Anti-Human CD47 antibody ( Lem

Lemzoparlimab（来佐利单抗、TJ011133) 是一种差异化靶向 CD47 的人源化抗体，具有抗肿瘤活性，可用于研究髓系白血病。

Lemzoparlimab (TJ011133) is a differentiated anti-CD47 humanized antibody with anti-tumor activity, used in the study of myeloid leukemia.lemzoparlimab
A human monoclonal antibody targeting the human cell surface antigen CD47, with potential phagocytosis-inducing and antineoplastic activities. Upon administration, lemzoparlimab preferentially binds to a unique epitope of CD47 on tumor cells. This blocks the interaction of CD47 with signal regulatory protein alpha (SIRPalpha), an inhibitory protein expressed on macrophages and dendritic cells (DCs), which prevents CD47/SIRPalpha-mediated signaling and abrogates the CD47/SIRPalpha-mediated inhibition of phagocytosis. This induces pro-phagocytic signaling mediated by the binding of calreticulin (CRT), which is specifically expressed on the surface of tumor cells, to low-density lipoprotein (LDL) receptor-related protein (LRP), expressed on macrophages, which results in macrophage activation and the specific phagocytosis of tumor cells. Additionally, blocking CD47 signaling activates an anti-tumor T-lymphocyte immune response and T-cell-mediated killing of CD47-expressing tumor cells. CD47, also called integrin-associated protein (IAP), is a tumor-associated antigen (TAA) expressed on normal, healthy hematopoietic stem cells (HSCs) and overexpressed on the surface of a variety of cancer cells. Expression of CD47, and its interaction with SIRPalpha, leads to the inhibition of macrophage activation and protects cancer cells from phagocytosis, which allows cancer cells to proliferate. TJC4, compared to other anti-CD47 monoclonal antibodies, is designed to minimize inherent binding to normal red blood cells (RBCs), which may results in a more advantageous hematologic safety profile.
anti-CD47 monoclonal antibody TJC4
TJ 011133
TJ-011133
TJC4

CD47 is overexpressed in various types of cancers and it can directly bind with SIRPα, which is mainly located on macrophages. The binding of CD47-SIRPα transmits a “don't eat me” signal, which can prevent cancer cells from immune clearance. In this case, the comprehensive understandings of the regulation of CD47 in cancer cells are essential for further developments. In this review, based on the current reports, we summarized that CD47 expression could be regulated by cytokines, oncogenes, microRNAs and enzymes in cancer cells. Likewise, CD47 expression could be regulated at the transcriptional level, post-transcriptional level, post-translational modification level, etc. However, further studies are required to determine other factors that regulate CD47 expression.

•Cytokines, oncogenes, microRNAs and enzymes regulate CD47 expression in cancer.

•CD47 expression could be regulated at the transcriptional, post-transcriptional and post-translational modification level.

•Further studies are required to determine other factors that regulate CD47 expression.