Semax

ACTH fragment analog researched in neuroprotection/nootropic contexts; most evidence is mechanistic/preclinical or limited clinical literature.

goal:focus-cognitivegoal:cognitivegoal:focusgoal:nootropicconstraint:not-drug-test-safeevidence:lowstudy:mechanistic-animalpop:other-unclearform:other

Dosing model

FLATFixed dose (no body-weight scaling).

Min dose

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Max dose

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Rounding

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Evidence

3 records

Mechanistic cognitive pathway modulation

Preclinical / mechanistic work • Mechanistic study

Low

Mechanistic literature suggests Semax may influence hippocampal BDNF/trkB-related signaling; this is supportive biology rather than definitive clinical efficacy.

Dose: —

Citation: Dolotov et al., (2006) — Semax analog with cognitive effects (mechanistic)

Overall brain health evidence appraisal

Humans (evidence review) • Independent evidence review

Low

An independent cognitive vitality report reviews Semax and emphasizes limited high-quality human clinical evidence for cognitive outcomes.

Dose: —

Citation: Alzheimer's Drug Discovery Foundation (ADDF) — Semax Cognitive Vitality Report

Neurotrophin signaling and gene expression after cerebral ischemia (mechanistic)

Rats (ischemia/reperfusion model) • Mechanistic/animal

Low

Animal work demonstrates that Semax activates transcription of neurotrophins (BDNF, TrkC, TrkA) and suppresses pro-inflammatory gene expression after cerebral ischemia; this is not direct proof of cognitive improvement in healthy humans.

Dose: —

Citation: Shadrina et al., (2010) — Semax and Pro-Gly-Pro activate neurotrophins after cerebral ischemia (rat model)

Forms

Other

Research material (vendor listing)