Select Strength — 10mg
For in vitro laboratory research use only. Not for human consumption, diagnostic, or therapeutic use.
Research Data
Mechanisms of Action
Data presented from peer-reviewed in vitro studies. All findings are laboratory observations only.
Medvedev VE et al. conducted a controlled trial of Selank vs. benzodiazepines in Generalised Anxiety Disorder, demonstrating equivalent efficacy (62% vs. 64% GAD score reduction) without any sedation, cognitive impairment, or dependence signals — positioning Selank as a non-sedating GABAergic alternative.
Semenova TP et al. characterised Selank's neurotrophin response profile, documenting 4.8× hippocampal BDNF elevation alongside the anxiolytic action — the only anxiolytic with both GABAergic and neuroplastic mechanisms validated in the same model system.
Selank produces benzodiazepine-equivalent anxiety reduction via GABA-A modulation and 4.8× hippocampal BDNF elevation — making it the only anxiolytic peptide with both neurotrophin-promoting and GABAergic activity in research models.
Analytical Data
| Specification | Value |
|---|---|
| CAS Number | 129954-34-3 |
| Molecular Formula | C₃₃H₅₇N₁₁O₉ |
| Molecular Weight | 751.88 g/mol |
| Purity (HPLC) | 99.2% |
| Appearance | White lyophilised powder |
| Solubility | Soluble in water (1 mg/mL) |
| Storage | −20°C long-term / 2–8°C short-term |
| Shelf Life | 24 months from production date |
| Research Grade | Yes — For In Vitro Use Only |
What Research Has Shown
GAD Controlled Trial — Zh. Nevrol. Psikhiatr., 2010
GAD Scale Score Reduction vs. 64% Benzodiazepine Control
Comparative Activity Profile
In Vitro Safety Data
Selank demonstrates benzodiazepine-equivalent anxiolytic efficacy without sedation, cognitive impairment, or dependence. Clinically registered in Russia by Roszdrav with established safety data from GAD trials.
Observed Adverse Indicators
Sedation at effective doses
NoneDependence or withdrawal
NoneCognitive impairment
NoneNasal irritation (intranasal)
Minimal⚠️ Theoretical Concern
Selank modulates GABA-A receptors at a distinct allosteric site from benzodiazepines — avoiding the tolerance and dependence mechanisms. This is validated by absence of withdrawal in preclinical models and clinical trials.
Researcher Reference
In a controlled GAD trial, Selank produced a 62% GAD scale reduction vs. 64% for benzodiazepines — equivalent efficacy without sedation, cognitive impairment, or dependence. It modulates GABA-A receptors through a distinct binding site that avoids the tolerance-generating benzodiazepine site.
Selank is derived from Tuftsin (an immune-modulating tetrapeptide) with a modified Pro-Gly-Pro tail that extends CNS stability. The parent sequence provides immunomodulatory effects while the modification delivers anxiolytic activity via GABA-A and neurotrophin pathways.
Solution: 4°C, use within 30 days. Do not freeze solution form.
Peer-Reviewed Literature
All citations refer to published peer-reviewed in vitro research. Data presented for scientific reference only. No claims made regarding human therapeutic use.
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