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Selank (11mg)

Price range: $61.25 through $64.59

Product Usage Disclaimer 

This material is supplied exclusively as a laboratory research chemical for in vitro scientific study. All descriptions and are provided for informational and educational purposes only.

This compound is not approved for human or animal consumption, injection, ingestion, inhalation, topical use, or any other biological application. It must be handled only by qualified, trained personnel in a properly equipped laboratory.

This product is not a drug, supplement, food, cosmetic, or therapeutic agent, and it may not be rebranded, repackaged, or marketed as any such item. Misuse, mislabeling, or unauthorized application is strictly prohibited.

Nothing on this website constitutes medical advice, professional guidance, or a recommendation of use.

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Description

Selank – Advanced Biochemical Mechanism Profile

(Synthetic Tuftsin Analog; Heptapeptide; Neuromodulatory Research Peptide)

Selank is a stabilized analog of the endogenous immunomodulatory peptide tuftsin (Thr-Lys-Pro-Arg). In research models, Selank influences GABAergic and monoaminergic neurotransmission and modulates transcription of neurotrophic and immune-related genes.


1. Primary Molecular Interactions (In-Vitro Models)

A. GABAA_A Receptor Allosteric Modulation

  • Binds allosteric sites on GABAA_A receptors

  • Enhances GABA binding affinity

  • Increases Cl⁻ influx

  • Produces inhibitory postsynaptic stabilization in neuronal cultures

Biochemical outcome:

  • ↑ GABAergic tone

  • ↓ Neuronal excitability

  • ↓ Ca²⁺ influx via voltage-gated Ca²⁺ channels


B. Monoamine Regulation

Selank has been shown to influence turnover and release of:

  • Serotonin

  • Dopamine

  • Norepinephrine

Likely via presynaptic modulation and feedback on monoamine transporters and synthesis enzymes (e.g., TPH2, MAOA, COMT) in research systems.


C. Enkephalin Metabolism

Selank may inhibit enkephalin-degrading peptidases (e.g., enkephalinase), increasing endogenous opioid peptide levels in vitro.
Effects observed:

  • ↑ enkephalin availability

  • ↑ opioid receptor signaling

  • Reduced excitatory neurotransmission


2. Intracellular Signaling Pathways

A. GABAA_A → Cl⁻ Currents

  • Hyperpolarization of neuronal membrane

  • Decreased Ca²⁺-dependent neurotransmitter release

B. Anti-inflammatory Cytokine Modulation

Cell-culture studies show altered expression of:

  • IL-6, TNF-α

  • IL-10
    Likely mediated by NF-κB pathway inhibition and cytokine-gene promoter regulation.

C. BDNF & Neurotrophic Signaling

Selank increases transcription of:

  • BDNF

  • GDNF

  • NGF-receptor–associated genes

Downstream pathways include:

  • CREB phosphorylation

  • ERK1/2 and Akt signaling in neuronal viability models


3. Second Messengers

Second Messenger Effect in Neuronal Systems
Cl⁻ Hyperpolarization via GABAA_A
Ca²⁺ ↓ Reduced neurotransmitter release
cAMP / PKA Modulated through monoamine signaling
ERK1/2 Induced for neurotrophic transcription
NF-κB Inhibited; impacts inflammation genes

4. Gene Targets Commonly Measured in Research

Functional Domain Representative Genes
GABA signaling GABRA1, GABRB2, GABRG2
Monoamine regulation TPH2, MAOA, SLC6A4 (serotonin transporter)
Neurotrophic support BDNF, GDNF, NGF, CREB1
Anti-inflammatory IL6, TNFA, IL10, NFKB1
Synaptic plasticity ARC, SYN1, CAMKII

Mechanistic Summary

  • Allosteric modulation of GABAA_A receptors

  • Influences monoamine turnover and transporter function

  • Modulates ERK/CREB signaling and neurotrophic gene transcription

  • Regulates NF-κB–linked cytokine genes in immune-neural crosstalk

  • Promotes synaptic stability and reduced excitatory drive in neuronal cultures


Research-Only Classification

Selank is supplied exclusively for in-vitro laboratory research.
Not approved for human or animal administration, therapeutic use, or biological application outside controlled research environments.

Additional information

Weight N/A
Size

10 Mg, 11 Mg