CAMBRIDGE, Mass., April 09, 2021 (GLOBE NEWSWIRE) -- Surface Oncology (NASDAQ:SURF), a clinical-stage immuno-oncology company developing next-generation immunotherapies that target the tumor microenvironment, will present preclinical findings supporting the company's lead product programs, SRF388 (targeting IL-27) and SRF617 (targeting CD39). These data will be presented as part of the American Association for Cancer Research (AACR) 2021 Annual Meeting, which is being held virtually April 10-15 and May 17-21, 2021.
"These findings further support the biological rationale that both of our lead product candidates, SRF388 and SRF617, promote increased proinflammatory activity within the tumor microenvironment in the hopes of ultimately providing novel treatment options to patients with cancer," said Vito Palombella, chief scientific officer. "We look forward to sharing data from the ongoing Phase 1 clinical trials for both programs this June."
The e-poster website will be launched at 8:30 a.m. ET on Saturday, April 10, and will remain available for viewing through Monday, June 21. The two e-posters will also be viewable on the Surface Oncology website.
Presentation Type: e-poster (Abstract: 1802)
Title: CD39 inhibition shapes the transcriptional landscape of myeloid cells and induces proinflammatory states in the CT26 syngeneic tumor model
Lead Authors: Devapregasan Moodley, Ph.D. and Mayra Carneiro
Summary:
- SRF617 is a potent inhibitor of CD39 enzymatic activity both in vitro and in vivo.
- Increased activity of CD39 results in significant reductions in extracellular ATP and subsequent accumulation of adenosine, contributing to tumor immune escape, induction of angiogenesis and metastatic progression.
- Immunological mechanisms associated with CD39 blockade reveal major changes to immunocyte transcriptional landscapes, including upregulation of several proinflammatory genes.
- CD39 inhibition predominantly shaped the transcriptional landscape of myeloid cells and dendritic cells, and generally induced proinflammatory conditions.
- These findings indicate that CD39 blockade induces proinflammatory responses, supporting future clinical studies of SRF617 for treating patients with cancer.
Presentation Type: e-poster (Abstract: 1607)
Title: IL-27 signaling serves as an immunological checkpoint for NK cells to promote hepatocellular carcinoma in multiple murine models
Lead Author: Turan Aghayev
Summary:
- IL-27 signaling suppresses natural killer (NK) cells within the tumor microenvironment, promoting hepatocellular carcinoma (HCC) development in vivo.
- Elevated IL-27RA expression in cancer tissue and elevated EBI3 serum levels are associated with poor prognosis in patients with HCC.
- Inhibiting IL-27 signaling leads to tumor growth inhibition and suppressed HCC development in a non-alcoholic steatohepatitis (NASH)-driven HCC model with concomitant enhancement of NK cell activity.
- These findings indicate that IL-27 blockade regulates NK cell-mediated control of HCC and is a promising therapeutic target in liver cancer.
Contacts:
Investors
Matt Lane
[email protected]
617-901-7698
Media
Chris Railey
[email protected]
617-460-3579
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