Our goal is to treat and prevent cancer, extend survival rates, and improve the quality of life for people with cancer and potentially malignant conditions.

Scientific Rationale

The current standard of care for cancer shows limited success rates, high toxicity and tolerability burdens. That is why we are committed to developing therapies that harness critical cell-to-cell communication, which revive the body’s ability to recognize, contain and eliminate abnormal cells found in cancer and potentially malignant conditions.

Through contact normalization, a cellular communication process that enables normal cells to not only inhibit tumor growth and spread, but also enables subsequent tumor elimination, the body is able to naturally evade cancer. Our therapies target specific receptors that precancerous and tumor cells use to escape contact normalization. This approach disables key pathways critical to disease progression.

We have performed comprehensive analyses to identify genes and proteins that are affected during contact normalization. Our technology can be used to accurately identify biomarkers that indicate cancer, prognostic indicators that determine the invasive and metastatic potential of cancer cells, and chemotherapeutic reagents that combat cancer cell growth, invasion, and metastasis.

We are currently discovering and developing therapies that target malignant and metastatic cancer cells. Our approach may halt cancer progression to the extent that patients would be spared from the harsh side effects of the standard of care including surgery, chemotherapy, and radiation.

Medical Approach

Our lead product, MASL, is a novel, orally dosed therapeutic that has been validated in preclinical studies conducted by major research institutions, including the NCI. MASL is a powerful inhibitor of podoplanin (PDPN) signaling. PDPN is a transmembrane receptor glycoprotein, that is overexpressed in many cancers and is critical in tumor activation and progression. It is an early expressed tumor biomarker correlated with poor prognosis in many cancers. By binding to PDPN, MASL inhibits tumor cell growth and invasion, and triggers cancer cell destruction.

The potential effects of MASL were demonstrated with the NCI-60 cell line panel as performed by the Developmental Therapeutics Program at the NCI. Cancer cells were plated, grown for 24 hours, and then treated with indicated concentrations of MASL for 48 hours before evaluation by Sulforhodamine B assay. These results showed that MASL was able to impact all 9 different types of cancer tested.  In a preclinical mouse model in melanoma, MASL provided 10-fold inhibition of tumor growth at 50 mg/kg without toxic side effects.

We are studying MASL with an initial focus in cancerous and potentially malignant oral lesions—where there is a significant opportunity to change the treatment paradigm from “watch and wait” to “treat and prevent.” Elevated PDPN expression in oral cancers aligns with poor prognosis.; 80% of leukoplakia patients with elevated PDPN expression go on to develop cancer. To date, there are more than 400,000 individuals in the U.S. living with oral cancer, with 54,000 new cases and over 11,000 deaths annually. Leukoplakia is the most common premalignant oral lesion with 6.6M cases in the U.S. and 2% prevalence worldwide.

MASL is dosed as an oral lozenge, where it can come in direct contact with oral cancer or leukoplakia on the inner surface of the mouth. Standard of care treatment approaches have not significantly reduced the high recurrence rates observed in oral cancer. Therefore, MASL has the potential to shift the treatment paradigm of oral cancer.

We also plan to explore MASL’s safety and efficacy in other cancers with high levels of PDPN expression such as skin, cutaneous, brain, and breast cancers.