7AA (modified) Preclinical (parent compound has limited human RCTs)
N-Acetyl Selank
A terminally-modified, more stable analog of Selank studied for anxiolytic and nootropic effects; direct human data on the acetylated form is absent—evidence is extrapolated from the parent heptapeptide.
In Plain English:
N-Acetyl Selank (also called Selank Amidate) is a lab-modified version of Selank—a synthetic peptide originally developed by the Russian Institute of Molecular Genetics as an analog of the immune peptide tuftsin. An acetyl group added to the N-terminus and an amide group at the C-terminus shield the chain from peptidases, giving it greater metabolic stability than unmodified Selank. Researchers study it for its potential to quiet anxiety through GABA and serotonin pathways, elevate BDNF (a brain growth protein important for memory), and modulate immune cytokines—all without the sedation or dependency risk of classical benzodiazepines.
Research Maturity
Preclinical (parent compound has limited human RCTs) (No studies on N-Acetyl Selank directly; parent Selank in ~30+ papers since 1999, incl. 3 clinical trials+ Studies)
Focus
Anxiety & Mood
Cognition
Stress Response
Origin
Synthetic heptapeptide; N-acetylated, C-amidated analog of Selank (TKPRPGP), which is itself an analog of the endogenous immunopeptide tuftsin. Developed at the Institute of Molecular Genetics, Russian Academy of Sciences.
Mechanism
Positive allosteric modulation of GABA-A receptors; upregulation of BDNF mRNA and protein in hippocampus; inhibition of enkephalin-degrading enzymes (boosting endogenous opioid tone); enhancement of serotonin metabolism in brainstem; suppression of pro-inflammatory cytokines IL-6 and TNF-α. N-terminal acetylation and C-terminal amidation block exopeptidase cleavage, extending exposure relative to parent Selank.
Outcome
Reduced anxiety (Hamilton Anxiety Scale); restored leu-enkephalin levels in GAD patients; antiasthenic and mild psychostimulant effects; BDNF elevation in hippocampus; immunomodulation (IL-6, Th1/Th2 balance); enhanced effect of concomitant benzodiazepines at lower doses.
