ID: semax
Aliases: ACTH(4-10) analog, MEHFPGP, Met-Glu-His-Phe-Pro-Gly-Pro, SEMAX
Type: compound
Route/form: intranasal in regional clinical/research literature; formulation varies by study and region
Status: regional_or_research
Evidence level: early human
Best data tier: early human
Support scope: human, non-human/mechanistic
Source types: human_trial, preclinical
Linked sources: 4
Broad outcomes: Brain / mood / sleep
Reading note: These are curation notes anchored to linked sources, not a clinical recommendation or protocol.
Targets / mechanism
- ACTH(4-10)-derived peptide signaling
- BDNF/trkB pathway hypotheses
- neuroprotection hypotheses
Optimization domains
- cognition
- stroke
- neuroprotection
- BDNF
- nootropic
- CNS
Research basis
- Regional clinical stroke literature and preclinical BDNF/neuroprotection work explain why Semax is discussed as a nootropic/neuroprotective peptide.
- It is a distinct ACTH-fragment analog, not interchangeable with Selank despite both being Russian-developed intranasal peptides.
Limits, risks, and missing evidence
- Healthy-human cognitive enhancement evidence is weak compared with the stroke/preclinical evidence base.
Risk flags
- regional evidence
- limited human data
- CNS
- intranasal delivery uncertainty
- unapproved context
Linked papers, labels, and reviews
- The efficacy of Semax in the treatment of patients at different stages of ischemic stroke
human_trial / pubmed_semax_rehab_2018
Russian clinical trial in ischemic stroke/rehabilitation with BDNF-related endpoints. - The heptapeptide Semax stimulates BDNF expression in different areas of the rat brain in vivo
preclinical / pubmed_semax_bdnf_2003
Rat BDNF-expression source for Semax neurotrophin rationale. - Semax, an analog of ACTH(4-7), regulates expression of immune response genes during ischemic brain injury in rats
preclinical / pubmed_semax_ischemia_genes_2017
Rat focal-cerebral-ischemia transcriptome study supporting Semax neuroprotection/inflammation pathway rationale. - Semax, synthetic ACTH(4-10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats
preclinical / pubmed_semax_cns_review_2021
Rat neurochemical/behavioral study providing additional Semax CNS mechanism context; not healthy-human nootropic evidence.