hTrkA-IN-1 is a potent and orally active inhibitor of TrkA kinase with an IC50 of 1.3 nM, compound 2. extracted from patent WO2015175788. hTrkA-IN-1 can be used for the study of inflammatory disease, such as prostatitis, pelvic, et al[1].
TRK-IN-17 is a potent inhibitor of TRK. Tropomyosin-related kinases (Trks) are a family of receptor tyrosine kinases activated by neurotrophins, a group of soluble growth factors including Nerve Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF) and Neurotrophin-3 (NT-3) and Neurotrophin-4/5 (NT-4/5). TRK-IN-17 has the potential for the research of cancer diseases (extracted from patent WO2021148807A1, compound 3)[1].
Entrectinib is a potent and orally available Trk, ROS1, and ALK inhibitor; inhibits TrkA, TrkB, TrkC, ROS1 and ALK with IC50 values of 1, 3, 5, 12 and 7 nM, respectively.
Lestaurtinib (CEP-701;KT-5555) is a multi-kinase inhibitor with potent activity against the Trk family of receptor tyrosine kinases. Lestaurtinib inhibits JAK2, FLT3 and TrkA with IC50s of 0.9, 3 and less than 25 nM, respectively.
Larotrectinib (LOXO-101) sulfate is an ATP-competitive oral, selective inhibitor of the tropomyosin-related kinase (TRK) family receptors, with low nanomolar 50% inhibitory concentrations against all three isoforms (TRKA, B, and C).
Repotrectinib (TPX-0005) is a potent ALK/ROS1/TRK inhibitor, with IC50 of 5.3 nM, 1.01 nM, 1.26 nM and 1.08 nM for SRC, WT ALK, ALK G1202R and ALK L1196M, respectively.
GNF-5837 is a potent pan-Trk inhibitor which display antiproliferative effects in cellular Ba/F3 assays (IC50 values are 7, 9 and 11 nM for cells containing the fusion proteins Tel-TrkC, Tel-TrkB and Tel-TrkA, respectively).IC50 Value: 7/9/11 nM (Tel-TrkC/Tel-TrkB/Tel-TrkA) [1]Target: pan-TrkGNF-5837 is an orally bioavailable oxindole compound that and acts as a potent, reversible and type II DFG-out inhibitor of pan-Trk activity (IC50 = 8 and 12 nM for TrkA and TrkB). Shown to target Trk (tropomyosin receptor kinase) ATP binding cleft and an immediately adjacent hydrophobic pocket. Preferentially arrests the proliferation of Ba/F3 cells fused with Tel-TrkA, Tel-TrkB and Tel-TrkC (IC50 = 11, 9 and 7 nM, respectively) and in Ba/F3 and RIE cells expressing both TrkA and NGF (IC50 = 42 and 17 nM, respectively) over Mo7e-c-Kit and Rat-A10-PDGFR (IC50 = 1 and 0.5 μM) and Ba/F3-Tel-KDR and wt-Ba/F3 cells (IC50 = 3.0 and 5.6 μM). GNF-5837 displays ~100-fold greater selectivity among a panel of 59 closely related kinases and in 33 cellular kinase assays. GNF-5837 weakly antagonize relevant cytochrome P450 isozymes and hERG channel, and exhibit adequate microsomal stability, pharmacokinetic profile and efficacy in mice and rats. GNF-5837 suppresses tumor growth in a mouse RIE-TrkAmNGF xenograft model (50 mg/kg, p.o.) [1].
PF-06273340 is a potent, selective, orally bioavailable and peripherally restricted pan Trk inhibitor[1].
Larotrectinib (LOXO-101) is an ATP-competitive oral, selective inhibitor of the tropomyosin-related kinase (TRK) family receptors, with low nanomolar 50% inhibitory concentrations against all three isoforms (TRKA, B, and C).
TRK-IN-18 is a potent inhibitor of TRK. Tropomyosin-related kinases (Trks) are a family of receptor tyrosine kinases activated by neurotrophins, a group of soluble growth factors including Nerve Growth Factor (NGF), Brain-Derived Neurotrophic Factor (BDNF) and Neurotrophin-3 (NT-3) and Neurotrophin-4/5 (NT-4/5). TRK-IN-18 has the potential for the research of cancer diseases (extracted from patent WO2021148805A1, compound 7)[1].
IHMT-TRK-284 (Compound 34) is a potent, orally active type II TRK kinase inhibitor with IC50 values of 10.5, 0.7, and 2.6 nM to TRKA, B, and C respectively. IHMT-TRK-284 displays great selectivity profile in the kinome and good in vivo antitumor efficacies[1].
Altiratinib (DCC-2701) is a multi-targeted kinase inhibitor with IC50s of 2.7, 8, 9.2, 9.3, 0.85, 4.6, 0.83 nM for MET, TIE2, VEGFR2, FLT3, Trk1, Trk2, and Trk3 respectively.
Paltimatrectinib (compound I-147) is a potent tyrosine kinase inhibitor with an IC50 of <10 nM for tropomyosin kinases A (TrkA). Paltimatrectinib has the potential for cancer and inflammatory diseases[1].
(R)-Larotrectinib is a potent TRK inhibitor with an IC50 value of 28.5 nM for TrkA. (R)-Larotrectinib can be used for researching cancer, inflammatory and certain infectious diseases[1]
BDNF (human) is a neurotrophin in the central nervous system and mediates survival and differentiation of neurons. BDNF (human) binds to TrkB and leads to the dimerization and autophosphorylation of tyrosine residues in the intracellular domain of the receptor. BDNF (human) can be used for study of neurodegenerative and psychiatric disorder[1][2].
TRK-IN-23 (compound 24b) is a potent and orally active TRK inhibitor with IC50 values of 0.5 nM, 9 nM, 14 nM, 4.4 nM, and 4.8 nM against TRKA, TRKC, TRKAG595R, TRKAF589L, and TRKAG667C, respectively. TRK-IN-23 indues apoptosis of Ba/F3-TRKAG595Rand Ba/F3-TRKAG667C cells[1].
Trk-IN-20 is a kind of 3-vinylindazole derivatives. Trk-IN-20 suppresses Trk kinases functions by phosphorylation inhibition of TrkA/B/C with IC50 values of 1.6 nM, 2.9 nM and 2.0 nM, respectively[1].
Trk-IN-6 shows excellent in vitro potency on a panel of TRK mutants (IC50 = 0.2-0.7 nM).
TRK-IN-13 is a potent inhibitor of TRK. Protein kinases play a critical role in the control of cell growth and differentiation and are responsible for the control of a wide variety of cellular signal transduction processes. TRK-IN-13 has the potential for the research of TRK-related diseases (extracted from patent WO2012034091A1, compound X-24)[1].
TRK-IN-21 (5n) is an orally activity TRK inhibitor. TRK-IN-21 inhibits TRKAWT, TRKAG667C, TRKAF589L, and TRKAG595 with IC50s of 0.3, 2.3, 0.4 and 0.5 nM, respectively. TRK-IN-21 can be used for the research of cancer[1].
D5261 is a potent, type III allosteric tropomyosin-related kinase A (TrkA) inhibitor[1].
CH7057288 is a potent and selective TRK inhibitor.
Compound cpd-1 is a small molecule Trks inhibitor with good antitumor activity[1].
ONO-7475 is a potent, selective, and orally active novel Axl/Mer inhibitor with IC50 values of 0.7 nM and 1.0 nM, respectively. ONO-7475 sensitizes AXL-overexpressing EGFR-mutant NSCLC cells to the EGFR-TKIs, suppresses the emergence and maintenance of tolerant cells. ONO-7475 combines with Osimertinib (HY-15772) provides a bright promise for the study of EGFR-mutated non-small cell lung cancer (NSCLC)[1].
GW 441756 is a specific Tropomyosin-related kinase A (TrkA) inhibitor with an IC50 value of 2 nM; little activity to c-Raf1 and CDK2.IC50 Value: 2 nM [1]Target: TrkAin vitro: GW441756 specifically blocked TrkA-induced cell death in a dose-dependent manner, but there was no effect in uninduced cells. TrkA ability to induce γH2AX production was significantly downregulated by both K-252a and GW441756 in the absence of DNA damage inducer. In addition, it was also suppressed by K-252a during DNA damage by doxorubicin treatment, but not by GW441756 [2].
TRK-IN-16 is a potent inhibitor of TRK. Protein kinases play a critical role in the control of cell growth and differentiation and are responsible for the control of a wide variety of cellular signal transduction processes. TRK-IN-16 has the potential for the research of TRK-related diseases (extracted from patent WO2012034091A1, compound X-21)[1].
TRK-IN-24 (compound 10g) is a Trk Receptor inhibitor that inhibits TRKA, TRKC, TRKAG595R, TRKAG667C and TRKAF589L IC50s are 5.21, 4.51, 6.77, 1.42 and 6.13 nM respectively. TRK-IN-24 has antitumor efficacy in BaF3-CD74-NTRK1G595R and BaF3-CD74-NTRK1G667C xenograft models. TRK-IN-24 inhibits the proliferation of Ba/F3 cells transfected with single mutants such as SF, GK, and xDFG, with an IC50 of 1.43-47.56 nM[1].
AZ-23 is an ATP-competitive and orally bioavailable Trk kinase A/B/C inhibitor with IC50s of 2 nM (TrkA), 8 nM (TrkB), 24 nM (FGFR1), 52 nM (Flt3), 55 nM (Ret), 84 nM (MuSk), 99 nM (Lck), respectively.
N-Acetyl-5-hydroxytryptamine is a Melatonin precursor, and that it can potently activate TrkB receptor.
HIOC is a potent and selective activator of TrkB (tropomyosin related kinase B) receptor. HIOC can pass the blood-brain and blood-retinal barriers.HIOC activates TrkB/ERK pathway and decreases neuronal cell apoptosis. HIOC attenuates early brain injury after SAH (subarachnoid hemorrhage). HIOC shows protective activity in an animal model for light-induced retinal degeneration[1][2][3].