Description
About Selank
Selank is a synthetic seven-amino-acid research peptide with the sequence Thr-Lys-Pro-Arg-Pro-Gly-Pro, commonly represented as TKPRPGP.
It was developed from tuftsin, an endogenous tetrapeptide with the sequence Thr-Lys-Pro-Arg. The addition of the Pro-Gly-Pro sequence extends the parent peptide into the seven-amino-acid Selank structure.
Selank has been investigated principally within neurochemical, behavioural and regulatory-peptide research.
Published studies have examined its relationship with GABAergic neurotransmission, enkephalin metabolism, serotonin and other monoamine systems, gene-expression changes and neurotrophin-associated signalling.
Experimental research has also investigated Selank in stress- and anxiety-associated behavioural models and in models examining memory, attention and neural adaptation.
Together, these research areas make Selank relevant to experimental studies examining how short regulatory peptides interact with neurotransmitter systems, neural stress responses and wider neurochemical regulation.
Pronoia supplies Selank in a 10mg lyophilised research format with batch traceability and supporting documentation available for the supplied material.
Product Specification
Product: Selank
Alternative name: TP-7
Strength: 10mg
Peptide class: Synthetic heptapeptide / tuftsin analogue
Peptide length: 7 amino acids
Sequence: H-Thr-Lys-Pro-Arg-Pro-Gly-Pro-OH
Sequence notation: TKPRPGP
Parent framework: Tuftsin-derived peptide
Research focus: GABAergic signalling, enkephalin metabolism, serotonin-related pathways, stress-response biology and neurotrophin regulation
Form: Lyophilised solid
Pronoia minimum purity standard: ≥99%
Batch traceability: Maintained
SKU: PB-SEL-10
Testing & Batch Documentation
Pronoia maintains a structured quality, testing and traceability process for Selank, with supporting documentation retained for the supplied research material.
- Batch-tested research material
- Pronoia minimum accepted purity standard of ≥99%
- Full batch traceability
- Batch-separated and labelled inventory
- Physical inventory routinely reconciled with digital stock records
- Temperature-controlled cold storage
- Certificate of Analysis (COA) and Safety Data Sheet (SDS) documentation available
The applicable Certificate of Analysis should be treated as the authoritative reference for the chemical form, identity, purity and analytical results reported for an individual batch.
Research Context
Selank has been investigated as a regulatory heptapeptide across neurochemical, molecular, behavioural and limited human research.
Its research profile is unusual because several different mechanisms have been proposed rather than one single established molecular target.
Tuftsin-derived peptide structure
Selank was developed from tuftsin, a naturally occurring tetrapeptide with the sequence Thr-Lys-Pro-Arg.
The Selank structure retains this four-amino-acid region and adds Pro-Gly-Pro at the C-terminus:
Thr-Lys-Pro-Arg-Pro-Gly-Pro
The resulting seven-amino-acid sequence has been used experimentally to investigate how modification of a short endogenous regulatory peptide changes its stability and biological activity.
GABAergic neurotransmission
One of the most extensively investigated areas of Selank research involves the GABAergic system.
GABA is the major inhibitory neurotransmitter within the mammalian central nervous system and signals through several receptor families, including GABA-A receptors.
Researchers studying Selank in rat frontal cortex reported changes in the expression of numerous genes involved in neurotransmission.
Under the experimental conditions used, Selank and GABA produced overlapping patterns of gene-expression change during the early stages of the experiment.
The affected systems included genes associated with:
- GABA receptor subunits
- GABA transport and metabolism
- Ion-channel signalling
- Dopamine receptors
- Serotonin receptors
- Wider neuronal signalling pathways
These findings contributed to the hypothesis that one component of Selank biology may involve modulation of GABAergic neurotransmission.
The mechanism should not be described as fully established.
Separate experiments using human neuroblastoma cells found that Selank alone did not reproduce the same direct gene-expression effects but altered cellular responses when combined with GABA.
Taken together, the research supports an interaction with GABA-associated signalling while indicating that the mechanism is more complex than direct activation of a single GABA receptor.
Enkephalin metabolism
Another distinctive area of Selank research concerns enkephalins.
Enkephalins are endogenous regulatory peptides involved in neural signalling and are normally broken down by several peptidase enzymes.
Laboratory experiments using human serum and plasma reported that Selank inhibited enzymes involved in enkephalin degradation.
Researchers observed dose-dependent inhibition of enkephalin breakdown and proposed that changes in endogenous peptide metabolism could contribute to the wider biological activity associated with Selank.
This has made Selank relevant to experimental studies examining:
- Regulatory-peptide metabolism
- Enkephalin degradation
- Peptidase activity
- Interactions between short peptides and endogenous neuropeptide systems
Serotonin and monoamine research
Selank has also been investigated in relation to monoamine neurotransmitter systems.
In rat experiments where serotonin synthesis had been experimentally reduced, researchers reported changes in serotonin metabolism following Selank exposure.
Additional gene-expression studies have identified changes involving dopamine- and serotonin-receptor-related genes.
These findings have supported investigation of Selank across:
- Serotonergic signalling
- Dopaminergic signalling
- Monoamine metabolism
- Interactions between inhibitory and monoaminergic neurotransmitter systems
The available evidence does not support reducing Selank to a simple “serotonin-boosting” or “GABA-boosting” peptide. Its effects appear to involve regulation across multiple signalling systems.
BDNF and neural-plasticity research
Brain-derived neurotrophic factor, or BDNF, is an important signalling protein involved in neuronal plasticity and adaptation.
Selank has been investigated in rat models examining relationships between behavioural responses, memory-associated tasks and BDNF concentrations in the hippocampus and prefrontal cortex.
In a chronic ethanol-exposure model, researchers reported effects on object-recognition performance together with changes in BDNF regulation in these brain regions.
This has contributed to wider experimental interest in relationships between Selank, neurotrophin signalling and neural adaptation.
These findings derive from specific animal models and should not be interpreted as demonstrating an established cognitive-enhancement or memory effect in humans.
Stress and behavioural research
Selank has been investigated extensively in animal models involving stress-associated and anxiety-associated behaviour.
These experiments have been used to explore relationships between behavioural responses and:
- GABAergic neurotransmission
- Enkephalin metabolism
- Monoamine systems
- Neurotrophin regulation
- Gene-expression changes
Some early human comparative research has also been published.
A study involving 62 patients with generalised anxiety disorder or neurasthenia compared Selank with the benzodiazepine-class compound medazepam and reported changes on psychometric measures under the study conditions.
This human literature is scientifically relevant but should be interpreted cautiously. It consists principally of relatively small studies from a limited number of research groups and does not provide the breadth of evidence associated with an established internationally authorised therapeutic intervention.
For this reason, Pronoia presents Selank as an experimental neuropeptide research material rather than as a treatment for anxiety, stress or cognitive disorders.
Broader regulatory-peptide research
Because Selank originates from the tuftsin framework, research has also extended into immune and regulatory signalling.
Published studies have investigated changes in cytokine-, chemokine- and receptor-associated gene expression alongside neural mechanisms.
This broader literature reinforces the view that Selank is a multi-system regulatory peptide rather than a compound with one fully resolved receptor mechanism.
Together, the available evidence makes Selank relevant to experimental research examining:
- GABAergic neurotransmission
- Enkephalin and regulatory-peptide metabolism
- Serotonin and monoamine signalling
- Stress-associated neural responses
- BDNF and neurotrophin regulation
- Neural gene-expression changes
- Short-peptide regulatory biology
The evidence base includes biochemical, cell-culture, animal and limited human research, but these evidence types differ substantially and should not be treated as equivalent.
The published findings do not establish clinical efficacy, safety or suitability for human or veterinary use.
Storage & Handling
Selank is supplied in lyophilised form and should be stored according to the conditions specified by Pronoia and the applicable batch documentation.
Pronoia stock is maintained in temperature-controlled cold storage and organised by identifiable batch prior to dispatch.
The material should be protected from unnecessary exposure to heat, moisture and light and handled using appropriate laboratory procedures.
Where batch-specific storage or handling information is supplied, that information should take precedence.
UK Delivery
Selank is dispatched from Pronoia’s UK stock using tracked delivery.
Current availability and dispatch information are shown directly on the product page, with tracking supplied following dispatch.
Orders are prepared through Pronoia’s established research-product fulfilment process, with applicable delivery conditions remaining subject to Pronoia’s current delivery terms.
Research Use
Selank supplied by Pronoia Bio is intended for laboratory research and experimental use only.
It is not supplied for human or veterinary use and should not be treated as a medicine, cognitive-enhancement product or consumer healthcare product.
Pronoia does not provide dosage, treatment or administration guidance for this research material.
