What is not known about Semax?

No double-blind randomised trial with a clinical primary endpoint was found for any indication; the only placebo-controlled human study measured brain imaging in healthy volunteers. No cognitive endpoint has been measured in healthy people, which is the use the compound is marketed for outside Russia. No replication of the stroke findings outside Russia was found in the indexed literature. The Russian-language full texts have not been read or translated for this entry; it rests on English abstracts and PubMed records. Human pharmacokinetics after intranasal administration were not retrieved, so nothing here establishes how much peptide reaches the brain. Whether the reported BDNF increase causes the reported functional recovery is unresolved, because every human study reporting both is unblinded. Registration status in Russia could not be verified against the state register while writing

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nootropic

Semax

Also known as: MEHFPGP, Met-Glu-His-Phe-Pro-Gly-Pro, ACTH(4-7)-Pro-Gly-Pro, semaks

Human trial draft

A seven-residue peptide built from a fragment of ACTH with a Pro-Gly-Pro tail added, developed in Moscow and used in Russian neurology for stroke recovery and cognitive complaints. It has more human data behind it than almost anything else on this site — and none of it is a double-blind randomised trial of a clinical outcome. The literature is concentrated in a few Moscow institutions, much of it in Russian, with one author recurring throughout.

Sequence

MEHFPGP

Met-Glu-His-Phe-Pro-Gly-Pro · 7 residues · 813.93 Da (computed)

Contains no lysine.

verified C37H51N9O10S 813.90 Da (published)

Sequence source: PubChem CID 9811102, synonym 'Met-Glu-His-Phe-Pro-Gly-Pro', corroborated by a second resolver rung parsing the record's IUPAC name, whose composition is consistent with MEHFPGP. The formula computed from the sequence (C37H51N9O10S) matches the record exactly. Status is 'verified' on two agreeing rungs; the sign-off flag stays false because no human has checked this entry.

Claimed vs established

Mechanism

Claimed

An ACTH fragment analogue stripped of the hormone's endocrine activity, said to improve attention, memory and stress resistance and to protect brain tissue after ischemia, largely by raising BDNF and other neurotrophin signalling.

Actually established

Increased transcription of neurotrophins and their receptors has been reported repeatedly in rat brain after experimental ischemia, and increased plasma BDNF was reported in a Russian stroke rehabilitation cohort. That the compound moves BDNF is the best-supported part of the story. That the BDNF change is what produces the clinical improvements claimed for it has not been shown — every human study reporting both is unblinded.

Honest appraisal

How good is the evidence

Human trial 0 human RCTs · 3 human trials · 3 animal

Unusually for this site, human studies exist and are not tiny: a stroke rehabilitation cohort of 110 patients, an imaging study in 52 healthy volunteers with a placebo comparison, and an open-label trial in 27 patients with motor neuron disease. What is missing is the design that would make them decisive — none is a blinded randomised trial with a pre-stated clinical primary endpoint. The most informative result may be the negative one: in motor neuron disease the compound did not change the disease measures, only a quality-of-life score in an open-label setting.

Where this evidence comes from

N.F. Myasoedov is a listed author on four of the six studies cited here and appears on most of the Semax records returned by PubMed; the work comes from a small cluster of Moscow institutions. The stroke rehabilitation cohort is from a different group (Pirogov Russian National Research Medical University and a Moscow rehabilitation centre) and is the nearest thing to independent work in this entry. One rodent study includes Finnish co-authors, so the literature is not entirely single-country.

What is said vs what was shown

Claims, one at a time

Each claim carries its own evidence tier. A compound is never simply "well studied" — some of its claims may be, others not at all.

Claim	Verdict	Evidence	Basis
Improves attention, memory and mental performance in healthy people	untested	Mechanistic	This is the claim that sells the compound outside Russia, and no study found here measured a cognitive endpoint in healthy people. The one placebo-controlled study in healthy volunteers measured resting-state brain connectivity, not performance on any cognitive task.
Changes brain activity in healthy people	mixed	Human trial	In 52 healthy participants scanned before and after injection of Semax, Selank or placebo, differences in connectivity between the right amygdala and right temporal regions were reported, described by the authors as a first finding. This is an imaging biomarker with no established link to any symptom or capability, from a study whose randomisation and blinding are not stated in the record.
Speeds recovery after ischemic stroke	mixed	Human trial	In 110 post-stroke patients, subgroups that received semax alongside rehabilitation showed higher plasma BDNF and faster improvement on the Barthel index than subgroups that did not. Patients were assigned to semax and non-semax subgroups without stated randomisation or blinding, so expectation, clinician attention and allocation are not controlled; the report is in Russian and only the abstract was read here.
Helps in motor neuron disease	contradicted	Human trial	Directly tested in 27 patients and reported not to influence the course of chronic partial denervation or the clinical measures, including the timing of major functional deficits. A total quality-of-life score did improve, attributed to emotional state and motivation, in an open-label design with no control group — the setting in which a mood-linked self-report is least interpretable.
Protects the brain after ischemia	mixed	Animal	Rat models of cerebral ischemia report increased transcription of neurotrophins and their receptors, altered immune-response gene expression, and changes in brain-cell morphology and proliferation, the last from a study its own authors call a pilot. Gene expression and histology are not the same as functional recovery, and none of these studies measured behaviour.

Primary sources

The studies themselves

Study	Design	Subjects	Quality
[The study of chronic partial denervation and quality of life in patients with motor neuron disease treated with semax]. Serdiuk AV, Levitskiĭ GN, Miasoedov NF, Skvortsova VI · Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova · 2007 PMID 18379501 ru	open_label_trial / human	27 — Patients with definite, probable or possible motor neuron disease	Human trial risk of bias: high
[The efficacy of semax in the tretament of patients at different stages of ischemic stroke]. Gusev EI, Martynov MY, Kostenko EV, Petrova LV, Bobyreva SN · Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova · 2018 PMID 29798983 ru	controlled_trial / human	110 — Adults after ischemic stroke, entering rehabilitation early or late, each group split into semax and non-semax subgroups	Human trial risk of bias: high
Functional Connectomic Approach to Studying Selank and Semax Effects. Panikratova YR, Lebedeva IS, Sokolov OY, Rumshiskaya AD, Kupriyanov DA, Kost NV, Myasoedov NF · Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2020 PMID 32342318	controlled_trial / human	52 — Healthy adult volunteers	Human trial risk of bias: high
Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia. Dmitrieva VG, Povarova OV, Skvortsova VI, Limborska SA, Myasoedov NF, Dergunova LV · Cellular and molecular neurobiology · 2010 PMID 19633950	unknown / rat	— Rats subjected to experimental cerebral ischemia	Animal risk of bias: unclear
The effect of Semax and its C-end peptide PGP on the morphology and proliferative activity of rat brain cells during experimental ischemia: a pilot study. Stavchansky VV, Yuzhakov VV, Botsina AY, Skvortsova VI, Bondurko LN, Tsyganova MG, Limborska SA, Myasoedov NF, Dergunova LV · Journal of molecular neuroscience : MN · 2011 PMID 20617398	unknown / rat	— Rats subjected to experimental cerebral ischemia	Animal risk of bias: unclear
Semax, an analog of ACTH((4-7)), regulates expression of immune response genes during ischemic brain injury in rats. Medvedeva EV, Dmitrieva VG, Limborska SA, Myasoedov NF, Dergunova LV · Molecular genetics and genomics : MGG · 2017 PMID 28255762	unknown / rat	— Rats with ischemic brain injury	Animal risk of bias: unclear

What we do not know

No double-blind randomised trial with a clinical primary endpoint was found for any indication; the only placebo-controlled human study measured brain imaging in healthy volunteers.
No cognitive endpoint has been measured in healthy people, which is the use the compound is marketed for outside Russia.
No replication of the stroke findings outside Russia was found in the indexed literature.
The Russian-language full texts have not been read or translated for this entry; it rests on English abstracts and PubMed records.
Human pharmacokinetics after intranasal administration were not retrieved, so nothing here establishes how much peptide reaches the brain.
Whether the reported BDNF increase causes the reported functional recovery is unresolved, because every human study reporting both is unblinded.
Registration status in Russia could not be verified against the state register while writing this entry.
No dose from any cited study is recorded here, and several of the abstracts state one.