WZH-17-002

WZH-17-002 (< 4.6 nM-10 μM; 48 h) potently inhibits the proliferation of Ba/F3 cells expressing EML4-ALK (wild-type) or Lorlatinib (HY-12215)-resistant EML4-ALK^{G1202R/L1196M}, with IC₅₀ values ranging from < 4.6 nM to 17.2 nM^[1].
WZH-17-002 (< 4.6 nM-10 μM; 48 h) selectively inhibits the proliferation of ALK-rearranged human non-small cell lung cancer cell lines (DFCI076, H3122, H2228), with IC₅₀ values ranging from 4.5 nM to 58.6 nM; it exhibits moderate activity against EGFR-mutated PC9 cells^[1].
WZH-17-002 (1-500 nM; 16 h) degrades ALK protein in ALK-rearranged human non-small cell lung cancer cells (DFCI076, H3122) with a DC₅₀ value of approximately 25 nM, while inhibiting the ALK signaling pathway, degrading the mutant ALK^G12C in ALK inhibitor-resistant Ba/F3 cells, and mediating degradation via a CRBN- and proteasome-dependent pathway^[1].
WZH-17-002 (5-20 nM; 14 days) inhibits colony formation of ALK-rearranged DFCI076 and H2228 non-small cell lung cancer (NSCLC) cells^[1].
WZH-17-002 (50 nM; 70 days) delays the emergence of drug resistance in ALK-rearranged H3122 non-small cell lung cancer cells^[1].

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