Abstract| Volume 92, SUPPLEMENT 1, S14-S15, March 2018

AB928, a dual antagonist of the A2aR and A2bR adenosine receptors, leads to greater immune activation and reduced tumor growth when combined with chemotherapy

      Background: In the tumor micro-environment, extracellular adenosine (ADO) suppresses immune responses through activation of the adenosine receptors A2aR and A2bR. ADO is generated by the consecutive action of two ectonucleotidases CD39 (ATP→AMP) and CD73 (AMP→ADO). Treatment of cancer cells with platinum-based and anthracycline chemotherapy has been shown to induce immunogenic cell death (ICD), characterized by increased extracellular ATP levels, and upregulation of CD39 and CD73, leading to the enhanced generation of adenosine. Here we describe the effects of AB928 plus ICD-inducing chemotherapy in mouse tumor models, as well as the relationship between plasma levels of the drug, receptor coverage in peripheral blood, tumor growth and anti-tumor immune response.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to European Journal of Cancer
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect