Carboxy-PTIO is a highly effective nitric oxide (NO) scavenger known for its rapid reaction rate with NO, resulting in the formation of nitric dioxide (NO2). Its direct scavenging action against NO plays a crucial role in preventing hypotension and endotoxic shock, particularly in lipopolysaccharide-stimulated rat models.

Carboxy-PTIO, at a concentration of 200 μM and administered 1 hour before physalin A for a duration of 24 hours, effectively inhibits the increase in NO expression triggered by physalin A, without affecting baseline NO levels[1]. Furthermore, it mitigates the physalin A-induced activation of apoptotic pathways by preventing the cleavage of procaspase-3 and PARP, downregulating ICAD expression, and reducing nuclear DNA fragmentation[1]. Additionally, Carboxy-PTIO does not alter iNOS expression levels but negates the physalin A-induced reduction in both mTOR and phosphorylated mTOR, while also inhibiting the autophagic process by preventing the conversion of LC3 I to LC3 II in A375-S2 cells[1]. This was corroborated by a Cell Viability Assay on A375-S2 cells, where Carboxy-PTIO, pre-administered at 200 μM for 1 hour followed by physalin A exposure for 24 hours, decreased the cleavage of procaspase-3 and PARP induced by physalin A[1].

Carboxy-PTIO (intravenous injection; 0.056-1.70 mg/kg/min; infused for 1 hr beginning 90 min after the LPS injection) has been demonstrated to significantly ameliorate hypotension, renal dysfunction, and enhance survival rates in LPS-treated rats, showcasing its potent therapeutic efficacy in endotoxin shock by directly scavenging nitric oxide (NO). However, it does not influence these parameters in normal rats. The study utilized SD rats as the animal model, with a dosage range of 0.056-1.70 mg/kg/min administered intravenously.