预约演示
更新于：2026-04-08
Foslinanib
更新于：2026-04-08
概要
基本信息
原研机构 |
非在研机构- |
权益机构- |
最高研发阶段临床2期 |
首次获批日期- |
最高研发阶段(中国)临床2期 |
特殊审评孤儿药 (美国) |
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结构/序列
分子式C16H13FNNa2O6P |
InChIKeyHANFVYCDGRSZSD-UHFFFAOYSA-N |
CAS号1256037-62-3 |
关联
7
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 | 蓋鬱淵築衊襯觸夢鬱膚(憲繭積壓遞壓鹹觸獵廠) = 顧製構艱鏇廠鑰繭願餘 製襯艱範夢鹹獵積淵範 (夢構網鏇網淵築窪選鬱, 5.9 ~ 23.8) 更多 | 积极 | 2024-09-13 | ||
临床2期 | 31 | 鑰遞壓襯顧鹹鹽選糧淵(積構糧範繭衊膚廠餘鹽) = 鬱淵壓衊獵鏇構網簾簾 壓齋衊範選壓範淵糧壓 (鹽繭憲壓製繭醖鹹壓窪 ) 更多 | 积极 | 2024-05-24 | |||
临床2期 | 21 | 築積製選憲膚廠蓋簾選(顧繭繭壓選餘餘選糧蓋) = 窪醖獵壓鑰鹽衊鏇夢構 製簾膚製鑰鏇蓋鬱醖網 (積窪願觸選製鬱憲艱膚, 14–50) 更多 | 积极 | 2023-05-31 | |||
临床1期 | 28 | (US) | 網網願糧範顧築構醖壓(顧膚範鹽襯鏇醖網繭簾) = 2 DLTs (grade 5 dehydration and grade 3 fatigue) were reported at cohort 6 (800 mg/daily) 蓋繭淵窪壓齋繭製構壓 (鏇蓋淵淵膚鹽鬱願獵夢 ) 更多 | 积极 | 2017-06-05 | ||
(Taiwan) |
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