Selank [Peptide]

Description

What is Selank?

Selank is a synthetic heptapeptide structurally derived from tuftsin, a naturally occurring immunomodulatory tetrapeptide (Thr-Lys-Pro-Arg, TKPR) located in the Fc region of the human immunoglobulin G heavy chain. The Selank sequence (Thr-Lys-Pro-Arg-Pro-Gly-Pro; TKPRPGP) extends the tuftsin tetrapeptide at the C-terminus with a Pro-Gly-Pro (PGP) tripeptide stabilisation sequence, significantly improving metabolic stability relative to the parent tuftsin by conferring resistance to peptidase-mediated hydrolysis. Selank was developed at the Institute of Molecular Genetics of the Russian Academy of Sciences, and represents one of the primary neuropeptide research compounds to emerge from the same programme that produced Semax.

Selank has been investigated in preclinical and clinical research contexts for its GABAergic pathway modulation, enkephalinase inhibition, monoaminergic system interactions, and immunomodulatory activity. It has been compared to benzodiazepine anxiolytics in clinical studies, demonstrating anxiolytic activity in generalised anxiety disorder (GAD) populations with a mechanistically distinct profile from benzodiazepine allosteric modulators. In preclinical models, a single administration of Selank has been associated with altered expression of 45 GABAergic genes in rat cortical preparations within one hour, alongside increased inhibitory postsynaptic currents in hippocampal neuron preparations.

Selank has been approved as a registered pharmaceutical in Russia since 2009 for the treatment of generalised anxiety disorders and neurasthenia, where it is available as a 0.15% nasal drop formulation (“Selank 0.15%”). Research-grade Selank supplied by RCDbio is not a pharmaceutical product and is not approved for any use outside laboratory research contexts. It is not approved by the Food and Drug Administration for human or veterinary use. It is not a dietary supplement and is not intended for human consumption or therapeutic self-administration. All RCDbio research compounds are supplied strictly for laboratory and research purposes only.

Chemical Properties

Property	Detail
Product Type	Synthetic Heptapeptide / Tuftsin Analogue Research Compound
Product Name	Selank
Application	Scientific / Research Use Only
CAS Number	129954-34-3
Molar Mass	751.887 g/mol
Chemical Formula	C33H57N11O9
PubChem CID	11765600
IUPAC Name	(2S)-1-[2-[[(2S)-1-[(2S)-2-[[(2S)-1-[(2S)-6-amino-2-[[(2S,3R)-2-amino-3-hydroxybutanoyl]amino]hexanoyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoyl]pyrrolidine-2-carbonyl]amino]acetyl]pyrrolidine-2-carboxylic acid
Amino Acid Sequence	Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP); 7 amino acids; tuftsin (TKPR) + C-terminal Pro-Gly-Pro extension
Parent Tetrapeptide	Tuftsin (TKPR; CAS 9063-57-4; MW 500.593 g/mol; C21H40N8O6) — IgG Fc region-derived immunomodulatory tetrapeptide
Synonyms	Selanc; TP-7; H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH; L-threonyl-L-lysyl-L-prolyl-L-arginyl-L-prolylglycyl-L-proline
Physical Form	Lyophilized white to off-white powder
Solubility	Freely soluble in water; soluble in PBS and standard aqueous buffers
Storage (Lyophilized)	−20°C; sealed container; protected from light and moisture
Storage (Reconstituted)	4°C; use within 48–72 hours; avoid repeated freeze-thaw cycles
Purity	≥98% (HPLC verified, independent third-party laboratory analysis)
WADA Status	Selank is not explicitly named on the 2026 WADA Prohibited List. As a non-approved research-grade peptide outside its Russian pharmaceutical approval context, S0 (Non-Approved Substances) provisions may apply in sport-adjacent research contexts. Verify current status at GlobalDRO.com before use.

How Does Selank Work?

Selank’s pharmacological activity is mediated through multiple intersecting pathways, including GABAergic system modulation, enkephalinase inhibition, monoaminergic neurotransmitter system interactions, and immunomodulatory activity via the preserved tuftsin sequence. Mechanistic data are derived from both preclinical rodent and limited clinical study preparations.

GABAergic Pathway Modulation

In isolated cell and rodent preclinical preparations, Selank has been investigated for modulation of GABAergic neurotransmission. A single administration increased GABA-A receptor binding sites by 38% in mouse frontal cortex preparations and altered the expression of 45 GABAergic genes in rat cortical tissue within one hour. Electrophysiology studies in rat hippocampal CA1 preparations confirmed increased amplitude and discharge rate of inhibitory postsynaptic currents at 1 μM Selank concentration. Mechanistically, Selank’s GABAergic interaction profile is distinct from benzodiazepine allosteric modulation — its binding site at GABA-A receptors has been characterised as separate from the benzodiazepine binding site in preclinical assay systems. This mechanistic distinction is proposed as the basis for Selank’s observed anxiolytic activity in preclinical models and clinical studies without the sedation, cognitive impairment, or dependence associated with benzodiazepines [Zozulya et al., 2001].

Enkephalinase Inhibition and Endogenous Opioid System

Selank dose-dependently inhibits enkephalin-degrading enzymes (enkephalinases) in plasma and brain tissue preparations, with an IC50 of approximately 15 μM — greater potency than standard peptidase inhibitors bacitracin and puromycin. By preserving endogenous leucine- and methionine-enkephalin concentrations through reduced enzymatic hydrolysis, Selank indirectly prolongs enkephalin-mediated inhibitory and analgesic signalling without direct opioid receptor agonism [Zozulya et al., 2001]. In clinical studies of patients with generalised anxiety disorder, decreased enkephalinase activity and shortened enkephalin half-life were observed in blood preparations, suggesting HPA dysregulation of the enkephalin system in anxiety pathophysiology.

Monoaminergic System Interactions

In rodent brain tissue preparations, Selank administration has been associated with modulation of serotonin metabolism, including interactions with catecholamine concentrations in specific brain regions [Semenova et al., 2010]. Effects on dopaminergic and noradrenergic neurotransmitter system concentrations have also been characterised in rodent in vivo models, contributing to the compound’s antidepressant-like and antistress profiles in preclinical behavioural paradigms.

Tuftsin-Derived Immunomodulatory Activity

The preserved tuftsin (TKPR) sequence in Selank retains the immunomodulatory activity of the parent tetrapeptide. In isolated cell preparations and rodent in vivo models, Selank has been shown to modulate interleukin-6 (IL-6) expression and influence T helper cell cytokine balance. Gene expression changes in chemokine and cytokine networks following single and repeated Selank administration have been characterised in murine spleen preparations, supporting the investigation of immune-neuroendocrine interaction pathways.

Key Research Findings

In preclinical and clinical research contexts, Selank has been associated with the following observations:

• GABAergic modulation: 38% increase in GABA-A receptor binding sites in mouse frontal cortex; 45 GABAergic genes altered in rat cortex within 1 hour; increased hippocampal inhibitory postsynaptic currents at 1 μM in CA1 preparations.
• Enkephalinase inhibition: Dose-dependent plasma enkephalin hydrolysis inhibition (IC50 ~15 μM) in preclinical and clinical preparations; greater potency than bacitracin and puromycin [Zozulya et al., 2001].
• GAD clinical study: In 62 patients, Selank anxiolytic efficacy comparable to medazepam with additional antiasthenic and mild stimulant effects; no sedation, cognitive impairment, or dependence observed [Zozulya et al., 2008].
• Phenazepam comparison: In 60 patients, Selank demonstrated pronounced anxiolytic effects plus mild nootropic activity persisting approximately one week after stopping; benzodiazepine side effects were absent [Medvedev et al., 2014].
• Serotonin metabolism: Selank modulated serotonin catabolism in specific rat brain regions; monoamine system interactions characterised in preclinical behavioural models [Semenova et al., 2010].

All findings listed above are derived from preclinical in vitro and in vivo data and limited clinical observations from Russian registered drug studies. No FDA-regulated clinical trial data have been established for research-grade Selank. These observations do not constitute evidence of efficacy or safety in any human condition or organism.

What are the Potential Research Applications of Selank?

In controlled laboratory environments, Selank has been investigated for the following research applications. These are observed in preclinical and in vitro contexts only and do not constitute claims of efficacy or safety in any organism.

GABAergic Pharmacology and Anxiolytic Mechanism Research. Selank is employed as a reference compound for studies characterising GABAergic modulation at a binding site distinct from the benzodiazepine allosteric site. Research employs GABA-A receptor binding assays, inhibitory postsynaptic current electrophysiology, gene expression profiling, and behavioural anxiety paradigms in rodent in vivo models to characterise Selank’s GABAergic mechanism profile.

Enkephalinase Inhibition and Endogenous Opioid Research. In plasma and brain tissue preparations, Selank is investigated for its capacity to inhibit enkephalin-degrading enzymes, preserving endogenous opioid peptide half-life without direct opioid receptor agonism. Research examines the relationship between enkephalinase inhibition, anxiety-related neuroendocrine changes, and behavioural outcomes in preclinical models.

Comparative Benzodiazepine Pharmacology As a compound with anxiolytic clinical data and a mechanistically distinct GABAergic profile, Selank is employed in comparative pharmacology studies examining benzodiazepine versus non-benzodiazepine GABAergic anxiolytic mechanisms in rodent models and isolated cell preparations.

Immune-Neuroendocrine Interaction Research Through its tuftsin-derived immunomodulatory sequence, Selank is investigated in studies examining the interface between immune system cytokine signalling and CNS anxiety-related pathway modulation. Research characterises IL-6, T helper cytokine balance, and chemokine expression changes in isolated cell and rodent in vivo model systems.

Nootropic Peptide Pharmacokinetics Selank’s PGP C-terminal extension is investigated as a model for understanding how tripeptide stabilisation sequences alter the plasma and brain tissue half-life of tuftsin-class peptides. Comparative pharmacokinetic studies examine the degradation kinetics of Selank versus parent tuftsin in preclinical plasma stability assays.

What are the Potential Side Effects of Selank?

Researchers in preclinical and clinical settings have noted the following observations. Research-grade Selank outside the Russian pharmaceutical context has no independently established human safety data.

• No sedation, amnesia, myorelaxation, or dependence observed in clinical studies of the pharmaceutical Selank formulation at anxiolytic doses — a key mechanistic distinction from benzodiazepine class effects
• No withdrawal syndrome observed in clinical research populations following Selank discontinuation in published clinical study data
• Headache was reported at low frequency in some clinical trial participants receiving the pharmaceutical Selank
• Mild transient dizziness was reported at low frequency in some preclinical and clinical preparations
• Immunomodulatory activity through tuftsin sequence may produce cytokine profile changes in cell-based research systems — a relevant confounding variable in immunology model experiments
• No human safety or tolerability data have been established for research-grade Selank outside the approved Russian pharmaceutical context. These observations are derived from pharmaceutical-grade formulation studies and should not be extrapolated to research-grade material or to any human or animal outcomes.

Risk & Handling

Handling Precautions

Selank should only be handled by trained laboratory personnel. Appropriate PPE is required: nitrile gloves, laboratory coat, and eye protection at a minimum. When working with lyophilized powder, use within a laminar flow cabinet or a clean area. Avoid aerosol generation during reconstitution. The compound’s GABAergic and CNS-active profile means that accidental intranasal or systemic exposure should be considered in laboratory risk assessments.

Exposure Risks

Risk Tier: LOW–MODERATE

Selank has demonstrated a generally low acute toxicity profile in preclinical rodent studies and in clinical studies of the registered pharmaceutical formulation. Its CNS-active GABAergic, enkephalinase, and monoaminergic mechanisms mean that accidental systemic exposure at research-relevant concentrations may produce pharmacological effects in tissues expressing relevant targets. No sedation, dependence, or significant adverse effects were observed in clinical study populations at anxiolytic doses. No human safety or tolerability data have been established for research-grade Selank.

Storage

• Lyophilized form: Store at −20°C in original sealed, light-protected container with desiccant
• Reconstituted form: Store at 4°C; use within 48–72 hours of reconstitution
• Do not subject to repeated freeze-thaw cycles; peptide integrity may be compromised
• Protect from prolonged light exposure and moisture
• PGP C-terminal extension provides enhanced aminopeptidase resistance; standard peptide storage precautions apply

Frequently Asked Questions

Q: What is Selank, and what is it investigated for in research? A: Selank (TKPRPGP) is a synthetic tuftsin-analogue heptapeptide investigated in preclinical and clinical research contexts for GABAergic pathway modulation, enkephalinase inhibition, monoaminergic system interactions, and immunomodulatory activity. It has been approved as a pharmaceutical in Russia since 2009 for generalised anxiety disorders. Research-grade Selank from RCDbio is not a pharmaceutical product and is intended strictly for laboratory and research purposes.

Q: How does Selank differ from benzodiazepines mechanistically? A: Benzodiazepines act as positive allosteric modulators at the benzodiazepine binding site on GABA-A receptors, producing sedation, myorelaxation, and dependence. Selank’s GABAergic interaction occurs at a distinct binding site in preclinical assay systems, characterised by increased GABA-A receptor binding sites and GABAergic gene expression without the sedation, cognitive impairment, or dependence profile of benzodiazepines in preclinical models and clinical study populations.

Q: Is Selank approved by the FDA? A: No. Selank has not received FDA approval for any indication. It is approved as a pharmaceutical in Russia since 2009 for generalised anxiety disorders and neurasthenia. Research-grade Selank from RCDbio is not a pharmaceutical product and is not intended for human use.

Q: What is the plasma half-life of Selank in preclinical models? A: Selank demonstrates enhanced plasma stability relative to parent tuftsin due to the C-terminal Pro-Gly-Pro extension, which confers resistance to carboxypeptidase degradation. Precise standardised pharmacokinetic half-life data from peer-reviewed preclinical studies in controlled conditions is limited in the published literature. These observations are from preclinical animal studies and do not represent human pharmacokinetic data for research-grade material.

Q: What is the enkephalinase inhibition mechanism of Selank? A: In plasma and brain tissue preparations, Selank dose-dependently inhibits enkephalin-degrading enzymes with an IC50 of approximately 15 μM — greater potency than standard peptidase inhibitors. By reducing the enzymatic hydrolysis of leucine- and methionine-enkephalins, Selank preserves their endogenous concentrations and prolongs their inhibitory and analgesic signalling without direct opioid receptor agonism. In clinical GAD populations, decreased enkephalinase activity was characterised as a pathogenic feature, suggesting DSIP-class dysregulation in anxiety pathophysiology [Zozulya et al., 2001].

Q: How should Selank be stored? A: Lyophilized Selank should be stored at −20°C in a sealed, light-protected container with desiccant. Once reconstituted, store at 4°C and use within 48–72 hours. Repeated freeze-thaw cycles are not recommended. The PGP C-terminal extension provides inherent stability advantages over unprotected peptides; standard lyophilized peptide storage precautions apply.

Related Research Compounds

Researchers investigating Selank may also be interested in the following compounds currently available for laboratory research at RCDbio:

• N-Acetyl Selank — The N-terminally acetylated derivative of Selank investigated for enhanced aminopeptidase resistance and comparative metabolic stability; the primary analogue for pharmacokinetic research alongside the parent compound.
• Semax — A synthetic ACTH(4-7) analogue developed by the same Russian institute as Selank; commonly investigated alongside Selank in comparative neuropeptide CNS pharmacology and BDNF pathway studies.
• DSIP — A synthetic neuroendocrine nonapeptide investigated for HPA axis modulation; shares the neuroendocrine anxiety pathway research context with Selank’s enkephalinase inhibition and HPA-axis interaction studies.

All products listed are for laboratory and research purposes only.

References

1. Zozulya, A. A., Kost, N. V., Sokolov, O. Yu., Gabaeva, M. V., Grivennikov, I. A., Andreeva, L. N., Zolotarev, Y. A., Ivanov, S. V., Andryushchenko, A. V., Myasoedov, N. F., & Smulevich, A. B. (2001). The inhibitory effect of Selank on enkephalin-degrading enzymes as a possible mechanism of its anxiolytic activity. Bulletin of Experimental Biology and Medicine, 131(4), 315–317. https://pubmed.ncbi.nlm.nih.gov/11550013/

2. Zozulya, A. A., Neznamov, G. G., Siuniakov, T. S., Kost, N. V., Gabaeva, M. V., Sokolov, O. Yu., Serebriakova, E. V., Siranchieva, O. A., Andriushenko, A. V., Telesheva, E. S., Siuniakov, S. A., Smulevich, A. B., Myasoedov, N. F., & Seredenin, S. B. (2008). Efficacy and possible mechanisms of action of a new peptide anxiolytic, Selank, in the therapy of generalized anxiety disorders and neurasthenia. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 108(4), 38–48. https://pubmed.ncbi.nlm.nih.gov/18454096/

3. Semenova, T. P., Kozlovskiy, I. I., Zakharova, N. M., & Kozlovskaya, M. M. (2010). Experimental optimization of learning and memory processes by Selank. Eksperimental’naya i Klinicheskaya Farmakologiya, 73(8), 2–5. https://pubmed.ncbi.nlm.nih.gov/20919548/

4. Medvedev, V. E., Tereshchenko, O. N., Israelian, A. Yu., Chobanu, I. K., Kost, N. V., Sokolov, O. Yu., & Myasoedov, N. F. (2014). A comparison of the anxiolytic effect and tolerability of Selank and phenazepam in the treatment of anxiety disorders. Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 114(7), 17–22. https://pubmed.ncbi.nlm.nih.gov/25176261/ 

Disclaimer

Selank is exclusively for laboratory research purposes. RCDbio products are not intended to diagnose, prevent, treat, or cure any disease or medical condition.

The Food and Drug Administration has not evaluated the statements on our website. This product is not approved for human or veterinary use. Researchers must comply with all applicable local, state, and federal laws and regulations governing the purchase and use of research compounds. By purchasing, you agree to our Terms and Conditions. RCDbio reserves the right to refuse sales to unauthorized individuals.

ATTENTION: All RCDbio products are strictly for LABORATORY AND RESEARCH PURPOSES ONLY. They are not intended for human consumption, veterinary use, or any other non-research application. For queries, complaints, or support, contact support@rcdbio.co