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From Wikipedia, the free encyclopedia

Cyclotraxin B
Clinical data
Other namesCTX-B
ATC code
  • None
Identifiers
  • (3S,6R,11R,17S,20S,23S,26S,32S,35S)-6-amino-20-(4-aminobutyl)-3-(2-amino-2-oxoethyl)-17-(2-carboxyethyl)-23-[(1R)-1-hydroxyethyl]-26-[(4-hydroxyphenyl)methyl]-32-(2-methylsulfanylethyl)-2,5,13,16,19,22,25,28,31,34-decaoxo-8,9-dithia-1,4,12,15,18,21,24,27,30,33-decazabicyclo[33.3.0]octatriacontane-11-carboxylic acid
CAS Number
PubChem CID
ChemSpider
Chemical and physical data
FormulaC48H73N13O17S3
Molar mass1200.37 g·mol−1
3D model (JSmol)
  • CC(C1C(=O)NC(C(=O)NC(C(=O)NCC(=O)NC(CSSCC(C(=O)NC(C(=O)N2CCCC2C(=O)NC(C(=O)NCC(=O)NC(C(=O)N1)CC3=CC=C(C=C3)O)CCSC)CC(=O)N)N)C(=O)O)CCC(=O)O)CCCCN)O
  • InChI=1S/C48H73N13O17S3/c1-24(62)39-46(75)58-28(6-3-4-15-49)43(72)56-29(12-13-38(67)68)41(70)52-21-37(66)55-33(48(77)78)23-81-80-22-27(50)40(69)59-32(19-35(51)64)47(76)61-16-5-7-34(61)45(74)57-30(14-17-79-2)42(71)53-20-36(65)54-31(44(73)60-39)18-25-8-10-26(63)11-9-25/h8-11,24,27-34,39,62-63H,3-7,12-23,49-50H2,1-2H3,(H2,51,64)(H,52,70)(H,53,71)(H,54,65)(H,55,66)(H,56,72)(H,57,74)(H,58,75)(H,59,69)(H,60,73)(H,67,68)(H,77,78)/t24-,27+,28+,29+,30+,31+,32+,33+,34+,39+/m1/s1
  • Key:JLBMMJHZUYBFGX-ZHTCEXBHSA-N

Cyclotraxin B (CTX-B) is a small (1200 Da) cyclic peptide and highly potent, selective, non-competitive antagonist or negative allosteric modulator of TrkB (IC50  = 0.30 nM),[1][2] the main receptor of brain-derived neurotrophic factor (BDNF), which itself was derived from BDNF.[1][3] It crosses the blood-brain-barrier with systemic administration and produces anxiolytic-like effects in animals, though notably not antidepressant-like effects.[1][4] The compound has also been found to produce analgesic effects in animal models of neuropathic pain.[5] In addition to TrkB, CTX-B has been found to be an allosteric modulator of VEGFR2, one of the receptors of vascular endothelial growth factor (VEGF).[2]

See also

References

  1. ^ a b c Cazorla M, Jouvenceau A, Rose C, Guilloux JP, Pilon C, Dranovsky A, Prémont J (March 2010). "Cyclotraxin-B, the first highly potent and selective TrkB inhibitor, has anxiolytic properties in mice". PLOS ONE. 5 (3): e9777. Bibcode:2010PLoSO...5.9777C. doi:10.1371/journal.pone.0009777. PMC 2841647. PMID 20333308.
  2. ^ a b De Smet F, Christopoulos A, Carmeliet P (November 2014). "Allosteric targeting of receptor tyrosine kinases". Nature Biotechnology. 32 (11): 1113–20. doi:10.1038/nbt.3028. PMID 25380447. S2CID 12609911.
  3. ^ Growth Factor Receptors—Advances in Research and Application: 2013 Edition. ScholarlyEditions. 21 June 2013. pp. 42–. ISBN 978-1-4816-7619-9.
  4. ^ Advances in Physiology Research and Application: 2011 Edition. ScholarlyEditions. 9 January 2012. pp. 1431–. ISBN 978-1-4649-2075-2.
  5. ^ Constandil L, Goich M, Hernández A, Bourgeais L, Cazorla M, Hamon M, et al. (June 2012). "Cyclotraxin-B, a new TrkB antagonist, and glial blockade by propentofylline, equally prevent and reverse cold allodynia induced by BDNF or partial infraorbital nerve constriction in mice". The Journal of Pain. 13 (6): 579–89. doi:10.1016/j.jpain.2012.03.008. hdl:10533/130454. PMID 22560237.
This page was last edited on 7 December 2023, at 19:11
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