B-cell antigen receptor complex-associated protein subunit beta (CD79B)

B-cell antigen receptor complex-associated protein subunit beta (CD79b) is a transmembrane protein that forms a disulfide-linked heterodimer with CD79a, serving as the essential signaling component of the B-cell receptor (BCR) complex [UniProt, https://www.uniprot.org/uniprotkb/P40259/entry]. It contains an immunoreceptor tyrosine-based activation motif (ITAM) in its cytoplasmic domain, which is phosphorylated upon antigen binding to initiate downstream signaling pathways such as NF-κB and PI3K/AKT, crucial for B-cell development, activation, and survival [NIH, https://pmc.ncbi.nlm.nih.gov/articles/PMC10729845/]. CD79b expression is highly restricted to B cells and is maintained across most B-cell malignancies, making it an ideal therapeutic target [CUSABIO, https://www.cusabio.com/c-21144.html]. In certain cancers, such as the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL), mutations in CD79B lead to chronic active BCR signaling that promotes tumor cell proliferation and resistance to apoptosis [NIH, https://pmc.ncbi.nlm.nih.gov/articles/PMC10729845/]. The most prominent drug targeting this molecule is polatuzumab vedotin, an antibody-drug conjugate (ADC) that binds to CD79b, induces internalization, and releases a cytotoxic payload to kill the malignant cell [CUSABIO, https://www.cusabio.com/c-21144.html]. Other emerging therapies include bispecific T-cell engagers and CAR-T cells designed to specifically recognize CD79b-expressing cells [NIH, https://pmc.ncbi.nlm.nih.gov/articles/PMC10668551/].

Other names

CD79bB29IGBIg-betaB-cell-specific glycoprotein B29Immunoglobulin-associated B29 proteinAGM6

Antibody-drug conjugate (ADC) mediated delivery of cytotoxic agents; Inhibition of B-cell receptor (BCR) signaling pathways; T-cell mediated cytotoxicity via bispecific antibodies or CAR-T cells [CUSABIO, https://www.cusabio.com/c-21144.html; Gosset.ai, https://gosset.ai/targets/CD79B; NIH, https://pmc.ncbi.nlm.nih.gov/articles/PMC10668551/]