Overview
Selank (also TP-7) is a synthetic heptapeptide, Thr-Lys-Pro-Arg-Pro-Gly-Pro, developed as an analogue of tuftsin: it comprises the tuftsin sequence (Thr-Lys-Pro-Arg) followed by Pro-Gly-Pro5,6. Most of the published work comes from groups at the Institute of Molecular Genetics of the Russian Academy of Sciences and collaborating Moscow institutes.
Research has been predominantly preclinical. Studies have examined gene expression in rat frontal cortex, mouse spleen and human neuroblastoma cells, GABA receptor binding in brain membrane preparations, inhibition of enkephalin-degrading enzymes, and rodent behavioural and stress models1,2,3,4,5,6,7.
Mechanism of action
As described in the research literature
As described in the research literature, much of the mechanistic work on Selank has focused on the GABAergic system. In radioligand binding experiments on brain membrane preparations, Selank altered [3H]GABA binding in a way the authors interpreted as positive allosteric modulation, and it interacted with the modulatory activity of diazepam and olanzapine; the authors proposed subtype-selective allosteric modulation of GABA receptors3.
Gene expression studies have examined the same question. In rat frontal cortex, real-time PCR analysis of 84 neurotransmission-related genes found changes in 45 genes one hour after Selank, with a positive correlation between the changes produced by Selank and by GABA1. In IMR-32 neuroblastoma cells, by contrast, Selank alone did not change mRNA levels of the genes studied, although it altered the expression changes produced by GABA and by olanzapine2.
Other proposed pathways include inhibition of enkephalin-degrading enzymes, measured as reduced enzymatic hydrolysis of plasma enkephalin in vitro4, and modulation of inflammation-related genes (C3, Casp1, Il2rg and Xcr1) in mouse spleen, where the dipeptide fragment Gly-Pro produced largely similar expression profiles5.
Research areas
What published studies have examined
GABAergic signalling and gene expression
Expression of 84 genes involved in neurotransmission was measured in rat frontal cortex at one and three hours after Selank or GABA1, and in IMR-32 neuroblastoma cells exposed to Selank, GABA, olanzapine and their combinations2. Radioligand binding studies examined [3H]GABA binding to brain membranes and its interaction with benzodiazepines3.
Sources [1] [2] [3]
Enkephalinase activity
Enzymatic hydrolysis of plasma enkephalin was measured in vitro in the presence of Selank and compared with the peptidase inhibitors bacitracin and puromycin4.
Sources [4]
Immune and inflammation-related genes
Studies in mouse spleen followed the time course of expression of genes involved in complement, apoptosis and immune cell signalling after Selank and its fragment Gly-Pro, using real-time PCR5.
Sources [5]
Rodent behavioural and stress models
A rat model of long-term ethanol consumption examined object recognition memory and BDNF content in the hippocampus and frontal cortex6. The elevated plus maze was used to examine anxiety-related behaviour in rats under unpredictable chronic mild stress, with Selank given alone and together with diazepam7.
Sources [6] [7]
Specifications
- Sequence
- Thr-Lys-Pro-Arg-Pro-Gly-Pro (TKPRPGP)
- Molecular formula
- C33H57N11O9
- Molecular weight
- 751.9 g/mol
- CAS number
- 129954-34-3
Vial
- Form
- White to off-white lyophilised powder in a sealed vial (10 mg)
- Storage
- Store lyophilised powder at -20 °C, protected from light and moisture. Once reconstituted, keep refrigerated at 2 to 8 °C and protect from light.
- Solubility and reconstitution
- Reconstitute with bacteriostatic water. Add the diluent slowly down the inside wall of the vial and swirl gently until clear; do not shake.
Mist Applicator
- Form
- 10 mg in a vial fitted with a 10 mL mist applicator
- Storage
- Store as directed on the product label, protected from light.
- Solubility and reconstitution
- Prepare and use as directed on the product label.