CDH17 Antibody (M03), clone 3H2
- Known as:
- CDH17 Antibody (M03), clonality 3H2
- Catalog number:
- bin-001015-m03
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CDH17 Antibody (M03) clone 3H2
Related genes to: CDH17 Antibody (M03), clone 3H2
- Gene:
- CDH17 NIH gene
- Name:
- cadherin 17
- Previous symbol:
- -
- Synonyms:
- HPT-1, cadherin
- Chromosome:
- 8q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-10
- Date modifiied:
- 2016-01-15
- Gene:
- CENPJ NIH gene
- Name:
- centromere protein J
- Previous symbol:
- MCPH6
- Synonyms:
- CPAP, BM032, LAP, LIP1, Sas-4, SASS4, SCKL4
- Chromosome:
- 13q12.12-q12.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-15
- Date modifiied:
- 2018-02-13
- Gene:
- CENPN NIH gene
- Name:
- centromere protein N
- Previous symbol:
- C16orf60
- Synonyms:
- FLJ13607, FLJ22660, BM039
- Chromosome:
- 16q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2006-02-20
- Date modifiied:
- 2015-08-24
- Gene:
- DONSON NIH gene
- Name:
- downstream neighbor of SON
- Previous symbol:
- C21orf60
- Synonyms:
- B17, C2TA, DKFZP434M035
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-18
- Date modifiied:
- 2017-03-30
- Gene:
- EAPP NIH gene
- Name:
- E2F associated phosphoprotein
- Previous symbol:
- C14orf11
- Synonyms:
- BM036, FLJ20578
- Chromosome:
- 14q13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-18
- Date modifiied:
- 2016-02-26
Related products to: CDH17 Antibody (M03), clone 3H2
Related articles to: CDH17 Antibody (M03), clone 3H2
- Potent and sustained inhibition of epidermal growth factor receptor (EGFR) signaling is critical for suppressing colorectal cancer (CRC) growth, yet current EGFR therapies are often limited by incomplete EGFR blockade and on-target/off-tumor toxicities, particularly skin rash. Here, we co-targeted EGFR and cadherin-17 (CDH17) with a bispecific antibody (bsAb), overcoming these limitations by reducing skin-related toxicities and achieving superior tumor growth inhibition compared to EGFR- or c-MET/EGFR-targeting antibodies. Mechanistically, the high-affinity CDH17-binding arm anchored the EGFR/CDH17 bsAb to the tumor cell surface, facilitating rapid engagement of unbound or newly synthesized EGFR. This "anchor and capture" mechanism allowed the EGFR/CDH17 bsAb to achieve superior and more sustained suppression of the EGFR pathway than cetuximab and amivantamab. Further incorporation of an anti-CD16A nanobody transformed the EGFR/CDH17 bsAb into a trispecific natural killer (NK)-cell engager. Extensive format screening revealed that NK cell activation is heavily influenced by the spatial distance between the tumor antigen-binding Fab and the anti-CD16A nanobody, with longer distances impairing the bulky CD45 phosphatase exclusion from the immunological synapse and leading to significantly reduced cytotoxicity. Consequently, the widely adopted Morrison-type antibody consistently underperformed compared to architectures with shorter CD16A-TAA-Fab spacing. The final optimized molecule was IBI3019, a CDH17/EGFR/CD16A trispecific antibody that integrates potent CDH17-enhanced EGFR blockade with optimal architecture for efficient NK cell engagement. It demonstrated superior in vivo efficacy and a good safety profile in cynomolgus monkeys, with no observable skin toxicity. These promising pre-clinical findings warrant the clinical development of IBI3019. . - Source: PubMed
Publication date: 2026/09/01
Liu JiaMa JingboLin ShumingDai WeiLu JiaWu MinWang YifanZheng HuilinZhou ShuaixiangLiu YangWang FeifeiLi BinWu ZhihaiLiu WangwangLyu JingYan YayaoXu JinlingGuan JianXia LiangyongLiu HuisiHe YuanqiaoZhou JihaoHe KaijieLi ZhijieChia Tiongsun - Cadherin-17 (CDH17, LI-cadherin) is a non-classical cadherin with an atypical structure and unique functions. CDH17 expression is restricted to normal intestinal epithelium. Furthermore, CDH17 functions as an oncoprotein that promotes tumor migration and invasion in colorectal, gastric, and pancreatic cancers. Therefore, CDH17 is an important diagnostic marker and therapeutic target. The CDH17-directed strategies, including monoclonal antibodies (mAbs), bispecific Abs, antibody-drug conjugates (ADCs), and chimeric antigen receptor (CAR) T cells, have been evaluated in preclinical and clinical studies. Therefore, developing mAbs that specifically recognize cell surface-expressing CDH17 is essential for advancing both tumor diagnosis and therapy. - Source: PubMed
Publication date: 2026/07/10
Ito ReinaSuzuki HiroyukiIshikawa KenichiroYagi KazutakeOhkoshi AkiraKatori YukioKaneko Mika KKato Yukinari - Antibody-drug conjugates (ADCs) represent an emerging class of targeted therapeutics with considerable potential in the management of colorectal cancer (CRC). By delivering highly potent cytotoxic agents to cancer cells via specific antibodies, ADCs enable precise tumor targeting while minimizing off-target toxicity. Recent advancements have identified several promising targets for ADC development in CRC, including human epidermal growth factor receptor 2 (HER2), carcinoembryonic antigen-related cell adhesion molecule 5 (CEACAM5), mesenchymal-epithelial transition factor (c-MET), epidermal growth factor receptor (EGFR), cadherin-17 (CDH17), and trophoblast cell surface antigen 2 (Trop-2). Clinical trials have demonstrated encouraging objective response rates and survival benefits with ADCs such as trastuzumab deruxtecan (T-DXd) and disitamab vedotin in patients with advanced CRC. Nonetheless, the clinical application of ADCs faces several challenges, including tumor heterogeneity leading to variable target expression, the emergence of diverse resistance mechanisms that limit long-term efficacy, and manageable but significant safety concerns. Future research should prioritize tumor-selective linker design, novel payload development, bispecific and dual-payload ADC platforms, and rational combination strategies to overcome resistance and further improve the therapeutic index of ADCs in CRC. - Source: PubMed
Publication date: 2026/07/20
Zeng LiliZhu YuanlinZhang KeLiu BinDing Jie - The therapeutic landscape of colorectal cancer (CRC) has evolved with the identification of molecular subtypes, including mismatch repair-deficient/microsatellite instability-high, POLE mutations, RAS/BRAF alterations, and HER2 amplification, enabling use of precision therapies and immune checkpoint inhibitors for selected populations. However, most microsatellite-stable (MSS) tumors remain resistant due to tumor heterogeneity, adaptive resistance, and an immunosuppressive tumor microenvironment (TME). Advances in molecular profiling, spatial biology, and immune characterization have revealed vulnerabilities beyond canonical signaling, facilitating novel strategies such as antibody-drug conjugates (ADCs), bispecific antibodies, DNA damage response (DDR) targeting, TME-directed therapies, cellular therapies, and epigenetic modulation. HER2-directed ADCs, notably trastuzumab deruxtecan, have shown clinically meaningful activity in HER2-positive metastatic CRC, providing proof of concept for ADC-based therapy. Additional targets under investigation include CEACAM5, LGR5, EGFR, HER3, MET, B7-H3, and CDH17. Bispecific antibodies and co-stimulatory agonists are being developed to overcome antigen heterogeneity and pathway redundancy, with the EGFR-MET bispecific antibody amivantamab showing initial clinical efficacy. Moreover, next-generation immune checkpoint inhibitors and multitarget combinations aim to reinvigorate T-cell responses in MSS tumors. Early chimeric antigen receptor T-cell studies targeting CEA and GUCY2C demonstrate feasibility and manageable toxicity, although tumor-intrinsic and TME barriers persist. Emerging strategies increasingly focus on modulating the TME to enhance immune infiltration and effector function, targeting CCR8, TGF-β, adenosine, CSF1R, CXCR1/2, STING, and CD47. DDR and epigenetic therapies offer additional opportunities to sensitize resistant tumors. Integrated, multidimensional biomarker approaches and artificial intelligence-driven interpretation of tumor and TME features are expected to guide personalized therapy, anticipate resistance, and broaden the benefit of targeted and immune-based interventions in CRC. - Source: PubMed
Publication date: 2026/07/16
Bartolini MAlgaze SLenz H-J - Immunohistochemistry (IHC) is essential in diagnostic pathology, but antibody reliability is often limited by insufficient validation and high variability between clones. Conventional validation approaches normally use only few tissues or cell lines which do not reflect tissue and cell type complexity. A high-throughput validation platform based on large-scale tissue microarrays (TMAs) was established to assess antibody specificity across 76 normal tissue types and to evaluate the diagnostic performance in > 15,000 tumours from > 130 entities. Comparative staining with independent antibodies on a full set of normal tissues enables robust detection of cross-reactivity. Comparative staining of critical tumour cohorts under different conditions enables protocol optimization to obtain the best possible sensitivity and specificity for the distinction of different tumour types. Large-scale tumour profiling studies on ≥ 15,000 cancers generated comprehensive datasets refining the diagnostic value of established markers (e.g., CK7/CK20, PLAP) and characterizing the impact of emerging diagnostic targets such as MTAP, CDH16, and CDH17. Furthermore, screening of over 6000 antibodies of previously unknown clinical significance identified various novel diagnostic markers, including CPA1, GAD2, and KDM6A, with high specificity for distinct tumour entities and/or neoplastic transformation. In conclusion, large-scale TMA-based validation improves antibody identification and characterization and provides a robust framework for integrating IHC into digital pathology solutions. - Source: PubMed
Sauter GuidoKluth MartinaTsourlakis Maria ChristinaSauter MarcoDieckert SandraSimon Ronald