Selank
Selank
Base Peptides are intended for licensed medical professionals and experienced researchers. Reconstitution required. Dosing and use instructions are not provided.
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Selank (TP-7) — Research-Grade Heptapeptide
Synthetic analogue of tuftsin (sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro) explored for anxiolytic, nootropic, and neuroimmune-modulating properties in preclinical and clinical studies primarily from Russian research groups.[1–4]
- Molecular mass: ~751.9 Da[5]
- Sequence: TKPRPGP (tuftsin-based)
- Form: Lyophilized powder or solution (per variant)
- Purity: 99%+ (HPLC/MS; see product lot)
- Origin of research: Institute of Molecular Genetics, RAS[1,4]
- • Anxiolytic effects comparable to low-dose benzodiazepines in studies, without classical sedative profile.[1,3,6]
- • Modulates GABAA signaling; evidence for subtype-selective positive allosteric modulation.[2,6,7]
- • Nootropic/neuroadaptive signals (BDNF/monoamines; route-dependent receptor effects).[4,8]
- Generalized anxiety & stress response[3,6]
- Cognition, attention, fatigue endpoints[4]
- Neurotransmission & receptor expression (GABA/NMDA)[2,8]
For laboratory research only. Not for human, clinical, or veterinary use.
Background & Rationale
Selank is a heptapeptide engineered from the endogenous immunopeptide tuftsin and developed by the Russian Academy of Sciences as a neuroactive research agent. Historical programs compared its anxiolytic profile to benzodiazepines while noting a distinct side-effect and dependence profile.[1,4,6]
Mechanistic Highlights
GABAergic Modulation
- Alters expression of genes tied to GABAergic neurotransmission in brain tissue and cell models.[2]
- Evidence for positive allosteric modulation of GABAA receptors (subtype-selective; concentration-dependent).[7]
Neuroadaptive & Route Effects
- Intranasal vs. systemic routes show differing receptor-binding adaptations (e.g., NMDA site density).[8]
- Reports of effects on monoamines/BDNF and stress-response markers in select studies.[4]
Selected Research Findings
- Clinical comparisons: Multiple studies report anxiolytic efficacy comparable to low-dose benzodiazepines, with a distinct side-effect profile.[1,6]
- GAD & neurasthenia cohorts: Clinical-biological work noted correlations between symptom changes and neuropeptide parameters during Selank administration.[3]
- Molecular studies: Rapid changes in expression of GABA-related genes and overlap with GABA’s transcriptomic signature.[2]
- Route-specific neurochemistry: Intranasal administration increased NMDA binding site density without altering GABA binding in a mouse model; effects differ by route and strain.[8]
Many primary studies originate from Russian research groups; access to full datasets and standardized endpoints may vary.
Regulatory & Use Notice
This material is sold for laboratory research use only. Not for human consumption, medical, or veterinary use. No instructions for reconstitution or administration are provided. Buyer assumes all responsibility for safe handling and compliance with local regulations.
References
- Kasian A, et al. Selank & diazepam context. 2017.
- Volkova A, et al. GABAergic gene expression after Selank. 2016.
- Zozulia AA, et al. Clinical observations in GAD/neurasthenia. 2008.
- Deigin VI, et al. Peptide biopharma in Russia (incl. Selank/Semax). 2022.
- ProSpec Bio — physico-chemical data.
- Frontiers Pharmacology review—efficacy comparisons.
- Vyunova TV, et al. GABAA positive allosteric modulation. 2018.
- Vasil’eva EV, et al. Intranasal vs intraperitoneal effects. 2016.
