A Potent and Selective Dual Inhibitor of AXL and MERTK Possesses Both Immunomodulatory and Tumor-Targeted Activity.

气体6 肿瘤微环境 CD47型 癌症 血管生成 生物 酪氨酸激酶 癌细胞 免疫检查点 医学 髓系白血病 免疫系统
作者
Jonathan Rios-Doria,Margaret F. Favata,Kerri Lasky,Patricia Feldman,Yvonne Lo,Gengjie Yang,Christina Stevens,Xiaoming Wen,Sarita Sehra,Kamna Katiyar,Ke Liu,Richard Wynn,Jennifer J. Harris,Min Ye,Susan M. Spitz,Xiaozhao Wang,Chunhong He,Yun-Long Li,Wenqing Yao,Maryanne B. Covington,Peggy Scherle,Holly Koblish
出处
期刊:Frontiers in Oncology [Frontiers Media]
卷期号:10: 598477- 被引量:4
标识
DOI:10.3389/fonc.2020.598477
摘要

TYRO3, AXL, and MERTK constitute the TAM family of receptor tyrosine kinases, which play important roles in tumor growth, survival, cell adhesion, as well as innate immunity, phagocytosis, and immune-suppressive activity. Therefore, targeting both AXL and MERTK kinases may directly impact tumor growth and relieve immunosuppression. We describe here the discovery of INCB081776, a potent and selective dual inhibitor of AXL and MERTK that is currently in phase 1 clinical trials. In cellular assays, INCB081776 effectively blocked autophosphorylation of AXL or MERTK with low nanomolar half maximal inhibitory concentration values in tumor cells and Ba/F3 cells transfected with constitutively active AXL or MERTK. INCB081776 inhibited activation of MERTK in primary human macrophages and partially reversed M2 macrophage-mediated suppression of T-cell proliferation, which was associated with increased interferon-γ production. In vivo, the antitumor activity of INCB081776 was enhanced in combination with checkpoint blockade in syngeneic models, and resulted in increased proliferation of intratumoral CD4+ and CD8+ T cells. Finally, antitumor activity of INCB081776 was observed in a subset of sarcoma patient-derived xenograft models, which was linked with inhibition of phospho-AKT. These data support the potential therapeutic utility of INCB081776 as an immunotherapeutic agent capable of both enhancing tumor immune surveillance and blocking tumor cell survival mechanisms.

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