Laboratory findings show DZX19 inhibits tumor growth in models with NTRK gene fusions, suggesting potential for treating resistant tumors.
Tropomyosin receptor kinase (TRK) is an important therapeutic target for tumors driven by NTRK gene fusions. However, the clinically approved TRK inhibitors, including Larotrectinib and Entrectinib, are limited by insufficient efficacy and resistance due to kinase mutations. Here, we report DZX19 (C02), a novel phenyl thiophene-3-carboxamide TRK inhibitor developed via a pharmacophore-guided scaffold-hopping approach combined with structure-based design, based on the key binding features of Entrectinib. DZX19 demonstrated stronger in vitro activity and an improved resistance profile against Entrectinib-resistant TRKA mutants, including G595R, F589L, and G667C. In the TPM3-NTRK1 fusion-positive Km-12 cell line, DZX19 induced G1 arrest, promoted apoptosis, and suppressed TRK downstream signaling. DZX19 displayed excellent plasma stability and moderate microsomal stability. In the Km-12 xenograft model, DZX19 significantly suppressed tumor growth. These results indicate that DZX19 serves as a novel TRK-targeting lead compound for further investigation.
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