Evidence Grade E — Very limited evidence. 0 published studies. 0 registered clinical trials.
Medically reviewed by a licensed medical professional
NA-Semax (N-Acetyl Semax) is a modified version of Semax, a Russian-developed neuropeptide. The modification is proposed to improve stability. No published clinical or preclinical studies exist specifically on NA-Semax — all claims are extrapolated from the parent compound Semax.
NA-Semax is also known by these brand and alternate names:
No published studies found on PubMed.
NA-Semax has no marketing authorisation in any jurisdiction. No published clinical or preclinical studies exist specifically on this compound. All claims about its activity are extrapolated from the parent compound Semax (#106).
The absence of any compound-specific data means that the effects of N-acetylation on pharmacology, safety, and efficacy are unknown. Products available through unregulated channels lack pharmaceutical quality assurance.
No studies specific to NA-Semax have been published. The proposed mechanism is derived entirely from research on the parent compound Semax, which suggests neurotrophic factor modulation including BDNF upregulation. Whether the N-acetyl modification alters the pharmacological profile is not established.
No studies of any kind have been published specifically on NA-Semax. The parent compound Semax has a larger evidence base than Selank, including clinical use in Russia since 1996 — but the Alzheimer's Drug Discovery Foundation assessed it and concluded that well-conducted published studies are lacking. No randomised, double-blind, placebo-controlled trials of either Semax or NA-Semax have been published in English-language journals. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 0 registered clinical trials for NA-Semax sourced from ClinicalTrials.gov.
No trials registered on ClinicalTrials.gov for this compound.
NA-Semax (N-Acetyl Semax) is the N-acetylated form of Semax, a synthetic analogue of ACTH(4-10) developed at the Institute of Molecular Genetics, Russian Academy of Sciences. Its sequence is Ac-Met-Glu-His-Phe-Pro-Gly-Pro, with molecular formula C39H53N9O11S and molecular weight approximately 855.95 g/mol (CAS: 2920938-90-3). The N-acetyl modification targets the dominant degradation pathway: aminopeptidase cleavage of the N-terminal methionine. In vitro stability experiments provide the strongest case for the modification: leucine aminopeptidase degrades 87.4% of Semax within 60 minutes, and nasal mucus enzymes destroy 96%. The N-acetyl group blocks this dominant pathway. Kolomin et al. (2013) identified N-acetyl-Semax as the 'most promising' modification for intranasal delivery. Administration is primarily intranasal. Not approved by any regulatory agency.
Research suggests NA-Semax shares the pharmacodynamic profile of parent Semax. The primary mechanisms derive from Semax research: antagonism of alpha-MSH at MC4 and MC5 melanocortin receptors (demonstrated in vitro and in vivo), rapid upregulation of BDNF and TrkB receptor expression in the hippocampus (a single intranasal dose of 50 ug/kg produced 1.4-fold increase in BDNF protein, 1.6-fold increase in TrkB phosphorylation, 3-fold increase in exon III BDNF mRNA, and 2-fold increase in TrkB mRNA). Research suggests Semax increases 5-HIAA (serotonin metabolite) levels by 25% at 2 hours and up to 180% at 4 hours, and inhibits enkephalin-degrading enzymes (IC50 = 10 uM). Genome-wide analysis identified over 1,500 differentially expressed genes in ischemic rat brain cortex following Semax treatment, with suppression of inflammatory pathways and activation of neurotransmission-related genes.
No published clinical or preclinical studies exist specifically on NA-Semax. All data derives from the parent compound Semax. The largest study (Gusev et al., 2018; N=110 stroke patients) showed Semax 6,000 ug/day for 10 days increased BDNF plasma levels with positive correlation to Barthel index score. An fMRI study in 24 healthy subjects (Lebedeva et al., 2018) showed increased resting-state signal in the default mode network after intranasal 1% Semax (1.2 mg). An RNA-Seq study demonstrated over 1,500 differentially expressed genes in hippocampus after Semax plus acute restraint stress, with behavioral attenuation significant at p = 0.048 (d = 1.48). Parent Semax is on Russia's List of Vital and Essential Drugs (approved December 7, 2011), marketed as 0.1% and 1% nasal drops by JSC Peptogen. NA-Semax has no brand name and is not approved in any jurisdiction.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
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Cerebrolysin has been studied in over 200 clinical trials involving more than 15,000 patients, primarily for stroke and Alzheimer's disease. The largest stroke trial (CASTA, 1,070 patients) showed no significant benefit on its primary endpoint. A Cochrane systematic review concluded that evidence was insufficient to support its routine use in stroke or dementia. Cerebrolysin is approved in some non-FDA/non-EMA jurisdictions for neurological conditions. Its clinical evidence base, despite being extensive in volume, has not met the standards required for FDA or EMA approval. The undefined molecular composition makes batch-to-batch consistency and quality standardisation inherently challenging compared to defined single-entity pharmaceuticals.
P21 has no marketing authorisation. No human clinical trials have been conducted. The evidence base consists entirely of studies in transgenic Alzheimer's disease mouse models, conducted primarily by a single research group. Animal studies reported behavioural and biochemical changes in AD mouse models following chronic oral administration. The translation of results from transgenic mouse models of Alzheimer's disease to human disease has historically been extremely poor — the vast majority of compounds showing efficacy in such models have failed in human trials. Products available through unregulated channels lack pharmaceutical quality assurance.
Semax is approved in Russia for stroke recovery and cognitive conditions. It has not been approved by the FDA, EMA, or other major Western regulatory agencies, and the clinical evidence base has not undergone Western regulatory review. Published clinical studies are predominantly Russian. The largest published study (110 stroke patients) reported correlations between treatment and BDNF levels. The evidence does not meet the standards typically required for FDA or EMA approval. Its regulatory status is limited to Russia and certain former Soviet states.
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.
