Tumor Cells Recruit an Immunosuppressive “Cloak” that Hides them from the Adaptive Immune System and Initiates Metastasis

Tumors secrete chemo-attractive proteins, or chemokines, that bind to the chemokine receptors CXCR1 and CXCR2 on the surface of neutrophils and myeloid-derived-suppressor-cells (together “myeloid cells”).  Chemokine-receptor binding recruits these myeloid cells to the tumor microenvironment, creating an immunosuppressive inflammatory “cloak” that hides the tumor from killing by T cells and natural killer cells (“effector cells”) of the adaptive immune system. Chemokine receptors CXCR1 and CXCR2 on MDSCs and tumor cells additionally drive tumor metastasis and resistance to chemotherapeutic and immunologic therapies through other mechanisms.

SX-682 Abrogates the Tumor Immunosuppressive Microenvironment

SX-682 is a potent small-molecule dual-inhibitor of CXCR1 and CXCR2, chemokine receptors pivotal to myeloid cell suppression of cancer surveillance by the adaptive immune system.  By blocking the CXCR1/2 pathway, SX-682 inactivates immunosuppressive myeloid cells, thereby cutting off “at the source” dozens of downstream pro-tumor mechanisms mediated by these cells.  The inactivation of suppressive myeloid cells liberates effector cells to kill and eliminate cancer cells.

CXCR1/2 Control Two Major Arms of Pro-Tumor Microenvironment:
(1) Immunosuppressive Shield and (2) Metastasis/Resistance

SX-682 is the only therapeutic in development for oncology that blocks all parts of the CXCR1/2 signaling axis.

In collaborations with a host of top academic collaborators, SX-682 has been validated in numerous tumor models, where it exhibits single-agent activity, synergizes with checkpoint inhibitors, and blocks metastasis.

SX-682 Clinical Program

SX-682 is being investigated in Phase 1 and Phase 2 trials in various clinical oncology indications.