Cantharidic acid disodium

Cantharidic acid (1.25-40 μM for FHC cells; 5-20 μM for SW480/HCT116 cells; 24-48 h) selectively reduces the viability of SW480 and HCT116 colorectal cancer cells, with an IC₅₀ of 10 μM against HCT116 cells at 48 h, while having no obvious effect on the viability of FHC cells^[1].
Cantharidic acid (5-20 μM) reduces colony formation in SW480 and HCT116 colorectal cancer cells^[1].
Cantharidic acid (5-20 μM) reduces PCNA, MMP2, and MMP9 protein levels in SW480 and HCT116 colorectal cancer cells^[1].
Cantharidic acid (5-20 μM; 24 h) disrupts the cell membrane integrity of SW480 and HCT116 colorectal cancer cells and increases LDH release^[1].
Cantharidic acid (5-40 µM; 24 h) inhibits the proliferation of SK-Hep-1 and Huh-7 HCC cells, with 10 µM causing >59% reduction in viability and 40 µM being the most toxic concentration tested^[2].
Cantharidic acid (24 h) inhibits the proliferation of UMSCC-1, UMSCC-23, HN12, and A-253 OSCC cells, with 24 h IC₅₀ values of 3.26-15.7 µM^[3].
Cantharidic acid (1-25 µM; 24-72 h) reduces LoVo cell viability in a time- and concentration-dependent manner, with 25 µM exposure for 24 h causing 40-60% viability loss and 5-10 µM exposure for 72 h causing 40% cell death^[4].

Cantharidic acid (5-20 μM; 24 h) induces apoptosis in SW480 and HCT116 colorectal cancer cells^[1].

Cantharidic acid (5-20 µM; 24 h) increases the percentage of apoptosis in SK-Hep-1 cells^[2].
Cantharidic acid (5-20 µM) activates caspase-3, caspase-8, and caspase-9 as well as PARP cleavage in SK-Hep-1 cells in a concentration-dependent manner^[2].
Cantharidic acid increases Caspase-3-like activity in LoVoDx cells^[4].

Cantharidic acid (20 µM; 24 h) increases the subG1 and S phase cell populations and decreases the G2/M and G1 phase cell populations in SK-Hep-1 cells^[2].

Cantharidic acid (5-20 µM) increases p-ERK, p-JNK, and p-p38 in SK-Hep-1 cells^[2].