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news.Tara Immuno-Oncology has acquired licenses from City of Hope for the development of p53MVA (modified vaccinia ankara) and a Salmonella-based therapy targeting Indoleamine 2,3-Dioxygenase (shIDO-ST), both for multiple oncology indication.
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Both technologies originate from the pioneering work of Don J. Diamond, Ph.D., chair of the Department of Experimental Therapeutics at City of Hope, an independent biomedical research institution and cancer treatment center. Tara I-O will pay City of Hope upfront and milestone payments in excess of $10 million, in addition to commercial royalties for the exclusive licenses.
Tara Immuno-Oncology founder and CEO Dhesh Govender said: "Our mission at Tara Immuno-Oncology is to utilize novel therapies to harness the body’s immune system to treat and potentially cure cancer patients.
"We recognized the thoughtful approach and hard work of Don Diamond and his team of scientists to advance both p53MVA and shIDO-ST as novel immuno-oncology assets. We are very encouraged by the compelling data and responses from patients thus far and look forward to working with City of Hope to rapidly advance both therapies."
City of Hope director of the office of technology licensing George Megaw said: "City of Hope believes Tara I-O’s development expertise uniquely positions it to advance both the p53MVA and the shIDO-ST technology, ultimately providing more effective treatments for cancer patients here and around the world."
About p53MVA:
TP53 mutations are present in the majority of solid tumors, resulting in the accumulation of mutant p53 protein. In contrast, the concentration of normal p53 in healthy cells is low, making p53 an attractive cancer target with potentially wide therapeutic applications.
A Phase 1 trial in patients with refractory gastrointestinal malignancies was completed in 2014 and published. p53MVA immunization was well-tolerated at both doses, with no adverse events above grade 2. CD4+ and CD8+ T cells showing enhanced recognition of a p53 overlapping peptide library were detectable after the first immunization, particularly in the CD8+ T-cell compartment (P=0.03).
The frequency of PD1+ T cells detectable in patients’ peripheral blood mononuclear cells (PBMC) was significantly higher than in healthy controls.
Furthermore, the frequency of PD1+ CD8+ T cells showed an inverse correlation with the peak CD8+ p53 response (P=0.02) and antibody blockade of PD1 in vitro increased the p53 immune responses detected after the second or third immunizations. Induction of strong T-cell and antibody responses to the MVA backbone were also apparent.
There are 2 ongoing clinical trials: one in combination with PD-1 blockade antibody in multiple indications (NCT02432963) and another in combination with gemcitabine for refractory ovarian patients (NCT02275039).