Peptide Evidence Index

Semax

Evidence last reviewed: September 2026

Quick answers

What is it?
Semax is a synthetic seven-amino-acid peptide built from a fragment of ACTH (ACTH 4-10) with a three-amino-acid tail added, developed in Russia and given as a nasal spray or nasal drops.
Why are people interested in it?
It is used and studied in Russia as a neuroprotective and cognitive-enhancing agent, and is marketed elsewhere for stroke recovery and nootropic use.
What has actually been studied?
Small, non-blinded, mostly open-label human studies conducted in Russia, covering ischemic stroke recovery, optic nerve disease, and motor neuron disease / ALS, plus rat studies on its effect on brain growth factors.
How strong is the evidence?
Early human data only — every located human study is Russian, small, and non-blinded, and zero trials are registered on ClinicalTrials.gov, so there is no controlled evidence confirming a real effect in people.
What don't we know yet?
Whether Semax does anything measurable against a real placebo under blinded conditions, whether its claimed stroke-recovery or cognitive effects hold up outside the researchers who developed it, and its long-term safety are all unestablished.
Where can I read the original research?
Sources at the bottom of this page: The efficacy of semax in the treatment of patients at different stages of ischemic stroke; Effectiveness of semax in acute period of hemispheric ischemic stroke.

Plain-English overview

Semax is a synthetic seven-amino-acid peptide built from a fragment of adrenocorticotropic hormone (ACTH 4-10) with a three-amino-acid tail (Pro-Gly-Pro) added on. It was developed in Russia, where it is described in the medical literature as a domestically registered drug, given as a nasal spray or nasal drops. In Russian clinical practice and research it has mainly been studied as a neuroprotective and cognitive-enhancing agent, particularly for ischemic stroke recovery. Every human study located for this profile was published in Russian-language journals, almost entirely in Zhurnal Nevrologii i Psikhiatrii, and none was double-blind or placebo-controlled. A separate line of Russian laboratory research has examined how Semax affects nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in rat brain, offering a possible mechanism for its neuroprotective claims without establishing that the same effect occurs in people. Semax is not approved as a medicine in the United States, the EU, or the UK.

What researchers are studying it for

Current evidence level

Early human data

Regulatory status: Not an approved medicine. Evidence strength and approval are scored separately; approval is a regulatory decision about a specific use, not a measure of how much research exists.

Human research

Four human studies were located, all non-blinded and all conducted in Russia. The largest, Gusev et al. (2018, n=110), examined patients at different stages of ischemic stroke, comparing Semax-treated subgroups rather than using a placebo arm. An earlier study by the same lead author (Gusev et al., 1997) compared 30 stroke patients given Semax against 80 patients receiving conventional therapy alone, using clinical and electrophysiological measures including EEG and evoked potentials, and reported that Semax was associated with faster regression of neurological deficits, particularly motor problems, at daily doses of 12–18 milligrams depending on stroke severity. A separate study in optic nerve disease (Polunin et al., 2000) compared three groups distinguished by route of administration — intranasal drops, endonasal electrophoresis, and a control group — rather than testing Semax against no treatment, and reported improved visual acuity, visual field, and color vision in the treated groups. The one study in motor neuron disease/ALS (Serdiuk et al., 2007, n=27) was explicitly described as an "open-label clinical trial"; Semax did not change the nerve-damage measurements tracked by needle electromyography, but patients reported improved quality-of-life scores, most notably 10 days into treatment. No trial of Semax is registered on ClinicalTrials.gov. Taken together, the human evidence for Semax consists of small, open-label, or non-blinded comparative studies, the largest involving about 110 people, none of which used a placebo control or was conducted outside Russia.

Animal and preclinical research

A series of Russian laboratory studies has examined how Semax affects the brain in rats. Dolotov et al. (2006, Journal of Neurochemistry) found that intranasal Semax bound to specific sites in the rat basal forebrain and increased levels of brain-derived neurotrophic factor (BDNF) protein there within three hours. A related study (Dmitrieva et al., 2009) found that Semax activated the transcription of neurotrophins and their receptor genes in the cortex of rats after an induced stroke (permanent middle cerebral artery occlusion). An earlier pharmacokinetic study in rats (Sheremet et al., 2004) found that intranasally applied Semax penetrated into the brain and eyes of the animals, offering a rationale for its use as an intranasal treatment for optic-nerve disease. These are laboratory and animal findings and do not establish that Semax produces the same neuroprotective effect in human patients.

Major findings

What has not been established

Important limitations

Regulatory status

Semax is described in Russian medical literature as a domestically registered drug and is used clinically there, chiefly as an intranasal stroke-recovery and nootropic treatment. It has not been evaluated or approved as a medicine by the FDA, the EMA, or the UK's MHRA, and no application for approval outside Russia is known.

Primary research sources

Gusev et al., "Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)"
Zhurnal Nevrologii i Psikhiatrii, 1997; PMID: 11517472
Polunin et al., "The study of therapeutic effect of new Russian drug semax in optic nerve disease"
Vestnik Oftalmologii, 2000; PMID: 10741256
Serdiuk et al., "The study of chronic partial denervation and quality of life in patients with motor neuron disease treated with semax"
Zhurnal Nevrologii i Psikhiatrii, 2007; PMID: 18379501
Gusev et al., "The efficacy of semax in the treatment of patients at different stages of ischemic stroke"
Zhurnal Nevrologii i Psikhiatrii, 2018; DOI: 10.17116/jnevro20181183261-68
Dolotov et al., "Semax, an analogue of adrenocorticotropin (4-10), binds specifically and increases levels of brain-derived neurotrophic factor protein in rat basal forebrain" (rat study)
Journal of Neurochemistry, 2006; PMID: 16635254; DOI: 10.1111/j.1471-4159.2006.03658.x
Dmitrieva et al., "Semax and Pro-Gly-Pro activate the transcription of neurotrophins and their receptor genes after cerebral ischemia" (rat study)
Cellular and Molecular Neurobiology, 2009; PMID: 19633950; DOI: 10.1007/s10571-009-9432-0
Sheremet et al., "An experimental substantiation for using the 'Semax' neuroprotector in the treatment of optic-nerve diseases" (rat pharmacokinetic study)
Vestnik Oftalmologii, 2004; PMID: 15678666
Full evidence entry (complete data, registry records, dosing evidence)
Early human data
Small or uncontrolled human studies only

At a glance

Also known as
Semax, ACTH(4-10)-Pro-Gly-Pro
Class
Synthetic heptapeptide (ACTH 4-10 analogue)
Derived from
A synthetic analogue of adrenocorticotropic hormone fragment 4-10, with a Pro-Gly-Pro sequence added to the end; developed in Russia
Registered human trials
0
…with published results
0
Largest human trial
None registered on ClinicalTrials.gov. The largest published human study found is 110 stroke-rehabilitation patients (Gusev et al., 2018), not blinded or placebo-controlled.
Studied for
ischemic stroke recovery, optic nerve disease, motor neuron disease / ALS (no benefit on nerve damage), cognitive / nootropic use
Dosing evidence
No human dose establishedNo blinded, placebo-controlled human trial has established an effective Semax dose; published amounts trace to open-label Russian clinical practice, not controlled dose-finding research.
Regulatory status
Described in the Russian medical literature as a registered domestic drug and used clinically there; not approved as a medicine in the United States, the EU, or the UK.

What it is

Semax is a synthetic seven-amino-acid peptide, built from a fragment of adrenocorticotropic hormone (ACTH 4-10) with a three-amino-acid tail added on. It was developed in Russia, where the medical literature describes it as a domestically registered drug, given as a nasal spray or nasal drops and studied mainly as a neuroprotective and cognitive-enhancing agent.

What the studies actually found

Every human study of Semax located for this profile was published in Russian-language medical journals, almost entirely in Zhurnal Nevrologii i Psikhiatrii. The topics covered include ischemic stroke recovery, optic nerve disease, and motor neuron disease (ALS).

None of these studies is described as double-blind or placebo-controlled. The stroke studies compared Semax-treated patients against patients receiving "conventional therapy," not a placebo. The optic-nerve study compared different routes of giving the same drug (nasal drops vs. electrophoresis) rather than testing Semax against no treatment. The one ALS/motor-neuron-disease study explicitly describes itself as "open-label." In that study, Semax did not change the underlying nerve-damage measurements the researchers tracked (needle EMG), although patients scored better on a quality-of-life questionnaire.

What exists in humans

No trial is registered on ClinicalTrials.gov. All human evidence located for Semax comes from a small number of open-label or non-blinded comparative studies conducted in Russia, the largest involving about 110 people recovering from stroke.

What doses have been studied in humans

The Russian studies used intranasal Semax at various total daily amounts, and in some cases compared administration routes rather than doses. Because none of these studies was double-blind and placebo-controlled, none of them can show that a given amount produces a real effect beyond what patients and observers expected, or what the underlying condition would have done on its own.

No dose-ranging study exists — no trial compared multiple Semax doses against each other, or against placebo, to establish how much (if any) is needed to produce an effect. The amounts referenced in the Russian clinical literature reflect what one national drug-registration and prescribing system settled on; they are not the product of a controlled trial that validated a specific effective dose.

What remains unknown

  • Whether Semax does anything measurable when tested against a real placebo under blinded conditions
  • Whether its claimed effects on stroke recovery or cognition hold up outside the researchers who developed the drug
  • Long-term safety — no study followed patients for more than a few months
  • What an unregulated vial sold outside Russia actually contains

Registry and study records

The efficacy of semax in the treatment of patients at different stages of ischemic stroke
PubMed · Gusev et al., 2018. n=110, stroke rehabilitation. Not blinded or placebo-controlled — compared semax+/- subgroups. DOI: 10.17116/jnevro20181183261-68
Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)
PubMed · Gusev et al., 1997. n=30 treated vs. 80 conventional-therapy controls. Not blinded.
The study of chronic partial denervation and quality of life in patients with motor neuron disease treated with semax
PubMed · Serdiuk et al., 2007. Explicitly described as an 'open-label clinical trial.' Semax did not change nerve-damage (EMG) measurements; patients reported better quality-of-life scores.
The study of therapeutic effect of new Russian drug semax in optic nerve disease
PubMed · Polunin et al., 2000. Controlled comparison of administration routes, not of semax vs. placebo.
See the full Evidence Index →

Evidence last reviewed: September 2026. Peptide Proof reports what studies found. We do not give medical advice, dosing guidance, or treatment recommendations.