Veru announces publication of data from 3 cancer studies as part of ASCO meeting
Veru Inc. announced the publication of data from preclinical studies of VERU-111, a novel oral alpha and beta tubulin inhibitor, that showed efficacy in chemotherapy resistant tumor types. Specifically, VERU-111 reduced tumor growth in a paclitaxel sensitive and resistant triple negative breast cancer model, as well as ovarian cancer and pancreatic cancer models. Three abstracts, which include data related to each of the three cancers, were published as part of the upcoming 2018 American Society of Clinical Oncology Annual Meeting in Chicago. Triple negative breast cancer is highly aggressive and has poor prognosis due to the frequent development of drug resistance. The study being published evaluated oral administration of VERU-111 compared with IV docetaxel in a paclitaxel resistant TNBC model. IV docetaxel had little impact on tumor growth whereas oral VERU-111 resulted in almost complete inhibition of TNBC tumor growth at 12.5 mg/kg, as well as significantly reduced tumor metastasis. Metastatic ovarian cancer is a highly lethal gynecological malignancy. Although many patients with ovarian cancer initially respond to treatment with taxane therapies, resistance is common. The study being published evaluated oral administration of VERU-111 in an orthotopic ovarian cancer model. Orally administered VERU-111 had a significant reduction in ovarian tumor growth and the animals receiving oral VERU-111 had no identifiable liver or spleen metastases. Likewise, the prognosis for pancreatic cancer is poor since pancreatic cancer usually does not cause recognizable symptoms in its early stages and the disease is typically not diagnosed until it has spread beyond the pancreas itself. The study being published evaluated oral administration of VERU-111 compared with paclitaxel, vinorelbine and colchicine in a pancreatic cancer model. Orally administered VERU-111 had significant impact on pancreatic tumor growth and mechanistically arrested the cell cycle and induced apoptotic pathways in this model.