N-Acetyl Selank

A free-acid N-acetylated analog of the Russian anxiolytic peptide Selank, capped at the N-terminus while retaining the native C-terminal carboxyl, sold in the research market with no published studies of its own.

Also referenced as: NA-Selank, N-Acetyl Selank Free Acid, Acetyl-Selank, Ac-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH

Also appears in: Neuroprotection · Immune

What is N-Acetyl Selank?

N-Acetyl Selank is the heptapeptide Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) carrying an acetyl group on its N-terminal threonine, with the native C-terminal carboxylic acid left intact — Ac-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH, C35H59N11O10, molecular weight roughly 793.9 (PubChem CID 133082488). Because the C-terminus is unmodified, it is described in the research market as the “free acid” member of the acetylated Selank family, and it is a different molecule from N-Acetyl Selank Amidate, which replaces that terminal –OH with –NH2. Acetylating an N-terminus is a routine peptide-chemistry tactic for blunting aminopeptidase attack, and it is the reason vendors list the capped forms separately from plain Selank.

How it works

No pharmacology has been published on the acetylated variant itself. The mechanisms below belong to unmodified Selank, whose backbone N-Acetyl Selank retains:

• Tuftsin scaffold — Selank extends tuftsin (Thr-Lys-Pro-Arg), the IgG-derived tetrapeptide first characterized as a phagocytosis-stimulating factor, with a C-terminal Pro-Gly-Pro (Najjar and Nishioka, Nature, 1970, 228:672–673)
• GABAergic allosteric modulation — radioligand-receptor analysis found Selank acts as a positive allosteric modulator of GABA binding, interacting non-additively with diazepam (Vyunova et al., Protein and Peptide Letters, 2018, 25(10):914–923); gene-expression work in the rat frontal cortex reported broad changes across GABAergic neurotransmission genes (Volkova et al., Frontiers in Pharmacology, 2016, 7:31)
• Enkephalin protection — Selank inhibits enkephalin-degrading enzymes in human serum with an IC50 near 20 µM, which the original authors proposed as a contributor to its anxiolytic effect (Kost et al., Bioorganicheskaia Khimiia, 2001, 27(3):180–183)
• BDNF regulation — intranasally administered Selank rapidly increased brain-derived neurotrophic factor mRNA expression in the rat hippocampus (Inozemtseva et al., Doklady Biological Sciences, 2008, 421:241–243)

Where the acetylated forms are supposed to differ from Selank is metabolic rather than receptor-level, and only the parent’s breakdown has actually been mapped. Uniformly tritium-labeled Selank degrades in blood plasma and brain tissue to the pentapeptide TKPRP, the tripeptide TKP, and the dipeptides RP and GP (Zolotarev et al., Bioorganicheskaia Khimiia, 2006, 32(2):183–191) — successive dipeptide losses, GP and then RP, that strip the molecule from its C-terminal end.

That pattern matters for how this particular variant is sold. Capping the N-terminus is intended to slow aminopeptidase clearance, but the degradation actually observed for Selank runs from the opposite end, and leaving the C-terminus as a free acid — the exact feature that defines this variant — leaves that C-terminal route open. It is the amidated version that is designed to close it. Whether either change alters activity, exposure, or duration in a living system has never been tested.

Research status

The acetylated free acid has no research record of its own. A PubMed phrase search returns zero records for “N-acetyl selank” and zero for “selank amidate” as of August 2026, and ClinicalTrials.gov lists no registered trial of Selank or any acetylated form of it.

The evidence usually cited for this compound belongs to unmodified Selank and is almost entirely Russian:

• Zozulya et al. (2008) compared Selank against the benzodiazepine medazepam in 62 patients with generalized anxiety disorder or neurasthenia (30 on Selank, 32 on medazepam). Anxiolytic effect was comparable between arms, with Selank additionally showing antiasthenic and psychostimulant effects; the serum leu-enkephalin half-life, reduced at baseline in proportion to symptom severity, rose during treatment, most markedly in the Selank arm (Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 108(4):38–48)
• Medvedev et al. (2014) compared Selank with phenazepam in 60 patients with phobic-anxiety and somatoform disorders, reporting anxiolytic and mild nootropic effects, with the anxiolytic effect reported to last a week after the last dose (Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 114(7):17–22); the same group published a further report in 2015 comparing phenazepam monotherapy against combined Selank-plus-phenazepam treatment (115(6):33–40)
• Uchakina et al. (2008) reported immunomodulatory and cytokine-regulating changes in patients with anxiety-asthenic disorders, the clinical thread connecting Selank back to its tuftsin origin (Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 108(5):71–75)
• Preclinical work continues alongside the clinical reports — for example, Kasian et al. (2017) found Selank enhanced diazepam’s anxiety-reducing effect in rats under unpredictable chronic mild stress (Behavioural Neurology, 2017:5091027)

These trials are small, and each tested Selank against an active comparator rather than placebo; the published abstracts do not report blinding. All appeared in Russian-language journals and none has been independently replicated outside Russia. A US pharmacology review grouped Selank with other GABA-active agents reaching American consumers outside any approval pathway and characterized it as poorly studied (Doyno and White, Journal of Clinical Pharmacology, 2021, 61 Suppl 2:S114–S128). Selank itself is a registered prescription drug in Russia, approved in 2009 as an intranasal solution for generalized anxiety disorder and neurasthenia — but that approval covers the unmodified peptide only, and neither Selank nor any acetylated variant has ever been FDA-approved.

Common dosage forms

Research suppliers list N-Acetyl Selank as a lyophilized powder in sealed vials at small milligram fills for reconstitution, and as pre-mixed intranasal spray bottles. The nasal format mirrors the route used in most of the Selank literature — comparative distribution work in rats, using tritium-labeled peptide across intranasal, intraperitoneal, intragastric, and intravenous dosing, supported intranasal administration as the most efficient of those routes for delivering this peptide class to the central nervous system (Ashmarin et al., Bioorganicheskaia Khimiia, 2008, 34(4):464–470). Free-acid and amidate versions are routinely sold side by side under nearly identical names, and the compound is frequently packaged alongside the acetylated Semax analogs. No FDA-approved product exists, and because Selank is not on the FDA’s section 503A bulk drug substances list there is no licensed US compounding route. This section describes formats only and is not dosing guidance.

Key considerations

• Free acid versus amidate is one terminal group, and neither is documented. N-Acetyl Selank ends in a carboxyl (–COOH, C35H59N11O10); N-Acetyl Selank Amidate ends in a carboxamide (–CONH2, C35H60N12O9) — an oxygen traded for a nitrogen plus a hydrogen, leaving the amidate about 1 Da lighter (roughly 792.9 versus 793.9). Neither has been characterized in any published pharmacokinetic, efficacy, or immunogenicity study, so the stability advantages attributed to each are design rationale, not measured results.
• Naming in this market is unreliable. “NA-Selank,” “N-Acetyl Selank,” and “N-Acetyl Selank Amidate” are used interchangeably by sellers even though they denote different molecules. A certificate of analysis reporting the observed mass, or the sequence written with its terminal group, is the only way to establish which one a given vial contains — and the two forms differ by roughly 1 Da, which a low-resolution mass spec may not cleanly resolve.
• Capping the N-terminus is not obviously neutral, and the analog data does not say which way it cuts. The tuftsin scaffold Selank is built on is sensitive to its N-terminal threonine: replacing that Thr with leucine produced an analog less able to stimulate phagocytosis than tuftsin, which the authors attributed to leucine aminopeptidase cleaving an N-terminal Leu more readily than Thr (Nishioka et al., International Journal of Biochemistry, 1991, 23(5–6):627–630). That is a degradation-rate explanation, so it does not predict what an acetyl cap does — a cap blocks aminopeptidase attack rather than inviting it. Acetylation could protect the immune arm of activity, blunt it by masking a residue the target reads, or do neither. None of this has been tested for Selank.
• FDA status of the parent compound. Selank acetate (TP-7) was nominated for the section 503A bulks list and placed in Category 2 — substances that may present significant safety risks — in September 2023, with FDA citing immunogenicity risk from aggregation and peptide-related impurities for certain routes of administration, plus a lack of important safety information in humans. The nominator later withdrew the nomination, and FDA removed Selank acetate from Category 2 effective September 2024 on that basis. Withdrawal is not approval: removal reflects the nomination being dropped, not a safety finding in the compound’s favor. It remains off the 503A bulks list, and the acetylated variants were never separately nominated.
• Human safety data is thin and route-specific. What exists comes from small Russian intranasal trials of the unmodified peptide. There is no published human safety, pharmacokinetic, or immunogenicity data for injected Selank or for either acetylated form.