This substitution drastically increases the IC50s for inhibition of COX1 (15 μM to >100 μM for celecoxib and TFM-C, respectively) and COX2 (0.04 μM to 8.2 μM, respectively), but does not affect the apoptotic index measured in PC3 prostate cancer cells, indicating independence between structural requirements for COX-2 inhibition and apoptosis induction [36]. Here, PTGS2 is linked to prostate carcinoma.