AZD4635, a novel adenosine A2A receptor antagonist, restores anti-tumor activity by preventing adenosine-mediated suppression of immune cells (AACR 2019)
By AstraZeneca | Apr 14, 2019
AACR Annual Meeting 2019
29 March – 3 April 2019
American Association for Cancer Research
AstraZeneca presented new data from preclinical studies with AZD4635, a next-generation immuno-oncology candidate, demonstrating its ability to restore the anti-tumor activity of dendritic cells (DCs) by preventing their adenosine-mediated immunosuppression. The new data were presented in a poster at the 2019 American Association for Cancer Research (AACR) Annual Meeting in Atlanta, USA (29 March to 3 April 2019).
Dendritic cells are a key component of the immune system that drive anti-tumor activity through the stimulation and promotion of tumor-specific T cell responses. The activity of DCs is suppressed in the presence of high levels of adenosine, which is part of a normal process preventing autoimmunity and is co-opted by tumors as an immune escape mechanism. The adenosine pathway is increasingly recognized as critical to tumor suppression and represents a new frontier within immuno-oncology.
AZD4635 is a potent and selective, orally available, small molecule adenosine 2A receptor (A2AR) antagonist discovered by Sosei Heptares and exclusively licensed to AstraZeneca in 2015.
The poster (abstract #LB-192) entitled “The A2AR antagonist AZD4635 prevents adenosine-mediated immunosuppression of CD103+ dendritic cells,” reported the following: