Complement component 1 q subcomponent receptor (CD93) (CD93)

Complement component 1 q subcomponent receptor, commonly known as CD93, is a 126-kDa Type I transmembrane glycoprotein belonging to the Group XIV C-type lectin family (UniProt: Q9NPY3) [1]. It is predominantly expressed on endothelial cells and myeloid lineages, including monocytes, macrophages, and dendritic cells, where it regulates vascular integrity, angiogenesis, and the clearance of apoptotic cells via efferocytosis (PubMed: 33432153) [2]. In the tumor microenvironment, CD93 is significantly upregulated in the vasculature and interacts with ligands such as IGFBP7 and Multimerin-2 to promote a pro-angiogenic and immunosuppressive state (PubMed: 28652405) [3]. Recent studies, particularly those utilizing specialized dendritic cell models like RENB-DC-11, have identified CD93 as an antigen-presentation co-receptor that modulates the priming and activation of T cells (Biocytogen Pharmaceuticals) [4]. Therapeutic targeting of CD93 with monoclonal antibodies, such as BCM001, is currently being explored to normalize tumor vessels and enhance the infiltration and activity of immune cells in solid tumors [4][5]. This approach aims to overcome resistance to traditional checkpoint inhibitors by addressing both vascular dysfunction and immune exclusion. Clinical and preclinical data suggest that CD93 inhibition can reprogram the tumor microenvironment toward a more immunostimulatory phenotype.

Other names

C1qRpC1qR(p)MXRA4AA4Ly68Cluster of differentiation 93

Monoclonal antibody-mediated inhibition of CD93 signaling to disrupt tumor angiogenesis and enhance T-cell infiltration.