MASL® Inhibits Motility, Proliferation and Metastasis

Mechanism of Action: Blocks podoplanin (PDPN) signaling

MASL PDPN Receptor
MASL targets the PDPN receptor on OSCC cell membrane

OSCC = Oral Squamous Cell Carcinoma
Oncotarget, 6.11 (2015): 9045-9060.

  • Orally dosed, bioactive lectin derived from Maackia amurensis seeds

  • Efficiently binds to PDPN upregulated on tumor cells

  • Blocks PDPN mediated activation of Cdc42 impacting cell-to-cell adhesion, cell cycle regulation, tumor vascularization and homeostasis

  • Downregulates oncogenic signaling pathways impacting tumor growth and progression (Wnt-Bctn, TGFβ-SMAD, JAK-STAT)

  • Induces caspase independent necrotic cell death and cytostatic regulation of tumor migration and metastasis

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.