$100

Peptides
Semax
ACTH(4-7)PGP / MEHFPGP, synthetic ACTH fragment — Institute of Molecular Genetics, Russia. Supplied as a lyophilised powder in 10mg vials.
Supplied as lyophilised powder in a 10mg specification. Storage: -20°C · Keep dry, avoid light. Dispatched from Sydney, Australia-wide.
Product information
About Semax
ACTH(4-7)PGP / MEHFPGP
Research background as published in the scientific literature. Supplied for in-vitro laboratory research only; nothing here is a claim about use in humans or animals.
Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) derived from the ACTH(4-10) fragment, developed at the Institute of Molecular Genetics of the Russian Academy of Sciences. Unlike the parent ACTH hormone, Semax lacks significant adrenocorticotropic activity, making it a selective CNS research tool.
Over three decades of preclinical and some clinical research have examined Semax in models of ischaemia, neurodegeneration, cognitive enhancement, and attention. It is considered one of the best-characterised nootropic peptides in the Russian scientific literature.
- Origin
- Synthetic ACTH fragment — Institute of Molecular Genetics, Russia
- Research Areas
- BDNF upregulation, neuroprotection, cognitive pathway research
- Amino Acids
- 7 residues (Met-Glu-His-Phe-Pro-Gly-Pro)
- CAS Number
- 80714-61-0
- Molecular Weight
- 805.9 g/mol
- Key Pathways
- BDNF · NGF · Dopamine · Serotonin
- Primary Research
- Neuroprotection, cognition, ischaemia
- Research Models
- Rodent stroke and cognitive models
- 01BDNF & NGF UpregulationSemax research has consistently examined its effects on brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression. Animal studies report upregulation in hippocampal tissues, with proposed implications for neuroplasticity and memory consolidation research.
- 02Dopaminergic & Serotonergic SystemsLaboratory studies have investigated Semax's modulation of dopaminergic and serotonergic neurotransmission. Research proposes interactions with D2/D3 receptor pathways and serotonin transporter expression in prefrontal and limbic regions.
- 03Ischaemia & Neuroprotection ModelsPreclinical research has examined Semax in cerebral ischaemia and hypoxia models. Studies report reduced infarct volumes and improved neurological outcomes in rodent stroke models, with proposed mechanisms involving anti-apoptotic gene expression.
References
- 1Ashmarin IP et al. Semax: from laboratory to clinical use. Zh Vyssh Nerv Deiat Im I P Pavlova. 1997;47(2):419-26.
- 2Grigoriev VV et al. Semax effects on BDNF in rat brain. Bull Exp Biol Med. 2006.
- 3PubMed: pubmed.ncbi.nlm.nih.gov/?term=Semax+neuroprotection
- 4Dolotov OV et al. Semax stimulates BDNF expression. J Neurochem. 2006;99(4):1080-8.
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