Our lead product, MASL, is a novel, orally dosed inhibitor of PDPN. MASL blocks PDPN mediated activation of Cell division control protein (Cdc42) a driver of metastasis and therapy resistance in multiple cancer types. Cdc42 plays an important role in cell-to-cell adhesion and cell cycle regulation by influencing cellular proliferation, transformation, and homeostasis, as well as the cellular migration and invasion processes underlying tumor formation. By efficiently binding to PDPN, contact normalization is revived by MASL to inhibit tumor cell growth and invasion, and activate tumor cell destruction signaling.
MASL Impacts Drug Resistant Tumor Cells
MASL has demonstrated both cytostatic effects (an 86% inhibition of cell motility) and cytotoxic effects (a 75% inhibition of cell viability) on drug resistant human oral squamous cell carcinoma (OSCC). In a melanoma mouse study, MASL provided a 10-fold inhibition of tumor growth. Animal studies have not produced any identifiable adverse effects and there have been no histological changes on heart, kidney, liver, lung, or small intestine tissue morphology with 15-week administration.