N-Acetyl Selank Amidate

Nootropic

Adalank — Synthetic Peptide

Amino Acid SequenceAc-Thr-Lys-Pro-Arg-Pro-Gly-Pro-NH2
2
Studies
9
Amino Acids
778.92
Mol. Weight
2
Routes

Overview

N-Acetyl Selank Amidate, also marketed under the name Adalank, is a doubly modified variant of Selank incorporating both N-terminal acetylation and C-terminal amidation. These are the two standard chemical modifications applied to extend peptide half-life: N-acetylation blocks aminopeptidase degradation from the N-terminus, while C-terminal amidation mimics the natural amide bond found in many endogenous neuropeptides (including oxytocin and vasopressin) and blocks carboxypeptidase activity.

Adalank is distinguished from N-Acetyl Selank (which carries only the N-terminal modification) by the additional C-terminal amide. It represents the most chemically stabilized version of the Selank peptide backbone commercially available. No independent published research exists for Adalank specifically. The compound is sold as a research peptide only and has no regulatory approval in any jurisdiction.

Mechanism of Action

Adalank is assumed to share the full mechanistic profile of Selank with enhanced in vivo stability:

**Dual enzymatic protection:** The N-acetyl group prevents aminopeptidase N (APN) cleavage from the N-terminus, while the C-terminal amide prevents carboxypeptidase cleavage from the C-terminus. Together, these modifications address the two primary routes of plasma peptide degradation, theoretically yielding a longer active half-life than either singly-modified or unmodified Selank.

**GABAergic neurotransmission modulation** via altered expression of GABA-A receptor subunit genes and GABA synthesis enzymes — the primary anxiolytic mechanism inherited from the Selank backbone.

**Immunomodulatory activity** from the tuftsin core sequence, modulating cytokine networks and neuroimmune gene expression in the brain.

**Enkephalin metabolism:** Inhibition of enkephalin-degrading enzymes, elevating endogenous opioid tone contributing to anxiolysis and mood stabilization.

The amide modification may additionally improve BBB permeability by reducing the net negative charge of the peptide at physiological pH, though this is inferred from general peptide chemistry principles rather than direct measurement for Adalank.

Research Dosing

Intranasal
250-600mcg

Dual terminal modification (N-acetyl + C-amide) is theorized to provide greater enzymatic resistance than either modification alone or than N-Acetyl Selank. No human clinical data exists for this specific compound. All dosing is extrapolated from approved Selank protocols.

1-2x daily·10-14 days per course
Subcutaneous
100-300mcg

Subcutaneous use inferred from Selank research. No published safety data specific to this modification.

Once daily·10-14 days

Research data only. These dosing ranges are derived from published studies, primarily in animal models. This is not medical advice. No peptide discussed on this site is approved for human therapeutic use unless otherwise noted.

Published Studies

Animal

Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission

Volkova A, Sharova EV, Kliashchenko GI, et al. Frontiers in Pharmacology, 2016

Core mechanistic study of the Selank parent compound demonstrating GABAergic gene modulation in rat hippocampus. N-Acetyl Selank Amidate (Adalank) carries no independent studies; this research is cited as its mechanistic basis.

PMID: 26924987
Animal

Anxiolytic-like effect of the neuropeptide Selank on behavior of animals in the elevated plus maze

Seredenin SB, Kozlovskaia MM, Blednov IuA, et al. Bulletin of Experimental Biology and Medicine, 2002

Demonstrated dose-dependent anxiolytic effects of unmodified Selank comparable to diazepam without sedation, amnesia, or muscle relaxation in rat models. The amidate form is presumed to share this effect profile with improved metabolic stability.