B7-H3 Antibody
- Known as:
- B7-H3 Antibody
- Catalog number:
- amm00012
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- B7-H3 Antibody
Related genes to: B7-H3 Antibody
- Gene:
- CD276 NIH gene
- Name:
- CD276 molecule
- Previous symbol:
- -
- Synonyms:
- B7-H3, B7H3, B7RP-2
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-04
- Date modifiied:
- 2016-10-05
Related products to: B7-H3 Antibody
Related articles to: B7-H3 Antibody
- Pancreatic cancer remains one of the most lethal malignancies worldwide, with pancreatic ductal adenocarcinoma (PDAC) accounting for the majority of cases and exhibiting a persistently poor prognosis. Although chimeric antigen receptor T (CAR-T) cell therapy has achieved remarkable success in hematological malignancies, its therapeutic efficacy in pancreatic cancer remains limited. This review summarizes recent advances in CAR-T cell therapy for pancreatic cancer, with a focus on representative tumor-associated targets, including mesothelin (MSLN), claudin 18.2 (CLDN18.2), prostate stem cell antigen (PSCA), CD155, CD276, growth arrest-specific protein 6 (GAS6), and glypican-1 (GPC1), while also highlighting emerging next-generation CAR-T engineering strategies, including nanobody-based antigen recognition, cytokine-armored CAR-T cells, allogeneic CAR-NKT platforms, dual-target and logic-gated CAR systems, and innovative delivery approaches. Current preclinical and early clinical evidence suggests that several targets, particularly MSLN and CLDN18.2, show promising antitumor activity; however, durable clinical responses remain difficult to achieve. The major barriers include the dense desmoplastic stroma, highly immunosuppressive tumor microenvironment (TME), antigen heterogeneity, antigen loss, limited CAR-T persistence and expansion, T-cell exhaustion, and on-target, off-tumor toxicity. To overcome these obstacles, emerging strategies have focused on remodeling the TME, engineering armored or dual-target CAR-T cells, developing logic-gated CAR systems, improving CAR-T persistence, and optimizing delivery approaches through nanomaterials, oncolytic viruses, in situ CAR-T generation, alternative immune-cell carriers, and locoregional administration. Overall, CAR-T therapy for pancreatic cancer is progressing from preclinical exploration toward clinical translation. Future success will likely depend on rational target selection, multi-dimensional TME modulation, advanced CAR engineering, precision delivery, and biomarker-guided patient stratification. - Source: PubMed
Publication date: 2026/08/07
Xiao Ru-YanJiang Ye-FanZhao WeiWang Qing-QingHuang You-QingLi Xin-YuXiao Yu-JieYao HaoDai Rui-Wu - Ewing sarcoma is a fusion-driven malignancy with low tumor mutational burden, making recurrent tumor-associated antigens with favorable tumor-to-normal contrast central to immunotherapy development. We converted the Deng -defined 32-gene Ewing Sarcoma Specific Signature (ESS32) into a practical target atlas by integrating tumor RNA expression with normal-tissue context, protein evidence, subcellular localization, and therapeutic accessibility. - Source: PubMed
Goldman Corey - Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal cell carcinoma, characterized by dysregulated lipid metabolism and therapy resistance, leading to a poorer prognosis than other subtypes. This study investigates the role of the immune checkpoint molecule CD276 in lipid metabolic reprogramming and the regulation of ferroptosis in ccRCC. Clinical sample analysis, in vitro experiments, and animal models revealed that CD276 is significantly overexpressed in ccRCC and positively correlated with an unfavorable prognosis. Mechanistically, CD276 activates the transcription factor sterol regulatory element-binding protein 1 (SREBP1), upregulates the expression of fatty acid synthase (FASN), promotes de novo fatty acid synthesis, and drives lipid accumulation. Concurrently, CD276-mediated lipid metabolic reprogramming suppresses ferroptosis in ccRCC cells by increasing reduced glutathione levels and enhancing glutathione peroxidase 4 activity. In vivo experiments confirmed that inhibiting CD276 significantly suppresses tumor growth and enhances the efficacy of ferroptosis inducers. This study reveals the pivotal role of the CD276-SREBP1-FASN axis in regulating lipid metabolism and ferroptosis in ccRCC, providing a theoretical basis for CD276-targeted therapy combined with ferroptosis induction as a treatment strategy for ccRCC. - Source: PubMed
Publication date: 2026/08/31
Zhang ZhiYuZhang FanYu YanHangZhang ChuanAoOuYang Jun - B7-H3-targeted antibody-drug conjugates (B7-H3-targeted ADCs) have shown promising antitumor effects in patients with previously treated small cell lung cancer (SCLC), yet the available evidence on their efficacy and safety has not been systematically synthesized. This study aimed to systematically evaluate the efficacy and safety of B7-H3-targeted ADCs and contextualize their clinical outcomes against standard-dose intravenous topotecan. - Source: PubMed
Publication date: 2026/08/13
Wang JiahuiJiang HongqinNiu JunziLiu LixiaWu YijunShi JianlinLiu LiyaYin ShouyanFeng ChunZhang LeiYang MeiYi Zihan - Clear cell renal cell carcinoma (ccRCC) is frequently vascular and immune-infiltrated, yet durable responses to immune checkpoint blockade remain limited. This suggests that immune resistance may reflect tumor microenvironmental organization and mechanotransduction state rather than immune infiltration alone. We aimed to determine whether matrix reorganization and branch-specific integrin mechanosensing define immune-regulatory states in ccRCC, with particular attention to adenosine-associated immune resistance. - Source: PubMed
Publication date: 2026/08/02
Karaca CanerArayici Mehmet EminSemiz Hüseyin SalihEllidokuz HulyaBasbinar Yasemin