Periplanetasin-4

Periplanetasin-4 (100 μg/mL, 48 h) significantly rescues the loss of cell viability and reduces cell rounding induced by Clostridium difficile toxin A in HT29 cells^[1].
Periplanetasin-4 (100 μg/mL, 48 h) markedly decreases the number of TUNEL-positive apoptotic HT29 cells and inhibits the activation of caspase-3 (a hallmark of apoptosis) induced by Clostridium difficile toxin A^[1].
Periplanetasin-4 (100 μg/mL, 45 min) completely inhibits the increase in ROS production induced by Clostridium difficile toxin A in HT29 cells^[1].
Periplanetasin-4 (100 μg/mL, 4 h) significantly blocks the activation of p38MAPK and the up-regulation of p21 in HT29 cells^[1].
Periplanetasin-4 (5 μM, 2-4 h) significantly increases PI influx and DiBAC4(3) accumulation in Candida albicans ATCC 90028 cells^[2].
Periplanetasin-4 (5 μM, 2 h) significantly elevates intracellular ROS level, increases mitochondrial superoxide radical and hydrogen peroxide production in Candida albicans ATCC 90028 cells^[2].
Periplanetasin-4 (5 μM, 2 h) significantly induces phosphatidylserine externalization and caspase activation in Candida albicans ATCC 90028 protoplasts^[2].
Periplanetasin-4 (5 μM, 2 h) significantly increases malondialdehyde (MDA) level, enhances catalase activity and total glutathione content, causes mitochondrial membrane potential collapse, increases mitochondrial biomass, and promotes mitochondrial fragmentation in Candida albicans ATCC 90028 cells^[2].
Periplanetasin-4 (5 μM, 2 h) significantly increases BCECF and C-DCFDA fluorescence intensity and mitochondrial calcium level, reduces DPH fluorescence intensity and vacuolar dysfunction in Candida albicans ATCC 90028 cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.