NA-Semax Amidate (N-Acetyl Semax Amidate)

Cognitive & Neurological · ['N-Acetyl Semax Amidate', 'NA-Semax', 'Ac-Semax-NH2', 'Ac-MEHFPGP-NH2']

A terminally modified analog of the ACTH(4-7)-derived heptapeptide Semax, with N-acetylation and C-amidation intended to increase stability, investigated for BDNF/TrkB pathway modulation and neuroplasticity in preclinical research.

🔬 Research use only — not for human or veterinary use. K4 Elite does not provide dosing instructions.

Molecular Formula

C39H54N10O10S

Molecular Weight

855.0 g/mol

PubChem

CID 172638603 ↗

Research Level

Emerging Research

Browse the store →

NA-Semax Amidate (N-Acetyl Semax Amidate) chemical structure

N-Acetyl Semax Amidate (NA-Semax Amidate) is a modified analog of Semax, a synthetic heptapeptide derived from the ACTH(4-7) fragment (Met-Glu-His-Phe) extended at the C-terminus with a Pro-Gly-Pro stabilizing sequence. The core sequence Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP) is identical to that of Semax.

What distinguishes this analog are two terminal modifications: acetylation at the N-terminus and amidation at the C-terminus (Ac-MEHFPGP-NH2). PubChem lists it under CID 172638603 with molecular formula C39H54N10O10S and a molecular weight of about 855 g/mol.

The terminal modifications are described in the literature as reducing susceptibility to exopeptidases and altering the peptide's net charge and stability profile. All information here is from preclinical research and product reference material and is provided for research and reference use only.

Based on its preserved MEHFPGP core, NA-Semax Amidate is investigated as an ACTH(4-7) analog acting on the brain-derived neurotrophic factor (BDNF) / TrkB signaling pathway. Parent-compound Semax research reports increased hippocampal BDNF and NGF expression and enhanced TrkB receptor activity, associated with neuroplasticity and neuroprotection in animal models.

The N-acetyl and C-amide modifications are proposed to slow enzymatic degradation, which researchers hypothesize could extend or amplify neurotrophin-pathway activation relative to unmodified Semax. Direct comparative data for the modified analog remain limited to preclinical and product-characterization contexts.

BDNF/TrkB pathway modulation: Studies (largely on the parent Semax) reporting increased hippocampal BDNF expression and TrkB activation.
Neuroplasticity and neuroprotection: Animal-model work on Semax-family peptides in ischemia and cognitive paradigms.
Enzymatic stability of terminal modifications: Research on how N-acetylation and C-amidation affect peptidase resistance.
NGF expression: Reports of increased nerve growth factor expression with Semax-class peptides.
Attention and cognitive endpoints: Clinical and preclinical Semax literature examining cognitive and attentional measures.

📋 How published studies were conducted — a research reference summarizing study designs from the literature. This is not usage, dosing, or administration guidance. K4 Elite does not provide dosing instructions; determining any research protocol is the sole responsibility of the qualified researcher.

Semax BDNF/NGF expression studies (Dolotov, Shadrina et al.): Reported that the parent peptide Semax increased BDNF and TrkB expression in the rat hippocampus, providing the mechanistic basis extended to the acetylated/amidated analog. Reported for reference only.

Semax neuroprotection in ischemia models: Animal studies of the Semax family reported neuroprotective and neurotrophic effects in cerebral ischemia paradigms. Described for information only; any dosing figures are experimental parameters, not recommendations.

Terminal-modification characterization: Peptide-chemistry literature and product characterization describe how N-acetylation and C-amidation reduce exopeptidase degradation of ACTH-derived peptides. This is reporting on stability properties, not a usage protocol.

Combinations examined in the research literature. Descriptive only — not a recommendation to combine compounds.

Semax (parent peptide)Compatible

Shares the identical MEHFPGP core sequence; used as the primary comparator in the research literature.

Selank / N-Acetyl Selank AmidateCompatible

Frequently studied and formulated alongside Semax-family peptides in neuropeptide research.

BDNF/TrkB pathway agentsSynergistic

Proposed action converges on the BDNF/TrkB pathway, overlapping with other neurotrophin-pathway tool compounds.

Dopaminergic modulatorsNeutral

Some Semax literature notes effects on dopaminergic and monoaminergic systems; interactions are not well characterized.

References are being compiled for this entry.

How is NA-Semax Amidate different from Semax?

It shares the identical MEHFPGP core sequence but adds N-terminal acetylation and C-terminal amidation, modifications described as reducing enzymatic breakdown and altering the peptide's stability and charge profile.

What pathway is it studied for?

Like Semax, it is investigated for modulation of the BDNF/TrkB neurotrophin pathway and associated neuroplasticity and neuroprotection endpoints in preclinical models.

Is it more potent than Semax?

Product and preclinical sources suggest the terminal modifications may increase per-microgram stability and activity, but rigorous head-to-head clinical comparisons are not established; this entry makes no efficacy claim.

What is the origin of the Semax sequence?

The core is derived from the ACTH(4-7) fragment (Met-Glu-His-Phe) extended with a Pro-Gly-Pro sequence to improve stability; it is an ACTH-analog neuropeptide.

Is NA-Semax Amidate approved for use?

No. It is a research-use-only compound. It is not approved by regulatory agencies in most jurisdictions for human or veterinary use, and this entry is for reference only, not medical advice or a usage recommendation.

Disclaimer: This profile summarizes published preclinical and laboratory research for reference only. It is not medical advice and makes no claim of safety or efficacy in humans. Determining any research protocol is the sole responsibility of the qualified researcher. Products are sold strictly for in-vitro research and have not been evaluated by the FDA.