NA-Semax Amidate

N-Acetyl Semax Amidate is a terminally modified Semax analog, typically represented as Ac-Met-Glu-His-Phe-Pro-Gly-Pro-NH2. PubChem provides a compound record for the modified analog, but defensible peer-reviewed biological studies or clinical trials directly testing N-Acetyl Semax Amidate were not found. The credible evidence base is therefore parent Semax evidence only. Parent Semax is an ACTH(4-10)-derived heptapeptide studied in rodents for BDNF/trkB signaling, NGF/BDNF gene-expression dynamics, and focal ischemia transcriptomics. A Russian clinical study in post-ischemic-stroke rehabilitation reported increased plasma BDNF and improved functional recovery measures with parent Semax. These data cannot be transferred to the acetylated/amidated analog without direct studies.

Parent Semax Neurotrophin Research

Parent Semax increased hippocampal BDNF protein, trkB phosphorylation, and BDNF/trkB mRNA measures in rats ^[2].

Ischemia and Clinical Context

Parent Semax affected immune- and vascular-system gene expression in a rat focal ischemia model, and a clinical parent-Semax study reported post-stroke rehabilitation signals ^[4][5].

Direct Variant Gap

These findings are Semax-family context, not proof for N-Acetyl Semax Amidate ^[1].

Compound Record Is Not Safety Evidence

PubChem supports identity of N-Acetyl Semax Amidate as a compound record, but not biological safety or efficacy ^[1].

Analog-Specific Translation Gap

Parent Semax studies cannot establish safety, dosing, or expected effects for N-Acetyl Semax Amidate because terminal modification can alter stability, exposure, and activity ^[2][3][4].