N-Acetyl Selank
Also known as: NA Selank Amidate
N-Acetyl Selank is a chemically stabilized (N-acetylated, C-amidated) analog of the tuftsin-derived peptide Selank, proposed to act via GABAergic modulation, inhibition of enkephalin-degrading enzymes that raises endogenous enkephalins, and BDNF-related effects, though these mechanisms were demonstrated for the parent Selank rather than the analog.
- Drug class
- Synthetic tuftsin-derived heptapeptide analog (anxiolytic neuropeptide)
- Primary targets
- GABAergic system, Enkephalin-degrading enzymes (enkephalinase), BDNF expression, Serotonergic/monoaminergic systems
- Dose reference
- No established human dose; research-only. Parent Selank was used intranasally in rodent studies at roughly 250-500 micrograms/kg, and Russian Selank nasal-drop clinical use is product-specific - neither is a validated guide for the acetylated analog and neither is a recommendation.
- Half-life
- Not validated for the analog. Parent Selank has a very short plasma half-life (on the order of minutes); N-terminal acetylation and C-terminal amidation are intended to slow enzymatic degradation, but no peer-reviewed human pharmacokinetic data exist for N-Acetyl Selank.
- Developer / origin
- Institute of Molecular Genetics, Russian Academy of Sciences with the V.V. Zakusov Research Institute of Pharmacology (parent Selank); the acetylated/amidated analog originates from the research-chemical market
- Reference year
- 2009
- Evidence score
- 2/5 - Preclinical / limited clinical for parent compound; research-only analog
Preclinical / limited clinical for parent compound; research-only analog
There is no published human or animal study of the N-Acetyl Selank analog itself. The evidence cited for it actually describes the parent peptide Selank: a small Russian clinical trial in generalized anxiety disorder/neurasthenia plus rodent and cell-culture mechanistic work on GABAergic gene expression, enkephalinase inhibition, and BDNF. None of it has been independently replicated in Western trials, and applying it to the acetylated analog is untested extrapolation.
Mostly animal, ex vivo, cell, or indirect evidence.
Evidence basis
- No direct human or animal data on the N-Acetyl Selank analog
- Parent Selank clinical evidence limited to small Russian trials (e.g., 62-patient GAD/neurasthenia comparison vs medazepam)
- Mechanistic data are mostly rodent and cell-culture studies from a small set of affiliated groups
- Not FDA-approved; parent Selank registered only in Russia
Key references
- PubMedEfficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia (PMID 18454096)
- PMCSelank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission
- PubMedThe inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity (PMID 11550013)
- SpringerIntranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo (Doklady Biological Sciences, 2008)
How to read this entry
Dose references and half-life values are pulled from trial protocols, labels, reviews, or published summaries where available. They are context for research and comparison, not a personal dosing recommendation.
Status matters: approved drugs have regulated indications; investigational compounds are still being studied; research-only peptides do not have established human dosing, safety, or efficacy for consumer use.
N-Acetyl Selank guides
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