EMU-116

EMU-116 (EMU-000116) is an orally bioavailable small-molecule antagonist of the chemokine receptor CXCR4, developed from a tetrahydroisoquinoline (TIQ) chemotype at Emory University as a best-in-class CXCR4 inhibitor for oncology and immuno-oncology applications.[1][5][11] By selectively blocking the CXCR4–CXCL12 axis, EMU-116 disrupts tumor-promoting chemokine signaling, mobilizes immune and myeloid cells (including neutrophils) from the bone marrow, and remodels the tumor microenvironment by increasing CD8+ T cells and reducing regulatory T cells, thereby enhancing antitumor immunity and potentiating combinations with agents such as VEGFR inhibitors (e.g., axitinib) and checkpoint/other systemic therapies.[1][5][11] Preclinical data indicate superior pharmacokinetic and drug-like properties versus the clinical CXCR4 antagonist mavorixafor (X4P-001), including improved human liver microsomal stability, permeability, solubility, and therapeutic index, together with strong oral efficacy in xenograft models of renal cell carcinoma and robust neutrophil mobilization at oral doses.[1][3][5]