预约演示
更新于：2025-03-29
LCL-161
更新于：2025-03-29
概要
基本信息
在研机构- |
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)- |
特殊审评- |
登录后查看时间轴
结构/序列
分子式C26H33FN4O3S |
InChIKeyUFPFGVNKHCLJJO-SSKFGXFMSA-N |
CAS号1005342-46-0 |
关联
8
项与 LCL-161 相关的临床试验NCT03111992
Phase I/Ib, Multi-center, Open-label, Study of Single Agent CJM112, and PDR001 in Combination With LCL161 or CJM112 in Patients With Relapsed and/or Refractory Multiple Myeloma
NCT02890069
Phase Ib, Open-label, Multi-center Study to Characterize the Safety, Tolerability and Pharmacodynamics (PD) of PDR001 in Combination With LCL161, Everolimus (RAD001) or Panobinostat (LBH589)
NCT02649673
Phase Ib Dose-Escalation Study of LCL161 in Combination With Oral Topotecan for Patients With Relapsed/Refractory Small Cell Lung Cancer (SCLC) and Select Gynecologic Malignancies
100 项与 LCL-161 相关的临床结果
登录后查看更多信息
100 项与 LCL-161 相关的转化医学
登录后查看更多信息
100 项与 LCL-161 相关的专利（医药）
登录后查看更多信息
175
项与 LCL-161 相关的文献（医药）2025-05-24Journal of biomolecular structure & dynamics
Integration analysis of PLAUR as a sunitinib resistance and macrophage related biomarker in ccRCC, an in silicon and experimental study
Article
作者: Gan, Sishun ; Li, Lin ; Jiang, Aimin ; Chu, Jian ; Yang, Qiwei ; Cao, Jianwei ; Ye, Fangdie ; Tian, Yijun
Sunitinib remains the preferred systemic treatment option for specific patients with advanced RCC who are ineligible for immune therapy. However, it's essential to recognize that Sunitinib fails to elicit a favourable response in all patients. Moreover, most patients eventually develop resistance to Sunitinib. Therefore, identifying new targets associated with Sunitinib resistance is crucial. Utilizing multiple datasets from public cohorts, we conducted an exhaustive analysis and identified a total of 8 microRNAs and 112 mRNAs displaying significant expression differences between Sunitinib responsive and resistant groups. A particular set of six genes, specifically NIPSNAP1, STK40, SDC4, NEU1, TBC1D9, and PLAUR, were identified as highly significant via WGCNA. To delve deeper into the resistance mechanisms, we performed additional investigations using cell, molecular, and flow cytometry tests. These studies confirmed PLAUR's pivotal role in fostering Sunitinib resistance, both in vitro and in vivo. Our findings suggest that PLAUR could be a promising therapeutic target across various cancer types. In conclusion, this investigation not only uncovers vital genes and microRNAs associated with Sunitinib resistance in RCC but also introduces PLAUR as a prospective therapeutic target for diverse cancers. The outcomes contribute to advancing personalized healthcare and developing superior therapeutic strategies.
2025-03-01BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
NetSDR: Drug repurposing for cancers based on subtype-specific network modularization and perturbation analysis
Article
作者: Li, Wei ; Li, Wanshi ; Hu, Guang ; Xu, Zhen ; Yang, Bin
Cancer, a heterogeneous disease, presents significant challenges for drug development due to its complex etiology. Drug repurposing, particularly through network medicine approaches, offers a promising avenue for cancer treatment by analyzing how drugs influence cellular networks on a systemic scale. The advent of large-scale proteomics data provides new opportunities to elucidate regulatory mechanisms specific to cancer subtypes. Herein, we present NetSDR, a Network-based Subtype-specific Drug Repurposing framework for prioritizing repurposed drugs specific to certain cancer subtypes, guided by subtype-specific proteomic signatures and network perturbations. First, by integrating cancer subtype information into a network-based method, we developed a pipeline to recognize subtype-specific functional modules. Next, we conducted drug response analysis for each module to identify the "therapeutic module" and then used deep learning to construct weighted drug response network for the particular subtype. Finally, we employed a perturbation response scanning-based drug repurposing method, which incorporates dynamic information, to facilitate the prioritization of candidate drugs. Applying the framework to gastric cancer, we attested the significance of the extracellular matrix module in treatment strategies and discovered a promising potential drug target, LAMB2, as well as a series of possible repurposed drugs. This study demonstrates a systems biology framework for precise drug repurposing in cancer and other complex diseases.
2025-01-01BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
cIAP2 supports the cell growth-promoting activity of FMR1 in gastric cancer via CARD-RING domains
Article
作者: Seo, Tae Woong ; Yoo, Soon Ji ; Kang, Ji Woo ; Lee, Yui Taek ; Heo, Jeong In
Fragile X Mental Retardation Protein 1 (FMR1) is a translational repressor crucial for regulating genes in the central nervous system. While a lack of FMR1 expression causes Fragile X Syndrome (FXS), its overexpression is implicated in various cancers, necessitating tight regulation of FMR1 protein levels for normal cell physiology. In this study, we report that FMR1 is upregulated in gastric cancer patients. Reducing FMR1 expression decreased cell growth in gastric cancer cell lines. The Smac Mimetic LCL161 reduced both FMR1 and cellular inhibitor of apoptosis protein 2 (cIAP2) levels. Suppressing cIAP2, but not cIAP1, led to decreased FMR1, while cIAP2 overexpression increased FMR1 in gastric cancer cells. We observed that cIAP2 is also upregulated in gastric cancer patients, with FMR1 and cIAP2 levels positively correlated in both gastric and colorectal cancers. Notably, cIAP2 binds FMR1 via its CARD domain, unlike most cIAP2 targets that bind the BIR domain. Furthermore, cIAP2 ubiquitinates FMR1 through its CARD-RING domains, stabilizing the protein without proteasomal degradation. FMR1, modulated by cIAP2, promotes gastric cancer cell growth. Collectively, our findings highlight FMR1's growth-promoting role in gastric cancer and reveal a novel function of cIAP2 in stabilizing FMR1 as an E3 ligase. These results suggest targeting cIAP2 could be an effective strategy for treating gastric cancer by downregulating both cIAP2 and FMR1.
1
项与 LCL-161 相关的新闻（医药）2022-07-20
免疫疗法放射疗法AACR会议突破性疗法First in Class
100 项与 LCL-161 相关的药物交易
登录后查看更多信息
外链
| KEGG | Wiki | ATC | Drug Bank |
|---|---|---|---|
| - | - | - |
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 |
|---|---|---|---|---|
| 三阴性乳腺癌 | 临床2期 | 美国 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 澳大利亚 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 巴西 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 捷克 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 德国 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 爱尔兰 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 意大利 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 俄罗斯 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 韩国 | 2012-08-01 | |
| 三阴性乳腺癌 | 临床2期 | 西班牙 | 2012-08-01 |
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
临床1期 | 35 | 醖獵窪窪鹽顧築壓淵觸(糧遞積糧夢窪積糧積遞) = 憲衊築繭鬱鬱窪觸願壓 鏇壓鹹範鹹蓋構糧選餘 (廠膚夢淵壓膚憲衊選繭 ) 更多 | 不佳 | 2023-05-02 | |||
临床2期 | 三阴性乳腺癌 ER Negative | PR Negative | HER2 Negative | 209 | 顧壓遞鑰鹽構餘鹹範網(築膚廠壓網鹽簾簾餘網) = 齋餘憲範遞衊醖夢鑰構 鹹醖鹹蓋獵築鏇糧網蓋 (鏇顧選顧壓選觸鬱鑰襯 ) 更多 | 积极 | 2018-09-20 | ||
顧壓遞鑰鹽構餘鹹範網(築膚廠壓網鹽簾簾餘網) = 餘餘製製觸夢選鹽遞簾 鹹醖鹹蓋獵築鏇糧網蓋 (鏇顧選顧壓選觸鬱鑰襯 ) 更多 | |||||||
临床2期 | 三阴性乳腺癌 新辅助 | 209 | 餘鏇範窪積簾窪鬱簾鏇(衊獵簾窪鏇壓廠鏇廠簾) = 鹽壓壓鏇糧獵餘壓憲夢 構鹹糧壓餘構襯觸襯齋 (鬱糧襯膚範蓋觸淵衊醖 ) | - | 2015-05-20 | ||
餘鏇範窪積簾窪鬱簾鏇(衊獵簾窪鏇壓廠鏇廠簾) = 膚鏇製鏇網糧鏇窪鹹鹽 構鹹糧壓餘構襯觸襯齋 (鬱糧襯膚範蓋觸淵衊醖 ) | |||||||
临床1期 | 27 | 夢憲艱觸構遞願淵築淵(鏇蓋糧衊艱醖糧願襯築) = 夢艱繭鏇夢築築簾糧齋 鑰糧構廠製製築壓蓋憲 (壓淵鬱憲築夢積網構築 ) | - | 2010-04-15 |
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
来和芽仔聊天吧
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