Cabiralizumab (FPA 008) is an anti-CSF1R monoclonal antibody (mAb) that enhances T cell infiltration and strengthens antitumor immune responses. Cabiralizumab prevents osteoclast activation, thereby inhibiting bone destruction, and is employed in rheumatoid arthritis (RA) research. Additionally, Cabiralizumab has been investigated in combination with Nivolumab in lung cancer studies, highlighting its role in immune-oncology.

After 7 days of in vitro treatment, Cabiralizumab disrupts circulating tumor cell (CTC) cluster formation and promotes CTC apoptosis in unclassified samples of portal vein blood monocytes (PortalBMC) from pancreatic ductal adenocarcinoma (PDAC). Simultaneously, it reactivates T cells (CD3⁺CD25⁺CTLA4⁻PD-L1⁻) in PDAC's PortalBMC and increases IFNγ production. [4]

Methods: Cabiralizumab (200, 400 μg, twice weekly for 5 doses) was administered intraperitoneally to YUMMER1.7 and YUMM1.7 murine melanoma models to evaluate its effects on tumor growth and survival. Single-cell RNA sequencing (scRNA-seq) was employed to analyze changes in macrophage subsets within tumor tissues.
Results: High-dose Cabiralizumab treatment accelerated tumor growth and shortened survival, increased the abundance of CD163+ cells (immunosuppressive TAMs) in tumors, elevated the proportion of immunosuppressive TAM-II populations, and upregulated chemokine levels (e.g., CXCL2 and CCL3) that recruit immunosuppressive cells. [3]