The research, conducted by Antengene in collaboration with the Department of Hematology at Peking University Third Hospital, identifies a critical resistance mechanism: selinexor treatment triggers an upregulation of CD73 in tumors, which fosters an immunosuppressive environment. By blocking CD73-dependent adenosine synthesis, ATG-037 disrupts this feedback loop, allowing for a more potent immune response.

In a J558-inoculated BALB/c mouse model, the combination therapy achieved a tumor growth inhibition rate of 62%, markedly outperforming both ATG-037 monotherapy at 31% and selinexor alone at 43%. Single-cell RNA sequencing confirmed that this synergy relies on the CD80–CD28 signaling pathway, which enhances the infiltration and activation of CD8+ T cells within tumor tissue. Co-culture experiments further validated these findings, showing elevated levels of Granzyme B and IFN-γ, suggesting that the dual approach successfully reinvigorates the body's natural cancer-killing mechanisms.