Carboxy-PTIO (200 μM; 1 h prior to physalin A; 24 hours) significantly suppresses the stimulation of NO expression induced by physalin A treatment, but no change is observed in Carboxy-PTIO treatment alone[1].

Carboxy-PTIO (200 μM; 1 h prior to physalin A; 24 hours) reduces physalin A-induced cleavage of procaspase-3 and PARP, down-regulated ICAD expression,diminishing DNA fragmentation in nuclei[1].

Carboxy-PTIO (200 μM; 1 h prior to physalin A; 24 hours) shows no effect on iNOS expression. However, decreased-mTOR and p-mTOR levels induced by physalin A is reversed by Carboxy-PTIO with concomitant suppression of LC3 I to LC3 II conversions in A375-S2 cells[1]. Cell Viability Assay[1]Cell Line: A375-S2 cells Concentration: 200 μM Incubation Time: 1 h prior to physalin A; 24 hours Result: Diminished physalin A-induced procaspase-3 and PARP cleavage.

Carboxy-PTIO (intravenous injection; 0.056-1.70 mg/kg/min; infused for 1 hr beginning 90 min after the LPS injection 90 min) treatment improves the hypotension, renal dysfunction and survival rate in Lps-treated rats. But it does not affect each parameter in naomal rats[3]. Animal Model: SD rats[3]Dosage: 0.056-1.70 mg/kg/min Administration: Intravenous injection; 0.056-1.70 mg/kg/min; infused for 1 hr beginning 90 min after the LPS injection 90 min Result: Exhibited a potent therapeutic value in endotoxin shock through the direct scavenging action against NO.