Trk Receptor
The NTRK1, NTRK2, and NTRK3 genes encode related single-pass transmembrane receptor tyrosine kinases, high affinity nerve growth factor receptor (TRKA), BDNF/NT-3 growth factor receptor (TRKB), and NT-3 growth factor receptor (TRKC), respectively, that function as high-affinity receptors for neurotrophins. TRK receptors contribute to neuronal development, function, survival, and proliferation during the development and into adulthood. Like other receptor tyrosine kinases, TRK proteins are activated following ligand binding to the extracellular domain of the receptor. Ligands for TRK proteins are the neurotrophins, a family of closely-related secreted proteins that were discovered and classified initially as proteins that were able to promote differentiation and survival in both sympathetic and sensory nerves.
Signaling via TRK proteins is achieved with specific neurotrophin ligands, which triggers receptor dimerization and phosphorylation, leading to the activation of downstream signaling cascades. Through binding to TRK receptors, neorotrophinss activate Ras, phosphatidylinositol-3 (PI3)-kinase, and phospholipase C-γ1 signaling pathways. By this signaling, neurotrophins ultimately regulate cell fate decisions, axon growth, dendrite growth, and pruning. In addition to the expression in the central nervous system (CNS), TRK proteins have also been identified in non-neuronal normal tissues and cells, including pancreatic beta cells, monocytes, lungs, and bone.
References
1.Hsiao SJ,et al. J Mol Diagn. 2019;21(4):553–571.
2.Lange AM, et al. Cancers (Basel). 2018;10(4):105.
Signaling via TRK proteins is achieved with specific neurotrophin ligands, which triggers receptor dimerization and phosphorylation, leading to the activation of downstream signaling cascades. Through binding to TRK receptors, neorotrophinss activate Ras, phosphatidylinositol-3 (PI3)-kinase, and phospholipase C-γ1 signaling pathways. By this signaling, neurotrophins ultimately regulate cell fate decisions, axon growth, dendrite growth, and pruning. In addition to the expression in the central nervous system (CNS), TRK proteins have also been identified in non-neuronal normal tissues and cells, including pancreatic beta cells, monocytes, lungs, and bone.
References
1.Hsiao SJ,et al. J Mol Diagn. 2019;21(4):553–571.
2.Lange AM, et al. Cancers (Basel). 2018;10(4):105.
Tyrosine Kinase
Trk Receptor
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ENT-C225
catalog no : M36522
cas no: 2919962-53-9
ENT-C225 is a potent TrkB neurotrophin receptor (TrkBR) activator with neuroprotective activity for the study of Alzheimer's disease and Parkinson's disease. -
CG 428
catalog no : M35263
cas no: 2412055-93-5
CG 428 is a potent tropomyosin receptor Kinase (TRK) Degrader (uSMITETM) with a DC50 of 0.36 nM. CG 428 comprises an analog of the pan-TRK inhibitor GNF-8625 joined by a linker to the cereblon E3 ligase ligand pomalidomide. -
GNF-8625 monopyridin-N-piperazine hydrochloride
catalog no : M35176
cas no: 2412055-62-8
GNF-8625 monopyridin-N-piperazine hydrochloride is a tropomyosin receptor kinase (TRK) inhibitor. -
Cyclotraxin B
catalog no : M30732
cas no: 1203586-72-4
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. -
(3aR)-Selitrectinib
catalog no : M28716
cas no: 1350884-56-8
(6RS)-LOXO-195 is a potent and selective Trk tyrosine kinase inhibitor.