Selank — Peptide Protocol Wiki reference

Selank doses Pre-filled reconstitution and dose math for Selank New to peptides?

Covers neurotrophic mechanisms, approvals in 40+ countries, dosing, and safety data.

These point to a multimodal mechanism but remain predominantly preclinical and variably strain- and dose-dependent.

Safety and tolerability Accessible clinical sources provide minimal systematic safety data.

Covers epigenetic gene regulation, cognitive enhancement research, and Khavinson science.

Accordingly, the certainty about human safety and adverse events is low.

Selank: Anxiolytic Nootropic Peptide Guide | Peptide Protocol Wiki Skip to main content 🧬 Peptide Protocol Wiki Peptides Side Effects New Learn Directory Tools Blog News About ⌘K ⌘K 🌱 New to Peptides?

Start the 7-step beginner guide Peptides Side Effects New Directory Learn Tools Blog News About Selank 📋 Overview 🧬 Molecule 🔄 Similar ⚠️ Side Effects 💉 Dosing 🔬 Research 🚨 Risks 👥 Community 📊 Community Data Home Peptides Selank Cognitive Enhancement Immune Support approved Selank Also known as: TP-7, Selanc, Thr-Lys-Pro-Arg-Pro-Gly-Pro Compare with 1 peptide Research compiled by Peptide Protocol Wiki 📅 Updated February 1, 2026 Citations Verified TL;DR Selank is a synthetic heptapeptide derived from the endogenous immunomodulatory peptide tuftsin, with an added Pro-Gly-Pro sequence for enhanced stability.

It is approved in Russia as an anxiolytic and nootropic medication and has been studied for effects on GABA, serotonin, and BDNF systems.

The mechanistic implication is potentiation of BDNF–TrkB signaling with downstream PI3K–AKT, MAPK/ERK, and PLCγ cascades that support synaptic plasticity and neuroprotection (inference from BDNF biology).

Browse all cognitive peptides → Table of Contents 📌 TL;DR • Approved as an anxiolytic in Russia (intranasal formulation) • Demonstrates anxiolytic effects without sedation or dependence in studies • Modulates BDNF expression and monoamine neurotransmitter systems • Retains immunomodulatory properties from parent compound tuftsin Community-Reported Side Effects Anecdotal ?

Anxiolytic and nootropic peptide for anxiety reduction and cognitive enhancement 💉 Dosing Amount 300-600 mcg per dose intranasal; 200-400 mcg per dose subcutaneous Frequency 2-3 times daily (intranasal); once daily (SC, 5 days per week) Duration 30 days on, 30 days off; approximately 6 cycles per year 💊 Administration Route Intranasal Schedule 2-3 times daily (intranasal); once daily (SC, 5 days per week) Timing Morning and early afternoon doses; avoid late evening due to potential activating effects ✓ Rotate injection sites 📅 Cycle Duration 30 days on, 30 days off; approximately 6 cycles per year Repeatable Yes Course-based protocol with rest periods Preparation & Storage ✓ Ready-to-use — no reconstitution required ⚗️ Suggested Bloodwork ( 5 tests) CBC with differential When: Baseline Why: Selank has immunomodulatory properties; baseline immune status CMP When: Baseline Why: Liver and kidney function baseline Thyroid panel When: Baseline Why: Rule out thyroid dysfunction as cause of anxiety/cognitive issues Cortisol (AM) When: Baseline Why: Baseline HPA axis assessment; Selank modulates stress response CBC When: End of 30-day cycle Why: Monitor immunomodulatory effects 💡 Key Considerations → Contraindication: Limited safety data outside Russian regulatory framework; caution in pregnancy and lactation; avoid in patients with bleeding disorders (tuftsin analog may affect immune/coagulation parameters) Subscribe to unlock this

Restore access No thanks, continue reading Related Reading Peptide Semax ACTH-derived neuroprotective peptide Peptide Pinealon neuroprotective bioregulatory tripeptide Peptide Oxytocin peptide How Selank works at the cellular level Overview of Selank benefits and applications Scientific Details Molecular Formula C33H57N11O9 Molecular Weight 751.9 Da CAS Number 129954-34-3 Sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro What is Selank?

Mechanism of Action # Selank is a synthetic heptapeptide derived from the endogenous immunomodulator tuftsin (Thr–Lys–Pro–Arg–Pro–Gly–Pro).

Current evidence supports a multimodal mechanism encompassing GABAergic allosteric modulation, indirect engagement of the opioid system via enkephalinase inhibition, neurotrophin-linked plasticity, and coordinated neuroimmune transcriptomic regulation, rather than a single high-affinity receptor target.

Primary receptor interactions and molecular targets GABAergic system: In vivo and cellular studies indicate that Selank modulates the GABAA receptor system in an allosteric manner.

ic binding sites in cortical tissue without changing affinity, and gene-expression changes after Selank show a positive correlation with those induced by exogenous GABA.

Functionally, Selank augments diazepam’s anxiolytic effect in stressed rats, consistent with facilitation of benzodiazepine-sensitive GABAA signaling.

Enkephalinase inhibition and opioid pathway: Biochemical data show that Selank inhibits serum enkephalin-degrading enzymes (including aminopeptidases, enkephalinase B/NEP 24-11, and ACE/enkephalinase A), increasing endogenous enkephalin levels and thereby indirectly engaging opioid receptors.

Neurotrophic factors: Selank upregulates Bdnf mRNA and increases BDNF protein in hippocampus following intranasal administration.

Transporters and ion homeostasis: Transcriptomic profiling identifies Selank-driven regulation of ion/neurotransmitter transporters, including upregulation of SLC8A3/NCX3 and modulation of SLC1A2 (EAAT2), SLC5A7 (choline transporter), and SLC6A20.

Neuroimmune targets: Selank modulates

the fractalkine receptor CX3CR1 and broad panels of cytokine/chemokine genes in spleen and brain, linking it to neuron–microglia communication and antiapoptotic NF-κB and AKT signaling axes.

Signaling pathways GABAergic potentiation: Allosteric enhancement of GABAA receptor function increases inhibitory tone, which can secondarily reshape activity-dependent transcription programs.

Correlated gene-expression signatures with GABA and increased [3H]GABA binding site number support this pathway.

Opioid signaling via preserved enkephalins: By inhibiting enkephalinases, Selank elevates endogenous enkephalin tone, activating Gi/o-coupled opioid receptors and impacting cAMP, ERK/MAPK, and AKT pathways that contribute to anxiolysis and stress resilience (inference consistent with observed pharmacology).

BDNF–TrkB cascades: Increased hippocampal BDNF suggests engagement of canonical TrkB pathways—PI3K–AKT, MAPK/ERK, PLCγ—promoting survival and synaptic plasticity, consistent with behavioral and neuroprotective profiles.

Ion/Ca2+ signaling and plasticity: Upregulated NCX3 (SLC8A3) predicts changes in intracellular Ca2+ dynamics that can influence AKT/CREB-dependent plasticity programs.

Neuroimmune NF-κB/AKT signaling: Changes in CX3CR1 and immune gene sets imply modulation of NF-κB and AKT within microglia-neuron crosstalk, aligning with reported antiapoptotic and immunocorrective effects.

uropilin‑1 and can signal via VEGF/TGF-β–related axes; however, there is no direct biochemical evidence that Selank itself binds neuropilin‑1.

Any neuropilin‑linked mechanisms for Selank remain speculative without direct binding data.

Integrated mechanism Collectively, Selank acts as a pleiotropic neuromodulator: it enhances inhibitory GABAergic transmission, preserves endogenous enkephalins to modulate opioid pathways, increases neurotrophic support (BDNF), and reprograms neural and immune transcriptomes, including ion transport and microglia–neuron communication genes.

Key uncertainties Direct, high-affinity receptor binding of Selank to GABAA or neuropilin‑1 has not been structurally demonstrated.

Thus, Selank should be considered a multimodal peptide with indirect and network-level mechanisms rather than a single-target ligand.

Mechanistic axis Primary molecular targets / receptors Key evidence and models Proposed signaling pathways Direction / effects Notes / limitations GABAergic modulation (GABAA allosteric effects) GABAA receptor (allosteric modulation; modulation of benzodiazepine-like effects) Changes in [3H]GABA binding sites and gene-expression correlations with GABA; Selank enhances diazepam anxiolysis in rats (in vivo, IMR‑32 cells, b...

Increased GABAergic inhibitory tone → altered neuronal excitability and downstream transcriptional responses (e.g., CREB-related cascades inferred) Net potentiation of inhibitory signaling → anxiolytic, sedative-modulating effects No single high‑affinity GABAA binding site proven; evidence from functional binding/site changes and transcriptomics rather than direct receptor co...

Enkephalinase inhibition / opioid-system engagement Enkephalin-degrading peptidases (enkephalinases; aminopeptidases, endopeptidase 24‑11, ACE) → increased enkephalin levels → opioid receptors (indir...

Biochemical inhibition of serum enkephalinases by Selank and active fragments; behavioral naloxone sensitivity and opioid-system involvement reported Increased endogenous enkephalins → activation of opioid receptor signaling (Gi/o) → downstream modulation of cAMP, MAPK/Akt pathways (proposed, inf...

Elevation of enkephalins → anxiolytic/protective behavioral effects; modulation of stress responses Direct binding to opioid receptors not demonstrated; mechanism inferred from peptidase inhibition and pharmacology Neurotrophic regulation (BDNF / TrkB-related) BDNF (expression levels); TrkB pathway (indirectly implicated) Intranasal Selank increases BDNF expression in hippocampus; transcriptomic upregulation of Bdnf and other neurotrophic genes after treatment (in vi...

Increased neurotrophic support → neuroprotective, pro-plasticity effects; may reverse stress-induced deficits Direct TrkB agonism not shown; effects reported at expression level (mRNA/protein), causal linkage inferred Ion homeostasis & neurotransmitter transporters (SLCs) NCX3 (SLC8A3), glutamate transporter EAAT2 (SLC1A2), choline transporter (SLC5A7), proline transporter (SLC6A20) Transcriptomic profiling after Selank (single/curative dosing) shows up/down regulation of SLC8A3, SLC1A2, SLC5A7, SLC6A20 and other ion/neurotrans...