REDWOOD CITY, Calif., Jan. 08, 2016 (GLOBE NEWSWIRE) -- OncoMed Pharmaceuticals Inc. (NASDAQ:OMED), a clinical-stage company developing novel anti-cancer stem cell and immuno-oncology therapeutics, today announced the publication of a manuscript in Cancer Research describing OncoMed's efforts to develop novel therapeutics against R-spondin (RSPO) targets and elucidating the link between expression of the RSPO cancer stem cell pathway and tumor growth. OncoMed is currently conducting a Phase 1a/b clinical trial of its anti-RSPO3 (OMP-131R10) antibody.
The article "Therapeutic Targeting of Tumor-Derived R-Spondin Attenuates beta-Catenin Signaling and Tumorigenesis in Multiple Cancer Types" (released online December 30, 2015) describes the generation of neutralizing monoclonal antibodies against RSPO-1, -2 or -3 and the successful use of these antibodies to treat diverse types of patient-derived xenografts, including colon, ovarian, pancreas and lung tumors. Of note, these anti-RSPO antibodies were effective in the tumor models regardless of whether the tumors overexpressed RSPO because of gene translocations or because of other tumor-intrinsic pathways. OncoMed is utilizing biomarker assays to prospectively screen patients for RSPO gene expression as part of its Phase 1a/b clinical program.
Mechanistically, the paper establishes a functional link between RSPO expression and tumor growth. Tumor-derived RSPO can activate beta-catenin, and antibody-mediated blocking of RSPO binding to its receptor potently inhibits tumor growth. This anti-tumor activity is associated with the modulation of beta-catenin and cancer stem cell pathways.
"R-spondins are emerging as an important cancer target. As key stimulators of beta-catenin activity in a variety of human tumor types, targeting the RSPO pathway may prove to be an effective approach to modulating this fundamental signaling axis," said John Lewicki, Ph.D., OncoMed's Chief Scientific Officer. "Our first anti-RSPO candidate is being studied in Phase 1a/b clinical trials with a strong biomarker hypothesis and we expect to establish a single-agent dose and treat biomarker-positive patients this year."
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