Semax
aka ACTH 4-10 analogue · Met-Glu-His-Phe-Pro-Gly-Pro · heptapeptide
A synthetic nootropic peptide researched for cognitive enhancement, neuroprotection, and BDNF upregulation.
Sequence
MEHFPGP
Met-Glu-His-Phe-Pro-Gly-Pro
Mechanism of action
Semax is a synthetic peptide that primarily acts as a neuroprotective agent by modulating the expression of brain-derived neurotrophic factor (BDNF) and other neurotrophins. It enhances the availability of neurotransmitters like dopamine and serotonin, which are crucial for cognitive processes. Semax also inhibits the breakdown of enkephalins, which are peptides that regulate pain and stress responses. Additionally, it may improve cerebral blood flow, contributing to its cognitive-enhancing effects.
What the evidence actually shows
There are several human trials conducted in Russia that suggest Semax improves cognitive function and mood, particularly in patients with neurological conditions. However, these studies are limited in number and often lack rigorous controls. More high-quality, placebo-controlled trials are needed to confirm these effects. | REGULATORY: FDA Category 2 reclassification to Category 1 expected (announced Feb 2026).
Regulatory status
In the UK, Semax is not approved for medical use and is considered a research compound. It is not licensed by the MHRA for any therapeutic indications.
Source ↗Pharmacokinetics
Dosing — what backs each figure
Semax is not approved by FDA, EMA or MHRA, but Russian clinical studies do document human intranasal regimens: 12 mg/day for moderate and 18 mg/day for severe acute ischaemic stroke over 5- to 10-day courses, and 6 mg/day as two 10-day courses 20 days apart in stroke rehabilitation. The published courses are short and indication-specific, not open-ended nootropic use.
Most effective daily doses 12 mg/day (moderate-severity stroke) and 18 mg/day (severe stroke), given as 5-day and 10-day treatment courses respectively
patients in the acute period of hemispheric ischaemic stroke (n=30 vs 80 conventionally treated controls) · intranasal
6000 mcg/day (6 mg/day) given as two 10-day courses separated by a 20-day interval
adults in early (89 days) or late (214 days) rehabilitation after ischaemic stroke (n=110) · intranasal (not stated explicitly in abstract; Semax is an intranasal formulation)
Gusev, Martynov et al., Zh Nevrol Psikhiatr 2018;118(3 Vyp 2):61-68 ↗
Single intranasal administration of 1% Semax (total mg not stated), imaged at 5 and 20 minutes post-dose
healthy volunteers aged ~44 (n=14 active, 10 placebo), resting-state fMRI study · intranasal
- Dose
- Research literature cites intranasal ~200 to 600 mcg/day
- Frequency
- 1-3x daily
Why this isn't evidence
Every human dose that could be sourced is 6-18 mg/day, i.e. 10-90 times higher than the 200-600 mcg/day claimed, so the ported figure does not come from the clinical literature it invokes - though the dosingNotes' incidental '10-14 day cycle' does coincidentally resemble the published 5-10 day treatment courses.
This figure is shown because it is what circulates and what people search for — not because it is supported. Cycle lengths in particular tend to be convention copied between compounds rather than anything derived from a compound's own pharmacokinetics.
Handling and storage
Safety
- ·Nasal irritation
- ·Headache
- ·Allergic reactions
- ·Hypersensitivity to Semax or any of its components
- ·MAO inhibitors: May enhance serotonergic effects, increasing the risk of serotonin syndrome
Generally well tolerated in studies
Reported combinations
- ·Piracetam: May enhance cognitive benefits
- ·Anticholinergics: May reduce cognitive enhancement effects
Combination claims in this dataset are largely unsourced and should be treated as folk knowledge until a citation appears beside them.
References (3)
- Dolotov OV, Karpenko EA, Inozemtseva LS, et al. (2006) Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus. ↗Brain ResearchPMID 16996037DOI
Rat study showing semax increases BDNF and trkB expression in the hippocampus, the most-cited mechanistic basis for its claimed nootropic effect.
- Gusev EI, Martynov MY, Kostenko EV, Petrova LV, et al. (2018) [The efficacy of semax in the treatment of patients at different stages of ischemic stroke]. ↗Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova (Russian)PMID 29798983DOI
Russian-language clinical report on semax across stages of ischaemic stroke. The principal human dataset, but Russian-language and not a Western-standard blinded RCT.
- Inozemtseva LS, Yatsenko KA, Glazova NY, et al. (2024) Antidepressant-like and antistress effects of the ACTH(4-10) synthetic analogs Semax and Melanotan II on male rats in a model of chronic unpredictable stress. ↗European Journal of PharmacologyPMID 39442746DOI
Rat chronic-unpredictable-stress model reporting antidepressant-like and antistress effects of semax.
Data provenance
Chemistry and citations on this page were checked against primary sources on 2026-08-14. Values that could not be verified were left blank rather than filled with a plausible guess.
Could not verify
storage, reconstitution, regulatory.wada, regulatory.russianApproval