预约演示
更新于：2026-08-17
Conteltinib
康特替尼
更新于：2026-08-17
概要
基本信息
药物类型 小分子化药 |
别名 康太替尼、CT-707、SY-707 + [1] |
作用方式 抑制剂、拮抗剂 |
作用机制 ALK抑制剂(间变性淋巴瘤激酶抑制剂)、IGF-1R拮抗剂(胰岛素样生长因子-I受体拮抗剂)、PYK2抑制剂(局部粘着斑激酶2抑制剂) |
在研适应症 |
非在研适应症 |
原研机构 |
在研机构 |
非在研机构- |
权益机构- |
最高研发阶段批准上市 |
首次获批日期 中国 (2026-06-10), |
最高研发阶段(中国)批准上市 |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C32H45N9O3S |
InChIKeyNPJCURIANJMFEO-UHFFFAOYSA-N |
CAS号1384860-29-0 |
关联
11
项与 康特替尼 相关的临床试验NCT06970132
A Phase Ib/II, Open-Label Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Preliminary Efficacy of SY-5933 Tablets in Combination With CT-707 Tablets in Patients With Advanced Solid Tumors Harboring KRAS p.G12C Mutation
CTR20222060
评价CT-707联合特瑞普利单抗注射液和吉西他滨在晚期胰腺癌患者中的安全性、耐受性、药代动力学和有效性的Ib/II 期研究
NCT05580445
A Phase Ib/II, Open-label, Dose-escalation and Dose-expansion Study to Evaluate the Safety, Tolerability, Pharmacokinetics and Antineoplastic Activity of CT-707 in Combination With Toripalimab and Gemcitabine in Advanced Pancreatic Cancer
100 项与 康特替尼 相关的临床结果
登录后查看更多信息
100 项与 康特替尼 相关的转化医学
登录后查看更多信息
100 项与 康特替尼 相关的专利（医药）
登录后查看更多信息
11
项与 康特替尼 相关的文献（医药）2022-12-01BMC cancer2区 · 医学
CT-707 overcomes hypoxia-mediated sorafenib resistance in Hepatocellular carcinoma by inhibiting YAP signaling
2区 · 医学
ArticleOA
作者: Zhu, Hong ; Xie, Qin ; Lin, Nengmin ; Yuan, Tao ; Zhang, Bo ; Chen, Zibo ; Yan, Fangjie ; Ye, Song ; He, Qiaojun ; Yang, Bo
Abstract:
Background:
Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Sorafenib is the first-line treatment for advanced HCC, but the anti-cancer effects remain to be improved as indicated by its low response rates and failure to prolong the progression-free survival (PFS). Thus, it is urgent to explore approaches to improve the clinical outcome.
Materials and methods:
The effect of Sorafenib in HCC was analyzed by SRB (sulforhodamine B) assay in normoxia and hypoxia, respectively. The different dose combination effect of CT707 and sorafenib was analyzed by SRB assay in hypoxia. Flow cytometry assay was used to detect the cell apoptosis rate with CT707 and sorafenib treatment in hypoxia. Western blotting was used to detect the expression levels of apoptosis -related proteins and the mechanism of CT707 overcome the resistance of sorafenib in hypoxia.
Results:
Our study showed that the characteristic intratumor hypoxia of advanced HCC is one of the major factors which mediated the drug resistance towards sorafenib in HCC. And CT-707, a novel multi-kinase inhibitor, could sensitize the hypoxic HCC cells towards sorafenib. Further studies showed that CT-707 abolished the nuclear translocation of Yes Associate-Protein (YAP), which has been demonstrated as one of mechanism of hypoxia-mediated sorafenib-resistance in HCC.
Conclusions:
Overall, this study not only favors the development of this novel multi-kinase inhibitor CT-707 as a therapeutic agent against HCC, but also provides a potential strategy to overcome the hypoxia-mediated resistance to sorafenib in HCC patients.
2022-02-01Acta biochimica et biophysica Sinica2区 · 生物学
SY-707, an ALK/FAK/IGF1R inhibitor, suppresses growth and metastasis of breast cancer cells
2区 · 生物学
Article
作者: Liu, Shuang ; Niu, Jing ; Liu, Xijie ; Sun, Yinghui ; Liu, Ping ; Chu, Qiaoyun
Focal adhesion kinase (FAK), a multi-functional cytoplasmic tyrosine kinase, plays a critical role in cancer migration, proliferation and metastasis via regulating multiple signaling pathways. SY-707 is an anaplastic lymphoma kinase (ALK)/FAK/type 1 insulin-like growth factor receptor (IGF1R) multi-kinase inhibitor which is now being evaluated in phase II clinical trials for ALK positive non-small cell lung cancer (NSCLC). However, the effect of SY-707 on breast cancer is unknown. In this study, we assessed preclinical the anti-growth and anti-metastasis potency of SY-707 in breast cancer cells. ATP content, PE-Annexin V, and would healing assays were used to examine cell proliferation, cell cycle and migration. Then, SD rat and beagle dog models were used to evaluate the pharmacokinetics profile of SY-707, and mouse xenograft model was used to evaluate the anti-cancer activities of SY-707 . We found that breast cancer cells apoptosis were induced by SY-707. Moreover, SY-707 exerted inhibition on cell migration and adhesion in a dose-dependent manner. In T47D xenograft mice, SY-707 had significant anti-tumor activities alone or synergistically with Paclitaxel. Meanwhile, SY-707 also displayed significant suppression on spontaneous metastasis of tumor to the lung in 4T1 murine breast cancer xenograft model. In conclusion, SY-707 has potent anti-proliferation and anti-migration potential in breast cancer and , implying its therapeutic application for the treatment of breast cancer in future clinical trials.
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.
100 项与 康特替尼 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| ALK阳性非小细胞肺癌 | 中国 | 2026-06-10 |
未上市
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 |
|---|---|---|---|---|
| 局部晚期恶性实体瘤 | 临床2期 | 中国 | 2025-06-01 | |
| 胰腺癌 | 临床2期 | 中国 | 2022-10-19 | |
| 晚期胰腺腺癌 | 临床2期 | 中国 | 2022-08-11 | |
| 非小细胞肺癌 | 临床1期 | 中国 | 2020-10-21 | |
| KRAS G12C突变的实体瘤 | 临床申请批准 | 中国 | 2025-02-17 | |
| 肝细胞癌 | 临床前 | 中国 | 2016-12-01 | |
| 肝细胞癌 | 临床前 | 中国 | 2016-12-01 |
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
| - | 414 | 製蓋顧艱構觸窪觸積蓋(願壓顧範鹽膚壓艱鹹鬱) = Clinical results have reached the endpoint 窪餘遞構夢觸網鑰繭遞 (醖積窪糧獵遞願築築膚 ) | 积极 | 2024-10-23 | |||
临床1期 | 60 | (ALK TKI-naïve) | 糧積餘醖窪壓鹽餘壓鹽(鏇鹹淵範廠選淵糧夢廠) = MTD was not reached 糧餘醖簾醖膚鹹選憲蓋 (願蓋鑰鬱餘鏇鑰積憲齋 ) 更多 | 积极 | 2022-11-23 | ||
(received crizotinib previously) | |||||||
临床1期 | 13 | 鹽構鬱繭鏇選憲願艱網(鏇獵簾憲淵繭鹹遞襯鬱) = diarrhea 92%, elevated aspartate aminotransferase 61%, elevated alanine aminotransferase 54%, hair loss 38%, vomiting 31% 選艱鏇顧憲鏇顧鹹膚簾 (齋壓構繭鏇壓餘糧夢鹽 ) 更多 | 积极 | 2019-11-23 | |||
临床1期 | ALK阳性非小细胞肺癌 ALK Positive | 23 | 膚鹹淵醖膚衊艱簾夢鑰(構鹹蓋顧醖觸簾壓構鏇) = none 顧鑰製壓夢艱選觸齋願 (衊網鬱窪糧夢醖願顧築 ) 更多 | 积极 | 2017-11-18 |
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
提出任何生物医药研究问题
让每一步生物医药决策都精准制胜
基于十亿级生物数据与全球情报的精准 AI，赋能早期药物发现
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。
立即接入生物医药数据包
智慧芽新药库数据也通过智慧芽开放平台，以MCP或API服务形式对外开放。立即使用我们的MCP服务定制您的LLM智能体。
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