Cyclotraxin B

Cyclotraxin B is highly potent and selective TrkB receptor antagonist that inhibits BDNF-induced TrkB activity (IC50 = 0.30 nM). It allosterically changes the conformation of TrkB receptor, but does not change BDNF binding.

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CAT#	R0881
CAS	1203586-72-4
Background	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),the main receptor of brain-derived neurotrophic factor (BDNF), which itself was derived from BDNF. It crosses the blood-brain-barrier with systemic administration and produces anxiolytic-like effects in animals, though notably not antidepressant-like effects. The compound has also been found to produce analgesic effects in animal models of neuropathic pain. 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). >> Read More
M.F/Formula	C48H73N13O17S3
M.W/Mr.	1200.36
Sequence	CNPMGYTKEGC(Disulfide bridge between Cys1-Cys11)
Labeling Target	TrkB receptor
Appearance	White lyophilised solid
Purity	>98 %
Activity	Antagonist

CAT#	Product Name	M.W	Molecular Formula	Inquiry
R1026	Z-Leu-Arg-Gly-Gly-AMC	692.77	C₃₄H₄₄N₈O₈	Inquiry
R1032	Chlorotoxin	599.64	C29H37N5O9S1	Inquiry
R1034	Ac-Trp-Leu-Ala-AMC	718.7	C35H38N6O11	Inquiry
R1054	Norleual	774.95	C41H58N8O7	Inquiry
R1080	st-Ht31	2798.27	C129H217N29O39	Inquiry

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Storage	-20°C
Long-term Storage Conditions	-20 °C
InChI	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
InChI Key	JLBMMJHZUYBFGX-ZHTCEXBHSA-N
Isomeric SMILES	C[C@H]([C@H]1C(=O)N[C@H](C(=O)N[C@H](C(=O)NCC(=O)N[C@@H](CSSC[C@@H](C(=O)N[C@H](C(=O)N2CCC[C@H]2C(=O)N[C@H](C(=O)NCC(=O)N[C@H](C(=O)N1)CC3=CC=C(C=C3)O)CCSC)CC(=O)N)N)C(=O)O)CCC(=O)O)CCCCN)O
References	Cocaine exposure alters brain-derived neurotrophic factor (BDNF) expression in the brain. BDNF signaling through TrkB receptors differentially modulates cocaine self-administration, depending on the brain regions involved. In the present study, we determined how brain-wide inhibition of TrkB signaling affects cocaine intake, the motivation for the drug, and reinstatement of drug taking after extinction. To overcome the inability of TrkB ligands to cross the blood–brain barrier, the TrkB antagonist cyclotraxin-B was fused to the nontoxictransduction domain ofthetat proteinfrom human immunodeficiency virustype 1 (tat-cyclotraxin-B). Intravenous injection of tat-cyclotraxin-B dose-dependently reduced cocaine intake, motivation for cocaine (as measured under a progressive ratio schedule of reinforcement), and reinstatement of cocainetaking in rats allowed either short or long accessto cocaine self-administration. Systemic Delivery of a Brain-Penetrant TrkB Antagonist Reduces Cocaine Self-Administration and Normalizes TrkB Signaling in the Nucleus Accumbens and Prefrontal Cortex By using a peptidomimetic approach, we developed a highly potent and selective TrkB inhibitor, cyclotraxin-B, capable of altering TrkB-dependent molecular and physiological processes such as synaptic plasticity, neuronal differentiation and BDNF-induced neurotoxicity. Cyclotraxin-B allosterically alters the conformation of TrkB, which leads to the inhibition of both BDNF-dependent and -independent (basal) activities. Cyclotraxin-B, the First Highly Potent and Selective TrkB Inhibitor, Has Anxiolytic Properties in Mice