TRK-IN-32 

TRK-IN-32 is a potent TRK inhibitor. TRK-IN-32 potently inhibits TRK^WT, TRK^G595R and TRK^G667C with IC₅₀ values of 0.08 nM, 2.14 nM and 0.68 nM, respectively. TRK-IN-32 also demonstrates antiproliferative activity against a panel of Ba/F3 cell lines transformed with wild type, xDFG, solvent-front as well as gatekeeper mutant TRK fusion proteins. TRK-IN-32 induces apoptosis of Ba/F3-TRKA^WT and Ba/F3-TRKA^G667C cells.TRK-IN-32 can be used for the study of various cancers (such as thyroid cancer, secretory breast carcinoma)^[1].

TRK-IN-32 (Compound 15m) exhibits moderate human liver microsomal stability (t_{1/2 = 33.8 min). TRK-IN-32 exhibits anti-proliferative efficacy against Ba/F3 cell lines, with an IC50s of 1.24 (Ba/F3-ETV6-TRKA^WT), 0.35 (Ba/F3-ETV6-TRKB^WT), 24.26 (Ba/F3-LMNA-TRKA^G595R), 10.24 (Ba/F3-LMNA-TRKA^G667C) and 1.06 (Ba/F3-LMNA-TRKA^F589L) nM^[1].
TRK-IN-32 (0-10 nM) effectively blocks the TRKA^WT and TRKA^G667C autophosphorylation in cells at relatively low concentrations as well as phosphorylation of their downstream molecules AKT, PLCγ1 and ERK in Ba/F3 cells expressing TRKA^WT and TRKA^G667C fusion mutant^[1].
TRK-IN-32 (0-500 nM, 48 h) strongly induces Ba/F3-CD74-TRKA and Ba/F3-CD74-TRKAG667C cells apoptosis^[1].}

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

363.39

C₁₉H₁₈FN₇

3044124-79-7

C[C@@H](C1=CC=C(C=N1)F)NC2=NN3C(C4=NNC(C5CC5)=C4)=CN=C3C=C2

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Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Xu Y, et al. Discovery of imidazo[1,2-b]pyridazine derivatives as potent TRK inhibitors for overcoming multiple resistant mutants. Bioorg Chem. 2025 Aug;163:108737.  [Content Brief]