CLM3, a pyrazolopyrimidine derivative, functions as a multitargeted tyrosine kinase inhibitor. It exhibits antiproliferative and proapoptotic activities on endothelial and cancer cells, activities that are synergistically enhanced by SN38. The primary mechanism of action for CLM3 involves the inhibition of phosphorylation in tyrosine kinases such as VEGFR-2, EGFR, and RET, along with their associated signaling pathways.

CLM3 (0-100 μM, 72 h)在处理过程中，有效下调活化内皮细胞和癌细胞中的磷酸化 VEGFR-2、磷酸化 EGFR、以及磷酸化 RET 的水平。此外，CLM3 (0-100 μM, 72 h) 还显著抑制了内皮细胞和癌细胞中细胞周期蛋白 D1 基因的表达，并减少了细胞内细胞周期蛋白 D1 蛋白的浓度。