195883-06-8

In a mouse model of cisplatin-induced AKI, omtriptolide results in a significant decrease in blood urea nitrogen (BUN), serum creatinine, and acute tubular necrosis (ATN) score, and a nonsignificant increase in tubular apoptosis score in AKI. The protection of omtriptolide against AKI is associated with a decrease in p-ERK and is independent of MKP-1 and proinflammatory cytokines^[1]. In a mouse heterotopic tracheal allograft model of obliterative airway disease, omtriptolide attenuates airway obliteration and inhibits accumulation of inflammatory cells, and therefore may have preventive or therapeutic benefits for patients with obliterative airway disease following lung transplantation^[2]. Omtriptolide inhibits fibrosis in the bleomycin group when given the same day or 5 days after bleomycin. Omtriptolide also markedly reduces the number of myofibroblasts in the bleomycin treatment group^[3]. Omtriptolide inhibits in vivo both CD4+Vbeta3+ and CD8+Vbeta3+ T cell (alloreactive T cells in this model) expansion in the spleen by 64.09 and 34.02%, respectively, at the time when Vbeta3+ cell expansion is in the logarithmic phase (day 3 after transplantation)^[4].