this form; use the route notes and full dosing chapter before comparing options.

Protocol anchor

Full dosing section

Open the full report at the dosing chapter for protocol rows, cycle context, and administration notes.

Typical dose snapshot

See route notes

Evidence varies by use case

Published literature

0human trials0human studies0animal0in vitro

Evidence reality check

Human evidence

No human studies

0 observational; RCT evidence not present in corpus.

Preclinical base

0 lab signals

0 animal; 0 in-vitro/mechanistic.

Risk posture

No major flags listed

Review route-specific cautions before use.

Categories

Cognition & Mood

Properties

Not injectable

Half-life

The resulting compound has an estimated half-life of 4-6 hours — a massive pharmacokinetic advantage over Semax's 3-5 minutes — without altering the core sequence that interacts…

Evidence

CAnimal replicated

The CRITICAL Naming Confusion

This chapter covers N-Acetyl Semax Amidate. NA Selank Amidate (Adamax) is a completely different compound — a dual-modified version of Selank (not Semax). The Compound Report file pbnasav4 covers NA Selank Amidate. The abbreviation 'NA-SA' or 'NASA' is used for both in community shorthand, causing persistent confusion. Semax and Selank are different peptides with different structures, mechanisms, and clinical evidence bases. Before ordering: confirm your vendor is supplying Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH₂ (Semax-based) and not the Selank-based compound.

Semax Background

Semax (Met-Glu-His-Phe-Pro-Gly-Pro) is a synthetic heptapeptide derived from the ACTH(4-10) fragment of adrenocorticotropic hormone with a C-terminal Pro-Gly-Pro extension for stability. Developed at the Institute of Molecular Genetics, Russian Academy of Sciences. Russian-approved for ischemic stroke recovery and cognitive impairment. Intranasal 0.1% spray for cognitive applications; 1% spray for stroke recovery at higher doses. The Pro-Gly-Pro extension adds stability against midchain cleavage and has independent pharmacological activity. N-Acetyl Semax Amidate adds two further modifications on top of this.

What the Modifications Do

N-acetylation: adds acetyl group (CH₃CO-) to the N-terminal methionine → blocks aminopeptidase access to the free N-terminus → protects against N-terminal exopeptidase degradation → extends plasma and tissue half-life; simultaneously increases lipophilicity, enhancing passive diffusion across the BBB. C-terminal amidation: converts the C-terminal carboxyl group (-COOH) to an amide (-CONH₂) → blocks carboxypeptidase degradation from the C-terminus → neutralizes the negative charge at the C-terminus, improving fit in receptor binding pockets where many neuropeptide receptors prefer neutral C-termini. Combined effect: protection from both directions of enzymatic attack + improved BBB crossing + improved receptor interaction = estimated 3-4x greater potency per microgram vs unmodified Semax.

Evidence Grade

NA Semax Amidate itself: Grade E (community consensus) + Grade X (theoretical extrapolation from modification chemistry). Human evidence: zero trials for this specific modification. Mechanism of the modifications: Grade D (chemical/biochemical; N-acetylation and amidation effects on peptide stability are well-established in peptide chemistry). Semax underlying pharmacology: Grade B (limited human; Russian clinical trials including Gusev 2018 stroke study; Russian regulatory approval). All NA Semax Amidate chapter content extrapolated from Semax data unless stated otherwise.

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Alternatives

Compare nearby options

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Adamax

Same class · Semax Analog

A Structural Modification of Semax With No Published Studies of Its Own. Being Sold as 'The Most Potent Semax Analog.' Every Claim Belongs to Its Parent Compound.

PE-22-28

Same class · Nootropic Peptide

The 7-Amino-Acid Antidepressant That Works in 4 Days Instead of 4 Weeks. TREK-1: The Potassium Channel That Keeps You Depressed. IC50 of 0.12 nM — 333x More Potent Than Its Parent Spadin. Duration Extended to 23 Hours vs 7 Hours. Hippocampal Neurogenesis in 4 Days. The Same One French Research Group Since 2010. Zero Human Trials. A Novel Mechanism That Bypasses the Serotonin Transporter Entirely.

9-ME-BC

Shared goal · cognition

Synthetic β-carboline heterocyclic amine with a compelling in vitro dopaminergic neuroprotective profile and zero human clinical trials. Also a MAO-A inhibitor (IC50 = 1 μM) with tyramine-reaction and serotonin-syndrome risk, plus photosensitizer concerns from UV-activated DNA damage potential.