# Selank: The Tuftsin-Analog Anxiolytic Peptide, Reviewed at Source > Selank is a synthetic tuftsin-analog heptapeptide (TP-7) studied as a non-benzodiazepine anxiolytic. A scholarly digest of the GABAergic, enkephalinase, BDNF, and monoaminergic findings, cited to source. A scholarly, evidence-first digest of Selank's GABAergic, enkephalinase, BDNF, and monoamine signals, with the single-region Russian evidence base named where it is thin rather than hidden. ## The short version Selank is a small lab-made peptide — a chain of seven amino-acid building blocks (Thr-Lys-Pro-Arg-Pro-Gly-Pro), also called TP-7. It was built in Russia by adding a short, stabilizing tail to tuftsin, a natural four-piece fragment our own antibodies release. People study it as an *anxiolytic* (a calm-the-nerves compound) and a *nootropic* (a compound looked at for focus and memory). In animal studies and a handful of small Russian human trials, it appears to ease anxiety without the heavy drowsiness of common sedatives. Reported upsides, the genuine downsides, and what to watch for are laid out on [Selank effects](/effects). One honest caution up front: Selank is **not** approved by the U.S. Food and Drug Administration (the agency that clears medicines). Almost all of the human evidence comes from one country, and it does not prove Selank treats any diagnosed anxiety condition. This site summarizes published research; it gives no doses and no medical advice. ## What the Selank literature describes Selank (full sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro; CAS 129954-34-3; molecular weight 751.9 Da) is a synthetic analog of tuftsin, an endogenous tetrapeptide (Thr-Lys-Pro-Arg) cleaved from the heavy chain of immunoglobulin G. Native tuftsin is degraded almost immediately by plasma peptidases; the C-terminal Pro-Gly-Pro extension that defines Selank slows that breakdown and is the molecule's core design rationale. The central pharmacological claim in the literature is that Selank exerts anxiolytic activity without acting as a benzodiazepine. A 2018 review characterizes it as a positive allosteric modulator (a molecule that binds a receptor away from its main site and tunes its response) of GABA receptor binding, with subtype-selective, concentration-dependent modulation distinct from classical sedatives [1]. A separate, independent line of work attributes part of the effect to inhibition of enkephalin-degrading enzymes — Selank inhibited plasma enkephalin hydrolysis in human plasma in vitro with an IC50 near 15 µM, stabilizing the body's own anti-stress peptides [2]. The evidence is real but it is not abundant, and it is concentrated. The great majority of Selank studies originate from a small set of Russian research groups, many in Russian-language journals with English abstracts only, and independent Western replication is limited [6]. That concentration is stated here as a finding in its own right, not buried. ## Selank peptide: a tuftsin analog, not a benzodiazepine As a peptide rather than a small-molecule sedative, the Selank peptide engages the nervous system across several axes at once. Beyond GABAergic modulation [1] and enkephalinase inhibition [2], intranasal Selank increased brain-derived neurotrophic factor (BDNF) expression in the rat hippocampus in vivo, linking the peptide to neurotrophic signaling [3]. Administration also shifted the expression of GABA-pathway genes in rat frontal cortex — 45 genes changed one hour after dosing and 22 at three hours, with the direction of change correlating positively with GABA's own effect [4]. This multi-system profile is why the literature treats Selank as mechanistically distinct from the agents people commonly compare it to. The comparison itself is covered on [Selank vs Semax](/vs-semax), and the speed-of-onset and duration questions on [Selank half life](/half-life). ## Where the evidence is strong, and where it is thin Strong, in the sense of genuinely measured and cited: the GABA positive-allosteric-modulation account [1], the human-plasma enkephalinase IC50 [2], the rat hippocampal BDNF increase [3], the GABA-pathway gene shift [4], and the Russian clinical reports in generalized anxiety disorder [6]. Each is a real result attached to a real paper, listed in full on [Selank references](/references). Thin, and stated as such: pharmacokinetics of intact Selank in humans are poorly characterized in mainstream literature; human efficacy data come almost entirely from single-region trials with limited replication; and a notable minority of users report little or no subjective effect [6]. None of this is a verdict against the compound — it is the accurate state of the record, which is what a digest is for. ## How to read this site Every quantitative claim here maps to a numbered citation, and the full source list lives on [Selank references](/references). Mechanism and the key studies are on [Selank research](/research); the doses and routes used in published work, in research context only, are on the dosage page; reported benefits, downsides, and cautions — including what people report anecdotally — are on [Selank effects](/effects). This is editorial commentary on publicly available science. It is not a clinic, it does not sell anything, and it makes no human dosing or treatment recommendation. --- A verification-minded reading of the Selank record — the GABA, enkephalinase and monoamine findings logged to source and tagged by evidence strength, the single-region Russian base and unknown human pharmacokinetics named without flinching; no clinic behind the console, and nothing here dispensed or sold.