On December 2, 2016 Surface Oncology, an immuno-oncology company developing next-generation immunotherapies that target the tumor microenvironment, reported that it will present preclinical data on its CD47 program at the 58th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting (Press release, Surface Oncology, DEC 2, 2016, View Source [SID1234516902]). The data demonstrate that SRF231, a fully human CD47 antibody, induces robust tumor cell phagocytosis and clearance, both alone and in combination with existing standard of care treatment.
Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:
Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing
Schedule Your 30 min Free Demo!
"These data highlight the strong anti-tumor activity of SRF231 in hematological disease models," said Vito Palombella, PhD, Chief Scientific Officer at Surface Oncology, "and further suggest that SRF231 has the potential to be the best-in-class CD47 antibody to help patients with a wide range of cancers."
CD47 is an important immune escape mechanism exploited by multiple tumor types, making it a target with broad therapeutic potential. CD47 acts as a macrophage checkpoint or "don’t eat me" signal that prevents cells from being eliminated by a macrophage-mediated process called phagocytosis.
The data presented at ASH (Free ASH Whitepaper) demonstrate that SRF231 enhances tumor cell phagocytosis alone and in combination with opsonizing antibodies (e.g., anti-CD20 Ab). SRF231 also leads to profound tumor growth inhibition in models of multiple myeloma and non-Hodgkin’s lymphoma.
Previously, Surface presented data at the Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper)’s annual meeting demonstrating that SRF231 binds with high affinity to CD47, stimulates phagocytosis of cancer cells in vitro, and has potent anti-tumor activity in multiple in vivo disease models. These data also demonstrate that SRF231 does not induce detectable hemagglutination or phagocytosis of red blood cells in vitro, a potentially important safety advantage. SRF231 is expected to enter clinical trials in 2017.