Semax

Semax Research Overview

Semax is a seven-amino-acid peptide based on a fragment of ACTH, developed in Russia as a nasal drug for stroke recovery and cognitive impairment. It is studied for focus, mental stamina, and mood support.

Also known as: Met-Glu-His-Phe-Pro-Gly-Pro, ACTH(4-10) analog, NA-Semax, N-Acetyl Semax

Background

Semax is a synthetic heptapeptide built from the 4-10 fragment of adrenocorticotropic hormone (ACTH), with the last two residues swapped for Pro-Gly-Pro to make it more stable in the body. It was created at the Institute of Molecular Genetics in Moscow in the 1980s and 1990s and has been an approved medicine in Russia since the mid 1990s, sold as a 0.1 percent nasal solution for cognitive complaints and a 1 percent solution for acute ischemic stroke. Unlike ACTH itself, Semax does not stimulate cortisol release, which is the whole point of the modification.

The Russian clinical literature is fairly large but mostly consists of open-label or small controlled studies published in Russian-language journals. Those report faster recovery after stroke, improved attention in healthy volunteers and in people with attention problems, and benefit in optic nerve disease. The methodology is generally weaker than what Western regulators expect, and there are essentially no large, independent, double-blind trials from outside Russia. That is the honest state of the human evidence.

Animal and cell work is more consistent. In rodents, Semax increases BDNF and its TrkB receptor in the hippocampus, protects neurons during ischemia, dampens inflammatory gene expression after stroke, and has mild anxiolytic and analgesic effects. Whether the doses researchers study at home reproduce those changes is not known. The community version comes as lyophilized powder for nasal or subcutaneous use, or as ready-made nasal sprays, sometimes in an N-acetyl form marketed as longer acting.

Mechanistic Profile

Semax is thought to act mostly through neurotrophin signaling. Within hours of administration it raises BDNF expression in the hippocampus and frontal cortex and increases TrkB receptor levels, which supports synaptic plasticity and neuronal survival. It also modulates the melanocortin system without the corticotropic effect of the parent hormone, and rodent gene expression studies show it shifting immune and vascular gene activity after ischemia toward a repair profile. Additional reported actions include reduced enkephalin breakdown, influence on serotonin and dopamine turnover, and antioxidant effects. Nasal delivery is favored because the peptide reaches the brain quickly along olfactory pathways and is degraded fast in blood.

Reported Research Findings

• Nasal Semax increased BDNF protein and TrkB receptor levels in rat hippocampus within hours of administration parameters. (rodent)

• In a rat stroke model, Semax shifted expression of hundreds of genes involved in immune response and vascular repair after ischemia. (rodent)

• Russian clinical studies report faster neurological recovery when 1 percent Semax is given during the first days after ischemic stroke. (human pilot)

• Healthy volunteers showed improved attention and memory task performance after a single nasal amount in small Russian studies. (human pilot)

• Semax reduced anxiety-like behavior and pain response in rodents without raising corticosterone. (rodent)

Analytical Validation, Formulation and Storage

• Purity: 99% or higher as verified by HPLC, with a third-party certificate of analysis available per batch.

• Formulation: lyophilised (freeze-dried) powder in a sterile sealed glass vial, to be reconstituted with an appropriate solvent for laboratory use.

• Reported half-life: A few minutes in blood, but effects on gene expression last many hours.

• Storage: keep lyophilised material cool, dark and dry (long-term at or below -20 °C). Store reconstituted solutions refrigerated, avoid repeated freeze-thaw cycles and use within laboratory-defined windows.

Selected Literature

• Semax, an analog of ACTH(4-10), induces BDNF expression and increases TrkB levels in rat hippocampus. Brain Research, 2006.

• Semax treatment alters expression of immune and vascular genes in rat brain after focal ischemia. BMC Genomics, 2013.

• Semax, an analogue of ACTH(4-10) with cognitive effects: clinical and experimental studies (review). Neuroscience and Behavioral Physiology, 1997.

• Use of Semax in acute ischemic stroke: Russian multicenter clinical experience. Zhurnal Nevrologii i Psikhiatrii, 2005.

Cloud Aminos supplies Semax as a high-purity research material intended strictly for controlled laboratory use in vitro or in established animal models. This compound is not approved as a drug, diagnostic or dietary ingredient and is not manufactured, packaged or marketed for human consumption, self-experimentation, clinical application or any use outside properly designed and ethically approved research protocols.