N-Acetyl Selank Amidate

A terminally protected, longer-acting analogue of the tuftsin-derived heptapeptide Selank, studied in research models for anxiolytic, GABAergic and neurotrophic activity.

What it is

N-Acetyl Selank Amidate (often shortened to NA-Selank) is a synthetic heptapeptide and a second-generation analogue of Selank, itself a stabilised derivative of the natural immunomodulatory tetrapeptide tuftsin. The parent Selank carries the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro; the acetylated, amidated variant adds an N-terminal acetyl group and a C-terminal amide to give the sequence Ac-Thr-Lys-Pro-Arg-Pro-Gly-Pro-NH₂. It belongs to the same Russian family of neuro-active research peptides as Semax and its own acetyl-amidate analogue.

The two terminal modifications are the whole point of the molecule. The N-terminal acetyl group blocks aminopeptidase cleavage and the C-terminal amide protects against carboxypeptidase attack, so the peptide resists the exopeptidases that rapidly clear unmodified Selank. Vendor and secondary-source material describes this as extending the effective plasma half-life from roughly 20-30 minutes for Selank into a substantially longer window, which is the rationale for studying the amidate as a more persistent probe of the same pathways. It is confirmed on PubChem as CID 133082488, molecular formula C₃₅H₅₉N₁₁O₁₀. Supplied strictly for laboratory research use only, not for human or veterinary use.

How it works

Selank and its analogues are not classical benzodiazepines: they do not bind the benzodiazepine site directly. Instead the research literature on the parent peptide points to a multi-pathway profile. Selank appears to act as a concentration-dependent modulator of GABA-ergic tone, to slow the breakdown of endogenous enkephalins by inhibiting enkephalin-degrading enzymes, and to shift expression of neurotrophic and cytokine genes. In the foundational clinical comparison against the benzodiazepine medazepam, Selank-treated patients showed rising leucine-enkephalin levels that tracked with improvement in anxiety scores, a neurochemical change absent in the benzodiazepine arm.

On the neurotrophic side, intranasal Selank was shown to regulate brain-derived neurotrophic factor (BDNF) in the rat hippocampus: single doses of 250 and 500 mcg/kg raised Bdnf mRNA within 3 hours and increased BDNF protein at 24 hours (Inozemtseva et al., 2008). On the GABA-receptor side, a Frontiers in Pharmacology study in IMR-32 neuroblastoma cells found that Selank alone did not change GABAergic gene transcription, but strongly reshaped it in combination with other agents, consistent with a modulatory rather than a directly transcription-driving role. N-Acetyl Selank Amidate is studied as a metabolically hardened version of this same pharmacology, on the premise that longer residence time lets these mechanisms be probed over an extended window.

What the research shows

Most controlled, quantitative data are on the parent Selank rather than on the acetyl-amidate analogue specifically, so the numbers below are foregrounded as Selank findings and should be read as the mechanistic backdrop for NA-Selank. They span the anxiolytic behaviour, the neurotrophic (BDNF) signal, and the GABAergic gene-expression work, each with a real published source.

Side Effects

There is no dedicated human safety or tolerability data for N-Acetyl Selank Amidate itself. A PubMed search for this modified analog returns no clinical or preclinical safety studies, so everything below is inferred from the parent peptide, Selank, and should be read as parent-compound data rather than evidence about the amidate. Selank was studied and used clinically in Russia and was generally described as well tolerated, but the acetylation and amidation that make this analog more metabolically stable could also change its distribution, duration, and off-target activity in ways that have not been characterized in humans.

In short, N-Acetyl Selank Amidate has no human side-effect profile of its own. The reassuring tolerability record belongs to the unmodified parent peptide, and it cannot be assumed to transfer to a structurally modified, longer-acting analog that has not been tested for safety in people.

At a glance

Molecular identity confirmed on PubChem (CID 133082488): molecular formula C₃₅H₅₉N₁₁O₁₀, sequence Ac-Thr-Lys-Pro-Arg-Pro-Gly-Pro-NH₂.

Compared with Selank

The parent Selank has a molecular weight of about 751.9 Da (CAS 129954-34-3) and an unprotected N- and C-terminus, which leaves it open to rapid exopeptidase clearance. N-Acetyl Selank Amidate keeps the same core heptapeptide but caps both ends, raising the molecular weight to about 793.9 Da and, per vendor and secondary sources, extending the metabolic window. The pharmacological hypotheses, GABAergic modulation, enkephalin stabilisation and BDNF-driven neurotrophic signalling, carry over from Selank; the amidate is essentially a stability-hardened tool for studying the same biology over a longer time course.

Dosing

No dedicated dosing study exists for N-Acetyl Selank Amidate. This modified analog was designed for greater metabolic stability than the parent peptide, but its dose-response has not been characterized in humans, so every figure below is inferred from clinical work on parent Selank and is not a regimen for the amidate. Parent Selank is registered in Russia as a 0.15% intranasal solution (roughly 75 µg per drop), and published trials cluster in the range of about 250 to 2,700 µg/day. These are study doses, presented as educational context, not instructions.

No established dose exists for N-Acetyl Selank Amidate itself: the values above describe parent Selank study protocols and do not transfer directly to the amidate, whose potency and duration may differ. This material is provided for laboratory research use only and as educational information, not as personalized medical advice.

Preparing it

N-Acetyl Selank Amidate is supplied as a lyophilised powder and is reconstituted with bacteriostatic or sterile water before use in research. See the reconstitution guide for mixing and storage, and the concentration guide for working out volume per target amount. Store lyophilised vials cold and keep reconstituted solution refrigerated at 2-8 C.

Where to go next

Last updated on July 3, 2026