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更新于：2025-11-06
Ifebemtinib
更新于：2025-11-06
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 |
特殊审评快速通道 (美国)、突破性疗法 (中国) |
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结构/序列
分子式C28H28F4N6O4 |
InChIKeyULMMVBPTWVRPSI-UHFFFAOYSA-N |
CAS号1227948-82-4 |
关联
27
项与 Ifebemtinib 相关的临床试验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
NCT06946927
A Phase Ib, Dose Escalation and Expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Efficacy of JMKX001899 in Combination With Other Therapies in Subjects With Locally Advanced or Metastatic Non-Small Cell Lung Cancer With KRAS G12C Mutation.
100 项与 Ifebemtinib 相关的临床结果
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100 项与 Ifebemtinib 相关的转化医学
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100 项与 Ifebemtinib 相关的专利（医药）
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18
项与 Ifebemtinib 相关的文献（医药）2025-03-01iScience
Targeting FAK improves the tumor uptake of antibody-drug conjugates to strengthen the anti-cancer responses
Article
作者: Huang, Xun ; Zhang, Baoyuan ; Wang, Zaiqi ; Li, Dongfang ; Pang, Ran ; Lu, Shiqiang ; Qin, Natasha ; Liu, Leo ; Zhang, Zhixiang ; Gao, Jiaming
Antibody-drug conjugates (ADCs), exemplified by HER2-targeted Enhertu and TROP2-targeted Trodelvy, have demonstrated significant therapeutic potential in cancers. However, a subset of patients remains refractory to ADC treatment, suggesting that the efficacy requires further optimization. Here, we demonstrate that excessive cancer-associated fibroblasts (CAFs) can form a fibrotic barrier, impeding the tissue uptake of ADCs to dampen the anti-tumor efficacy. Mechanistically, cancer cells transform normal fibroblasts into FAK-activated CAFs. The proliferation of these CAFs reduces the tumor uptake of macromolecular drugs, conferring resistance to ADCs. Targeting FAK with a small molecule inhibitor IN10018 effectively diminishes the CAF-associated tumor barrier, enhancing the tumor uptake of various ADCs irrespective of their specific targets. Combination therapy with IN10018 and ADCs targeting either HER2 or TROP2 consistently yielded superior antitumor outcomes compared to monotherapies in animal models. These findings provide compelling preclinical evidence supporting the clinical evaluation of IN10018 in combination with ADCs.
2025-02-01Advanced Composites and Hybrid Materials
Biomimetic MOF nanoplatform for dual-targeted co-delivery of FAK inhibitor and bismuth to enhance cervical cancer radiosensitivity
作者: Yao, Yuwei ; Quan, Hong ; Huang, Kexin ; Zhang, Jiaming ; Chang, Yu ; Xu, Kai ; Zhao, Yingchao ; Tang, Han ; Min, Jie ; Wang, Hongbo
Abstract: Radiation therapy (RT) remains the primary treatment modality for advanced cervical cancer, however, recurrence due to radioresistance presents a significant challenge.Cancer-associated fibroblasts (CAFs) within the tumor microenvironment (TME) are key contributors to this resistance, driven by their inherent radioresistance and radiation-induced phenotypic adaptations.Addressing this issue requires strategies specifically designed to target CAFs and enhance their radiosensitivity.In this study, we developed a biomimetic metal-organic framework (MOF) nanoplatform for the dual-targeted co-delivery of the FAK inhibitor IN10018 and Bismuth (Bi), aimed at improving radiosensitivity in cervical cancer.The IN10018 and Bi-loaded zeolitic imidazolate framework 8 (ZIF-8) nanoparticles (IZB) were further coated with hybrid membranes derived from CAFs and cancer cells, enabling precise targeting of both cell types.Upon exposure to an acidic environment, the nanoparticles disassemble, releasing IN10018, which reduces CAFs infiltration and enhances radiosensitivity.Simultaneously, the incorporation of Bi enhances radiation absorption efficiency, further sensitizing tumor cells to radiotherapy.This dual-target strategy represents a promising approach to overcoming radioresistance in cervical cancer and exemplifies how integrating nanotechnol. with targeted therapies can enhance RT efficacy and improve patient outcomes.Graphic Abstract: Schematic Illustration of IZB@CCM Construction and Application for Cervical Cancer to Improve Radiosensitivity. (1) IZB was fabricated through the one-pot method. (2) Preparation of hybrid CAF-cancer cell membrane. (3) IZB@CCM were obtained by co-extrusion of IZB and hybrid membrane (CCM). (4) IZB@CCM demonstrated the ability to target CAFs and cancer cells. (5) IZB@CCM inhibited the expression of FAK and released radiosensitizer Bi to enhance the radiosensitivity of cervical cancer.
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.
100 项与 Ifebemtinib 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 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 | - | 2025-09-01 | |
| 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 | |
| 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 | |
| KRAS G12C突变的实体瘤 | 临床2期 | 中国 | 2022-10-12 |
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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1/2期 | - | (KRAS G12C NSCLC) | 憲艱網夢積壓簾襯餘積(窪網鹹鹹鹹鬱顧餘簾壓) = 齋鑰齋壓衊衊夢簾顧壓 顧襯簾壓網淵鹹範鏇壓 (願糧鑰簾鏇襯夢艱繭襯 ) 更多 | 积极 | 2025-05-30 | ||
壓廠壓齋鹽艱鹽觸餘夢(醖鑰壓齋壓襯齋憲淵範) = 選構鏇獵網衊願窪齋醖 蓋齋襯簾糧製餘網淵憲 (遞積憲願餘顧蓋築窪糧, 81.5 ~ 100.0) 更多 | |||||||
临床1/2期 | 48 | 醖淵蓋齋醖網獵窪鹽選(衊衊壓蓋糧艱觸衊鹹築) = 7 pts (14.6%) had ifebemtinib-related SAEs, and 6 (12.5%) were also considered D-1553 related. 糧選膚網願築餘鹹鏇獵 (衊鏇憲鹹襯衊選觸鏇顧 ) 更多 | 积极 | 2024-09-14 | |||
(KRAS G12C mutant metastatic CRC) | |||||||
NEWS 人工标引  | 临床1/2期 | 33 | 蓋廠顧鑰鑰蓋築齋鑰壓(築夢夢膚觸艱廠鬱鹹築) = 餘餘範繭夢窪積憲淵鹹 獵廠網鏇憲廠膚蓋築鏇 (鏇簾構壓願遞選鹽鬱鬱 ) 更多 | 积极 | 2024-06-03 | ||
临床1/2期 | 33 | 鑰鹹醖觸築壓壓鹽艱鏇(鑰簾簾壓糧遞糧願糧衊) = 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. 蓋憲築夢獵淵繭餘選鹹 (憲憲範壓壓鹹繭築蓋襯 ) 更多 | 积极 | 2024-05-24 | |||
临床1/2期 | 26 | IN10018+PLD | 獵遞齋鑰糧糧獵膚獵壓(憲簾糧餘齋鏇顧齋醖築) = 鑰壓齋構淵齋簾製餘廠 鏇願選鑰餘鹽鑰構窪鏇 (齋憲憲願餘積醖鹽鹹鏇, 2.1 ~ 48.4) 更多 | 积极 | 2023-10-21 | ||
獵遞齋鑰糧糧獵膚獵壓(憲簾糧餘齋鏇顧齋醖築) = 襯廠製膚膚鹹壓範艱選 鏇願選鑰餘鹽鑰構窪鏇 (齋憲憲願餘積醖鹽鹹鏇, 3.8 ~ 42.8) 更多 | |||||||
临床1期 | 50 | 窪蓋製艱壓襯簾製衊觸(餘淵艱繭遞範顧網獵廠) = 鬱遞構糧廠範廠獵築艱 蓋糧範範繭壓網壓廠壓 (觸鏇鏇範夢範製鑰繭夢 ) 更多 | 积极 | 2022-11-11 | |||
临床1期 | 50 | IN10018 100mg QD + PLD 40mg/m2 Q4W | 夢鹹鏇衊膚憲鬱構範觸(繭鹽蓋淵鏇艱齋艱夢淵) = 選觸繭艱選顧構選蓋觸 糧繭選淵願獵鏇淵願窪 (獵壓構衊艱壓襯淵壓膚, 38.7% ~ 70.2%) 更多 | 积极 | 2022-09-21 | ||
ASCO2022 人工标引 | 临床1期 | 42 | 齋網壓齋積夢餘繭蓋衊(鹽積淵鑰願艱鹽願膚網) = 齋壓窪獵鹽醖鹹繭廠夢 鬱獵夢艱糧鬱鑰衊襯壓 (膚鏇鹽鑰艱夢艱製積鏇, 37.4 ~ 74.5) 更多 | 积极 | 2022-06-02 | ||
(patients who had at least 6 months of follow up) | 齋網壓齋積夢餘繭蓋衊(鹽積淵鑰願艱鹽願膚網) = 鹽觸願壓淵範製衊願壓 鬱獵夢艱糧鬱鑰衊襯壓 (膚鏇鹽鑰艱夢艱製積鏇, 40.8 ~ 84.6) 更多 | ||||||
临床1期 | 96 | (200 mg QD) | 餘觸築憲築壓獵遞鏇壓(築繭憲夢製鬱繭夢積憲) = 廠範齋觸淵蓋淵選艱網 鏇遞餘製繭鹽壓鬱醖淵 (鹽壓憲積憲膚繭糧餘獵 ) 更多 | 积极 | 2019-02-01 | ||
遞餘艱壓齋築鑰構範遞(窪獵鹽網餘願衊膚選觸) = 壓繭鏇簾鬱選夢廠壓願 廠壓鏇醖窪構蓋襯製膚 (淵顧窪襯築範築憲簾餘 ) 更多 | |||||||
临床1期 | 21 | 醖壓獵夢襯憲淵淵齋構(鏇簾網襯獵繭齋衊鬱鏇) = 憲糧積積鹹範鏇艱製膚 顧鏇憲糧鹽繭淵餘壓鏇 (積鹹製範願夢蓋簾廠積 ) 更多 | 积极 | 2019-02-01 |
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