PD-1 (camrelizumab) plus VEGFR2/PDGFR-β/c-Kit (famitinib)

Class

PD-1 immune checkpoint inhibitor combined with a multi-target receptor tyrosine kinase (anti-angiogenic) inhibitor

Pathway

Camrelizumab blocks the PD-1/PD-L1 immune checkpoint; famitinib inhibits VEGFR2/PDGFR-β/c-Kit-driven angiogenesis, normalizing tumor vasculature and enhancing T-cell infiltration to synergize with checkpoint blockade

This mechanism combines two complementary approaches to cancer treatment. The first component blocks PD-1, a checkpoint receptor on T cells that, when engaged by its ligand PD-L1, restrains T-cell activity and allows tumors to evade immune attack; blocking this interaction restores the capacity of T cells to recognize and destroy malignant cells. The second component inhibits several receptor tyrosine kinases—VEGFR2, PDGFR-β, and c-Kit—that drive formation of new blood vessels (angiogenesis) and support the disorganized, leaky vasculature typical of tumors. By inhibiting these receptors, blood vessels within the tumor become more normalized in structure and function, which improves oxygen delivery, reduces pressure that impedes cell movement, and facilitates infiltration of immune cells into the tumor. The rationale for pairing these mechanisms is that abnormal tumor vasculature and an immunosuppressive microenvironment reinforce one another; normalizing vessels can enhance T-cell trafficking into the tumor, thereby amplifying the effect of checkpoint blockade beyond what either approach achieves alone. This combined mechanism is broadly relevant across solid tumor types in which both vascular abnormality and immune exclusion limit response to single-agent immunotherapy, particularly cancers with limited baseline immune infiltration.