N-Acetyl-Selank

N-Acetyl-Selank is Selank (Thr-Lys-Pro-Arg-Pro-Gly-Pro) carrying an acetyl group on its N-terminal threonine, as recorded in PubChem. The published animal work uses the unmodified parent peptide, and much of it concerns the nasal route: receptor-binding changes in mouse brain after intranasal versus intraperitoneal delivery, hippocampal transcriptome shifts after a single intranasal application in rats, and how Selank is broken down into shorter fragments. Research Market supplies this N-Acetyl-Selank spray in solution in a spray bottle, with a lot-specific certificate of analysis. It is sold strictly for laboratory research use.

Chemical structure and identification

• Molecular formula: C₃₅H₅₉N₁₁O₁₀
• Molecular weight: 793.9 g/mol
• CAS number: Not assigned in PubChem
• PubChem CID: 133082488
• Amino acid sequence: Ac-Thr-Lys-Pro-Arg-Pro-Gly-Pro (N-acetyl TKPRPGP)
• Parent peptide: Selank, CAS 129954-34-3, PubChem CID 11765600
• Form: Supplied in solution in a spray bottle
• Analytical methods: RP-HPLC for purity and mass spectrometry for identity, reported on the batch certificate of analysis

Research applications

• Intranasal versus intraperitoneal route: In BALB/c mice, intraperitoneal Selank increased GABA-receptor binding sites in the frontal cortex by 38%, while intranasal Selank increased hippocampal NMDA-receptor ([³H]MK-801) binding density by 23%; behavioral effects appeared in BALB/c but not C57BL/6 mice [1]
• Hippocampal transcriptome: cDNA microarrays showed that 36 genes in rat hippocampus changed more than 2-fold after a single intranasal Selank application and 20 after a course, many of them encoding plasma-membrane proteins [2]
• Biodegradation: With evenly tritium-labeled peptide, researchers traced Selank breakdown in blood plasma and in brain tissue after intranasal application; TKPRP, TKP, RP and GP were the major products [3]
• Spleen inflammation genes: 34 of 84 inflammation-related genes in mouse spleen changed expression 6 to 24 hours after a single intraperitoneal Selank injection, with Bcl6 responding to Selank and to its fragments [4]
• BDNF and chronic ethanol: In rats given ethanol for 30 weeks, Selank prevented the ethanol-induced rise in BDNF content in the hippocampus and frontal cortex and was studied in an object recognition test [5]

Reference citations

1. Vasil’eva E.V. et al. (2016). [Comparison of pharmacological effects of heptapeptide selank after intranasal and intraperitoneal administration to BALB/c and C57BL/6 mice]. Eksp Klin Farmakol, 79(9):3–11. PMID 29787664
2. Kolomin T.A. et al. (2013). [Transcriptome alteration in hippocampus under the treatment of tuftsin analog Selank]. Zh Vyssh Nerv Deiat Im I P Pavlova, 63(3):365–374. PMID 24450168 · DOI
3. Zolotarev Iu.A. et al. (2006). [Evenly tritium-labeled peptides and their in vivo and in vitro biodegradation]. Bioorg Khim, 32(2):183–191. PMID 16637290
4. Kolomin T. et al. (2011). Expression of inflammation-related genes in mouse spleen under tuftsin analog Selank. Regul Pept, 170(1-3):18–23. PMID 21609736 · DOI
5. Kolik L.G. et al. (2019). Selank, peptide analogue of tuftsin, protects against ethanol-induced memory impairment by regulating of BDNF content in the hippocampus and prefrontal cortex in rats. Bull Exp Biol Med, 167(5):641–644. PMID 31625062 · DOI

Compound data from PubChem CID 133082488. Literature summaries describe published preclinical research and are not claims about this product’s effects in humans or animals.