Evidence Grade C — Moderate human evidence. 205 published studies, 45 human. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
Semax is a synthetic peptide derived from a fragment of ACTH, developed in Russia in the 1980s. It is used clinically in Russia as a nasal spray for stroke recovery and cognitive conditions but has never been evaluated by the FDA, EMA, or other major Western regulatory agencies. The clinical evidence is predominantly Russian-language.
Semax is also known by these brand and alternate names:
205 published studies: 45 human, 144 animal, 12 in-vitro, 10 reviews
Semax is approved in Russia for stroke recovery and cognitive conditions. It has not been approved by the FDA, EMA, or other major Western regulatory agencies, and the clinical evidence base has not undergone Western regulatory review.
Published clinical studies are predominantly Russian. The largest published study (110 stroke patients) reported correlations between treatment and BDNF levels. The evidence does not meet the standards typically required for FDA or EMA approval. Its regulatory status is limited to Russia and certain former Soviet states.
Research suggests Semax may interact with neurotrophic factor pathways, including upregulation of BDNF expression. These proposed mechanisms are based primarily on animal studies and a limited number of human studies conducted predominantly in Russia. The evidence has not been evaluated through FDA or EMA regulatory review processes.
Research suggests Semax has been in clinical use in Russia since 1996, with the largest published study involving 110 stroke patients. The Alzheimer's Drug Discovery Foundation assessed Semax and concluded that well-conducted published studies are lacking. Most clinical studies are available only as Russian-language abstracts, making full quality assessment difficult. No randomised, double-blind, placebo-controlled trials have been published in English-language journals. Reported side effects include nasal discolouration (about 10% of patients) and blood sugar elevation in people with diabetes. Widespread Russian use suggests an acceptable safety profile in that context, but data meeting Western regulatory standards are absent.
PeptideTrace tracks 0 registered clinical trials for Semax sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
Semax is a synthetic analogue of ACTH(4-10) with a Pro-Gly-Pro C-terminal extension. Its 7 amino acid sequence is Met-Glu-His-Phe-Pro-Gly-Pro (MEHFPGP), with molecular formula C37H51N9O10S and molecular weight 813.93 Da (CAS: 80714-61-0). Developed in the 1980s by N.F. Myasoedov and I.P. Ashmarin at the Institute of Molecular Genetics, Russian Academy of Sciences. Approved for clinical use in Russia in 1996 and added to the Russian List of Vital and Essential Drugs in 2011. Plasma half-life is very short (minutes), yet research suggests therapeutic effects persist for 20-24 hours after a single intranasal dose. The Pro-Gly-Pro extension dramatically increased duration versus native ACTH(4-10). Administration is primarily intranasal (0.1% solution for cognitive indications; 1% solution for stroke indications). Manufactured by JSC Peptogen (Moscow). Not approved by the FDA, EMA, or MHRA.
Research suggests Semax operates through multiple pathways. The primary mechanism involves rapid upregulation of BDNF and TrkB receptor expression in the hippocampus (Dolotov et al., 2006), with BDNF and NGF mRNA increases peaking at approximately 8 hours post-administration in frontal cortex, hippocampus, and retina. Semax lacks ACTH's hormonal activity (no cortisol stimulation) but research suggests it acts as an antagonist or partial agonist at MC4 and MC5 melanocortin receptors. In monoamine systems, animal studies indicate it significantly increased striatal 5-HIAA (serotonin metabolite) by approximately 25% at 2 hours and extracellular 5-HIAA up to 180% within 1-4 hours, while potentiating amphetamine's dopaminergic effects. Transcriptomic analysis in ischemia models revealed modulation of over 1,500 genes, suppressing inflammatory pathways and activating neurotransmission-related genes. Both Semax and Selank inhibit enkephalin-degrading enzymes with IC50 = 10 uM.
Clinical evidence is predominantly Russian. The largest published study (Gusev et al., 2018; N=110 stroke patients) showed Semax increased plasma BDNF levels regardless of rehabilitation timing, with positive correlation between BDNF and Barthel index scores. An fMRI study in 24 healthy subjects showed increased resting-state signal in the default mode network after intranasal 1% Semax versus placebo. Kaplan et al. (1996) reported improved attention and short-term memory in healthy volunteers at 250-1,000 ug/kg. Russian-approved indications include ischemic stroke, TIA, cognitive disorders, dyscirculatory encephalopathy, and optic nerve disease. Semax is not approved by the FDA, EMA, or MHRA and no Western clinical trials have been identified.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
Compare prices from 36 vendor listings
View pricing data across vendors and countries for Semax
Cerebrolysin has been studied in over 200 clinical trials involving more than 15,000 patients, primarily for stroke and Alzheimer's disease. The largest stroke trial (CASTA, 1,070 patients) showed no significant benefit on its primary endpoint. A Cochrane systematic review concluded that evidence was insufficient to support its routine use in stroke or dementia. Cerebrolysin is approved in some non-FDA/non-EMA jurisdictions for neurological conditions. Its clinical evidence base, despite being extensive in volume, has not met the standards required for FDA or EMA approval. The undefined molecular composition makes batch-to-batch consistency and quality standardisation inherently challenging compared to defined single-entity pharmaceuticals.
FGL has no marketing authorisation. A Phase I trial (24 healthy volunteers) of intranasal FGL demonstrated tolerability with only mild adverse events. Preclinical studies reported effects on memory in animal models. The compound has progressed further through formal development than many research peptides, having completed a Phase I safety study. However, no efficacy trials have been conducted in patients, and clinical development beyond Phase I has not been reported.
P21 has no marketing authorisation. No human clinical trials have been conducted. The evidence base consists entirely of studies in transgenic Alzheimer's disease mouse models, conducted primarily by a single research group. Animal studies reported behavioural and biochemical changes in AD mouse models following chronic oral administration. The translation of results from transgenic mouse models of Alzheimer's disease to human disease has historically been extremely poor — the vast majority of compounds showing efficacy in such models have failed in human trials. Products available through unregulated channels lack pharmaceutical quality assurance.
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
