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
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Binds allosteric sites on GABAA_A receptors
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Enhances GABA binding affinity
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Increases Cl⁻ influx
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Produces inhibitory postsynaptic stabilization in neuronal cultures
Biochemical outcome:
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↑ GABAergic tone
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↓ Neuronal excitability
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↓ Ca²⁺ influx via voltage-gated Ca²⁺ channels
B. Monoamine Regulation
Selank has been shown to influence turnover and release of:
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Serotonin
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Dopamine
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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:
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↑ enkephalin availability
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↑ opioid receptor signaling
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Reduced excitatory neurotransmission
✅ 2. Intracellular Signaling Pathways
A. GABAA_A → Cl⁻ Currents
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Hyperpolarization of neuronal membrane
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Decreased Ca²⁺-dependent neurotransmitter release
B. Anti-inflammatory Cytokine Modulation
Cell-culture studies show altered expression of:
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↓ IL-6, TNF-α
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↑ IL-10
Likely mediated by NF-κB pathway inhibition and cytokine-gene promoter regulation.
C. BDNF & Neurotrophic Signaling
Selank increases transcription of:
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BDNF
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GDNF
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NGF-receptor–associated genes
Downstream pathways include:
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CREB phosphorylation
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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
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Allosteric modulation of GABAA_A receptors
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Influences monoamine turnover and transporter function
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Modulates ERK/CREB signaling and neurotrophic gene transcription
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Regulates NF-κB–linked cytokine genes in immune-neural crosstalk
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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.


