• Extracellular adenosine in the TME may limit antitumor activity of T cells and myeloid cells through A2AR-mediated cAMP signaling in the cells.1,2
  • A2BR, having lower affinity to adenosine compared to A2AR, is also involved in immune suppression, tumor proliferation, tumor angiogenesis, tumor cell invasion, and metastasis in adenosine-high TME, whereas A2BR acts complementary or compensatory to A2AR.3,4
  • Dual A2AR/A2BR antagonism is expected to limit adenosine-driven immuno-suppression/tumor promotion at the receptor level regardless of the mechanism of adenosine accumulation.
  • M1069 is an investigational small molecule, dual adenosine receptor antagonist. M1069 is thought to block immunosuppressive signaling through the A2AR/A2BR adenosine receptors, thus enhancing antitumor immune activity.



Investigational compounds are not approved by any health authority. Safety and efficacy have not been established.


A2A/A2B, A2A and A2B receptors; AMP, adenosine monophosphate; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; PD-L1, programmed death-ligand 1; TIGIT, T-cell immunoglobulin; TME, tumor microenvironment.


  1. Leone RD, Emens LA. Targeting adenosine for cancer immunotherapy. J Immunother Cancer. 2018;6(1):57. 
  2. Augustin RC, Leone RD, Naing A, et al. Next steps for clinical translation of adenosine pathway inhibition in cancer immunotherapy. J Immunother Cancer. 2022;10(2):e004089.
  3. Novitskiy SV, Ryzhov S, Zaynagetdinov R, et al. Adenosine receptors in regulation of dendritic cell differentiation and function. Blood. 2008;112(5):1822-1831. 
  4. Ryzhov S, Novitskiy SV, Zaynagetdinov R, et al. Host A(2B) adenosine receptors promote carcinoma growth. Neoplasia. 2008;10(9):987-995.