Name: Cyclotraxin B
Brand: Creative Peptides
SKU: R0881
Availability: MadeToOrder

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 No: R0881

CAS No: 1203586-72-4

Synonyms/Alias: Cyclotraxin B;1203586-72-4;Cyclotraxin B acetate;(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;DTXSID501045820;AKOS024458477;AS-85368;DA-72492;PD079892;G14323;S-1203586-72-4;

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M.F/Formula	C48H73N13O17S3
M.W/Mr.	1200.4
Sequence	One Letter Code:CNPMGYTKEGC Three Letter Code:H-Cys(1)-Asn-Pro-Met-Gly-Tyr-Thr-Lys-Glu-Gly-Cys(1)-OH
Labeling Target	TrkB receptor
Appearance	White lyophilised solid
Purity	>98 %
Activity	Antagonist

Solubility	-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

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