Ir-CA is an antitumor agent that accumulates in mitochondria, inducing mitochondrial dysfunction, apoptosis, and autophagy. It initiates mitophagy and cell cycle arrest to kill Cisplatin-resistant A549R cells and effectively inhibits metastasis by inhibiting MMP-2/MMP-9 [1].

Ir-CA exhibits cytotoxic effects on A549, A549R, HLF, BEAS-2B, MCF-7, and 4T1 cells, with IC 50 values of 4.4, 4.5, 6.6, 2.3, 2.6, and 5.7 μM, respectively [1]. It is rapidly taken up by A549R cells, as indicated by red fluorescence after 1 hour of incubation [1]. At a concentration of 10 μM for 2 hours, Ir-CA accumulates in the mitochondria of live A549 and A549R cells, as shown by co-staining with Mito-Tracker [1]. Exposure to Ir-CA (10 μM) for 24 hours damages the mitochondrial morphology and function of A549R cells and induces ROS production [1]. Ir-CA at the same concentration induces apoptosis in A549R cells via a non-apoptotic/necrotic pathway and increases the conversion of LC3-I to LC3-II, indicating autophagy [1]. Additionally, Ir-CA (2.5 μM, 24 hours) resensitizes A549R cells to cisplatin [1], and at 5 μM for 24 hours, it inhibits A549R cell metastasis by downregulating MMP [1].

Ir-CA (5 mg/kg, administered intraperitoneally every other day for 8 days) reduces lung metastasis of A549 cells in a metastatic mouse model (via tail vein injection of A549 cells) [1]. Ir-CA (5 mg/kg, administered intraperitoneally every other day for 14 days) suppresses tumor growth in A549 tumor-bearing Balb/c nude mice [1].