CDH17 Antibody (monoclonal) (M01)
- Known as:
- CDH17 Antibody (mab) (M01)
- Catalog number:
- AT1472a
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- CDH17 Antibody (monoclonal) (M01)
Related genes to: CDH17 Antibody (monoclonal) (M01)
- 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:
- GTF2H2B NIH gene
- Name:
- general transcription factor IIH subunit 2B (pseudogene)
- Previous symbol:
- -
- Synonyms:
- DKFZP686M0199
- Chromosome:
- 5q13.2
- Locus Type:
- pseudogene
- Date approved:
- 2008-07-04
- Date modifiied:
- 2015-11-09
- Gene:
- POLR1A NIH gene
- Name:
- RNA polymerase I subunit A
- Previous symbol:
- -
- Synonyms:
- DKFZP586M0122, FLJ21915, RPO1-4, RPA1
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-01
- Date modifiied:
- 2017-06-28
- Gene:
- TDRP NIH gene
- Name:
- testis development related protein
- Previous symbol:
- C8orf42
- Synonyms:
- INM01, TDRP1, TDRP2
- Chromosome:
- 8p23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-28
- Date modifiied:
- 2015-08-26
Related products to: CDH17 Antibody (monoclonal) (M01)
Related articles to: CDH17 Antibody (monoclonal) (M01)
- Advanced-stage gastrointestinal (GI) cancers present an unmet need for innovative therapies, and antibody-drug conjugates (ADCs) offer promising solutions. This study investigates the antitumor efficacy and toxicity of AMT-676, a novel ADC targeting Cadherin 17 (CDH17), in GI cancers. Utilizing MabArray screening and immunohistochemistry, CDH17 was identified as a promising ADC target in GI tumors with minimal expression in healthy organs. The ADC was optimized through comprehensive in vitro and in vivo evaluations of binding affinity, cytotoxicity, pharmacokinetics, and toxicity, with antitumor potential evaluated using cell line-derived (CDX) and patient-derived tumor xenograft (PDX) models. Leveraging the T moiety-exatecan platform, we synthesized AMT-676, comprising a high-affinity CDH17-specific antibody, a hydrophilic self-immolative T1000 linker, and exatecan with a Drug-to-Antibody Ratio (DAR) of 4. AMT-676 demonstrated sustained antitumor responses across CDX and PDX GI models with diverse CDH17 expression, notably inhibiting metastatic growth in a colorectal cancer model. Cynomolgus monkey studies revealed favorable pharmacokinetics and manageable toxicity associated with AMT-676. In conclusion, we developed a novel CDH17-targeting ADC characterized by a high therapeutic index and tolerable toxicity profile, highlighting its promise for GI cancer treatment. A first-in-human, phase I clinical trial of AMT-676 in patients with advanced solid tumors is currently underway (NCT06400485). - Source: PubMed
Publication date: 2026/09/09
Wang Ying-NanRuan Dan-YunShi JingHuang YueSheng HuiHuang Ya-LingMa LinjieWang LijunChen CaiweiWang YixuanZhang YueShen YiZhang QingZhang JianjianTang YanfangZhang Jin-LingHu Jia-JiaWu Chen-YiChen Jia-YingMeng XunLiu Shu-HuiWang Feng - 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