ASTX660, an antagonist of cIAP1/2 and XIAP, increases antigen processing machinery and can enhance radiation-induced immunogenic cell death in preclinical models of head and neck cancer.

While there were no significant differences in intratumoral CD11b + CD11c + dendritic cell numbers among treatment groups, expression of co-stimulatory molecule CD80 was significantly increased in the XRT group and approached significance in the ASTX660 + XRT group ( p = .058, Suppl.

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In comparison, cells killed by ASTX660 + XRT induced an even greater immune response with rejection of tumor formation in 72% (8/11) of mice, though the increase in % tumor-free mice did not reach statistical significance ( p = .24).

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The number of CD8 + T lymphocytes increased to a significant degree in the draining lymph nodes of animals treated with XRT alone, and to a near-significant degree in animals treated with combination therapy ( Figure 3(c )).

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