Peptigrade

Anxiolytic & Nootropic

Selank

Selank — heptapeptide Thr-Lys-Pro-Arg-Pro-Gly-Pro (tuftsin + C-terminal Pro-Gly-Pro)·Also known as: Селанк, TP-7, TP7, Tuftsin analog TKPRPGP

FDARegulatory status

Not approved. Has never been filed with FDA for any indication. Sold in the United States only as a research chemical for in-vitro and animal study. No IND on file in the FDA Drugs@FDA registry as of the April 15, 2026 503A Categories Update.

WADARegulatory status

Not specifically named on the 2026 WADA Prohibited List, but captured by the catch-all S0 category (non-approved substances with no current regulatory approval by any governmental health authority for human therapeutic use) for athletes in competition governed by WADA. Treat as prohibited.

Regulatory note ·Selank's approval status is jurisdiction-specific and frequently mis-stated online. In the Russian Federation it is registered as a nasal-drop anxiolytic (Селанк 0.15%) by the V.V. Zakusov Research Institute of Pharmacology via Peptogen, indicated for generalized anxiety disorder and neurasthenia; the registration dates to the late-2000s Russian Phase III program. No equivalent registration exists in the United States, European Union, United Kingdom, Canada, Australia, or Japan. Nearly all published efficacy trials originate from a single group of collaborating Russian institutes (Institute of Molecular Genetics RAS + Zakusov Research Institute) and have not been independently replicated in Western peer-reviewed journals. The single-lab-provenance problem is the dominant methodological limitation on every outcome grade on this page.

§ The quick take

TL;DR · Editor’s summary

Selank is a Russian-developed heptapeptide (Thr-Lys-Pro-Arg-Pro-Gly-Pro — the tuftsin tetrapeptide with a stabilizing C-terminal Pro-Gly-Pro) registered in the Russian Federation as a nasal-drop anxiolytic for generalized anxiety disorder and neurasthenia since approximately 2009. The registration rests primarily on Zozulia 2008, an open-label comparator study (n=62) in which Selank produced anxiolytic effects described as non-inferior to medazepam with fewer benzodiazepine-class adverse effects, and on a preclinical body of work from the Institute of Molecular Genetics of the Russian Academy of Sciences and the V.V. Zakusov Research Institute of Pharmacology characterizing GABA-A allosteric modulation (Volkova 2016: altered Gabra6 and Slc6a13 expression in IMR-32 cells), BDNF upregulation in the hippocampus and frontal cortex (Inozemtseva 2008; Kozlovskii 2019 ethanol-memory paradigm), enkephalinase inhibition (Kozlovskaya 2003 BALB/c vs C57BL/6 differential response), and cytokine modulation in depressive-disorder patients (Uchakina 2008, IL-6 suppression). The honest problem is that nearly every efficacy and mechanism publication comes from a single collaborating-institute group in one country, written in Russian, and has not been replicated in Western peer-reviewed journals or by an independent lab.

No double-blind placebo-controlled RCT has been published for any indication. Human pharmacokinetics for intranasal delivery — the approved clinical route — are not formally characterized in the English-language peer-reviewed literature. There is no FDA filing, no EMA filing, and no Phase 2 or Phase 3 program outside Russia. Under the Peptigrade rubric single-lab provenance caps efficacy grades at C regardless of reported effect size; this is not a judgment that the molecule does not work, but a reflection that the evidence base has not been independently stress-tested.

Safety signals from the Russian program are reassuring (non-sedating, no tolerance, no dependence, benign adverse-effect profile) but similarly single-source. Selank is not FDA-approved, is captured by WADA S0, and should be treated as an investigational compound outside the Russian Federation.

§ Grade matrix

The grade
per outcome.

One peptide can earn very different grades for different uses. Here is every outcome we’ve graded for Selank, sorted by strength of evidence.

C

Generalized anxiety disorder (GAD) and neurasthenia

Mixed

Zozulia 2008 open-label comparator trial (n=62, Russian) reported anxiolytic effect non-inferior to medazepam with fewer benzodiazepine-type adverse effects; basis of the 2009 Russian registration. No double-blind placebo-controlled trial has been published in a Western journal and the trial has not been replicated outside the originating Russian institutes. Under the Peptigrade rubric the single-lab-single-trial evidence does not clear the B threshold.

4 studiesUpdated 2026-04-20
C

GABA-A receptor allosteric modulation (mechanistic)

Mixed

Volkova 2016 and Kolik 2017 gene-expression work in IMR-32 cells and rat brain documented Selank-induced changes in Gabra6 and Slc6a13 transcript levels consistent with allosteric — not orthosteric — modulation. Supports mechanism but is in-vitro / rodent and from the originating-institute group. No radioligand binding study has localized a Selank binding site on the GABA-A receptor.

6 studiesUpdated 2026-04-20
D

BDNF upregulation and cognitive / neuroprotective effects

Weak

Inozemtseva 2008 and Volkova 2016 showed increased BDNF mRNA and protein in rat hippocampus and frontal cortex; Kozlovskii 2019 reported Selank (0.3 mg/kg/day IP × 7 d) prevented ethanol-induced BDNF reduction and object-recognition memory impairment in rats. All rodent, all originating-institute, and not paired with human cognitive-outcome trials.

5 studiesUpdated 2026-04-20
D

Cytokine / immunomodulatory effects (IL-6, TNF-α)

Weak

Uchakina 2008 reported IL-6 suppression in depressive-disorder patients (n small, open-label) without affecting healthy controls, framed as adaptogenic cytokine modulation. Kolomin 2011 reviewed T-helper cytokine shifts. No randomized comparator; consistent with tuftsin-analog immunology but does not establish clinical benefit.

4 studiesUpdated 2026-04-20
D

Enkephalinase inhibition and endogenous opioid modulation

Weak

Kozlovskaya 2003 and follow-ups: anxiolytic effect observed in high-enkephalinase BALB/c but not low-enkephalinase C57BL/6 mice, supporting enkephalinase inhibition as a contributing mechanism. Mechanistic plausibility only; no human analgesia or opioid-axis outcome data.

3 studiesUpdated 2026-04-20
D

Antiviral activity (H3N2 influenza, in vitro / animal)

Weak

Russian group reported Selank more effective than recombinant interferon-α at suppressing H3N2 replication in cell culture and mouse models. Single-lab, not replicated in Western virology literature, and no human antiviral trial.

2 studiesUpdated 2026-04-20
Ins.

Major depressive disorder and mood disorders

Insufficient

Cited as adjunct in small Russian open-label observations within the broader anxiety-spectrum literature. No controlled antidepressant trial. Online claims of standalone antidepressant effect are not supported by the published evidence.

1 studiesUpdated 2026-04-20

§ Why this grade

Sub-scores for this outcome.

Generalized anxiety disorder (GAD) and neurasthenia

Every grade rolls up six weighted sub-scores, each rated 1 to 5 with a written justification. Here is how the top-outcome grade was constructed.

Mechanism understood

3 / 5

GABA-A allosteric modulation (Volkova 2016 transcriptional, Semenova 2019 behavioral synergy with diazepam), enkephalinase inhibition (Kozlovskaya 2003), monoamine normalization (Semenova 2010), and BDNF upregulation (Inozemtseva 2008) are all characterized at the pathway level. No Selank-specific receptor identified. Human PK for the intranasal formulation is not published in Western literature. Partial mechanism score reflects functional-but-not-structural understanding.

Human studies (count + quality)

2 / 5

One registration-supporting open-label comparator trial (Zozulia 2008, n=62 including 30 on Selank) plus small open-label observations. No double-blind placebo-controlled RCT. All from the originating Russian institute group. Under the source hierarchy this is a tier-5 (open-label / pilot) evidence base — C-band at best regardless of effect size.

Effect vs placebo

2 / 5

No placebo arm in the pivotal trial; comparator is medazepam. The anxiolytic effect is reported as non-inferior to medazepam, but without placebo control the expectancy/regression-to-the-mean contribution cannot be separated. A B-grade requires placebo-controlled human data this program has not produced.

Long-term safety data

3 / 5

Russian post-marketing use dates to approximately 2009, giving roughly 17 years of real-world exposure in the Russian Federation. Formal long-term cohort data in Western peer-reviewed literature is absent. Reassuring but under-documented from an independent-surveillance standpoint.

Side effect profile

4 / 5

Russian clinical reports consistently describe a benign adverse-effect profile: non-sedating, no tolerance, no dependence, no withdrawal, minimal psychomotor effect. Favorable vs benzodiazepines on every axis studied. Score held at 4 rather than 5 because the entire safety narrative is single-source and lacks independent post-marketing surveillance.

Regulatory status

2 / 5

Registered in the Russian Federation as a nasal-drop anxiolytic for GAD and neurasthenia. Not FDA-approved, not EMA-approved, not approved in the UK, Canada, Australia, or Japan. WADA S0 applies by default. Regulatory recognition is real but jurisdiction-limited and not convertible to Western prescribing.

§ What the science says

How Selank
works.

The scientific explanation of the molecule and its proposed mechanism, with a plain-English translation — written at an 8th-grade reading level — in the teal callouts below each section. Every claim is linked to a primary source below.

What it is

Selank is a synthetic heptapeptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP), molecular formula C₃₃H₅₇N₁₁O₉, molecular weight 751.9 Da, CAS 129954-34-3. It was designed at the Institute of Molecular Genetics of the Russian Academy of Sciences by extending the endogenous immunomodulatory tetrapeptide tuftsin (Thr-Lys-Pro-Arg, cleaved from the Fc region of IgG heavy chain) with a C-terminal Pro-Gly-Pro tripeptide. The Pro-Gly-Pro tail confers resistance to serum and brain aminopeptidases and extends plasma half-life relative to native tuftsin, enabling practical intranasal administration (the approved Russian formulation is a 0.15% nasal-drop solution). Selank is used clinically only in the Russian Federation, where it is marketed as Selank / Селанк and is indicated for generalized anxiety disorder and neurasthenia.

In plain English

Selank is a synthetic seven-amino-acid peptide (TKPRPGP). It was built by taking tuftsin — a natural immune peptide the body clips from antibodies — and adding a short protective tail. That tail stops the body from breaking Selank down too quickly, making it stable enough to spray in the nose and reach the brain. The approved Russian formulation is a 0.15% nasal-drop solution. It was developed at the Institute of Molecular Genetics in Moscow. Selank is used as a prescription drug only in Russia, where it is approved for generalized anxiety disorder and neurasthenia (chronic fatigue combined with anxiety).

How it works

  1. 01

    GABA-A allosteric modulation (gene-expression evidence)

    Volkova (2016, Frontiers in Pharmacology) showed that Selank administration to IMR-32 neuroblastoma cells altered expression of GABAergic genes including Gabra6 (GABA-A α6 subunit) and Slc6a13 (GABA transporter GAT-2) in a pattern consistent with positive allosteric modulation rather than direct orthosteric agonism. Kolik (2017) and Semenova (2019) extended this to rat brain regions, observing Gabra6 expression shifts and enhanced diazepam effect in the elevated plus maze when Selank was co-administered — supporting the clinical-trial-level observation (Zozulia 2008) that Selank behaves like an anxiolytic without the sedative/cognitive liabilities of benzodiazepines. No radioligand study has identified a specific Selank binding pocket on the GABA-A receptor, so the 'allosteric modulator' designation is inferred from functional and transcriptional readouts, not from binding data.

    In plain English

    It may calm the brain's GABA system — but indirectly

    GABA is the brain's main calming chemical. Benzodiazepines work by directly activating GABA receptors. Selank works differently: it shifts which GABA-related genes are active, without directly turning on the receptor. Lab studies in human nerve cells and rat brains showed that Selank changed specific GABA receptor and transporter gene activity in a way that suggests it boosts — but doesn't directly trigger — the GABA system. Supporting this: when rats were given Selank plus a small dose of Valium, the calming effect was much bigger than either alone. That boosting behavior fits what scientists call an 'allosteric modulator.' The key gap: no study has found the specific spot on the receptor where Selank docks to produce this effect.

  2. 02

    BDNF upregulation in hippocampus and frontal cortex

    Inozemtseva (2008) and Volkova (2016) reported increased BDNF mRNA and protein in rat hippocampus following Selank. Kozlovskii (2019, Bulletin of Experimental Biology and Medicine) showed that Selank (0.3 mg/kg/day IP × 7 days) prevented ethanol-induced reductions in hippocampal and prefrontal-cortex BDNF content and corresponding object-recognition memory deficits. This is the mechanistic basis for claimed nootropic and neuroprotective effects, but is entirely rodent and from the originating-institute group.

    In plain English

    It raises a brain-growth protein that helps protect memory

    BDNF is a protein that helps brain cells grow, survive, and connect — it's closely tied to mood and memory. In rats, Selank raised BDNF levels in the hippocampus and frontal cortex (two key memory and mood areas). In a separate study, Selank prevented alcohol from reducing BDNF and from erasing object memory in rats. This is the basis for calling Selank 'memory-protective.' All of it is animal data from the same Russian lab — no human cognitive trial has been run.

  3. 03

    Monoamine (serotonin, dopamine, norepinephrine) modulation

    Semenova (2010, Neurochemical Journal) and follow-up work documented Selank-induced normalization of serotonin, dopamine, and norepinephrine concentrations in mouse hypothalamus, hippocampus, and frontal cortex, with effects most pronounced in anxiety-susceptible strains. Serotonin turnover appears to be the most consistent signal and is proposed as a contributor to the mood-stabilizing component of the anxiolytic profile.

    In plain English

    It normalizes mood-related brain chemicals in stressed animals

    In anxiety-prone mice, Selank moved serotonin, dopamine, and norepinephrine levels in key brain areas closer to normal. Serotonin was the most consistent signal. This is proposed as part of why Selank may stabilize mood. All of it is rodent data — the effect was most pronounced in strains of mice bred to be anxious, which suggests the drug may mainly correct an abnormal baseline rather than acting on a normal one.

  4. 04

    Enkephalinase inhibition

    Kozlovskaya (2003) reported that Selank produced robust anxiolytic effects in BALB/c mice (which express high enkephalin-degrading enzyme activity) but not in C57BL/6 mice (low activity), consistent with Selank preserving endogenous enkephalins by inhibiting their degradation. This provides a plausible mechanism for an opioid-system contribution to the anxiolytic effect distinct from the GABAergic arm. No human enkephalin pharmacodynamics have been measured.

    In plain English

    It may preserve the body's own natural calming molecules

    The body makes its own natural calming molecules called enkephalins. An enzyme called enkephalinase breaks them down. In mice with lots of this enzyme, Selank strongly reduced anxiety. In mice with low levels of it, Selank barely worked. This suggests Selank works partly by slowing down the breakdown of the body's own calming chemicals — essentially letting them last longer. This is a separate anxiety-relief pathway from the GABA effect. No human data has tested this.

  5. 05

    Immunomodulation and cytokine effects (tuftsin pharmacology)

    Because Selank contains the complete tuftsin sequence at its N-terminus, it retains tuftsin-like engagement of macrophage/neutrophil tuftsin receptors. Uchakina (2008) reported IL-6 suppression in patients with depressive disorder who had baseline IL-6 elevation, without cytokine changes in healthy controls — characterized as 'adaptogenic' immunomodulation. Kolomin (2011) reviewed T-helper cytokine rebalancing and reduced TNF-α signaling. These effects link the CNS-anxiolytic profile to the peripheral immune system and are one of the more distinctive features of the molecule compared with benzodiazepines.

    In plain English

    It inherits immune effects from the tuftsin part of its structure

    The first four amino acids of Selank's sequence are identical to tuftsin — a natural immune peptide the body clips from antibodies to activate immune cells. Because of this, Selank can bind to immune cells the way tuftsin does. In depressed patients with elevated inflammation (high IL-6), Selank lowered that marker — but did nothing in healthy people. This is called 'adaptogenic' because it only seems to correct an abnormality, not suppress a healthy immune system. This immune angle makes Selank different from benzodiazepines, which have no immune effects at all.

  6. 06

    What is NOT known about the mechanism

    No Selank-specific receptor has been molecularly identified. The allosteric-modulator designation is functional/transcriptional, not structural. Intranasal human pharmacokinetics (Cmax, Tmax, CNS penetration, half-life) are not characterized in Western peer-reviewed literature. The extent to which the reported CNS effects in rodents reflect central vs peripheral (tuftsin-receptor-mediated vagal / immune) signaling has not been dissected. Receptor pharmacology, PK, and blinded mechanistic replication are the three missing pillars that would move the grade upward.

    In plain English

    What we still don't know about how it works

    No one has identified the specific molecular target Selank binds to. The 'GABA booster' label is based on changes in gene activity, not on finding an actual receptor site. How much Selank reaches the brain when sprayed in the nose hasn't been published in any Western journal. It's also unknown whether the calming effects seen in rodents come from direct brain action or from signaling through the immune system. Those three gaps — molecular target, nose-to-brain delivery, and central vs peripheral action — are the main reasons the evidence grade stays capped at C.

§ Investigated uses

What it’s
been studied for.

Investigated does not mean proven. This list shows every use that appears in the published literature, regardless of evidence strength. See the grade matrix above for which ones have actually held up.

  • Generalized anxiety disorder (GAD)

    Zozulia 2008 open-label comparator vs medazepam (n=62); basis of 2009 Russian registration. No blinded placebo-controlled trial.

  • Neurasthenia

    Included in the Zozulia 2008 program as a co-indication; registered in Russia for this use. No Western diagnostic analog trial.

  • Cognitive function / memory protection

    Rodent object-recognition and ethanol-memory paradigms (Kozlovskii 2019). No human cognitive-endpoint trial.

  • Major depressive disorder (adjunct, exploratory)

    Small Russian open-label observations; insufficient for any efficacy claim.

  • Neuroinflammation / cytokine modulation

    Uchakina 2008 IL-6 suppression in depressive-disorder patients; mechanistic signal only.

  • H3N2 influenza (antiviral, preclinical)

    Russian in-vitro and mouse model work; not replicated in Western virology literature.

  • Substance-use withdrawal / craving (exploratory)

    Ethanol-memory model (Kozlovskii 2019) cited as rationale. No controlled addiction-medicine trial.

§ The honest gaps

What we don’t
know yet.

Every peptide page on this site is required to include this section. Absence of evidence is information. If we don’t flag the gaps, we’re lying by omission.

  • !

    No double-blind, placebo-controlled RCT has been published for any Selank indication in a Western peer-reviewed journal. The 2009 Russian registration for GAD rests on open-label comparator data (Zozulia 2008) that has never been independently replicated outside the originating institutes.

  • !

    Independent-lab replication is the central gap. Nearly every efficacy and mechanism paper on this page shares authors or institutional affiliation with the Institute of Molecular Genetics RAS or the V.V. Zakusov Research Institute of Pharmacology. Single-lab evidence — even extensive single-lab evidence — does not satisfy the replication requirement in the Peptigrade source hierarchy.

  • !

    Human pharmacokinetics for the approved intranasal route are not formally characterized in English-language peer-reviewed literature. Cmax, Tmax, brain exposure, and half-life for the 0.15% nasal-drop formulation are available only in Russian-language internal documentation and regulatory summaries.

  • !

    No Selank-specific molecular receptor has been identified. The GABA-A 'allosteric modulator' designation is inferred from functional assays and gene-expression changes, not from radioligand binding or cryo-EM. This limits dose-finding and structure-activity optimization.

  • !

    Long-term human safety beyond the Russian registration dossier is not documented in the Western literature. Multi-year cohorts, pregnancy exposure, pediatric exposure, and drug–drug interaction studies are absent.

  • !

    The relative contribution of the GABAergic, enkephalinergic, serotonergic, and peripheral-tuftsin-receptor arms to the clinical anxiolytic effect has not been dissected. This matters for predicting interactions with benzodiazepines, SSRIs, and opioids.

  • !

    The relationship between the preclinical cytokine / antiviral signal and clinical outcomes in humans is uncharacterized. Uchakina 2008 is suggestive but underpowered.

  • !

    No head-to-head trial vs modern first-line anxiolytics (SSRIs, SNRIs, buspirone) has been conducted. The only comparator in the pivotal trial is medazepam, a benzodiazepine no longer in first-line use in most of the world.

§ On YouTube

What experts and
influencers say.

We index YouTube content discussing Selankand tag every speaker by credential and trust level. The goal is not to summarize the internet — it’s to tell you which voices to weight.

  • Selank and Semax — the Russian nootropic peptides, and what the evidence actually says

    Huberman Lab·PhD Neurobiology, Stanford

    Walks through the Russian-literature provenance problem and is explicit that no double-blind placebo-controlled RCT exists for Selank in Western journals. Describes the tuftsin-analog origin and contrasts with benzodiazepine pharmacology.

    Verified credentials

  • Selank clinical use in anxiety — what a U.S. physician should know before recommending it

    Dr. Kyle Gillett·MD, Family Medicine

    Frames Selank as investigational in the U.S. and flags the single-lab-evidence issue. Notes the Russian intranasal formulation and the absence of FDA filings. Recommends against self-administration without a prescriber familiar with the literature.

    Verified credentials

  • I used Selank nasal spray for 30 days — here's what happened

    Anonymous biohacker·Unverified

    First-person anecdotal report with no methodology, no objective measure, and no independent verification of product identity or purity. Common in the Selank online content ecosystem. Do not weight against published evidence.

    Caution — anecdotal

  • Selank vs Semax — which Russian peptide for anxiety vs focus?

    Unverified peptide channel·Unverified

    Comparison content built from marketing copy rather than primary literature. Mischaracterizes the Russian registration as FDA-equivalent and omits the replication problem. Representative of the lower-quality content that dominates the Selank search results.

    Caution — anecdotal

§ Citations

Every claim,
linked to source.

All 12 sources informing this page, with DOI or PubMed identifiers. Click through to the primary literature.

  1. [01]

    Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia

    Zozulia AA, Neznamov GG, Siuniakov TS, et al. · Zh Nevrol Psikhiatr Im S S Korsakova · 2008

    Open-labelPMID 18454096
  2. [02]

    Peptide-based anxiolytics: the molecular aspects of heptapeptide Selank biological activity

    Kolomin T, Shadrina M, Slominsky P, Limborska S, Myasoedov N · Protein Pept Lett · 2018

    Systematic reviewPMID 30255741
  3. [03]

    Selank administration affects the expression of some genes involved in GABAergic neurotransmission

    Volkova A, Shadrina M, Kolomin T, et al. · Front Pharmacol · 2016

    In vitroDOI
  4. [04]

    GABA, Selank, and olanzapine affect the expression of genes involved in GABAergic neurotransmission in IMR-32 cells

    Kolomin T, Shadrina M, Andreeva L, et al. · Front Pharmacol · 2017

    In vitroDOI
  5. [05]

    Peptide Selank enhances the effect of diazepam in reducing anxiety in unpredictable chronic mild stress conditions in rats

    Semenova TP, Kozlovskaya MM, Zuikov AV, Kozlovskii II · Behav Neurol · 2017

    AnimalDOI
  6. [06]

    Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating BDNF content in the hippocampus and prefrontal cortex in rats

    Kozlovskii II, Andreeva LA, Kolomin TA, et al. · Bull Exp Biol Med · 2019

    AnimalPMID 31625062
  7. [07]

    Effect of the peptide Selank on cytokine balance in patients with anxiety-asthenic disorders

    Uchakina ON, Uchakin PN, Miasoedov NF, et al. · Zh Nevrol Psikhiatr Im S S Korsakova · 2008

    Open-labelPMID 19240853
  8. [08]

    Selank and short peptides of the tuftsin family in the regulation of adaptive behavior in stress

    Kozlovskaya MM, Kozlovskii II, Val'dman EA, Seredenin SB · Neurosci Behav Physiol · 2003

    AnimalPMID 14533009
  9. [09]

    Transcriptomic response to Selank: changes in expression of genes encoding for GABA-A receptor subunits and GABA transporters in rat brain

    Kolomin T, Agapova T, Agniullin Y, et al. · Mol Biol (Mosk) · 2011

    AnimalPMID 22160037
  10. [10]

    Selank — overview, development history, and Russian registration

    Wikipedia contributors · Wikipedia · 2026

    RegulatoryLink
  11. [11]

    WADA 2026 Prohibited List (in force January 1, 2026) — Section S0 Non-Approved Substances

    World Anti-Doping Agency · WADA · 2026

    RegulatoryLink
  12. [12]

    FDA 503A Bulk Drug Substances Categories — April 15, 2026 Update (Selank not listed in Category 1)

    U.S. Food and Drug Administration · FDA · 2026

    RegulatoryLink

§ Adjacent peptides

Worth reading
alongside this.

Compare

Semax

Sister Russian heptapeptide developed by the same Institute of Molecular Genetics program. Same evidence-quality pattern (Russian single-lab, registered in Russia, not Western-registered) and the closest peer for cross-reference on Selank's provenance story.

Read its grades

Compare

DSIP

Another CNS-active small peptide with a similarly Russian- and Eastern-European-dominated literature base. Useful peer for thinking about how to weight non-Western clinical evidence under the Peptigrade rubric.

Read its grades

Compare

Epitalon

A third Russian-developed peptide with a heavy originating-institute literature footprint and limited Western replication. Reads the same single-lab-provenance caution pattern as Selank.

Read its grades

Where to research further

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for laboratory research?

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