🧠 Tuftsin Analog • Anxiolytic/Nootropic

Selank (TKPRPGP)

Synthetic tuftsin-derived heptapeptide studied for reducing anxiety and sharpening cognition while sparing alertness. Multi-system profile: GABA modulation, BDNF, enkephalin preservation, and immune balancing.

Sequence TKPRPGP MW ~751.9 Da CAS 129954-34-3

⚡ Executive Summary

Selank (TKPRPGP) is a synthetic heptapeptide derived from tuftsin studied for anxiolytic and nootropic effects without sedation. In clinical studies, it matched benzodiazepine anxiolysis while adding antiasthenic/psychostimulant benefits. Mechanisms include GABA-related gene modulation, ↑BDNF, enkephalinase inhibition, and cytokine balancing. ✓ Calm Without Sedation

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01 Overview 02 Properties 03 Mechanism 04 Evidence 05 Handling 06 Comparison 📋

Overview

🧠 What is Selank?

Selank is a seven-amino-acid analog of the immune peptide tuftsin, engineered to provide anxiolysis without sedative trade-offs.

Features a glyproline (PGP) motif that aids stability and CNS penetration.

🎯 Key Effects

• 😌 Anxiolysis — without sedation
• 🧠 Nootropic — preserved/improved cognition
• ⚡ Antiasthenic — psychostimulant signal

💡

Why “calm without sedation” matters: Across clinical and translational work, Selank reduces anxiety without typical benzodiazepine downsides (amnesia, withdrawal). This has been explicitly noted in mechanistic studies and patient-level data showing preserved — or improved — mental energy.

🌍

Clinical status: Selank is used clinically in Russia (including GAD contexts). Outside Russia, it’s primarily a research compound. You may see “Selanc” or “TP-7” — these refer to the same peptide.

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Entity Properties

Aliases	Selank, Selanc, TP-7, UNII: TS9JR8EP1G
Sequence	Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP)
Length	7 amino acids (heptapeptide)
Molecular Weight	~751.9 Da
CAS Number	129954-34-3
Family	Tuftsin analog (immunomodulatory) with glyproline (PGP) motif
Diluent(s)	Bacteriostatic water (0.9% benzyl alcohol) or 0.9% saline
Concentration	5 mg + 2 mL = 2.5 mg/mL → 0.10 mL = 250 µg (example)
Storage (dry)	Refrigerated or frozen; stable long-term
Storage (solution)	2–8°C; minimize freeze-thaw; use relatively soon

⚙️

Mechanism of Action

🧠 Multi-System Neurochemistry

Selank influences GABA-related and monoaminergic signaling in ways that reduce anxiety while preserving cognition. Transcriptomic work shows broad regulation of GABAergic genes — indirect GABAergic modulation, not classic benzodiazepine receptor agonism.

🧬

GABA Gene Modulation

Broad regulation of GABAergic genes; indirect modulation (not classic benzo agonism) — anxiolysis without sedation

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↑ BDNF (Hippocampus)

Intranasal Selank increases BDNF in vivo — key neuroplasticity factor supporting pro-cognitive effects

🛡️

Enkephalinase Inhibition

IC₅₀ ~20 µM — prolongs endogenous enkephalin tone linked to stress relief and analgesia

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Immune/Cytokine Balancing

As tuftsin analog: alters ~34 cytokine/chemokine genes in spleen; normalizes inflammatory signals under stress

🦠

Bonus finding: Selank demonstrated antiviral activity against influenza A/H3N2 in vitro and in vivo with strongest effect via preventive pre-exposure — hinting at innate-immunity priming. This strengthens the “stress-immune” narrative.

📊

Research Evidence

📚 Clinical Signals

• ✓ GAD comparison: Selank’s anxiolytic effect matched medazepam (benzodiazepine) while adding antiasthenic/psychostimulant benefits
• ✓ Rapid responders: Clinical observations in GAD cohorts report rapid response within days in some patients
• ✓ No benzo downsides: Preserved — or improved — mental energy; no amnesia/withdrawal signals
• ✓ BDNF mechanism: Intranasal dosing alters hippocampal BDNF expression in vivo — substrate for cognitive/affective change

🧪 Preclinical

• 📊 GABA-related gene expression changes
• 📊 Enkephalinase inhibition IC₅₀ ~20 µM
• 📊 Cytokine gene normalization (~34 targets)

🌍 Clinical (Russia)

• ✓ Used in GAD treatment protocols
• ✓ Rapid vs slow responder phenotypes
• ✓ HAM-A / Zung scale improvements

🧪

Research Handling

📘

Research use only. The steps below outline laboratory-style handling common in peptide research. Educational only — no medical advice.

💉 Administration Routes

💉

Subcutaneous (SC)

Common in research for reliable bioavailability

👃

Intranasal (IN)

Supported by BDNF data; widely used in Russian clinical practice

1

Plan Concentration

5 mg + 2 mL = 2.5 mg/mL (0.10 mL = 250 µg). Or 5 mg + 4 mL = 1.25 mg/mL for smaller volumes.

2

Reconstitute Sterile

Bac water or 0.9% saline. Clean stopper with alcohol; direct along vial wall; swirl gently.

3

Select Route

SC for reliable bioavailability; IN if modeling translational use (hippocampal BDNF data).

4

Dosing Range

Literature explores hundreds of µg/day. Some protocols use multiple daily IN. Onset can be rapid (days).

5

Track Outcomes

Use standardized scales (HAM-A, Zung). Log time-of-day, route, and response patterns.

6

Store Properly

Lyophilized: refrigerated/frozen. Solutions: 2–8°C, minimize freeze-thaw, use soon or prepare fresh.

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Comparison

Selank vs Semax vs Benzodiazepines boils down to: calm-focus vs active-focus vs sedative-anxiolysis.

Selank

Tuftsin Analog (TKPRPGP) 😌 Anxiolysis + 🧠 Cognition

GABA gene modulation, ↑BDNF, enkephalinase inhibition. Matched medazepam anxiolysis without sedation.

No Sedation Pro-Cognitive No Dependence

Semax

ACTH(4-10) Analog (MEHFPGP) 🧠 Cognition + 🛡️ Neuroprotection

↑BDNF/TrkB signaling; dopaminergic/serotonergic effects. Clinical use post-stroke in Russia.

Enhanced Focus Potential Stimulation No Dependence

Benzodiazepines

GABA_A PAMs (Small Molecules) 😌 Anxiolysis + 😴 Sedation

Direct GABA_A receptor boost → broad CNS depression. Effective for acute anxiety.

Sedation Memory Impairment Dependence Risk 💡

Best choice? Selank when anxiety + cognitive clarity are dual aims. Semax when pure cognition/neuroprotection is paramount. Benzodiazepines remain potent but sedating and potentially habit-forming.

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FAQ

What is Selank? A synthetic heptapeptide (TKPRPGP) derived from tuftsin studied for anxiolytic and cognitive effects without sedation. Core mechanisms: GABA-related gene modulation, BDNF increases, enkephalinase inhibition, and cytokine balancing. How fast can Selank work? Clinical observations in GAD cohorts report rapid responders within days. Intranasal dosing alters hippocampal BDNF expression in vivo — a plausible substrate for earlier cognitive/affective change. Does it cause sedation like benzos? No — Selank is non-sedating and has even shown antiasthenic/psychostimulant signals. In comparative clinical study, it matched medazepam’s anxiolysis WITHOUT sedative downsides. What makes it unique vs. other nootropics? Selank uniquely combines neurochemical (GABA/monoamines/BDNF) and immunomodulatory actions AND inhibits enkephalinases, prolonging endogenous anti-stress peptides — an uncommon multi-axis profile. Is Selank approved anywhere? Yes — Selank is used clinically in Russia (including GAD contexts) with documented rapid- vs slow-response phenotypes. Outside Russia, it’s primarily a research compound. How is it different from Semax? Selank = calm-focus (anxiolysis + cognition). Semax = active-focus (pure cognition/neuroprotection, potential stimulation). Selank is tuftsin-derived; Semax is ACTH(4-10)-derived. Both are non-habit-forming. ✅

Bottom line: Selank’s value is its rare combination of anxiolysis without sedation plus cognitive support, underpinned by GABA/BDNF/enkephalin/immune mechanisms. Clinical data shows it matched benzodiazepine anxiolysis while preserving mental clarity — making it a compelling peptide when calm clarity is the goal.