Selank
10mg
A naturally occurring peptide found in the human immune system, studied for its interactions with the brain's stress and calming pathways. Research models have examined its potential role in anxiety reduction, cognitive support, and mood regulation — without the sedation or dependence associated with traditional options.
Transparency
Certificate of Analysis
Every batch independently verified by third-party laboratories.
Batch #TL-2406449-P
Selank Lab Certificates
All Trident Labs products are independently tested by accredited third-party laboratories. Results are batch-specific and provided for research transparency only. This product is not approved for human use.
Five pathways. Seven amino acids. In vitro research.
A synthetic peptide analogue of tuftsin — a naturally occurring molecule in the human immune system. Research has examined Selank's interactions with the brain's calming (GABAergic) and neurotrophic (BDNF) signaling systems, making it a studied compound in anxiety, cognition, and neuroimmune research models.
Kasian et al. Front Pharmacol 2017 · Seredenin et al. 1998 · Shadrina et al. 2018. All data from peer-reviewed literature. For Research Use Only — Not for Human Consumption.
Manufactured in US
US-formulated & filled
Endotoxin Tested
<0.05 EU/mL verified
Independently Tested
Horizon Analytical · 6-panel COA
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Selank is supplied exclusively for qualified in vitro laboratory research. Not for human administration.
This product is a research-grade synthetic heptapeptide supplied under research use only (RUO) designation. It is not approved by the FDA as a drug for any indication in the United States, not evaluated for safety or efficacy in humans under US regulatory standards, and not intended to diagnose, treat, cure, or prevent any disease or condition. By purchasing, the buyer represents they are a qualified researcher using this compound solely for lawful in vitro laboratory research. This product is not a dietary supplement, food, drug, or medical device. Trident Labs supplies Selank exclusively for cell-based, in vitro, or analytical research applications.
Mechanism of Action
From tuftsin to
five active pathways.
Selank (TKPRPGP) was engineered by appending a Pro-Gly-Pro tripeptide to the C-terminus of tuftsin — a naturally occurring immunomodulatory tetrapeptide fragment of IgG. The PGP extension dramatically increases metabolic stability while unlocking neurobiological activity not present in the parent molecule. The result is a single heptapeptide that simultaneously engages five distinct signaling systems.
GABAergic Modulation — GABA-A Receptor Gene Expression
Selank does not directly bind GABA-A receptors as a classical agonist. Instead, it modulates the expression of GABA-A receptor subunit genes — specifically influencing the affinity of the receptor for GABA. Kasian et al. (2017) found Selank affects 7 GABA signaling genes directly, with 45 genes showing expression changes and 52 GABA-related genes impacted overall. This indirect modulation may explain the separation of anxiolytic effects from benzodiazepine side effects.
BDNF Upregulation — Hippocampal Neuroplasticity
Selank rapidly upregulates BDNF mRNA in the rat hippocampus within hours of administration — with transcript levels climbing before a transient protein dip followed by a sustained rise above baseline. Kolik et al. (2019) demonstrated Selank normalizes pathologically altered BDNF levels in ethanol-exposed rats rather than simply elevating them — a regulatory rather than stimulatory effect. BDNF modulation provides mechanistic basis for observed nootropic and potential antidepressant effects.
Enkephalinase Inhibition — Endogenous Opioid Preservation
Selank concentration-dependently inhibits enkephalinase enzymes that normally degrade endogenous enkephalins. By slowing enkephalin breakdown, Selank increases availability of these endogenous anxiolytic neuropeptides without directly binding opioid receptors. Radioreceptor assays show Selank's actions are antagonized by naloxone — confirming opioid pathway involvement via enkephalin metabolism modulation, not direct receptor agonism.
Serotonin & Dopamine System Modulation
Zolotarev et al. (2003) characterized Selank's effects on monoamine neurotransmitter systems — serotonin metabolism, dopaminergic pathway interactions, and norepinephrine modulation in brain tissue models. Serotonergic modulation and BDNF upregulation act in concert to support neuroplasticity and emotional regulation pathways studied in preclinical depression models.
Tuftsin-Derived Immune Regulation — IL-6 · Th1/Th2
Selank retains the immunomodulatory heritage of its parent tuftsin. Ershov et al. showed Selank modulates interferon-related gene expression and influences cytokine profiles including IL-6. It stimulates phagocytic activity and modulates Th1/Th2 immune balance — a dual neurological and immunological profile from a single compound. CX3CR1 gene expression alterations observed in spleen and hippocampus suggest inflammatory pathway regulation via transcriptional mechanisms.
Sequence & Structure
TKPRPGP.
Seven residues.
The four N-terminal residues (TKPR) are the tuftsin core — retained intact from the immunomodulatory parent peptide. The C-terminal Pro-Gly-Pro tripeptide is the synthetic addition that confers metabolic stability and unlocks the neurobiological activity profile.
Primary Sequence — 7 Residues
Kasian et al. Front Pharmacol 2017 · Peptidebiologix.com. Research use only.
Molecular Identity
7 AA
TKPRPGP sequence
902 Da
MW — C₃₃H₅₇N₉O₈
4+3
Tuftsin core + PGP tail
5
Signaling pathways
Full Sequence
Thr-Lys-Pro-Arg-Pro-Gly-Pro
Tuftsin (TKPR) + PGP stability extension
Developed — Institute of Molecular Genetics, Russian Academy of Sciences
Compound Profile
Full specification.
Molecular and analytical specification from peer-reviewed literature and Trident Labs batch records.
| Common Name | Selank / TP-7 / Selanc |
| Sequence | Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP) |
| CAS Number | 129954-34-3 |
| Molecular Formula | C₃₃H₅₇N₉O₈ |
| Molecular Weight | 902.09 Da |
| Structure | Synthetic heptapeptide · Tuftsin (TKPR) + Pro-Gly-Pro C-terminal extension |
| Origin | Institute of Molecular Genetics, Russian Academy of Sciences |
| Primary Pathways | GABAergic · BDNF/neurotrophic · Enkephalinergic · Monoaminergic · Immunomodulatory |
| GABA Mechanism | GABA-A receptor subunit gene expression modulation · 52 GABA genes affected |
| Plasma t½ | ~minutes — complete clearance within 10 min · downstream effects persist hours |
| Form | Lyophilized powder · sealed glass vial |
| Purity | ≥99% HPLC · Mass Spec verified · 6-panel COA · Horizon Analytical |
| Endotoxin | <0.05 EU/mL · LAL-tested · Horizon Analytical |
| Solubility | Water, PBS · 1 mg/mL typical stock concentration |
| Regulatory | RUOIn Vitro Research Use Only — Not for Human Consumption |
Signaling Profile
Five pathways.
One compound.
Each arm is independently measurable in standard cell-based assay formats — from cAMP reporter assays for GABAergic modulation to ELISA for BDNF protein quantification and enkephalinase activity assays.
GABAergic Modulation — GABA-A Subunit Expression
Indirect modulation of GABA-A receptor subunit genes — 52 GABA-related genes impacted. No direct receptor binding, no sedation, no dependence. Anxiolytic efficacy comparable to diazepam in elevated plus maze without motor impairment.
BDNF Upregulation — Hippocampal Neuroplasticity
Rapid hippocampal BDNF mRNA increase within hours. Regulatory (normalizing) rather than simply stimulatory — documented in ethanol exposure models. Mechanistic basis for nootropic and antidepressant research interest.
Enkephalinase Inhibition — Endogenous Opioid Preservation
Concentration-dependent inhibition of enkephalin-degrading enzymes. Increases endogenous enkephalin availability without direct opioid receptor binding. Effect naloxone-reversible. Contributes to "clean" anxiolytic profile.
Monoamine System — Serotonin · Dopamine · Norepinephrine
Serotonin metabolite modulation and dopaminergic pathway interactions characterized in brain tissue models. Works in concert with BDNF upregulation for neuroplasticity and emotional regulation research endpoints.
Kasian et al. Front Pharmacol 2017 · Kolik et al. 2019 · Seredenin et al. 1998. In vitro data — research use only.
7 AA
Peptide Length
TKPRPGP sequence
5
Signaling Pathways
From one heptapeptide
52
GABA Genes Affected
Kasian et al. Front Pharmacol 2017
0
Direct Receptor Agonism
No BZD binding · No dependence
Research Observations
What the data
demonstrates.
Independent observations from preclinical behavioral studies, gene expression assays, and pharmacological models. Not Trident Labs claims. All data from peer-reviewed literature.
In elevated plus maze and light-dark transition tests, Selank produced anxiolytic efficacy comparable to diazepam (medazepam) without associated benzodiazepine effects — no sedation, no motor impairment, no amnesia, and no observable dependence or withdrawal in chronic administration models. This pharmacological separation is mechanistically explained by Selank's indirect GABAergic modulation versus the direct GABA-A allosteric potentiation of benzodiazepines.
Seredenin et al., Neurosci Behav Physiol 1998;28(3):321–6
Inozemtseva et al. documented rapid BDNF mRNA upregulation in rat hippocampus following Selank administration — transcript levels elevated within hours. Kolik et al. (2019) showed that in ethanol-exposed rats where BDNF is pathologically suppressed, Selank restored BDNF toward normal ranges rather than elevating beyond them — a regulatory effect suggesting Selank engages feedback mechanisms rather than simply driving expression upward.
Kolik LG et al., Bull Exp Biol Med 2019;167(5):641–644. PMID: 31625062
Kasian et al. (2017) used PCR analysis of RNA from rat spleen and hippocampus following single and repeated Selank exposure. Of 84 genes linked to GABA signaling examined, Selank directly regulated 7 genes, induced expression changes in 45, and impacted 52 total. CX3CR1 expression — a gene implicated in inflammatory pathways — was notably altered, suggesting simultaneous neuroimmune pathway engagement from a single compound at standard research concentrations.
Kasian A et al., Front Pharmacol 2017;8:782. PMID: 26847159
Radioreceptor assay data from Meshavkin et al. showed Selank's effects are fully antagonized by naloxone — a non-selective opioid receptor blocker — even though Selank does not compete for binding at δ- or μ-opioid receptors in displacement assays. This confirms Selank's anxiolytic activity involves opioid pathway modulation via enkephalin metabolism rather than direct agonism — a mechanistically distinct mode of action from both benzodiazepines and opioid analgesics.
Meshavkin VK et al. · Zozulya AA et al. — enkephalinase inhibition kinetics
Pharmacological Comparison
Selank vs
benzodiazepines.
Key mechanistic and pharmacological distinctions relevant to in vitro assay design and interpretation. Research data only — not clinical claims.
| Property | Selank | Diazepam (BZD) |
|---|---|---|
| Mechanism | Indirect GABA-A gene modulation | Direct GABA-A allosteric agonism |
| Anxiolytic efficacy | ✓ Comparable | ✓ Established |
| Sedation | None observed | Present |
| Motor impairment | None observed | Present |
| Amnesia | None observed | Present |
| Dependence potential | None observed | High |
| BDNF modulation | ✓ Upregulates | None |
| Immunomodulation | ✓ IL-6, Th1/Th2 | None |
| Enkephalin system | ✓ Enkephalinase inhibition | None |
| Plasma t½ | ~minutes | 20–100 hrs |
Seredenin et al. 1998 · Kasian et al. 2017. Preclinical comparison — research use only. Not clinical guidance.
Storage & Handling
Long-term
−20°C
Lyophilized, sealed. Stable 24 months. Avoid repeated freeze-thaw cycles.
In solution
4°C
Reconstituted in sterile water or PBS. Stable 7–14 days. Aliquot for single use.
For Research Use Only — Not for Human Consumption. Selank is supplied exclusively for in vitro laboratory research. Not a drug, dietary supplement, food, or medical device. For lawful in vitro laboratory research use only by qualified researchers.
Published Literature
Indexed research
on Selank.
Independent peer-reviewed studies. Not Trident Labs claims. For Research Use Only.
Selank Administration Affects the Expression of Some Genes Involved in GABAergic Neurotransmission
PCR analysis of RNA from rat hippocampus and spleen following single and repeated Selank exposure. Of 84 GABA signaling genes examined, Selank directly regulated 7 genes, induced expression changes in 45, and impacted 52 total. CX3CR1 gene alterations observed in both spleen and hippocampus — suggesting simultaneous neuroimmune pathway engagement. Provides molecular basis for Selank's anxiolytic effects via indirect GABA-A receptor subunit modulation rather than direct binding — mechanistically distinguishing it from benzodiazepines. Front Pharmacol 2017;8:782. PMID: 26847159.
Selank Protects Against Ethanol-Induced Memory Impairment by Regulating BDNF Content
In ethanol-exposed rats where BDNF is pathologically suppressed in hippocampus and prefrontal cortex, Selank administration normalized BDNF content toward baseline levels — restoring rather than simply elevating neurotrophic factor expression. This regulatory mechanism distinguishes Selank from crude BDNF upregulators and suggests engagement of endogenous feedback systems. Protective effects on working and spatial memory documented in Morris water maze and Y-maze paradigms. Bull Exp Biol Med 2019;167(5):641–644. PMID: 31625062.
Comparative Anxiolytic Activity of Selank vs Medazepam in Animal Models
Foundational comparative study demonstrating Selank matches medazepam (benzodiazepine) in anxiolytic efficacy across elevated plus maze, light-dark transition, and conflict test paradigms. Critically, Selank produced no sedation, no motor impairment, no amnesia, and no dependence — pharmacological profile incompatible with direct GABA-A agonism. Established Selank as the first research-grade peptide anxiolytic with benzodiazepine-equivalent efficacy and none of the signature side effects. Neurosci Behav Physiol 1998;28(3):321–326.
Neuroprotective and Neurotrophin Effects of Selank — BDNF Expression Analysis
Characterization of Selank's BDNF upregulation kinetics — rapid mRNA elevation (hours post-administration) followed by complex protein dynamics with a transient dip then sustained rise above baseline. Provides evidence that Selank engages fast signaling cascades first (mRNA transcription) followed by slower genomic effects (protein accumulation). Context for interpreting timing of downstream neuroplasticity and cognitive endpoints in in vitro and ex vivo assay systems. Linked to Selank's proposed nootropic mechanism.
From Tuftsin to Selank: Neurochemical and Immunological Dimensions of a Synthetic Heptapeptide
2025 review covering the structural basis and biological activity of Selank as a tuftsin analogue. Details the PGP C-terminal motif's role in membrane interactions and metabolic stability. Reviews immunological activity — T helper cell modulation, IL-6 signaling, Th1/Th2 balance — inherited from parent tuftsin. Covers neurobiological mechanisms: GABA subunit gene modulation, enkephalinase inhibition kinetics, BDNF regulation, and monoamine system interactions. Positions Selank as a model compound for studying peptide-based neuroimmune crosstalk. Biotechpeptides.com 2025.
Selank Enhances Effect of Diazepam in Unpredictable Chronic Mild Stress in Rats
Examines Selank's interaction with diazepam in an unpredictable chronic mild stress (UCMS) rat model. Selank showed additive rather than antagonistic interaction with diazepam — consistent with distinct but complementary mechanisms of action (indirect gene modulation + direct allosteric potentiation). Validates that Selank and classical benzodiazepines engage separable pathways within the GABAergic system, with implications for combinatorial pharmacology research in anxiety models. PMC5322660.
Independent peer-reviewed research — not Trident Labs claims. Selank is supplied for in vitro research use only. Not for human consumption. For lawful in vitro laboratory research use only by qualified researchers.
Cited Sources
References
All scientific claims sourced from peer-reviewed literature.
Selank administration affects the expression of some genes involved in GABAergic neurotransmission
Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating BDNF content
Comparative anxiolytic activity of Selank and medazepam in animal models
Neuroprotective effects of Selank — BDNF expression and neuroplasticity analysis
From Tuftsin to Selank: Exploring the Neurochemical and Immunological Dimensions of a Synthetic Heptapeptide
Peptide Selank Enhances the Effect of Diazepam in Reducing Anxiety in Unpredictable Chronic Mild Stress Conditions in Rats
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