Semax

What it is

Semax is a synthetic seven-amino-acid peptide built from a small fragment of ACTH (the pituitary hormone that stimulates the adrenal glands), modified so it retains ACTH's effects on the brain without its hormonal (steroid-stimulating) activity. It was developed in Russia in the 1980s and has been used there since the 1990s as a prescription intranasal drug for ischemic stroke recovery, certain cognitive disorders, and optic nerve disease. It is not approved by the FDA or EMA and is not available as an approved drug in the United States or Europe; there it exists only as an unregulated research chemical sold by peptide vendors. Animal and cell studies show Semax increases BDNF and NGF (proteins that support neuron survival and growth) in the brain, and a Russian human clinical study of post-stroke patients found that Semax raised blood BDNF levels alongside better recovery scores. The peptide is degraded very quickly in the body, within minutes, so its behavioral effects likely outlast its physical presence. Most of the supporting evidence comes from Russian-language research connected to its original development group, so independent Western replication is limited, and no rigorous modern human pharmacokinetic study has been published.

Dose ranges

Study-backed ranges carry a source you can open. Community ranges are widely reported but not clinically established - treat them as what people do, not as advice.

Storage

Common stacks

Interactions & cautions

No formal human drug-interaction studies were located. The clearest sourced signal is preclinical: in rodents, Semax markedly potentiated D-amphetamine's effect on extracellular striatal dopamine and locomotor activity, and increased striatal serotonin turnover on its own (Eremin et al., 2005, Neurochem Res). This suggests a plausible mechanistic basis for caution when combining Semax with dopaminergic/serotonergic stimulant drugs, but this has not been studied in humans or in combination with specific medications (e.g., SSRIs, MAOIs, stimulants), so no specific human interaction can be stated as established.

Questions people ask

Sources

1. [1]Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents PMID 16362768studySemax increases striatal serotonin metabolite levels and dramatically potentiates D-amphetamine-induced dopamine release/locomotor activity in rodents; basis for the interaction caution note.
2. [2]Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus PMID 16996037studyIntranasal Semax (50 mcg/kg) increases hippocampal BDNF protein and trkB activation in rats and improves avoidance learning; supports the BDNF-mechanism claims in the overview.
3. [3]Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia PMID 19633950studySemax and its active metabolite Pro-Gly-Pro upregulate neurotrophin/neurotrophin-receptor gene transcription in rat cortex after induced stroke; supports the neuroprotective mechanism claims.
4. [4]The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis PMID 24661604studyGenome-wide analysis showing Semax predominantly modulates immune-response and vascular genes after focal cerebral ischemia in rats; supports the mechanistic/neuroprotective evidence base.
5. [5]Semax, an analog of ACTH(4-7), regulates expression of immune response genes during ischemic brain injury in rats PMID 28255762studyFurther genome-wide evidence that Semax and its PGP fragment act through distinct neuroimmune gene-expression pathways after ischemic brain injury in rats.
6. [6]Comparative study of analgesic potency of ACTH4-10 fragment and its analog semax PMID 18018999studySemax (0.015-0.500 mg/kg) shows analgesic activity across its full tested dose range in rodent pain models, unlike the parent ACTH(4-10) fragment; preclinical dose-response data.
7. [7]Kinetics of Semax penetration into the brain and blood of rats after its intranasal administration PMID 16523722studyRadiolabeled Semax reaches rat brain within 2 minutes of intranasal dosing and is rapidly metabolized, with Pro-Gly-Pro becoming the predominant species; basis for the short-half-life / rapid-degradation statement.
8. [8]The efficacy of semax in the treatment of patients at different stages of ischemic stroke PMID 29798983studyRussian trial of 110 post-stroke patients: Semax (6 mg/day, two 10-day courses) raised plasma BDNF and was associated with improved Barthel index recovery scores; source for the clinical dose range and Russian clinical-use claim.
9. [9]Evaluation of therapeutic effect of new Russian drug semax in optic nerve disease PMID 10741256studyRussian clinical study finding intranasal Semax improved visual acuity, visual field, and optic nerve conductivity when added to therapy for optic nerve disease; source for the optic-nerve indication and confirms it is described as a 'Russian drug'.
10. [10]A New Generation of Drugs: Synthetic Peptides Based on Natural Regulatory PeptidesreviewReview by the Semax development group (Kolomin, Myasoedov et al.) characterizing Semax as a synthetic regulatory peptide effective in stroke therapy, composed only of natural amino acids; general background/overview source.
11. [11]DailyMed drug label search: 'semax'regulatoryConfirms zero FDA drug label results for Semax, i.e. no FDA-approved product exists; basis for the 'not FDA-approved' statement.
12. [12]PubChem Compound Summary for CID 9811102 (Semax / ACTH(4-7)-PGP)referenceChemical identity reference (molecular formula C37H51N9O10S) for Semax.
13. [13]Semax peptide overview and dosing/storage guidance (community reference site)communityCommunity-reported intranasal dosing range (200-600 mcg/day) and community storage guidance (frozen powder, refrigerated prepared solution); explicitly labeled community, not clinical evidence.
14. [14]Efficacy of Semax in acute ischaemic stroke (Gusev EI, Skvortsova VI, et al., 1997) PMID 11517472studyRussian clinical study of intranasal Semax in acute ischemic stroke reporting that the most effective daily doses were 12 mg for strokes of moderate severity and 18 mg for severe strokes.