Immune checkpoint inhibitors have revolutionized the treatment of cancer over the last decade, allowing a subset of patients to have sustained treatment responses, and some advanced cancers were even made “curable”. Despite the increasing success, a substantial number of patients do not benefit from checkpoint inhibitor immunotherapy. Their tumors are either resistant in the beginning or develop resistance after initial response. Resistance to checkpoint inhibitors may occur due to various factors within the tumor cells or the tumor microenvironment (TME).

Emerging evidence indicates that myeloid cells with regulatory activity in TME are key players in limiting host antitumor immunity and reducing the efficacy of immunotherapies. AXL, a member of the TAM receptor kinase family, is expressed in both tumor cells and immune cells (e.g. myeloid cells) in the tumor microenvironment. Due to its pro-oncogenic and immune-inhibitory features, AXL is a promising target for cancer treatment and its inhibition may enhance checkpoint inhibitor therapy.


AB-329 is a potent and selective AXL inhibitor potentially to be used in combination with other therapeutic agents to overcome resistance in multiple solid tumors and hematological cancers. The candidate has demonstrated a favorable safety profile in Phase 1 studies. We plan to evaluate AB-329 in combination with checkpoint inhibitors or chemotherapy in NSCLC and other solid tumors.