Semax Acetate is a synthetic heptapeptide (Met-Glu-His-Phe-Pro-Gly-Pro, MEHFPGP) derived from ACTH(4-10) with a C-terminal Pro-Gly-Pro extension. It is a neuroprotective nootropic peptide that upregulates BDNF and trkB phosphorylation, inhibits enkephalinase (IC50 ~10 μM), and acts as a partial antagonist at MC4R/MC5R melanocortin receptors. Unlike native ACTH, Semax does not stimulate cortisol secretion. Its half-life is 20-24 hours in animal models, far longer than native ACTH fragments (minutes). It is clinically approved in Russia for stroke, cognitive impairment, and optic nerve disease.

Semax and Selank are both Russian-developed synthetic peptides, but they have distinct pharmacological profiles. Semax (ACTH 4-10 analog) primarily enhances cognitive function and neuroprotection via BDNF upregulation and enkephalinase inhibition. Selank (tuftsin analog) is primarily anxiolytic and immunomodulatory. Semax is more cognitively focused (nootropic), while Selank is more anxiolytic. Both can be administered intranasally and have extended half-lives compared to their parent peptides. They are sometimes studied together for complementary cognitive and anxiolytic effects.

Intranasal administration is the primary route for Semax, as it allows direct nose-to-brain delivery bypassing the blood-brain barrier. The intranasal route provides CNS bioavailability that oral administration cannot achieve for peptides. Semax's extended half-life of 20-24 hours in animal models (versus minutes for native ACTH fragments) makes it pharmacologically practical. The Pro-Gly-Pro C-terminal extension confers resistance to proteolytic degradation, enabling sustained bioactivity after intranasal dosing.

Yes. Semax is classified as a nootropic (cognitive enhancer) and neuroprotective agent. It enhances memory consolidation, learning, and attention without stimulant side effects. Its nootropic effects are mediated through BDNF/trkB upregulation (1.4-fold BDNF increase, 1.6-fold trkB phosphorylation), enkephalinase inhibition, and modulation of central cholinergic systems. Unlike stimulants, Semax does not cause agitation, tolerance, or cortisol elevation, making it a non-stimulant cognitive enhancer — a profile of interest for ADHD and cognitive decline research.

Semax is clinically approved and widely used in Russia for: acute ischemic stroke (to improve neurological recovery), transient ischemic attacks, cognitive disorders including mild cognitive impairment, and optic nerve disease (optic neuropathy/atrophy). It is administered intranasally. Extensive Russian clinical literature supports its use in post-stroke rehabilitation, where it improves motor and functional recovery. Note that Semax is not FDA or EMA approved and is sold for research use only outside of Russia.

Native ACTH activates melanocortin type 2 receptors (MC2R) on adrenal cortex cells, triggering cortisol release. Semax, despite being an ACTH(4-10) analog, has a modified structure due to the C-terminal Pro-Gly-Pro extension. This modification shifts its receptor selectivity: Semax acts as a partial antagonist at MC4R and MC5R rather than activating MC2R. As a result, Semax provides the cognitive and neuroprotective benefits of melanocortin signaling without the HPA-axis activation and cortisol release that limits native ACTH therapeutic use.

Semax is soluble in DMSO (250 mg/mL) and water (>2 mg/mL). For cell-based assays, prepare a concentrated stock in sterile water or DMSO and dilute into culture media. For in vivo studies, aqueous solutions are typically used for intranasal or subcutaneous administration. Stock solutions should be aliquoted and stored at -20°C. Avoid repeated freeze-thaw cycles. Use aseptic technique when reconstituting the lyophilized powder.

Every batch ships with a Certificate of Analysis (COA) including HPLC purity and MS confirmation. MSDS/SDS, solubility datasheets, and Certificates of Origin are available on request. Sample evaluation policy is available for qualified institutions — please contact us for details.