CIL-102 is an apoptosis inducer that functions as an MMP-2/MMP-9 inhibitor, effectively reducing both the protein expression and mRNA levels of MMP-2/MMP-9. CIL-102 also demonstrates anticancer activity.

CIL-102 activates JNK and p38 MAPK in human leukemia K562 cells while reducing phosphorylated ERK levels. The activation of p38 MAPK/JNK by CIL-102 leads to the downregulation of tetratricopeptide (TTP) mediated by protein phosphatase 2A. Additionally, it decreases invasion and MMP-2/MMP-9 expression in breast and liver cancer cells [1]. In DLD-1 cells, CIL-102 induces an extrinsic apoptotic pathway in a time-dependent manner by activating Fas-L, caspase-8, and inducing Bid cleavage and cytochrome c release. Apoptosis and G2/M arrest are mediated via the phosphorylation of the JNK1/2 signaling pathway, resulting in altered levels of NFκB p50, p300, and CREB binding protein (CBP), along with the induction of p21 and GADD45 and reduced association of cdc2/cyclin B. Overall, CIL-102 induces cell cycle arrest and apoptosis in colon cancer cells by upregulating p21 and GADD45 expression and activating JNK1/2, NFκB p50, and p300 [2].