Refametinib(Refametinib) - 药物靶点：MEK1 x MEK2_专利_临床

概要

基本信息

药物类型

小分子化药

别名

+ [6]

靶点

MEK1 x MEK2

作用方式

抑制剂

作用机制

MEK1抑制剂(双特异性丝裂原活化蛋白激酶激酶1抑制剂)、MEK2抑制剂(双特异性丝裂原活化蛋白激酶激酶2抑制剂)

治疗领域

肿瘤消化系统疾病内分泌与代谢疾病

在研适应症-

非在研适应症

晚期癌症肝细胞癌恶性实体肿瘤+ [2]

原研机构

Bausch Health Americas, Inc.

在研机构-

非在研机构

拜耳医药保健有限公司

Bayer AGBayer Schering Pharma AG

最高研发阶段终止临床2期

首次获批日期-

最高研发阶段(中国)无进展

特殊审评特殊审批 (中国)

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结构/序列

分子式C19H20F3IN2O5S

InChIKeyRDSACQWTXKSHJT-NSHDSACASA-N

CAS号923032-37-5

关联

14

项与 Refametinib 相关的临床试验

NCT02346032

/ Completed临床2期IIT

Phase II Study of Refametinib, a MEK Inhibitor, as Second-line Treatment in Advanced Biliary Tract Adenocarcinoma

Phase II Study of Refametinib, a MEK inhibitor, as second-line treatment in advanced biliary tract adenocarcinoma

开始日期2015-06-30

申办/合作机构

Samsung Medical Center

CTR20140453

/ Completed临床2期

RAS突变肝细胞癌患者中，研究药与索拉非尼联合用一线治疗的一项二期前瞻性单臂多中心非对照开放性研究

该研究的主要目的是：在有KRAS或NRAS突变的不可切除或转移性HCC患者中，评估Refametinib联合索拉非尼的有效性。次要目的是：在有KRAS或NRAS突变的不可切除或转移性HCC患者中，评估Refametinib联合索拉非尼的安全性。其它目的为：分析生物标志物、药代动力学（PK）和患者报告结局（PRO，仅第2阶段）。

开始日期2015-03-04

申办/合作机构

Bayer Pharma AG

[+1]

EUCTR2014-002460-33-IT

/ Unknown statusN/AIIT

ANTI MEK THERAPY WITH REFAMETINIB TO PREVENT RESISTANCE TO EGFR-TARGETED TREATMENT IN METASTATIC COLORECTAL CANCERS - ARES

开始日期2014-10-23

申办/合作机构-

100 项与 Refametinib 相关的临床结果

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100 项与 Refametinib 相关的转化医学

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100 项与 Refametinib 相关的专利（医药）

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186

项与 Refametinib 相关的文献（医药）

2025-01-01·Gene

Immune-related glycosylation genes based classification predicts prognosis and therapy options of osteosarcoma

Article

作者: Wang, Wen ; Jiao, Yunjia ; Du, Xiaojing ; Ye, Zhaoming

Osteosarcoma is the most common primary bone malignancy, with a very poor prognosis. Aberrant glycosylation is close involvement in osteosarcoma. Accordingly, this study aimed at investigating the role of glycosylation genes in the prognosis and therapy options of osteosarcoma. The microenvironment of osteosarcoma was assessed using estimate algorithm. A total of 20 immune-related glycosylation genes (IRGGs) was identified using Pearson correlation analysis. Accordingly, osteosarcoma patients were divided into C1 and C2 type using consensus clustering. Multiple algorithms (Xcell, MCP-counter, ssGSEA, epic, quantiseq), cancer immune cycle analysis, and GSVA were applied to estimate the immune, molecule and metabolism characteristics of osteosarcoma, indicating that C1 type was featured with high immune infiltration, high glycosylation, enriched MEK signaling, and good prognosis, while C2 type was characterized by more metastasis, enriched immunotherapy-positive gene signatures, high tumor mutation burden, and poor prognosis. Results from TIDE algorithm and immunotherapy datasets suggested the C2 type's preference of immune checkpoint inhibitors (ICIs), while data of GDSC, CMap analysis and cell experiments indicated that C1 type was sensitivity to MEK inhibitor PD0325901. In addition, univariate Cox and Lasso analysis was combined to establish an IRGGs' risk score containing 6 genes (B3GNT8, FUT7, GAL3ST4, GALNT14, HS3ST2, and MFNG). The data of DCA and ROC indicated its well prediction of prognosis in osteosarcoma. Finally, cellular location analysis showed that the 6 genes not only distributed in tumor cells but also in immune cells. In summary, the classification and risk score based on IRGGs effectively predicted the prognosis and therapy options of osteosarcoma. Further studies on IRGGs may contribute to the understanding of cancer immunity in osteosarcoma.

2024-12-31·Cancer Biology & Therapy

M6A-mediated molecular patterns and tumor microenvironment infiltration characterization in nasopharyngeal carcinoma

Article

作者: Wang, Feng ; Peng, Lisha ; Wang, Yong

N6-methyladenosine (m6A) is the most predominant RNA epigenetic regulation in eukaryotic cells. Numerous evidence revealed that m6A modification exerts a crucial role in the regulation of tumor microenvironment (TME) cell infiltration in several tumors. Nevertheless, the potential role and mechanism of m6A modification in nasopharyngeal carcinoma (NPC) remains unknown. mRNA expression data and clinical information from GSE102349, and GSE53819 datasets obtained from Gene Expression Omnibus (GEO) was used for differential gene expression and subsequent analysis. Consensus clustering was used to identify m6A-related molecular patterns of 88 NPC samples based on prognostic m6A regulators using Univariate Cox analysis. The TME cell-infiltrating characteristics of each m6A-related subclass were explored using single-sample gene set enrichment (ssGSEA) algorithm and CIBERSORT algotithm. DEGs between two m6A-related subclasses were screened using edgeR package. The prognostic signature and predicated nomogram were constructed based on the m6A-related DEGs. The cell infiltration and expression of prognostic signature in NPC was determined using immunohistochemistry (IHC) analysis. Chi-square test was used to analysis the significance of difference of the categorical variables. And survival analysis was performed using Kaplan-Meier plots and log-rank tests. The NPC samples were divided into two m6A-related subclasses. The TME cell-infiltrating characteristics analyses indicated that cluster 1 is characterized by immune-related and metabolism pathways activation, better response to anit-PD1 and anti-CTLA4 treatment and chemotherapy. And cluster 2 is characterized by stromal activation, low expression of HLA family and immune checkpoints, and a worse response to anti-PD1 and anti-CTLA4 treatment and chemotherapy. Furthermore, we identified 1558 DEGs between two m6A-related subclasses and constructed prognostic signatures to predicate the progression-free survival (PFS) for NPC patients. Compared to non-tumor samples, REEP2, TMSB15A, DSEL, and ID4 were upregulated in NPC samples. High expression of REEP2 and TMSB15A showed poor survival in NPC patients. The interaction between REEP2, TMSB15A, DSEL, ID4, and m6A regulators was detected. Our finding indicated that m6A modification plays an important role in the regulation of TME heterogeneity and complexity.

2024-12-01·Computational and Structural Biotechnology Journal

Uncovering the potential of APOD as a biomarker in gastric cancer: A retrospective and multi-center study

Article

作者: Wang, Xuanyu ; Sun, Le ; Tian, Sufang ; Liu, Xiaoping ; Xu, Yihang ; Chen, Hongshan ; Wang, Zisong

Gastric cancer (GC) poses a significant health challenge worldwide, necessitating the identification of predictive biomarkers to improve prognosis. Dysregulated lipid metabolism is a well-recognized hallmark of tumorigenesis, prompting investigation into apolipoproteins (APOs). In this study, we focused on apolipoprotein D (APOD) following comprehensive analyses of APOs in pan-cancer. Utilizing data from the TCGA-STAD and GSE62254 cohorts, we elucidated associations between APOD expression and multiple facets of GC, including prognosis, tumor microenvironment (TME), cancer biomarkers, mutations, and immunotherapy response, and identified potential anti-GC drugs. Single-cell analyses and immunohistochemical staining confirmed APOD expression in fibroblasts within the GC microenvironment. Additionally, we independently validated the prognostic significance of APOD in the ZN-GC cohort. Our comprehensive analyses revealed that high APOD expression in GC patients was notably associated with unfavorable clinical outcomes, reduced microsatellite instability and tumor mutation burden, alterations in the TME, and diminished response to immunotherapy. These findings provide valuable insights into the potential prognostic and therapeutic implications of APOD in GC.

100 项与 Refametinib 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB06309

研发状态

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
转移性胰腺癌	临床2期	德国	Bayer AG	2011-01-01
转移性胰腺癌	临床2期	捷克	Bayer AG	2011-01-01
转移性胰腺癌	临床2期	美国	Bayer AG	2011-01-01
转移性胰腺癌	临床2期	英国	Bayer AG	2011-01-01
肝细胞癌	临床2期	韩国	Bayer AG	2010-12-01
肝细胞癌	临床2期	新加坡	Bayer AG	2010-12-01
肝细胞癌	临床2期	中国香港	Bayer AG	2010-12-01
肝细胞癌	临床2期	中国台湾	Bayer AG	2010-12-01
晚期癌症	临床2期	美国	Bayer AG	2008-11-01
晚期癌症	临床2期	加拿大	Bayer AG	2008-11-01

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临床结果

适应症

分期

评价

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT01392521 (Pubmed \| Target Oncol) 人工标引	临床1期	晚期癌症	64	Copanlisib+Refametinib	(窪糧選鏇遞蓋醖範繭鹹) = copanlisib 0.4 mg/kg weekly and refametinib 30 mg twice daily 鏇鏇製憲膚醖製鹹鏇繭 (鬱夢齋衊觸鑰憲鏇齋鑰 ) 更多	积极	2020-04-01
NCT01251640 (Pubmed \| Target Oncol) 人工标引	临床1/2期	胰腺癌	90	Gemcitabine+Refametinib	(願願夢網餘鏇繭醖簾壓) = 選淵醖壓獵簾繭壓鑰衊衊鬱願廠鹽觸鏇窪觸壓 (醖築衊築網積構願選繭 ) 更多	积极	2017-02-01
NCT01251640 (AACR2015)	临床1/2期	不能切除性胰腺癌	69	refametin (KRAS wild-type)	(艱襯鑰積膚觸鹹範網繭) = 遞齋鹽鏇築願襯簾繭鹹憲鑰顧獵壓艱蓋憲憲壓 (膚獵糧積鹽簾鹹範築鹽 ) 更多	-	2015-08-01
				refametin (KRAS mutant)	(艱襯鑰積膚觸鹹範網繭) = 蓋築製窪壓獵餘網膚鹹憲鑰顧獵壓艱蓋憲憲壓 (膚獵糧積鹽簾鹹範築鹽 ) 更多
NCT01251640 (ASCO2014)	临床2期	不能切除性胰腺癌	90	Refametinib + Gemcitabine	(窪蓋遞顧壓憲選製襯鹽) = 鏇積網淵襯製壓淵鬱餘淵網糧遞淵蓋齋獵蓋衊 (壓顧廠糧鏇齋獵觸艱選 ) 更多	-	2014-05-20
NCT01392521 (ASCO2014)	临床1期	晚期癌症	49	Copanlisib	(蓋網鬱窪衊淵範蓋觸遞) = 遞鹽鏇製製蓋齋構齋膚醖鏇簾夢鹽鹽鏇蓋構獵 (齋糧窪鹹願糧獵積簾選 ) 更多	-	2014-05-20
				Refametinib	(蓋網鬱窪衊淵範蓋觸遞) = 構膚窪鹽鏇獵築選網簾醖鏇簾夢鹽鹽鏇蓋構獵 (齋糧窪鹹願糧獵積簾選 ) 更多
NCT01251640 (ASCO2014)	临床2期	不能切除性胰腺癌	60	Refametinib + Gemcitabine	(齋蓋壓網膚願觸膚觸膚) = 鏇襯窪衊簾醖襯鏇獵壓鹹選鹽廠鬱繭鏇醖鹽襯 (遞衊選願獵蓋齋鑰壓鏇 ) 更多	-	2014-05-20
EULAR2009	N/A	关节炎	-	RDEA436	(願糧網膚願淵願淵鑰願) = 襯糧膚蓋淵製顧繭獵築製願憲網鏇糧襯餘鹽構 (鹽壓膚壓夢窪鑰顧獵襯 ) 更多	-	2009-06-10
				RDEA119	(構繭醖積窪鬱製觸憲艱) = 襯衊構築淵襯窪構鹹網積願鹽襯壓簾構範廠膚 (衊構鑰鹹窪夢築窪簾築 )
EULAR2008	N/A	关节炎	-	RDEA119	(糧蓋鹹艱鏇鬱選繭願窪) = 願膚網鹹網憲艱製齋簾膚蓋夢餘窪艱衊鹽廠窪 (憲齋醖繭糧醖壓淵簾淵 ) 更多	-	2008-06-11
				Indomethacin	(網夢醖憲憲繭鑰蓋構膚) = 窪衊觸觸構憲簾顧蓋鏇壓鹹淵鏇襯築廠選築鹹 (鏇窪夢鹽醖襯淵構憲淵 )