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更新于：2025-05-31
CC-90001
更新于：2025-05-31
概要
基本信息
原研机构 |
在研机构- |
非在研机构 |
权益机构- |
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- |
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结构/序列
分子式C16H27N5O2 |
InChIKeyQBBRJRLJWXRSHQ-CKYFFXLPSA-N |
CAS号1403859-14-2 |
关联
10
项与 CC-90001 相关的临床试验CTIS2022-500930-27-00
- IM043-004
NCT04655898
A Phase 1, Single-Center, Open-label Study to Evaluate the Metabolism and Exception of [14C]-CC-90001 in Healthy Male Subjects
NCT04048876
A Phase 2, Randomized, Double-Blind, Placebo-Controlled, Multicenter, Dose-Finding Study To Evaluate The Efficacy and Safety Of CC-90001 In Subjects With Non-Alcoholic Steatohepatitis (NASH) and Liver Fibrosis
100 项与 CC-90001 相关的临床结果
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100 项与 CC-90001 相关的转化医学
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100 项与 CC-90001 相关的专利（医药）
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13
项与 CC-90001 相关的文献（医药）2025-02-01BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
Discovery of a selective and potent inhibitor of c-Jun N-terminal kinase 1 with anti-pulmonary fibrosis effect
Article
作者: Yuan, Yaxia ; Liu, Jinfeng ; Huang, Weiwei ; Chen, Xiabin ; Huang, Yi ; Ren, Shuhua ; Hou, Shurong ; Liu, Fengling ; Ma, Lei ; Gu, Wenjing ; Chi, Man
We synthesized and evaluated a series of derivatives based on the pyrimidine-2,4-diamine scaffold as potential JNK1 inhibitors, incorporating bridging rings and spirocyclic modifications to enhance their inhibitory activity. These compounds were biologically assessed through JNK enzyme inhibition assays and Western Blot analysis. Compounds 13, 14 and 19 demonstrated significant inhibitory activity at both the enzyme and cellular level compared to the lead compound 1 and clinical candidate CC-90001. Notably, 14 exhibited strong inhibitory potency against JNK1 with sub-nanomolar efficacy and suppresses TGF-β-induced epithelial-mesenchymal transition, indicating its potential as a promising candidate for further development as an anti-pulmonary fibrosis agent targeting JNK1.
2024-12-01Molecular diversity
Identification of potential JNK3 inhibitors through virtual screening, molecular docking and molecular dynamics simulation as therapeutics for Alzheimer’s disease
Article
作者: Kumar, Vinod ; Jangid, Kailash ; Devi, Bharti ; Kumar, Naveen ; Kumar, Vinay
Alzheimer's disease (AD) is a complex neurological disorder and no effective drug is available for its treatment. Numerous pathological conditions are believed to be responsible for the initiation and development of AD including c-Jun N-terminal kinases (JNKs). The JNKs are one of the enzymes from the mitogen-activated protein kinase (MAPK) family that controls the phosphorylation of various transcription factors on serine and threonine residues, and hold significant responsibilities in tasks like gene expression, cell proliferation, differentiation, and apoptosis. Since, JNK3 is primarily expressed in the brain hence its increased levels in the brain are associated with the AD pathology promoting neurofibrillary tangles, senile plaques, neuroinflammation, and nerve cell apoptosis. The current research work is focused on the development of novel JNK inhibitors as therapeutics for AD employing a structure-based virtual screening (SBVS) approach. The ZINC database (14634052 compounds) was investigated after employing pan assay interference (PAINs), drug-likeness, and diversity picking filter to distinguish molecules interacting with JNK3 by following three docking precision criteria: High Throughput Virtual Screening (HTVS), Standard Precision (SP), and Extra Precision (XP) & MMGBSA. Five lead molecules showed a better docking score in the range of -13.091 to -14.051 kcal/mol better than the reference compound (- 11.828 kcal/mol). The lead compounds displayed acceptable pharmacokinetic properties and were subjected to molecular dynamic simulations of 100 ns and binding free energy calculations. All the lead molecules showed stable RMSD and hydrogen bond interactions throughout the trajectory. The ∆GMM/PBSA_total score for the lead compounds ZINC220382956, ZINC147071339, ZINC207081127, ZINC205151456, ZINC1228819126, and CC-930 was calculated and found to be - 31.39, - 42.8, - 37.04, - 39.01, - 36.5, - 34.16 kcal/mol, respectively. Thus, it was concluded that the lead molecules identified in these studies have the potential to be explored as potent JNK3 inhibitors.
2024-10-10JOURNAL OF MEDICINAL CHEMISTRY
Structure Optimization of c-Jun N-terminal Kinase 1 Inhibitors for Treating Idiopathic Pulmonary Fibrosis
Article
作者: Yuan, Yaxia ; Qian, Hewen ; Huang, Weiwei ; Ren, Shuhua ; Chen, Xiabin ; Ding, Yuanqing ; Hou, Shurong ; Ma, Lei ; Liu, Fengling ; Huang, Yi ; Chi, Man ; Gu, Wenjing
Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease with an elusive etiology. Aberrant activation of c-Jun N-terminal kinase 1 (JNK1) has been implicated in its pathogenesis. Through a combination of structure-based drug design and structure-activity relationship (SAR) optimization, a series of pyrimidine-2,4-diamine scaffold derivatives have been developed as potent JNK1 inhibitors. Compound E1 was identified with low nanomolar JNK1 inhibitory potency (IC50 = 2.7 nM). The introduction of a dimethylamine side chain has significantly enhanced the ability of E1 to inhibit c-Jun phosphorylation, surpassing the clinical candidate CC-90001. Molecular dynamics simulations revealed a binding free energy of -50.46 kcal/mol for E1. Moreover, E1 displayed satisfactory pharmacokinetic properties, with a bioavailability of 69% in rats. Furthermore, compound E1 exerted significant antifibrotic effects in a bleomycin-induced IPF mouse model and prevented a TGF-β-induced epithelial-to-mesenchymal transition in vitro. These findings position E1 as a promising lead for further drug development targeting IPF.
3
项与 CC-90001 相关的新闻（医药）100 项与 CC-90001 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 肝纤维化 | 临床2期 | 美国 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 日本 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 澳大利亚 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 加拿大 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 法国 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 德国 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 波兰 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 西班牙 | 2019-08-14 | |
| 肝纤维化 | 临床2期 | 英国 | 2019-08-14 | |
| 肝硬化 | 临床2期 | 美国 | 2019-08-14 |
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临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 112 | 構窪製構鑰衊範艱衊鑰(餘獵襯積鑰製膚窪鹹窪) = 製鑰顧餘廠製願範艱繭 網糧廠淵遞艱廠糧窪簾 (壓鑰觸鹹築壓廠鏇鹹鏇 ) | 积极 | 2024-03-14 | |||
構窪製構鑰衊範艱衊鑰(餘獵襯積鑰製膚窪鹹窪) = 遞製窪鑰齋膚製鬱鏇簾 網糧廠淵遞艱廠糧窪簾 (壓鑰觸鹹築壓廠鏇鹹鏇 ) | |||||||
临床1期 | 16 | (100mg) | 構膚廠鑰淵鹹襯獵膚遞(齋選蓋餘繭選膚鏇築獵) = The most common AEs were GI in nature (all mild to moderate). 壓醖衊艱壓膚艱遞膚鏇 (積製廠選夢顧選簾廠網 ) | 积极 | 2017-12-06 | ||
(200/400mg) |
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