ArticleFrontiers in immunology2024
An Fc-modified monoclonal antibody as novel treatment option for pancreatic cancer.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Generation of an NG2 targeting bispecific antibody for the induction of T-cell immunity against melanoma.Journal of translational medicine · 2026Article
- Dual metabolic intervention nanoplatform co-delivering BAY-876 and L-cystine for Wilms tumor therapy via disulfidptosis-associated cytoskeletal collapse.Journal of nanobiotechnology · 2026Article
- Enhancing NK Cell Activity in Colorectal Cancer with an Fc-Optimized Antibody Targeting CD276 (B7-H3).ImmunoTargets and therapy · 2026Article
- Review
- Preclinical Evaluation of a B7-H3 Targeting Antibody Enhancing NK Cell-Mediated Cytotoxicity for Ovarian Cancer Treatment.ImmunoTargets and therapy · 2025Article
- Fc-optimized CD276 antibody enhances NK cell activation against non-small cell lung cancer.Frontiers in immunology · 2025Article
- B7 homolog 3 in pancreatic cancer.World journal of gastroenterology · 2024Review
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Pancreatic cancer is a highly lethal disease with limited treatment options. Hence, there is a considerable medical need for novel treatment strategies. Monoclonal antibodies (mAbs) have significantly improved cancer therapy, primarily due to their ability to stimulate antibody-dependent cellular cytotoxicity (ADCC), which plays a crucial role in their therapeutic efficacy. As a result, significant effort has been focused on improving this critical function by engineering mAbs with Fc regions that have increased affinity for the Fc receptor CD16 expressed on natural killer (NK) cells, the major cell population that mediates ADCC in humans. Here we report on the preclinical characterization of a mAb directed to the target antigen B7-H3 (CD276) containing an Fc part with the amino acid substitutions S239D/I332E to increase affinity for CD16 (B7-H3-SDIE) for the treatment of pancreatic cancer. B7-H3 (CD276) is highly expressed in many tumor entities, whereas expression on healthy tissues is more limited. Our findings confirm high expression of B7-H3 on pancreatic cancer cells. Furthermore, our study shows that B7-H3-SDIE effectively activates NK cells against pancreatic cancer cells in an antigen-dependent manner, as demonstrated by the analysis of NK cell activation, degranulation and cytokine release. The activation of NK cells resulted in significant tumor cell lysis in both short-term and long-term cytotoxicity assays. In conclusion, B7-H3-SDIE constitutes a promising agent for the treatment of pancreatic cancer.
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