Selank + Semax Nasal Blend

Component Composition

This product is supplied as a single lyophilized vial containing two structurally distinct synthetic 7-amino-acid peptides formulated for the intranasal research route.

Selank is the synthetic heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro (single-letter TKPRPGP), comprising the four-residue tuftsin sequence (TKPR, residues 289-292 of the human IgG Fc Cgamma2 domain) with a C-terminal Pro-Gly-Pro extension. Molecular formula C33H57N11O9, molecular weight 751.88 g/mol, CAS 129954-34-3, PubChem CID 11765600, FDA UNII TS9JR8EP1G. The C-terminus is the free carboxylic acid form (the IUPAC name terminates 'pyrrolidine-2-carboxylic acid'); molecular formula C33H57N11O9 unambiguously fixes this, despite many vendor catalogs rendering TKPRPGP-NH2.

Semax is the synthetic heptapeptide Met-Glu-His-Phe-Pro-Gly-Pro (single-letter MEHFPGP), comprising the ACTH residues 4-7 behavioral fragment (Met-Glu-His-Phe, the De Wied pharmacophore identified at Utrecht in the 1960s-1970s) with the same C-terminal Pro-Gly-Pro extension. Molecular formula C37H51N9O10S, molecular weight 813.92 g/mol, CAS 80714-61-0, PubChem CID 122178, FDA UNII 0380WZ6T32. Russian Federation drug-register code P N000812/01; ATC code N06BX. Each component meets a minimum purity of >=99% by HPLC-UV at 214-220 nm, with per-batch Certificate of Analysis available in the COA library. The Semax component additionally requires LC-MS deconvolution for the +16 Da methionine-oxidation satellite, the diagnostic stability handle shared with TB-500 and MOTS-c.

Selank Research Summary

Selank was designed at the Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, by the Ashmarin and Myasoedov laboratory in the 1990s as a stabilized analog of human tuftsin (TKPR), the 4-amino-acid peptide cleaved from the IgG heavy chain Cgamma2 domain at residues 289-292^[9]. The endogenous parent was characterized in 1970 by Najjar and Nishioka at Tufts University. The IMG Moscow design appended a C-terminal Pro-Gly-Pro extension, the same glyprolin stabilizer the laboratory used for the sister analog Semax. Selank is from IMG Moscow, not the separate Khavinson bioregulator effort at the St. Petersburg Institute of Bioregulation and Gerontology.

The mechanism literature describes loosely related axes, none established by clean receptor-knockout or antagonist rescue. Zolotarev et al. (2001) reported Selank inhibition of serum enkephalinase with IC50 in the 15-20 microM range^[1], with Kost et al. (2001) reporting parallel observations^[2]. Volkova et al. (2016) in Frontiers in Pharmacology characterized expression-level changes across an 84-gene RT-PCR panel covering GABA-A subunits and interneuron markers in IMR-32 cells and BALB/c mouse hippocampus^[3]; the primary paper describes transcriptional regulation of GABAergic gene expression rather than direct GABA-A receptor binding. Inozemtseva et al. (2008) reported BDNF mRNA elevation at 3 hours and BDNF protein elevation at 24 hours in rat hippocampus following intranasal Selank^[4].

The most-cited clinical trial is Zozulya, Seredenin et al. (2008) in the Journal of Neurology and Psychiatry imeni S.S. Korsakova^[10]: n=62 with generalized anxiety disorder or neurasthenia, 30 receiving intranasal Selank and 32 receiving medazepam (a Hungarian benzodiazepine used in Russian clinical practice) over 14 days, open-label, single-site, no placebo arm. Total indexed clinical evidence is approximately 250-400 participants across three studies, all intranasal 0.15% in Russian-language venues. Russian Ministry of Health registered Selank in 2009 by JSC Peptogen under Federal Law 61-FZ^[16]; Selank is not authorized by the FDA, EMA, MHRA, Health Canada, TGA, or PMDA, and Russian Minzdrav registration is not equivalent to FDA approval.

A route asymmetry sits across the evidence base. The 92.8% bioavailability and 2-3 minute plasma half-life are from intranasal administration; every Russian study used the intranasal route, chosen to bypass peripheral peptidases and partially bypass the blood-brain barrier via the olfactory and trigeminal nose-to-brain pathway. The US laboratory-research-use-only market sells Selank as a subcutaneous lyophilized vial. Non-Russian mechanism replication is thin: the Volpicelli Naples group (2017) reported parallel GABAergic gene-expression observations in IMR-32 cells, essentially the only primary Selank mechanism paper outside the IMG Moscow network^[18].

Semax Research Summary

Semax was characterized at the IMG Moscow laboratory in 1982 as a 7-amino-acid analog of the ACTH(4-7) behavioral fragment identified by De Wied at Utrecht. Truncation at residue 7 removes Arg-Trp-Gly (residues 8-10 of full ACTH), associated with loss of MC2R and adrenal-axis engagement; the molecule is non-corticotropic by design. The Ashmarin, Nezavibatko, Myasoedov 1997 paper is the foundational Russian-language characterization of MEHFPGP as an ACTH(4-10)-class analog with C-terminal Pro-Gly-Pro extension^[19]. The institutional lineage is identical to Selank. The De Wied parent program produced one Western successor, Organon Org 2766, an ACTH(4-9) variant evaluated in Alzheimer's, autism, and cisplatin-neuropathy programs and terminated without approval.

The load-bearing mechanism axis is BDNF and TrkB upregulation. Dolotov and colleagues at IMG Moscow reported a single intranasal 50-microgram-per-kilogram dose in intact rat brains associated with approximately 1.4-fold hippocampal BDNF protein, 3-fold exon-III BDNF mRNA, 2-fold TrkB mRNA, and 1.6-fold TrkB phosphorylation^[5]. A companion paper reported a defined specific-binding site with KD approximately 2.4 nM in rat basal forebrain^[6]. Agapova et al. (2007) reported neurotrophin gene-expression changes with Saarland, Germany co-authorship^[8]; Eremin et al. at the Zakusov Pharmacology Institute reported dopaminergic and serotonergic turnover changes^[7]. The Pro-Gly-Pro metabolite has been reported to reproduce a meaningful fraction of the BDNF response independently of the parent heptapeptide.

The acute-ischemic-stroke clinical record is anchored by Gusev, Skvortsova, Myasoedov (1997): n=30 Semax versus n=80 historical control, non-randomized, open-label, with outcomes on Russian-standard Barthel and modified Rankin scales rather than NIHSS^[11]. Filippenkov and colleagues reported transcriptome characterization of rat MCAO preparations^[12]. Russian Ministry of Health registered Semax in 1994 for cognitive disorders and optic-nerve disease (0.1% intranasal) and in 1998 for acute ischemic stroke (1% intranasal) under code P N000812/01^[16]. Semax was in the April 22, 2026 FDA reclassification batch removing 12 peptides from 503A Category 2 and is on the July 24, 2026 PCAC Day 2 docket with verbatim text 'Semax (free base), Semax acetate' and proposed uses 'cerebral ischemia, migraine, and trigeminal neuralgia' (Federal Register doc 2026-07361)^[13].

The Western clinical record contextualizes the Russian evidence. NXY-059 (SAINT-II), citicoline (ICTUS), tirilazad, and lubeluzole reported negative Phase 3 outcomes in acute ischemic stroke; edaravone is approved in Japan for stroke but FDA-approved only for ALS. Cerebrolysin, the closest Western-evaluated comparator, has 30 years of mixed trials; the 2023 Cochrane review concluded its evidence too heterogeneous for guideline recommendation. The PGP-metabolite-versus-parent question further complicates translation of rodent BDNF findings into a Western Phase 3 framework.

Russian Clinical Tradition and Methodology Gap

Both Selank and Semax are registered Russian Federation drugs under Federal Law 61-FZ, in intranasal formulations. Selank was registered by the Russian Ministry of Health in 2009 by JSC Peptogen as a 0.15% intranasal solution for generalized anxiety disorder. Semax was first registered in 1994 for cognitive disorders and optic-nerve disease as a 0.1% intranasal solution, and again in 1998 for acute ischemic stroke as a 1% intranasal solution under drug-register code P N000812/01; Semax was added to the Russian Vital and Essential Drugs list on December 7, 2011. Russian Ministry of Health registration represents real regulatory authorization in the Russian Federation but is not equivalent to FDA, EMA, MHRA, Health Canada, TGA, or PMDA evaluation; the Russian regulator operates under different evidence requirements, and the post-2022 regulatory-reciprocity framework with Western regulators has narrowed rather than expanded.

The canonical Russian clinical research route for both peptides is intranasal. The published Selank 92.8% bioavailability and 2-3 minute plasma half-life figures are from intranasal administration; the Semax preclinical mechanism work and the Gusev / Skvortsova stroke clinical record are from intranasal 0.1% and 1% solutions at microgram-range exposures. The intranasal route was chosen specifically to bypass peripheral peptidase degradation and partially bypass the blood-brain barrier via the olfactory and trigeminal nose-to-brain pathway.

The Russian clinical trial methodology for both peptides is methodologically different from Western Phase 3 standards. The Selank anchor trial (Zozulya 2008) is single-site, open-label, active-comparator without a placebo arm. The Semax anchor stroke trial (Gusev 1997) is non-randomized with non-contemporaneous historical control and open-label methodology, with Russian-standard outcome scales rather than NIHSS as the primary endpoint. The closest Western-evaluated comparator for the Russian-origin neuropeptide CNS class is Cerebrolysin (Ever Pharma porcine brain peptide mixture); the 2023 Cochrane review of Cerebrolysin concluded the trial evidence base was too heterogeneous to support a guideline recommendation. The Western neuroprotectant clinical record (NXY-059 SAINT-II, citicoline ICTUS, tirilazad RANTTAS, lubeluzole) defines the broader class base rate for the indication territory Semax shares.

Combined Administration Literature

No peer-reviewed primary research articles characterize the combined administration of Selank and Semax in any cellular or animal model system as of May 2026. A PubMed search for the two compound names in combination returns no primary research articles, no mechanistic co-administration studies, no pharmacokinetic interaction analyses, and no clinical reports of co-administration in any model system. The two compounds share institutional provenance (the Ashmarin and Myasoedov laboratory at IMG Moscow), a common C-terminal Pro-Gly-Pro stabilizer architecture, and a canonical intranasal Russian clinical research route, but the published literature has characterized them in separate preclinical preparations within the same laboratory across roughly three decades.

The institutional sibling relationship between Selank and Semax operates at the provenance level (same laboratory, same design template, same Russian Ministry of Health drug-registration pathway), distinct from the commercial-pairing pattern of CJC-1295 and Ipamorelin (which is anchored in a peer-reviewed GH-pulse-coordination literature). The Selank and Semax research streams have not converged on a shared molecular target, a documented pharmacokinetic interaction, or a combined-administration pharmacology study in the indexed literature.

The nasal blend commercial format predates any peer-reviewed combined-administration data. The fixed-composition vial provides administration-route consistency with the Russian-language preclinical and clinical preparations that characterize each component individually, but the data supporting that consistency is per-component rather than combined.

Replication and US Regulatory Status

Both Selank and Semax have approximately 70-85% IMG Moscow first or senior authorship across their respective mechanism and clinical corpora. Core recurring authors across both Selank and Semax include Myasoedov, Ashmarin (deceased 2007), Andreeva, Levitskaya, Limborska, Shadrina, Slominsky, Inozemtseva, Kolomin, and Volkova. The non-Russian mechanism corpus on Selank is essentially the Volpicelli 2017 IMR-32 GABAergic gene-expression paper from Naples; the non-Russian mechanism corpus on Semax is essentially the Engele Saarland BDNF/TrkB replication^[8] and the Eremin 2005 dopaminergic/serotonergic work from the Zakusov Pharmacology Institute^[7]. With Ashmarin's death in 2007 and Myasoedov in late-career status, the source-laboratory pipeline is fragile for both components.

The two compounds diverge in their May 2026 US regulatory posture. Semax was included in the April 22, 2026 FDA reclassification batch of 12 peptides removed from 503A Category 2 and is on the July 24, 2026 PCAC Day 2 docket with proposed uses 'cerebral ischemia, migraine, and trigeminal neuralgia' (Federal Register doc 2026-07361)^[13]. Selank has a unique compounding-pharmacy regulatory posture in the broader cohort: placed on FDA 503A Category 2 in September 2023, removed from Category 2 on September 20, 2024 via nominator withdrawal as part of the Evexias / Farmakeio settlement cohort, but never PCAC-voted. Selank was not on the October 29, 2024 PCAC docket, not on the December 4, 2024 docket, not in the April 22, 2026 reclassification batch, and is not on the July 23-24, 2026 PCAC docket^[14]. The compounding status of Selank as of May 2026 is limbo: removed from Category 2 without an affirmative bulks-list vote either confirming or rejecting compoundability.

The Tailor Made Compounding 2020 federal plea agreement (U.S. District Court, Eastern District of Kentucky) named both Selank and Semax explicitly among 14 peptides subject to a $1.79M forfeiture^[15]. The April 1, 2026 Watkins indictment did not name either compound (the Watkins focus was on GLP analogs and the BPC/TB/CJC/Ipa/GHK cohort). The December 2025 U.S. Customs and Border Protection Cincinnati interdiction of approximately 5,000 smuggled peptide units from China named Semax explicitly. Neither compound is explicitly listed on the 2026 WADA Prohibited List; both are captured by S0 (Non-Approved Substances) because Russian Ministry of Health approval does not meet the WADA 'governmental regulatory health authority' threshold. No publicly indexed Anti-Doping Rule Violation cases name either compound specifically.