Semax
Semax is a synthetic heptapeptide based on the ACTH(4-10) fragment, extended with a proline-glycine-proline tail. The published record is largely preclinical and examines neurotrophin expression and monoamine systems in rodents. It holds no FDA or EMA marketing authorisation.
Synthetic melanocortin-fragment peptide
Research overview
Semax is a synthetic peptide corresponding to a modified fragment of adrenocorticotropic hormone, ACTH(4-10), extended at the C-terminus with a proline-glycine-proline sequence. It is characterised in the literature as lacking the corticotropic activity of the parent hormone. Dolotov and colleagues reported specific binding in rat basal forebrain and measured increases in brain-derived neurotrophic factor protein. Eremin and colleagues examined dopaminergic and serotonergic systems in rodents. Dmitrieva and colleagues measured transcription of neurotrophins and their receptor genes in a rodent cerebral-ischaemia model. The great majority of the published record is preclinical, and Semax holds no marketing authorisation from the FDA or the EMA.
What the literature studies
- Binding in rat basal forebrain and BDNF protein levels
- Transcription of neurotrophins and their receptor genes in rodent ischaemia models
- Dopaminergic and serotonergic activity measured in rodents
- Structural relationship to the ACTH(4-10) fragment and absence of corticotropic activity
From the Ironfield research guide
Neuropeptide research tools discussed around cognition, stress, and neurobiology models.
Sources
- 01Dolotov OV, et al. Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain. J Neurochem. 2006;97 Suppl 1:82-6. PubMed 16635254
- 02Eremin KO, et al. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res. 2005;30(12):1493-500. PubMed 16362768
- 03Dmitrieva VG, et al. Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Cell Mol Neurobiol. 2010;30(1):71-9. PubMed 19633950
Current evidence varies by compound. Many products discussed in this guide remain investigational, are not approved for general clinical use, and should only be handled under qualified research protocols.
No dosing, administration, or treatment instructions are provided.
The Ironfield research guide carries 11 further cited sources. See the guide.