预约演示
更新于：2026-02-27
Foslinanib
更新于：2026-02-27
概要
基本信息
结构/序列
分子式C16H13FNNa2O6P |
InChIKeyHANFVYCDGRSZSD-UHFFFAOYSA-N |
CAS号1256037-62-3 |
关联
6
项与 Foslinanib 相关的临床试验NCT05257590
A Phase 2, Open-Label Study of CVM-1118 in Combination With Nivolumab in Subjects With Unresectable Advanced Hepatocellular Carcinoma
NCT04336124
A Phase I Safety and Pharmacokinetic Study of CVM-1118 Extended-Release Capsules Administered Orally to Patients With Advanced Cancers
NCT03600233
A Phase II, Open-label Study of CVM-1118 Administered Orally to Patients With Advanced Neuroendocrine Tumors
100 项与 Foslinanib 相关的临床结果
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100 项与 Foslinanib 相关的转化医学
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100 项与 Foslinanib 相关的专利（医药）
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2
项与 Foslinanib 相关的文献（医药）2016-03-01Pharmacology & therapeutics1区 · 医学
Tumor cell vascular mimicry: Novel targeting opportunity in melanoma
1区 · 医学
Review
作者: Chao, Jun-Tzu ; Chien, Du-Shieng ; Chu, Yi-Wen ; Hendrix, Mary J C ; Seftor, Richard E B ; Seftor, Elisabeth A
In 1999, the American Journal of Pathology published an article, entitled "Vascular channel formation by human melanoma cells in vivo and in vitro: vasculogenic mimicry" by Maniotis and colleagues, which ignited a spirited debate for several years and earned the journal's distinction of a "citation classic" (Maniotis et al., 1999). Tumor cell vasculogenic mimicry (VM), also known as vascular mimicry, describes the plasticity of aggressive cancer cells forming de novo vascular networks and is associated with the malignant phenotype and poor clinical outcome. The tumor cells capable of VM share the commonality of a stem cell-like, transendothelial phenotype, which may be induced by hypoxia. Since its introduction as a novel paradigm for melanoma tumor perfusion, many studies have contributed new findings illuminating the underlying molecular pathways supporting VM in a variety of tumors, including carcinomas, sarcomas, glioblastomas, astrocytomas, and melanomas. Of special significance is the lack of effectiveness of angiogenesis inhibitors on tumor cell VM, suggesting a selective resistance by this phenotype to conventional therapy. Facilitating the functional plasticity of tumor cell VM are key proteins associated with vascular, stem cell, extracellular matrix, and hypoxia-related signaling pathways--each deserving serious consideration as potential therapeutic targets and diagnostic indicators of the aggressive, metastatic phenotype. This review highlights seminal findings pertinent to VM, including the effects of a novel, small molecular compound, CVM-1118, currently under clinical development to target VM, and illuminates important molecular pathways involved in the suppression of this plastic, aggressive phenotype, using melanoma as a model.
PATHOLOGY & ONCOLOGY RESEARCH
CVM-1118 (foslinanib), a 2-phenyl-4-quinolone derivative, promotes apoptosis and inhibits vasculogenic mimicry via targeting TRAP1
Article
作者: Shen, Lifen ; Huang, Chu-Chun ; Chien, Du-Shieng ; Chu, Yi-Wen ; Seftor, Richard E B ; Chen, Yen-Ling ; Shyu, Yu-Chiau ; Hendrix, Mary J C ; Seftor, Elisabeth A
CVM-1118 (foslinanib) is a phosphoric ester compound selected from 2-phenyl-4-quinolone derivatives. The NCI 60 cancer panel screening showed CVM-1125, the major active metabolite of CVM-1118, to exhibit growth inhibitory and cytotoxic effects at nanomolar range. CVM-1118 possesses multiple bioactivities, including inducing cellular apoptosis, cell cycle arrest at G2/M, as well as inhibiting vasculogenic mimicry (VM) formation. The TNF receptor associated protein 1 (TRAP1) was identified as the binding target of CVM-1125 using nematic protein organization technique (NPOT) interactome analysis. Further studies demonstrated CVM-1125 reduced the protein level of TRAP1 and impeded its downstream signaling by reduction of cellular succinate levels and destabilization of HIF-1α. The pharmacogenomic biomarkers associated with CVM-1118 were also examined by Whole Genome CRISPR Knock-Out Screening. Two hits (STK11 and NF2) were confirmed with higher sensitivity to the drug in cell knock-down experiments. Biological assays indicate that the mechanism of action of CVM-1118 is via targeting TRAP1 to induce mitochondrial apoptosis, suppress tumor cell growth, and inhibit vasculogenic mimicry formation. Most importantly, the loss-of-function mutations of STK11 and NF2 are potential biomarkers of CVM-1118 which can be applied in the selection of cancer patients for CVM-1118 treatment. CVM-1118 is currently in its Phase 2a clinical development.
100 项与 Foslinanib 相关的药物交易
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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 |
|---|---|---|---|---|
| 局部晚期不可切除癌 | 临床2期 | 中国台湾 | 2022-05-23 | |
| 不可切除的肝细胞癌 | 临床2期 | 中国台湾 | 2022-05-23 | |
| 晚期神经内分泌肿瘤 | 临床2期 | 中国台湾 | 2018-12-15 | |
| 胃肠胰神经内分泌肿瘤 | 临床2期 | 中国台湾 | 2018-12-15 | |
| 肺癌 | 临床2期 | 中国 | 2018-12-15 | |
| 神经内分泌癌 | 临床2期 | 中国台湾 | 2018-12-15 | |
| 肺神经内分泌肿瘤 | 临床2期 | 中国台湾 | 2018-12-15 | |
| 胰腺神经内分泌肿瘤 | 临床2期 | 中国台湾 | 2018-12-15 | |
| 晚期癌症 | 临床2期 | 美国 | 2018-07-12 | |
| 晚期肝细胞癌 | 临床2期 | 美国 | 2018-07-12 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 34 | CVM-1118 200mg BID | 選獵觸艱淵窪製齋築範(衊鬱鹹獵遞鑰壓憲壓選) = 簾淵網夢繭遞簾積簾網 廠鹽餘窪選鑰艱構餘遞 (衊鑰觸鬱顧繭範窪觸糧, 5.9 ~ 23.8) 更多 | 积极 | 2024-09-13 | ||
临床2期 | 31 | 鑰簾願窪鏇糧獵遞顧憲(鹽選顧醖築網選鏇憲鬱) = 鏇築餘繭衊夢淵觸簾憲 獵構壓壓餘繭齋製選衊 (構膚糧鬱鏇糧繭築窪顧 ) 更多 | 积极 | 2024-05-24 | |||
临床2期 | 21 | 窪鹹鏇繭築簾觸醖艱糧(願淵糧齋觸襯衊網獵廠) = 蓋鬱鹽淵鏇壓鹹夢鑰繭 蓋構簾構構簾醖鬱夢餘 (襯鹽鬱齋淵襯衊觸築廠, 14–50) 更多 | 积极 | 2023-05-31 | |||
临床1期 | 28 | (US) | 鹽簾廠鹽憲餘淵顧夢壓(鏇膚構鏇觸範網衊遞構) = 2 DLTs (grade 5 dehydration and grade 3 fatigue) were reported at cohort 6 (800 mg/daily) 築網廠壓繭獵艱廠夢糧 (糧壓鏇獵獵觸艱壓衊醖 ) 更多 | 积极 | 2017-06-05 | ||
(Taiwan) |
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