Description

Semax is a synthetic heptapeptide derived from a fragment of adrenocorticotropic hormone (ACTH 4-10) with a Pro-Gly-Pro C-terminal extension for metabolic stability. Developed at the Institute of Molecular Genetics in Moscow and approved in Russia for clinical use since 2011, Semax has accumulated significant research data across neurology, cognitive science, and neuroprotection.

Research Profile

Semax’s primary mechanism involves robust upregulation of BDNF and its receptor TrkB — with studies showing increases of 300-800% above baseline in specific brain regions. Unlike its ACTH parent molecule, Semax does not affect cortisol or adrenal function at research doses. Additional documented effects include modulation of dopaminergic and serotonergic systems, enhancement of NGF expression, and neuroprotective activity in ischemic models.

Key Research Areas

BDNF and NGF upregulation (300-800% increases documented)
Cognitive enhancement — attention, memory, processing speed
Neuroprotection in ischemic stroke models
Optic nerve recovery and visual processing
Dopamine and serotonin system modulation

Specifications

Sequence	Met-Glu-His-Phe-Pro-Gly-Pro
Molecular Weight	813.93 g/mol
Purity	≥99% (HPLC verified)
Form	Lyophilized powder
Quantity	5mg per vial
Storage	-20°C pre-reconstitution

Related Research Peptides

Semax and Selank represent complementary cognitive peptides — stimulatory vs. anxiolytic. For sleep-focused research, see DSIP. Full comparison at our nootropic peptides guide.

Research Dosage Protocols

Semax is approved in Russia as a nasal spray for cognitive impairment and stroke recovery, with a standard clinical preparation of 0.1% and 1% solutions. Research doses in published studies range from 50–300mcg intranasally or subcutaneously, with effects on BDNF and cognitive markers measured over 1–30 day windows. A 30mg vial reconstituted in 3mL bacteriostatic water yields 10mg/mL for injectable research, or can be diluted to a 0.1% nasal solution (1mg/mL) in saline for intranasal protocols. Effects on BDNF gene expression in hippocampal tissue appear within 24 hours of administration in rodent studies.

Frequently Asked Questions

What BDNF increase has been measured in Semax research?

Russian studies measuring BDNF mRNA in rat hippocampal tissue after Semax administration reported increases of 150–200% above baseline, depending on dose and measurement timepoint. A key study from Shadrina et al. (2010) showed significant BDNF and NGF (nerve growth factor) upregulation in multiple brain regions. The magnitude is notable because most pharmacological interventions show more modest BDNF effects. Whether this translates proportionally to protein levels and synaptic BDNF concentration — which is what matters functionally — involves additional steps in the regulatory cascade, but the gene expression data is the most cited figure in Semax BDNF research.

How is intranasal administration used in Semax research?

Intranasal delivery is the clinically-approved route for Semax in Russia and is preferred for CNS-focused research because it allows partial direct brain access via olfactory and trigeminal nerve pathways. This bypasses first-pass hepatic metabolism and avoids the blood-brain barrier limitations that reduce CNS penetration with intravenous or subcutaneous delivery. Research using intranasal Semax for neuroprotection, cognitive, and anxiety studies mirrors the clinical delivery route. Subcutaneous injection is used in studies measuring peripheral effects or when precise systemic dose control is required. Intranasal administration volumes are typically 10–50µL per nostril for small rodent models.

What is the ACTH relationship, and why doesn’t Semax elevate cortisol?

Semax is derived from the ACTH(4-7) fragment — the middle portion of adrenocorticotropin hormone. Full-length ACTH stimulates the adrenal cortex to produce cortisol. The 4-7 fragment of ACTH contains the sequence responsible for neuroprotective and cognitive effects (binding to melanocortin receptors in the CNS) but lacks the portions required to activate adrenal cortisol production. Semax extends this fragment to ACTH(4-7)-Pro-Gly-Pro to improve stability. The result: Semax activates CNS melanocortin receptors and neurotrophin pathways without adrenal stimulation. This makes it a tool for studying ACTH-related neuroprotection while avoiding the HPA axis confound that full ACTH would introduce.

What is N-Acetyl Semax, and how does it differ?

N-Acetyl Semax adds an acetyl group to the N-terminus of the Semax peptide. This modification increases lipophilicity, improving cell membrane permeability and potentially enhancing CNS penetration across the blood-brain barrier compared to standard Semax. N-Acetyl Semax Amidate (which adds both acetylation and C-terminal amidation) takes this further, with amidation protecting the C-terminus from carboxypeptidase cleavage and extending plasma half-life. Research comparing standard Semax to acetylated variants suggests enhanced potency per microgram for the modified forms. The base mechanism (BDNF upregulation, MC receptor activation) is preserved — the modifications affect pharmacokinetics more than pharmacodynamics.

How quickly are effects observed in Semax research?

Semax’s effects on gene expression (BDNF, NGF) appear within 24 hours of administration in rodent tissue sampling studies. Behavioral effects in maze and anxiety tests are measurable within the first 1–3 days of dosing protocols. This is faster than many neuroprotective interventions that require weeks of treatment before measurable outcomes. The rapid onset is consistent with Semax’s mechanism — receptor activation and transcription factor modulation rather than structural neuroplasticity changes that require longer timelines. Cognitive effects in stroke recovery models build over 7–14 days as neuroprotection and BDNF-driven repair accumulate.

What storage conditions does Semax require?

Lyophilized Semax powder should be stored at -20°C for long-term stability, protected from moisture. After reconstitution, refrigerate at 2–8°C. Working stability is approximately 3–4 weeks — somewhat shorter than more stable peptides because Semax’s proline-glycine-proline extension, while protecting against some enzymatic degradation, doesn’t eliminate hydrolytic breakdown over time. The pharmaceutical nasal spray preparation (approved Semax) uses preservatives and pH adjustment to maintain stability at refrigerated temperatures. Research-grade reconstituted solutions without these additives have shorter working windows. For multi-week protocols, aliquot and freeze at -20°C, thawing daily doses as needed.

For research and laboratory use only. Not for human consumption. All peptides are sold strictly as research chemicals.

Semax