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Antagonist of TrkB receptors; inhibits BDNF-induced TrkB activity (IC50 = 0.30 nM). Allosterically alters TrkB receptor conformation but does not alter BDNF binding. Prevents BDNF-induced cold allodynia in mice. Also shown to exhibit putative anxiolytic properties in mice.
(Modifications: Disulfide bridge between 1 - 11)
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solubility||Soluble to 2 mg/ml in water|
References are publications that support the biological activity of the product.
Constandil et al (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. J.Pain 13 579 PMID: 22560237
Cazorla et al (2010) Cyclotraxin-B, the first highly potent and selective TrkB antagonist, has anxiolytic properties in mice. PLoS One 5 e9777 PMID: 20333308
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Keywords: Cyclotraxin B, Cyclotraxin B supplier, anxiolytic, antagonists, TrkB, receptors, Trk, Receptors, 5062, Tocris Bioscience
2 Citations for Cyclotraxin B
Citations are publications that use Tocris products. Selected citations for Cyclotraxin B include:
Merk et al (2018) Opposing Effects of CREBBP Mutations Govern the Phenotype of Rubinstein-Taybi Syndrome and Adult SHH Medulloblastoma. Dev Cell 44 709 PMID: 29551561
Zhong et al (2015) BDNF interacts with endocannabinoids to regulate cocaine-induced synaptic plasticity in mouse midbrain DA neurons. Oncotarget 35 4469 PMID: 25762688
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Literature in this Area
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Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Huntington's Disease Poster
Huntington's disease (HD) is a monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the MSN intracellular signaling pathways implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.