CD276 Specific Neutra™ Antibody Products

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CD276, alias B7-H3, a member of the immunoglobulin superfamily, is implicated in the regulation of T-cell-mediated immune responses. While the gene transcript is broadly expressed in normal tissues and solid tumors, the protein exhibits selective expression in tumor tissues. CD276 suppresses both T cell proliferation and activation in non-malignant tissues, which predominantly plays an inhibitory role in adaptive immunity. Conversely, in malignant tissues, CD276 serves as an immune checkpoint molecule, hindering tumor antigen-specific immune responses. Additionally, CD276 exhibits non-immunological pro-tumorigenic functions, including the promotion of invasion, chemoresistance, migration, angiogenesis, and more.

Its Gene ID: 80381, UniProtKB ID: Q5ZPR3, and OMIM ID: 605715.

CD276 Drives Tumor-Promoting Pathways

In tumor cells, CD276 is implicated in the regulation of apoptosis, cell autophagy, invasion, cell differentiation, and cell cycle. It triggers elevated levels of ROS and HIF-1a by suppressing Nrf2, leading to reduced expression of SOD1, SOD2, and PRX3. This, in turn, promotes aerobic glycolysis in cancer cells, fostering tumor growth. CD276 additionally enhances the expression levels of its downstream signaling molecules and key enzymes in the glycolysis pathway associated with HIF-1a.

Fig.1 CD276 pathways. (Liu, et al., 2021) Fig.1 CD276 (B7-H3) is involved in several pathways that result in tumor growth.¹

Inhibitory Treatment with CD276 Antibody

Anti-CD276 antibodies have undergone development and animal testing, and are currently in clinical trials for immunotherapy. Strategies for human cancer immunotherapy targeting CD276 encompass CD276 blockade using monoclonal antibodies (mAbs), CD276-specific antibody-dependent cell-mediated cytotoxicity (ADCC), CD3/CD276 bispecific antibodies, small molecule inhibitors, engineered chimeric antigen receptor (CAR) T cells, and combination therapies with other modalities.

CD276 as a Target in Cancer Immunotherapy Strategies

Despite substantial evidence highlighting the tumorigenic role of B7-H3, there is currently no FDA-approved therapeutic targeting this molecule. The absence of a known receptor for B7-H3 poses challenges in developing pharmacological interventions. Various anti-B7-H3 strategies, employing diverse mechanisms such as mAbs, antibody-dependent cell-mediated cytotoxicity (ADCC), CAR-T therapy, and Antibody Drug Conjugate (ADC), have been investigated.

Fig.2 CD276 function in cancer immunotherapy. (Getu, et al., 2023) Fig.2 CD276 (B7-H3) as a target in cancer immunotherapy strategies.²

Targeting Over-Expressed CD276 Cells with Anti-CD276 Antibody Inhibits Tumor Growth

CD276 is expressed in a broad spectrum of human tumor cells. CD276Bi-Ab, binding to activated T-cells (ATC), markedly enhances the production of IFN-g, TNF-a, and IL-2. Elevated cytotoxicity mediated by CD276bi-Ab is evident in diverse human tumor cell lines and primary cells from breast and lung cancer patients. In vivo experiments demonstrate that, in comparison to regular activated T cells, CD276Bi-Ab-equipped ATCs significantly restrain tumor growth and extend survival. CD276-armed ATC emerges as a promising approach for treating CD276-positive cancer patients, yielding clinically meaningful antitumor effects.

Creative Biolabs offers a diverse selection of more than 30 anti-CD276 antibody products, engineered using recombinant techniques. Additionally, customization options are available for crafting CD276-based neutralizing or blocking antibodies to meet specific needs.

REFERENCES

Liu, Shengzhuo, et al. "The role of CD276 in cancers." Frontiers in Oncology 11 (2021): 654684.
Getu, Ayechew Adera, et al. "New frontiers in immune checkpoint B7-H3 (CD276) research and drug development." Molecular Cancer 22.1 (2023): 43.

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