Selank

Selank is a synthetic heptapeptide derived from the endogenous immunomodulatory peptide tuftsin. It is studied in research settings for its effects on anxiety-related behavior models, neurochemical signaling modulation (including GABAergic and monoaminergic systems), and immune regulation pathways. Selank has been investigated for nootropic and stress-modulating properties in experimental and clinical research contexts. For research use only.

10MG | PHYSICIAN USE ONLY

$73.10

Confirm compounded formula & unique dosing are necessary for the patient

Research Profile

At a Glance

  • Type: Synthetic Heptapeptide (Tuftsin Analog)
  • Also Known As: Thr-Lys-Pro-Arg-Pro-Gly-Pro
  • Sequence: Thr-Lys-Pro-Arg-Pro-Gly-Pro
  • Length: 7 amino acids
  • Molecular Weight: ~751.9 Da
  • Primary Target: GABAergic signaling pathways; immune modulation pathways
  • Research Focus: Anxiety-model behavior research, cognitive signaling pathways, stress modulation, immune response regulation
  • Regulatory Status: Not FDA-approved; Research Use Only (RUO) outside approved pharmaceutical systems
  • Categories: Recovery & Repair; Immune Support; Anti-Aging Research; Hormone Research

What Research Shows

  • Demonstrates anxiolytic-like activity in animal behavioral models without the sedative or myorelaxant effects commonly observed with benzodiazepines.
  • Influences GABAergic signaling, with research suggesting modulation of GABA receptor expression and related neurochemical pathways.
  • Studied for effects on monoamine neurotransmitter systems, including serotonin and dopamine turnover in preclinical models.
  • Exhibits immunomodulatory properties associated with its tuftsin-derived structure, influencing cytokine signaling pathways.
  • Investigated in clinical research settings for generalized anxiety disorder and stress-related conditions in controlled trials.

Mechanistic Notes

  • GABA system modulation: Alters GABA receptor subunit expression and influences inhibitory neurotransmission in research models.
  • Monoamine pathway interaction: Affects serotonin and dopamine metabolism in preclinical neurochemical studies.
  • Tuftsin lineage: Derived from the immunomodulatory peptide tuftsin, contributing to immune-regulatory signaling effects.
  • Neuroprotective signaling: Demonstrates regulation of brain-derived neurotrophic factor (BDNF) and related pathways in experimental models.
  • Non-benzodiazepine mechanism: Does not bind directly to benzodiazepine sites but produces anxiolytic-like effects through alternative signaling modulation.

What Remains Unknown

  • Long-term safety data outside limited clinical studies
  • Precise receptor binding interactions across central nervous system regions
  • Standardized dosing paradigms across different experimental contexts
  • Translational applicability beyond research settings