SymBio Pharmaceuticals negotiated rights to develop Onconova Therapeutics’ rigosertib (EstybonTM ; ON 1910 Na) in Japan and Korea. The styryl benzyl sulfone multikinase inhibitor is currently in late-stage clinical trials in the U.S., Europe, and India for treating myelodysplastic syndromes (MDS) and solid tumors. It is also undergoing a pivotal study as monotherapy against refractory/relapsed MDS in the U.S and Europe under an SPA agreement with FDA.
Under terms of its license agreement with Onconovoa, Tokyo-based SymBio has an exclusive license to develop and commercialize rigosertib in Japan and Korea, in return for paying an up-front fee and development milestones plus future sales royalties.
“This is the first commercial transaction for our lead product rigosertib,” comments Ramesh Kumar, Ph.D., Onconova president and CEO. “The broad reach of rigosertib across blood cancers as well as solid tumors and the ability to address previously intractable indications with single agent and combination therapies will provide multiple opportunities to serve the unmet medical needs of patients worldwide.”
Onconova is focused on developing drugs against cancer and radiation injury. Its anticancer pipeline is focused on treatments that target cell cycle regulation in tumor cells. Lead drug rigosertib is in addition being evaluated in combination with chemotherapy against multiple solid tumor types. Clinical studies have indicated that combining the candidate with either oxaliplatin or gemcitabine is associated with a rapid response in breast, colon, and ovarian cancer as well as lymphoma patients, Onconova states.
In June the firm initiated a Phase II/III trial evaluating the drug in combination with gemcitabine in patients with previously untreated metastatic pancreatic cancer. In June 2010 the Leukemia & Lymphoma Society (LLS) agreed to provide up to $10 million in funding to support the pivotal clinical trial evaluating rigosertib in high-risk MDS patients.
Onconova says candidate Estybon has a multitargeted mechanism of action that results in mitotic block and cell death selectively in cancer cells. The drug impacts on the polo-like kinase (PLK) pathway, causing polynumeric centrosomes and dysregulation of mitosis, and inhibits the PI-3 kinase, ERK, and AKT.