Treatment of nude mice bearing xenografts from women with endometriosis (BWE) with 30 mg/kg Bentamapimod (AS 602801) results in a 29% reduction in lesion size. Neither Medroxyprogesterone acetate (MPA) nor progesterone (PR) alone reduced BWE lesions; however, combining 10 mg/kg Bentamapimod with MPA achieved a 38% lesion regression. In human endometrial organ cultures from healthy women, both Bentamapimod and MPA decrease matrix metalloproteinase-3 (MMP-3) release. In BWE organ cultures, PR and MPA do not inhibit MMP-3 secretion, while AS 602801 alone or combined with MPA reduces MMP-3 production. In an autologous rat endometriosis model, AS 602801 reduces lesions by 48% compared to 84% with the GnRH antagonist Antide. Bentamapimod also lowers inflammatory cytokines in endometriotic lesions and enhances natural killer cell activity without negatively affecting the uterus[3].

Bentamapimod (AS 602801) induces cell death in a dose-dependent manner across various cancer cell lines including human pancreatic, non-small cell lung, ovarian cancer, and glioblastoma cells, without affecting the viability of normal human fibroblasts. It also hinders the self-renewal and tumor-initiating capabilities of cancer stem cells that survive treatment with Bentamapimod (AS 602801)^[2].