| Code | CSB-RA733578MB1HU |
| Size | US$9799 |
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This recombinant monoclonal antibody is developed as a research-grade biosimilar to Enoblizumab, targeting CD276 (B7-H3), a member of the B7 family of immune checkpoint proteins. CD276 is a type I transmembrane glycoprotein that functions as an immunoregulatory molecule, modulating T-cell activation and immune responses. While its precise immunological role remains complex, CD276 is widely overexpressed across multiple solid tumors including non-small cell lung cancer, renal cell carcinoma, prostate cancer, and various other malignancies, where it correlates with poor prognosis and promotes tumor immune evasion. Its restricted expression in normal tissues makes it an attractive target for cancer immunotherapy research.
Enoblizumab is a humanized IgG1 monoclonal antibody designed to bind CD276 and has been investigated in clinical trials for advanced solid tumors. This biosimilar antibody serves as a valuable research tool for investigating CD276-mediated immune regulation, exploring tumor microenvironment interactions, and evaluating potential therapeutic strategies targeting this immune checkpoint molecule. It enables researchers to study CD276 biology and its role in cancer progression and immune suppression.
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Earlier studies found that B7H3 (also known as B7H3) promotes the activation of T cells. Chapoval et al. confirmed that in the presence of anti-CD3 antibodies, B7H3 can promote the proliferation of CD4 and CD8+ T cells and selectively promote the secretion of IFN-γ. And B7H3 transfection into tumor cells can enhance the killing ability of CTL. Further research found that only TLT-2 transgenic cells could bind to mouse B7H3 with high affinity, and TLT-2 was determined to be the receptor molecule of B7H3. Moreover, Hashiguchi et al. confirmed that the B7H3-TLT-2 pathway enhanced T cell activation. However, Leitner et al. did not find the specific binding of B7H3 to TLT-2 by flow cytometry, therefore, the exact receptor molecule of B7H3 is still unclear.
On the other hand, studies have found that B7H3 can also suppress T-cell immune responses. Some studies have shown that B7H3 can inhibit human and mouse T cells by activating or inhibiting NFTA (nuclear factor for activated T cells), NF-KB (nuclear factor kB) and AP-1 (activator protein-1) pathways. activation. In addition, results have demonstrated that B7H3 may inhibit T cell immune responses by inhibiting the activity of Thl. The study of Leiner et al. also found that B7H3 can down-regulate the secretion of IL-2 in T cells to inhibit the activity of T cells.