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
- Malignant peripheral nerve sheath tumor (MPNST) carries the highest excess mortality of the cancers associated with neurofibromatosis Type 1, and usually arises from a neurofibroma. We asked whether the transcriptomic differences that distinguish MPNST from neurofibroma reproduce across independent cohorts, and whether a compact score derived from them transports between platforms. We meta-analyzed five public discovery cohorts of primary nerve-sheath tissue (113 MPNST, 79 neurofibromas; 3 platforms) and held out a sixth, independently generated cohort. Neurofibroma and MPNST tissue differed at 1489 genes in two opposing themes: up-regulated mitotic machinery (TOP2A, EZH2, AURKA) and loss of Schwann-cell identity (the transcription factors SOX10 and EGR2, and the myelin genes PMP2 and MPZ). These differences were reproducible. Among the significant genes assayed in all five cohorts, almost all changed in the same direction in everyone, and 93.3% of those detectable in the held-out cohort agreed in direction. Leave-one-cohort-out re-derivation of the pipeline gave a mean AUC of 0.90 across five folds (per-fold 0.84 to 0.97). CD276 (B7-H3) was selectively up-regulated, whereas CD274 and PDCD1LG2 were not. The myelin marker PMP2, a readout chosen retrospectively after the held-out results were known, separated MPNST from neurofibroma in that cohort but left atypical and conventional neurofibromas unseparated (AUC 0.67, p = 0.10). A program score derived without the discovery cohort carrying survival data was associated with shorter survival there, an exploratory single-cohort association. The composition of a compact score varied with platform and preprocessing, so no fixed single-sample classifier is warranted. - Source: PubMed
Jin QuanyuGao ZhenxuanZhang ZeKong ChenchenLiu JiaxinAbudurezhake AermanKou LeiCai ShuguangYang WenqiangWang QiLi ZhitaoZhang Li - B7-H3/CD276 is an emerging immunotherapy target in cancers. However, limited knowledge of B7-H3 signaling and its role in modulating the tumor microenvironment hinders the clinical application of B7-H3-targeting therapy. Here, we report that B7-H3 plays dual roles in regulating myeloid-derived suppressor cells (MDSCs) and cancer-associated fibroblasts (CAFs), thereby promoting tumor progression and therapy resistance, respectively. We comprehensively characterized a non-canonical function of B7-H3 that triggers MAPK signaling in monocytic MDSCs and induces cellular senescence. The senescent monocytic M-MDSCs secreted chemokines to recruit immunosuppressive granulocytic MDSCs. Genetic deletion or pharmacological inhibition of B7-H3/Cd276 reduced Gr-MDSCs and delayed tumor progression. Nevertheless, the secretory factor SPINK1 derived from MDSCs compensatorily activates EGFR/MEK/ERK signaling in CAFs and promotes their extracellular matrix remodeling features, dampening B7-H3-targeting immunotherapy. Combining the B7-H3 monoclonal antibody with the FDA-approved MEK inhibitor trametinib showed durable anti-tumor effects in preclinical models of castration-resistant prostate cancer by fully attenuating immunosuppressive mechanisms. - Source: PubMed
Publication date: 2026/09/18
Shi WeiXu PingGu QianlinFan ZhenLiang XinWang YinZhao YuehuiMeng ChenlingLeo JavierKim Justin JTeng HongqiZhang JieChen FeiyuChen YangNavin Nicholas EZhao Di - Chimeric antigen receptor (CAR) T cell therapy for acute myeloid leukemia (AML) faces critical challenges, including severe on-target off-tumor toxicities, antigen heterogeneity, and primary immune evasion mechanisms. To address these limitations, we previously developed an adapter CAR (AdCAR) platform that enables transient and combinatorial targeting to improve the safety and efficacy of CAR-T-cell therapy in AML. In this study, we further optimized the AdCAR system by investigating the role of immune checkpoint receptors (ICRs), particularly PD-1, CD96, LAG-3, TIM-3, and TIGIT, as well as the immunomodulatory molecule CD276, in suppressing AdCAR-T-cell function. Using multiparametric flow cytometry, we analyzed the expression of immune checkpoint ligands (ICLs) across multiple cancer entities, including three well-characterized AML cell lines, primary AML bone marrow samples, and healthy bone marrow as a reference. We then examined the inducibility of ICLs on AML cells after AdCAR-T-cell engagement. To evaluate the functional impact of immune checkpoint inhibition (ICI), we generated AdCAR-T-cells with CRISPR/Cas9-mediated knockouts (KOs) of PD-1, CD96, CD276, LAG-3, TIM-3, or TIGIT, and analyzed their cytotoxic potential in vitro. In our setting, PD-1 disruption did not significantly enhance AdCAR-T cytotoxicity against MOLM-13 wildtype, while TIGIT KO significantly enhanced AdCAR-T cytotoxicity specifically across five leukemia- and lymphoma-cell lines. Notably, pharmacological PD-1 blockade resulted in greater cytotoxicity than PD-1 gene disruption, whereas TIGIT blockade showed comparable effects to TIGIT KO. Our study identified TIGIT KO as a potent enhancer of AdCAR-T-cell function and supports ICR gene disruption as a promising approach to improve therapeutic efficacy while reducing the systemic toxicities commonly associated with ICI therapy. - Source: PubMed
Publication date: 2026/09/17
Mast Anna-SophiaAtar DanielRuoff LaraScheuermann SophiaKristmann BeateLang PeterSeitz Christian MartinSchlegel Patrick - Bispecific antibody-drug conjugates (BsADCs) represent a promising strategy to enhance tumor selectivity and overcome the limitations of monospecific ADCs. Here, we report the preclinical development of ABL206 (NEOK001), a novel BsADC targeting B7-H3 and ROR1, which are frequently co-expressed in various solid tumors. ABL206 was engineered in a 2 + 2 format and site-specifically conjugated with tavatecan, an exatecan-based linker-payload, utilizing GlycoConnect® technology to yield a highly homogeneous molecule with a drug-to-antibody ratio (DAR) of 4. , ABL206 demonstrated specific dual antigen binding, internalization, potent target-dependent cytotoxicity and a bystander killing effect. , ABL206 induced superior tumor regression, outperforming exact-matched monospecific ADCs at equimolar doses. Across 38 patient-derived xenograft (PDX) models spanning nine tumor types, ABL206 demonstrated broad translational potential with strong tumor regression. ABL206 consistently outperformed clinical-stage benchmark monospecific ADCs, ifinatamab deruxtecan (I-DXd) and zilovertamab vedotin, and effectively induced regression in I-DXd-pretreated regrowing tumors. Furthermore, ABL206 exhibited excellent plasma stability, a robust pharmacokinetic profile in rodents and non-human primates, and a favorable safety profile with the highest non-severely toxic dose (HNSTD) of 60 mg/kg in cynomolgus monkeys. Collectively, these data provide a comprehensive preclinical proof-of-concept for ABL206, supporting its advancement into a Phase 1 clinical trial for patients with advanced solid tumors (NCT07612176). - Source: PubMed
Publication date: 2026/09/12
Kwon Jung ALee SuyounKim JuheeYoo Byeong MinPark Hyeon JiRyu IlhwanKim JunyoungEom JaeHyunSon Yong-GyuYeom DonghoonSung ByungjeYoo MyeonghanSeo ArimYoo JiseonPark Jin YoungJung JinwonAhn JinhyungYou Weon-KyooLee Sang HoonKo Min Ji - HMGA1 is a chromatin-associated oncogenic factor implicated in tumor progression, epithelial-mesenchymal transition (EMT), stemness, and metastasis. However, its pan-cancer expression and prognostic patterns, epigenetic activation, and relationship with malignant-cell stemness/plasticity and tumor microenvironment (TME) remodeling in pancreatic adenocarcinoma (PAAD) remain incompletely defined. This study aimed to systematically characterize HMGA1 across cancers and clarify its clinical and biological relevance in PAAD. - Source: PubMed
Publication date: 2026/07/23
Liu HuanDai ShiyangLv ChaoxiangDeng MingmingZou XiaopanLi Xiaoling