预约演示
更新于：2026-04-27
Ifebemtinib
更新于：2026-04-27
概要
基本信息
药物类型 小分子化药 |
别名 BI 853520、BI-853520、IN 10018 + [2] |
靶点 |
作用方式 抑制剂 |
作用机制 FAK抑制剂(粘着斑蛋白酪氨酸激酶抑制剂) |
在研适应症 |
非在研适应症 |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评突破性疗法 (中国)、快速通道 (美国) |
登录后查看时间轴
结构/序列
分子式C28H28F4N6O4 |
InChIKeyULMMVBPTWVRPSI-UHFFFAOYSA-N |
CAS号1227948-82-4 |
关联
22
项与 Ifebemtinib 相关的临床试验NCT07441174
A Multicenter, Open-Label, Phase Ib/II Clinical Trial of IN10018 in Combination With RNK08954 for the Treatment of KRASG12D Mutation-Positive Locally Advanced or Metastatic Solid Tumors
NCT07174908
A Phase 3 Multicenter, Randomized, Controlled, and Open-Label Study of IN10018 in Combination With D-1553 Versus Standard Therapy for the Treatment of First Line Locally-advanced or Metastatic Non-squamous Non-small Cell Lung Cancer With KRAS G12C Mutation
NCT05982522
A Multicenter, Open-Label, Randomized, Phase Ib/II Clinical Trial to Evaluate the Efficacy, Safety, Tolerability, and Pharmacokinetics of IN10018 Combined With Taxane and Anti-PD-1/L1 Monoclonal Antibody in Previously-treated Solid Tumors
100 项与 Ifebemtinib 相关的临床结果
登录后查看更多信息
100 项与 Ifebemtinib 相关的转化医学
登录后查看更多信息
100 项与 Ifebemtinib 相关的专利（医药）
登录后查看更多信息
14
项与 Ifebemtinib 相关的文献（医药）2021-12-01Discover. Oncology
Focal adhesion kinase inhibitor BI 853520 inhibits cell proliferation, migration and EMT process through PI3K/AKT/mTOR signaling pathway in ovarian cancer
Article
作者: Li, Hong ; Ren, Chenchen ; Gao, Yizhi
Abstract:
Focal adhesion kinase (FAK) activation has been reported to be associated with cell progression and metastasis in a wide variety of cancer cells. Target treatment by inhibiting FAK has achieved remarkable effects in several cancers, but the effect in ovarian cancer has not been reported. In this study, we determined the role and the underlying molecular mechanism of BI853520, a novel small chemical FAK inhibitor against ovarian cancer. Results show that phosphorylated FAK tyrosine 397 (p-FAK Y397) is highly expressed in ovarian cancer tumor tissues and cell lines (SKOV3 and OVCAR3). BI853520 treatment greatly suppresses cell proliferation, viability, migration, invasion, decreases anchorage-independent growth and motility in vitro. Besides, treatment with BI853520 increases biologic effects following combination with chemotherapy in ovarian cancer cell lines. In addition, BI853520 suppresses EMT in ovarian cancer cell lines. Mechanically, BI853520 treatment downregulates the activation of PI3K/AKT/mTOR signal pathway. Finally, mice model experiments confirm BI853520 treatment dramatically reduces tumor growth in vivo and suppresses the activation of PI3K/AKT/mTOR signal pathway. Taken together, our findings demonstrate that focal adhesion kinase inhibitor BI853520 inhibits cell proliferation, migration, invasion and EMT process through PI3K/AKT/mTOR signaling pathway in ovarian cancer, and BI853520 can offer a preclinical rationale for targeting repression of FAK in ovarian cancer.
2021-08-01Advanced science (Weinheim, Baden-Wurttemberg, Germany)1区 · 材料科学
Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling
1区 · 材料科学
ArticleOA
作者: Jiangwei Zhang ; Ruibao Ren ; Bo Jiao ; Baoyuan Zhang ; Yan Zhang ; Ping Liu ; Zaiqi Wang
Abstract:
KRAS mutation is one of the most prevalent genetic drivers of cancer development, yet KRAS mutations are until very recently considered undruggable. There are ongoing trials of drugs that target the KRAS G12C mutation, yet acquired drug resistance from the extended use has already become a major concern. Here, it is demonstrated that KRAS G12C inhibition induces sustained activation of focal adhesive kinase (FAK) and show that a combination therapy comprising KRAS G12C inhibition and a FAK inhibitor (IN10018) achieves synergistic anticancer effects. It can simultaneously reduce the extent of drug resistance. Diverse CDX and PDX models of KRAS G12C mutant cancer are examined and synergistic benefits from the combination therapy are consistently observed. Mechanistically, it is found that both aberrant FAK–YAP signaling and FAK‐related fibrogenesis impact on the development of KRAS G12C inhibitor resistance. This study thus illustrates the mechanism of resistance of cancer to the treatment of KRAS G12C inhibitor, as well as an innovative combination therapy to improve treatment outcomes for KRAS G12C mutant cancers.
2021-06-01Arabian Journal of Chemistry
Molecular description of pyrimidine-based inhibitors with activity against FAK combining 3D-QSAR analysis, molecular docking and molecular dynamics
作者: Guijuan Cheng ; Zhihai Sui ; Ran Li ; Wei Yang ; Fangfang Wang ; Bo Zhou
Focal adhesion kinase (FAK) is a promising target for developing more effective anticancer drugs.To better understand the structure-activity relationships and mechanism of actions of FAK inhibitors, a mol. modeling study using 3D-QSAR, mol. docking, mol. dynamics simulations, and binding free energy anal. were conducted.Two types of satisfactory 3D-QSAR models were generated, comprising the CoMFA model (R2cv = 0.528, R2pred = 0.7557) and CoMSIA model (R2cv = 0.757, R2pred = 0.8362), for predicting the inhibitory activities of novel inhibitors.The derived contour maps indicate structural characteristics for substituents on the template.Mol. docking, mol. dynamic simulations and binding free energy calculations further reveal that the binding of inhibitors to FAK is mainly contributed from hydrophobic, electrostatic and hydrogen bonding interactions.In addition, some key residues (Arg14, Glu88, Cys90, Arg138, Asn139, Leu141, and Leu155) responsible for ligand-receptor binding are highlighted.All structural information obtained from 3D-QSAR models and mol. dynamics is consist with the available exptl. activities.All the results will facilitate the optimization of this series of FAK inhibitors with higher inhibitory activities.
160
项与 Ifebemtinib 相关的新闻（医药）2026-04-23
AACR会议临床结果临床1期
100 项与 Ifebemtinib 相关的药物交易
登录后查看更多信息
研发状态
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| KRAS G12C突变非鳞状非小细胞肺癌 | 临床3期 | 中国 | 2025-10-09 | |
| 非鳞状非小细胞肺癌 | 临床3期 | 中国 | 2025-09-10 | |
| 复发性铂耐药性卵巢癌 | 临床3期 | 中国 | 2022-08-29 | |
| 复发性铂耐药性卵巢癌 | 临床3期 | 中国香港 | 2022-08-29 | |
| KRAS G12D突变实体瘤 | 临床2期 | 中国 | 2026-01-19 | |
| 广泛期小细胞肺癌 | 临床2期 | 中国 | 2023-10-30 | |
| EGFR阳性非小细胞肺癌 | 临床2期 | 中国 | 2023-07-13 | |
| 不能切除性胰腺癌 | 临床2期 | 中国 | 2022-12-08 | |
| 胰腺导管腺癌 | 临床2期 | 中国 | 2022-12-08 | |
| 晚期结直肠腺癌 | 临床2期 | 中国 | 2022-10-12 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床1/2期 | - | (KRAS G12C NSCLC) | 窪窪夢鏇淵膚衊鬱繭齋(遞艱蓋襯範鏇襯選艱鹹) = 選選窪艱構顧鹽鹹膚積 鹹遞鏇鑰淵願範鹹糧鹹 (襯築壓淵選夢觸顧窪糧 ) 更多 | 积极 | 2025-05-30 | ||
廠鹽鹹鹽憲獵齋願鑰淵(鏇壓鹹觸蓋築醖觸顧蓋) = 衊簾壓簾艱醖窪鏇餘繭 獵鑰範範簾遞顧膚積廠 (鹹蓋餘簾窪蓋願廠遞製, 81.5 ~ 100.0) 更多 | |||||||
临床1/2期 | 48 | 蓋憲廠鑰鏇鹽選壓顧願(鑰壓鹽膚淵餘衊觸積襯) = 7 pts (14.6%) had ifebemtinib-related SAEs, and 6 (12.5%) were also considered D-1553 related. 構鬱鏇網糧艱繭積蓋鏇 (範憲糧醖衊願齋衊膚鏇 ) 更多 | 积极 | 2024-09-14 | |||
(KRAS G12C mutant metastatic CRC) | |||||||
NEWS 人工标引  | 临床1/2期 | 33 | 襯獵積顧顧構遞鹹獵廠(鬱願淵製憲鑰遞餘鏇夢) = 選淵蓋窪淵願積壓簾糧 襯憲鑰築築淵齋艱築鹽 (鏇鬱鑰餘淵鹹齋網鏇繭 ) 更多 | 积极 | 2024-06-03 | ||
临床1/2期 | 33 | 衊觸製膚獵繭製壓獵觸(鹽糧築願衊壓鑰選鬱衊) = Four subjects (12.1%) had ifebemtinib-related SAEs (diarrhea, enteritis, oedema peripheral and proteinuria) as assessed by investigators, and all SAEs were also considered D-1553 related. 廠範鬱鏇壓鑰襯衊壓顧 (遞窪廠醖製鏇觸願衊淵 ) 更多 | 积极 | 2024-05-24 | |||
临床1/2期 | 26 | IN10018+PLD | 鹽醖衊鏇憲鬱憲鹹醖網(淵糧範鑰襯憲鑰夢鹽膚) = 壓餘鹽鏇簾顧築餘蓋鹽 鹽餘窪憲顧範願鹽繭鹹 (壓廠積餘艱獵淵選糧選, 2.1 ~ 48.4) 更多 | 积极 | 2023-10-21 | ||
鹽醖衊鏇憲鬱憲鹹醖網(淵糧範鑰襯憲鑰夢鹽膚) = 鹹艱蓋廠襯觸糧築簾齋 鹽餘窪憲顧範願鹽繭鹹 (壓廠積餘艱獵淵選糧選, 3.8 ~ 42.8) 更多 | |||||||
临床1期 | 50 | 糧淵鹽艱範顧衊鬱觸廠(鑰積憲鹽網觸糧選憲醖) = 醖選醖夢醖醖觸鹹積艱 淵積壓夢壓鹽繭構選簾 (構範製鹹壓鑰網製齋鹽 ) 更多 | 积极 | 2022-11-11 | |||
临床1期 | 50 | IN10018 100mg QD + PLD 40mg/m2 Q4W | 夢衊選艱築鬱製獵淵淵(齋襯壓艱選壓顧鑰醖繭) = 醖膚憲鹽築蓋鹹鹽憲製 糧膚淵淵構衊獵鬱夢願 (醖齋選齋夢艱觸鹹顧窪, 38.7% ~ 70.2%) 更多 | 积极 | 2022-09-21 | ||
ASCO2022 人工标引 | 临床1期 | 42 | 範遞艱繭網衊顧廠鬱顧(繭鏇選積蓋遞齋顧選廠) = 襯鬱鑰遞鹽網鏇膚選鏇 齋鬱構構積觸壓鏇餘夢 (鏇膚廠繭鏇選齋衊繭網, 37.4 ~ 74.5) 更多 | 积极 | 2022-06-02 | ||
(patients who had at least 6 months of follow up) | 範遞艱繭網衊顧廠鬱顧(繭鏇選積蓋遞齋顧選廠) = 網網築襯襯製夢齋糧築 齋鬱構構積觸壓鏇餘夢 (鏇膚廠繭鏇選齋衊繭網, 40.8 ~ 84.6) 更多 | ||||||
临床1期 | 96 | (200 mg QD) | 淵鬱築鹹簾鬱淵衊簾憲(憲廠餘願築淵窪選觸構) = 鏇齋廠淵齋艱糧遞鹹襯 網蓋選鹽襯顧選衊壓蓋 (淵壓繭鬱鏇憲鹽構鑰鹽 ) 更多 | 积极 | 2019-02-01 | ||
構襯鏇繭繭遞築願窪獵(觸構醖鏇醖觸構夢觸窪) = 顧簾獵襯糧鏇構廠窪齋 膚鏇簾鑰鏇製遞鹹壓夢 (積築簾繭範鏇獵網鹽觸 ) 更多 | |||||||
临床1期 | 21 | 淵艱廠鑰衊獵範襯襯築(鏇鏇餘鏇鬱憲鹹鹹願餘) = 膚蓋鬱獵膚鬱構鏇選繭 憲齋餘觸齋鑰願壓蓋艱 (鑰鏇積願構夢淵鹽餘願 ) 更多 | 积极 | 2019-02-01 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用