NA-Selank Amidate Dosage Calculator
NA-Selank Amidate is a stabilized derivative of Selank, itself a synthetic heptapeptide analog of the endogenous immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg).
200mcg · 2x Daily
Summary: Add 0mL BAC water to your 5mg vial. Draw to < 0.1 units on a U-100 syringe for a 200mcg dose. This vial will last 0 doses.
Cycle Planner
NA-Selank Amidate Pharmacokinetics
Pharmacokinetics — Active Dose Over Time
t½ = ~2-3 min (plasma); functional effects persist 6-8 hours via downstream gene expressionDisclaimer: This curve is a simplified first-order exponential decay model. Actual pharmacokinetics vary based on injection site, individual metabolism, body composition, and other factors. Half-life values are approximate and based on available preclinical and clinical literature. Many research peptides lack formal human pharmacokinetic studies. This is for educational purposes only — not medical advice.
NA-Selank Amidate Dosing Protocol
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 200mcg | 2x Daily |
| Moderate | 400mcg | 2x Daily |
| Aggressive | 600mcg | 3x Daily |
Note: N-acetylated, C-amidated analog of Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro). The acetyl and amide modifications improve enzymatic stability and nasal membrane permeability compared to native Selank. Administered intranasally as a pre-mixed nasal spray — no reconstitution needed. Approved in Russia as an anxiolytic for GAD and neurasthenia under the parent Selank formulation.
About NA-Selank Amidate
NA-Selank Amidate is a stabilized derivative of Selank, itself a synthetic heptapeptide analog of the endogenous immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg). The N-terminal acetylation and C-terminal amidation modifications protect the peptide from rapid degradation by aminopeptidases and carboxypeptidases, extending its functional half-life after intranasal delivery. NA-Selank Amidate acts through multiple converging mechanisms: positive allosteric modulation of GABA-A receptors (producing anxiolytic effects comparable to low-dose benzodiazepines without sedation or dependence), inhibition of enkephalin-degrading enzymes (raising endogenous enkephalin levels), upregulation of BDNF expression in the hippocampus, and modulation of pro-inflammatory cytokines including IL-6, IL-1-beta, and TNF-alpha. Clinical trials of the parent compound Selank in patients with generalized anxiety disorder demonstrated efficacy comparable to medazepam, with additional antiasthenic and mild nootropic properties not seen with benzodiazepine comparators.