Complement decay-accelerating factor (CD55) (CD55)

Complement decay-accelerating factor (CD55), also known as DAF, is a membrane-bound glycoprotein that protects host cells from autologous complement-mediated damage by inhibiting C3 and C5 convertases [1, 3]. In many malignancies, including colorectal, ovarian, and gastric cancers, CD55 is significantly overexpressed, serving as a mechanism for immune evasion by preventing complement-dependent cytotoxicity [1, 5]. This overexpression makes CD55 a specific target for receptor-targeted therapies, such as the oncolytic RNA virus IVX037 [3, 6]. IVX037 is a bioselected, non-genetically modified picornavirus that utilizes its capsid to bind specifically to CD55 on tumor cells, leading to selective viral entry, replication, and subsequent cell lysis (oncolysis) [1, 7]. The resulting tumor destruction releases antigens and induces a pro-inflammatory response, characterized by the upregulation of CXCL10 and PD-L1, which can sensitize "cold" tumors to immune checkpoint inhibitors like sintilimab [1, 9, 10]. Clinical studies have demonstrated that targeting CD55 with IVX037 is generally well-tolerated and shows promising activity, particularly in tumors with KRAS or BRAF mutations that correlate with high CD55 expression [1, 13].

Other names

DAFComplement decay-accelerating factorCromer blood group antigenCD55 molecule

Viral capsid binding to CD55 facilitates selective tumor cell entry, replication, and oncolysis [1, 6].