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更新于：2025-11-08
Codrituzumab
更新于：2025-11-08
概要
基本信息
权益机构- |
最高研发阶段临床1期 |
首次获批日期- |
最高研发阶段(中国)- |
特殊审评- |
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结构/序列
Sequence Code 13574H
来源: *****
Sequence Code 13592L
来源: *****
关联
6
项与 Codrituzumab 相关的临床试验NCT04928677
A Multi-Center Phase I Study of Codrituzumab in Pediatric Patients With Relapsed or Refractory Glypican 3 (GPC3) Expressing Extra-cranial Solid Tumors
JPRN-jRCT2080221779
A Randomized, Placebo-controlled, Double-blind, Multicenter Phase II Trial of Intravenous GC33 at 1600 mg Q2W in Previously Treated Patients with Unresectable Advanced or Metastatic Hepatocellular Carcinoma (HCC)
NCT01507168
A Randomised, Placebo-controlled, Double-blind, Multicenter Phase II Trial of Intravenous GC33 at 1600 mg Q2W in Previously Treated Patients With Unresectable Advanced or Metastatic Hepatocellular Carcinoma (HCC)
100 项与 Codrituzumab 相关的临床结果
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100 项与 Codrituzumab 相关的转化医学
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100 项与 Codrituzumab 相关的专利（医药）
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25
项与 Codrituzumab 相关的文献（医药）2025-04-24Cureus Journal of Medical Science
Hepatocellular Carcinoma and Antibody Drug Conjugates: A Systematic Review
Review
作者: Patel, Tirath ; Maddukuri, Srivarshini ; Battula, Naga Spandana ; Haddad, Ryan R ; Chay, Timmie ; Mohammed, Lubna ; Dumaru, Nabina
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths, primarily associated with liver cirrhosis from factors like hepatitis B virus (HBV), hepatitis C virus (HCV), alcohol abuse, metabolic syndrome, and genetic disorders. With the rising incidence of liver cancer, particularly in HBV-endemic regions, research into novel therapies like antibody-drug conjugates (ADCs) has gained momentum. ADCs target cancer cells by attaching cytotoxic drugs to antibodies, minimizing damage to healthy tissue. Recent clinical trials have demonstrated that ADCs targeting GPC3, such as GC33 and 32A9, show promising results in reducing tumor growth and improving patient outcomes in advanced HCC. These therapies offer a potential alternative to conventional chemotherapy, marking a significant advancement in precision oncology. This systematic review was implemented using various databases like PubMed, Google Scholar, Science Direct, EBSCO, and Public Library of Science (PLoS) using regular keywords and MeSH keywords. Eligibility criteria were restricted to free full texts in the English language, humans, and publications between 2019-2024. The exclusion criteria included languages other than English and publications before 2019. A total of 26 articles were identified, and 12 articles were selected after quality assessment.
2025-04-01Small science
Therapeutic Glypican‐3 CRISPR Genome‐Editing Using UltraLarge Porous Silica Nano‐Depot for the Treatment of Hepatocellular Carcinoma
Article
作者: Lee, Hyojin ; Kim, Seongchan ; Lee, Sanghee ; Kim, Dong‐Hyun ; Lee, Sian
Glypican‐3 (GPC3) is a key diagnostic marker and therapeutic target in hepatocellular carcinoma (HCC), interacting with Wnt and Hippo/YAP pathways related to cancer proliferation. Modulating GPC3 gene expression can induce liver cancer cell death by disrupting growth factor signaling, cell adhesion, and metabolic regulation. This study presents the development of a non‐viral ultralarge porous CRISPR‐Cas9 silica nano‐depot to perform targeted GPC3 genome editing for the treatment of HCC. The synthesized ultralarge porous silica nano‐depot (UPSND) encapsulates substantial CRISPR‐Cas9‐ribonucleoprotein complexes with a remarkable 98.3% loading efficiency. The UPSND‐mediated GPC3 CRISPR‐Cas9 therapy significantly suppresses cancer cell proliferation by modulating the Wnt and Hippo/YAP pathways. The efficiency of GPC3 gene deletion is observed to be 5.1‐fold higher than that of commercial lipid‐based GPC3 CRISPR‐Cas9 in both human and murine genes, with minimal off‐target effects. In vivo systemic administration of GPC3 Cas9‐RNP@UPSND resulted in preferential accumulation within hepatic tissues in orthotopic HCC mouse models, leading to complete tumor eradication and enhancing T‐cell tumor‐infiltration. Furthermore, the GPC3 CRISPR‐Cas9@UPSND treatment exhibits superior anti‐proliferative efficacy in tumor‐growth prevention compared to Codrituzumab, as evidenced by the analysis of Ki67 and GPC3 expression, along with serum GPC3 levels. These findings underscore the translational potential of the non‐viral UPSND nanoplatform‐based CRISPR GPC3 genome editing, offering a promising targeted therapeutic strategy for HCC treatment.
2025-01-01Heliyon
Glypican-3 is a key tuner of the Hedgehog pathway in COPD
Article
作者: Ruaux, Christophe ; Mérol, Jean-Claude ; Polette, Myriam ; Hatoum, Sarah ; Petit, Laure M G ; Deslée, Gaëtan ; Dubernard, Xavier ; Saber Cherif, Lynda ; Dormoy, Valérian ; Delepine, Gonzague ; Ancel, Julien ; Durlach, Anne ; Devilliers, Maëva A ; Perotin, Jeanne-Marie
Hedgehog (HH) pathway is involved in pulmonary development and lung homeostasis. It orchestrates airway epithelial cell (AEC) differentiation and contributes to respiratory pathogenesis. The core elements Gli2, Smo, and Shh were found altered in the bronchial epithelium of patients with chronic obstructive pulmonary disease (COPD). Here, we investigated the co-receptors to fully decipher the complex machinery of airway HH pathway activation in health and COPD. The core elements and co-receptors of HH signalling were investigated in lung cell populations using single-cell RNAseq analysis. The transcript levels of the principal co-receptor GPC3 were investigated on public RNAseq datasets and by RT-qPCR. The localisation of GPC3 was evaluated through immunofluorescent stainings on isolated bronchial AEC and tissues from non-COPD and COPD patients. GPC3 pharmacological modulation was achieved with Codrituzumab during AEC differentiation. We demonstrated that the core elements were not abundant in pulmonary cell populations. Focusing on co-receptors, GPC3 was the most expressed transcript in tracheobronchial epithelial cells. The decrease in GPC3 transcript levels correlated with the severity of airway obstrution in COPD patients. Finally, interfering with GPC3 signalling during AEC differentiation induced downregulation of the HH pathway attested by a decrease of Gli2 leading to reduced ciliogenesis and altered mucin production. GPC3 appears as a crucial co-receptor for the HH pathway in the respiratory context. The modulation of GPC3 may represent a novel experimental strategy to tune HH signalling in therapeutic perspectives.
100 项与 Codrituzumab 相关的药物交易
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外链
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 转移性肝细胞癌 | 临床2期 | 美国 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 日本 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 比利时 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 法国 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 德国 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 中国香港 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 意大利 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 新西兰 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 新加坡 | 2012-02-02 | |
| 转移性肝细胞癌 | 临床2期 | 西班牙 | 2012-02-02 |
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临床结果
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临床1期 | 20 | 願遞顧夢膚膚鬱淵顧範(鏇膚積鏇淵鏇淵鏇簾夢) = 0% vs 15% vs 0% 網顧糧築積獵淵構築繭 (壓鑰鹹遞艱選網構淵簾 ) 更多 | 积极 | 2018-10-21 | |||
临床2期 | 185 | 顧窪廠衊鹽餘衊鹹顧鬱(網淵憲蓋糧鏇艱蓋壓鏇) = 網憲鹹網醖遞鑰齋積鹹 製壓鑰積齋糧鹹製蓋壓 (鹹襯觸獵積觸糧衊廠選 ) 更多 | 不佳 | 2016-08-01 | |||
Placebo | 顧窪廠衊鹽餘衊鹹顧鬱(網淵憲蓋糧鏇艱蓋壓鏇) = 選窪憲範鏇觸廠築鹹鏇 製壓鑰積齋糧鹹製蓋壓 (鹹襯觸獵積觸糧衊廠選 ) 更多 | ||||||
临床2期 | 185 | 鑰壓壓遞鏇鏇製壓築製(鏇積淵鏇餘糧壓廠繭淵) = 鏇衊顧鏇願積構糧遞衊 鹹齋廠選糧淵衊淵築醖 (構襯鹽糧製鹹壓顧網網 ) 更多 | - | 2014-05-20 | |||
Placebo | 鑰壓壓遞鏇鏇製壓築製(鏇積淵鏇餘糧壓廠繭淵) = 窪築蓋選蓋窪衊蓋鑰襯 鹹齋廠選糧淵衊淵築醖 (構襯鹽糧製鹹壓顧網網 ) 更多 |
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