Selank: Tuftsin Analogue — Peptide Anxiolytic Without Sedation
Educational Content Only
The information on this page is based on scientific publications and is for educational purposes only. It does not constitute medical prescription, diagnosis, therapeutic guidance, or recommendation for use. Any clinical intervention must be individualized by a qualified healthcare professional.
⚠️ The information on this page is based on scientific publications and is for educational purposes only. It does not constitute medical prescription, diagnosis, therapeutic guidance, or recommendation for use. Any clinical intervention must be individualized by a qualified healthcare professional.
Scientific analysis of Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro): analogue of endogenous tuftsin, preclinical and phase III clinical trial data documenting anxiolytic-antidepressant effect via BDNF modulation and monoaminergic systems.
Mechanism of Action
Selank is a synthetic heptapeptide of sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP, also called TP-7), analogue of endogenous tuftsin (TKPR) with the Pro-Gly-Pro tripeptide added for enzymatic stability. Co-developed by the Institute of Molecular Genetics (Russian Academy of Sciences) and Zakusov Institute of Pharmacology, it is described in the literature as a peptide anxiolytic with a profile distinct from benzodiazepines.
1. Endogenous tuftsin analogue
Tuftsin (Thr-Lys-Pro-Arg) is an endogenous tetrapeptide derived from IgG cleavage in the spleen, with described immunomodulatory action. Selank adds Pro-Gly-Pro to tuftsin, extending its half-life and directing activity to the CNS.
2. BDNF modulation in hippocampus and cortex
Kolik et al. (2019) demonstrated that Selank prevents ethanol-induced BDNF alterations in hippocampus and prefrontal cortex in rats. BDNF modulation is one of the proposed mechanisms for its anxiolytic and cognitive effects.
3. GABAergic action without BZD receptor
Studies describe GABA potentiation by Selank in neuronal cultures — without binding to the benzodiazepine site of the GABA-A receptor. This is proposed as the explanation for anxiolytic effect without sedation, dependence and cognitive impairment typical of BZDs.
4. Monoaminergic modulation and antidepressant component
Sarkisova et al. (2008) document antidepressant effect in genetic depression model (WAG/Rij rats) and situationally induced model (BALB/c mice). The mechanism involves activation of monoaminergic systems (dopamine, serotonin) and modulation of tyrosine hydroxylase activity.
- •Heptapeptide tuftsin analogue with added Pro-Gly-Pro.
- •Anxiolytic action without sedation and without effect on benzodiazepine site.
- •Modulates BDNF, dopaminergic and serotonergic systems.
- •Completed phase III clinical trial in Russia for generalized anxiety disorder.
Applications Described in Literature
Generalized anxiety — Russian clinical trials
Moderate evidenceIn Russia, Selank completed phase III clinical trials for generalized anxiety disorder and was approved for intranasal use. Western literature is still limited, predominantly preclinical studies and Russian data. Czabak-Garbacz et al. (2006), published in Pharmacological Reports (outside Russia), replicated 4-week sustained anxiolytic effect in Wistar rats.
Memory and cognitive function — preclinical literature
Preliminary evidenceKolik et al. (2019) demonstrated in rats that chronic ethanol intake (30 weeks) impairs object recognition memory. Selank (0.3 mg/kg/day, 7 days) prevented cognitive impairment and normalized BDNF levels in hippocampus and prefrontal cortex. A neurotrophic effect is suggested as the cognitive mechanism.
Withdrawal syndrome — preclinical data
Preliminary evidenceKonstantinopolsky et al. (2022) describe Selank at anxiolytic dose (0.3 mg/kg IP) reduced total morphine withdrawal syndrome index by 39.6% in dependent rats. Effect comparable to diazepam (2 mg/kg) in attenuating convulsions, ptosis and postural disorders.
Relevant Studies
4 curated studies · 2006–2022
Peer-reviewed evidence with PMID verifiable on PubMed
Selank, Peptide Analogue of Tuftsin, Protects Against Ethanol-Induced Memory Impairment by Regulating of BDNF Content in the Hippocampus and Prefrontal Cortex in Rats
Kolik LG, Nadorova AV, et al. · Bulletin of Experimental Biology and Medicine
In rats with chronic ethanol intake (30 weeks), Selank (0.3 mg/kg/day, 7 days IP) prevented object recognition memory impairment and normalized BDNF in hippocampus and prefrontal cortex.
Selank, a Peptide Analog of Tuftsin, Attenuates Aversive Signs of Morphine Withdrawal in Rats
Konstantinopolsky MA, Chernyakova IV, Kolik LG · Bulletin of Experimental Biology and Medicine
Single IP injection of Selank (0.3 mg/kg) reduced morphine withdrawal syndrome index by 39.6% in rats. Significantly attenuated convulsions, ptosis and postural disorders, with efficacy close to diazepam 2 mg/kg.
Effects of heptapeptide selank on genetically-based and situation-provoked symptoms of depression in behavior in WAG/Rij and Wistar rats, and in BALB/c mice
Sarkisova KIu, Kozlovskii II, Kozlovskaia MM · Zh Vyssh Nerv Deiat Im I P Pavlova
Selank at high doses (1000-2000 μg/kg) reversed forced swim test immobility and anhedonia in WAG/Rij rats (genetic model). In BALB/c mice, low doses (100-300 μg/kg) reduced immobility — indicating antidepressant component.
Influence of long-term treatment with tuftsin analogue TP-7 on the anxiety-phobic states and body weight
Czabak-Garbacz R, Cygan B, et al. · Pharmacological Reports
TP-7 (Selank) 0.3 mg/kg IP daily for 4 weeks reduced anxiety-phobic states in Wistar rats with high emotional reactivity, starting day 2. Sustained effect for 4 weeks. No weight change.
Latest literature review: 2026-04 · PubMed
FAQ
What is Selank?
Selank is a synthetic heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro, also called TP-7) analogue of endogenous tuftsin. Developed at the Institute of Molecular Genetics and Zakusov Institute of Pharmacology (Russia), it is described in the literature as a peptide anxiolytic with a profile distinct from benzodiazepines — without sedation and with no documented dependence potential in trials.
What is the mechanism of Selank?
Preclinical studies indicate action on BDNF in the hippocampus and prefrontal cortex (Kolik et al., 2019), modulation of monoaminergic systems (dopamine, serotonin) and GABA receptor interaction. Sarkisova et al. (2008) document an antidepressant component in its action spectrum.
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