Semax

Overview

Semax is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro) developed in the 1980s and early 1990s by the Institute of Molecular Genetics at the Russian Academy of Sciences. It was engineered as a stabilized analog of the adrenocorticotropic hormone fragment ACTH(4-10) — the core sequence responsible for cognitive and neuroprotective activity [1].

A Pro-Gly-Pro protective tail was attached to the C-terminus to prevent rapid enzymatic breakdown in the bloodstream, significantly extending bioavailability and central activity compared to native ACTH(4-10). Semax is approved for medical use in Russia as a nasal drop solution for stroke rehabilitation and optic nerve atrophy. It remains unapproved by Western regulatory agencies including the FDA.

Compound Variants

Three distinct variants of Semax are sold in the research-chemical market. They are chemically different compounds. All published clinical data used standard Semax intranasally:

Research Areas and Claims

Semax is heavily marketed as a nootropic in the biohacking community. Its most defensible research use cases — supported by indexed human data — are:

• Stroke Rehabilitation (Primary Evidence Base): The strongest human evidence for Semax is as an adjunct in acute ischemic stroke. Two clinical trials (1997, 2018) demonstrated dose-linked neuroprotection, elevated BDNF levels, and faster functional recovery compared to standard therapy alone [5][6].

• Acute CNS Activity in Healthy Adults: A placebo-controlled fMRI study showed that intranasal Semax significantly altered Default Mode Network (DMN) resting-state connectivity in healthy volunteers — providing measurable imaging evidence of central activity in a non-clinical population [3].

• Quality of Life in Motor Neuron Disease: In patients with ALS/MND, Semax paired with standard therapy improved composite quality-of-life scores, particularly emotional state and motivation [7].

• Nootropic / Cognitive Enhancement (Less Supported): Claims of focus improvement, memory enhancement, and ADHD symptom reduction in healthy adults are widely marketed but lack large, controlled, Western-indexed RCT evidence. Russian-language studies suggest benefit, but have not been independently replicated in Western cohorts [4].

Mechanism of Action

1. BDNF and NGF Upregulation: Semax rapidly stimulates the expression of Brain-Derived Neurotrophic Factor (BDNF) and Nerve Growth Factor (NGF) in the hippocampus and cortex [2]. Elevated BDNF promotes neuroplasticity, neuronal survival under hypoxic stress, and prevention of excitotoxicity — the primary mechanism thought to underlie its neuroprotection in stroke [6].
2. Default Mode Network (DMN) Modulation: Acute intranasal administration measurably alters resting-state functional connectivity in the DMN — a brain network central to resting cognition, attention, and self-referential thought. This was demonstrated directly via fMRI in healthy volunteers [3].
3. Antihypoxic Protection: Semax acts as an antihypoxic agent, protecting neurons against cell death caused by reduced oxygen supply — relevant to its stroke application [4].

Dosing Schedule (Clinical Context)

Clinical Trials & Evidence

Semax is an officially approved medication in Russia with a substantial regional research base. The studies below are peer-reviewed and indexed in PubMed. Many older foundational nootropic studies are published exclusively in Russian-language journals or non-indexed proceedings.

Regulatory Status & Limitations

Vendor Directory

Data collected March 2026. Tables sorted by $/mg ascending within each section.

SC Injection — Standard Semax

No Finnrick A vendor carries Semax. All listings below are non-Finnrick.

† Quantity-tiered pricing. Single-unit rate shown.

SC Injection — N-Acetyl Semax (NA-Semax) & NA-Semax-Amidate (NASSA)

† Quantity-tiered pricing. Single-unit rate shown.

Nasal Spray

Sublingual Tablets & Dissolving Strips

Combination Products (SC Injection)

No Public Price / Not Available

References

1. [1]

   Potaman VN, et al. "N-terminal degradation of ACTH(4-10) and its synthetic analog semax by the rat blood enzymes." Biochem Biophys Res Commun. 1991. pubmed.ncbi.nlm.nih.gov/1851003

2. [2]

   Dolotov OV, et al. "Semax, an analog of ACTH(4-10) with cognitive effects, regulates BDNF and trkB expression in the rat hippocampus." Brain Res. 2006. pubmed.ncbi.nlm.nih.gov/16996699

3. [3]

   Lebedeva IS, et al. "Effects of Semax on the Default Mode Network of the Brain." Bull Exp Biol Med. 2018. pubmed.ncbi.nlm.nih.gov/30225715

4. [4]

   Tsai SJ. "Semax, an analogue of adrenocorticotropin (4-10), is a nootropic peptide with pleiotropic neuroprotective properties and evolutionary-based mechanisms of action." Med Hypotheses. 2007. pubmed.ncbi.nlm.nih.gov/17030401

5. [5]

   Gusev EI, et al. "Effectiveness of semax in acute period of hemispheric ischemic stroke." Zh Nevrol Psikhiatr Im S S Korsakova. 1997. pubmed.ncbi.nlm.nih.gov/11517472

6. [6]

   Gusev EI, et al. "The efficacy of semax in the treatment of patients at different stages of ischemic stroke." Zh Nevrol Psikhiatr Im S S Korsakova. 2018. pubmed.ncbi.nlm.nih.gov/29798983

7. [7]

   Serdiuk AV, et al. "The study of chronic partial denervation and quality of life in patients with motor neuron disease." Zh Nevrol Psikhiatr Im S S Korsakova. 2007. pubmed.ncbi.nlm.nih.gov/18379501