tpm3-trka

Ensartinib hydrochloride (X-396 dihydrochloride) is a potent new-generation ALK inhibitor with high activity against CNS metastases and a broad range of known crizotinib-resistant ALK mutations. It potently inhibits both wild-type ALK and ALK variants (C1156Y, F1174, G1202R, L1196M, S1206R, and T1151 mutants) with in vitro IC50s of <4 nM.

NMS-P626 functions as an inhibitor targeting TRKA, TRKB, and TRKC, exhibiting IC 50 values of 8 nM, 7 nM, and 3 nM respectively. It effectively suppresses KM12 cell growth by inhibiting the phosphorylation of TPM3-TRKA and the subsequent downstream signaling, demonstrating an IC 50 of 19 nM specifically for KM12 cells. This compound is applicable in the study of colorectal cancer.

CG428-NEG is a negative control for TRK degraders. CG428 inhibits cell growth and reduces levels of TPM3-TRKA.

JWJ-01-378 is a selective TRK PROTAC degrader. It effectively degrades wild-type TRK and TPM3-TRKA fusion proteins while inhibiting downstream pERK signaling, but shows limited degradation effects on TRK inhibitor-resistant mutants and ALK fusion proteins. Additionally, JWJ-01-378 effectively suppresses cancer cell proliferation.

ALK-IN-9 (compound 40) is a highly effective ALK inhibitor, demonstrating remarkable inhibitory activity against cell proliferation, with IC50 values of <0.2 nM for Ba/F3-EML4-ALK, KM 12 (TPM3-TRKA), and KG-1 cell (OP2-FGFR1).