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Last update 31 May 2025
CC-90001
Last update 31 May 2025
Overview
Basic Info
Drug Type Small molecule drug |
Synonyms CC 90001, CC-539, CC90001 |
Target |
Action inhibitors |
Mechanism JNK1 inhibitors(c-Jun N-terminal kinase 1 inhibitors) |
Therapeutic Areas |
Active Indication- |
Inactive Indication |
Originator Organization |
Active Organization- |
Inactive Organization |
License Organization- |
Drug Highest PhaseDiscontinuedPhase 2 |
First Approval Date- |
Regulation- |
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Structure/Sequence
Molecular FormulaC16H27N5O2 |
InChIKeyQBBRJRLJWXRSHQ-CKYFFXLPSA-N |
CAS Registry1403859-14-2 |
Related
10
Clinical Trials associated with CC-90001CTIS2022-500930-27-00
- 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 Clinical Results associated with CC-90001
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100 Translational Medicine associated with CC-90001
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100 Patents (Medical) associated with CC-90001
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13
Literatures (Medical) associated with CC-9000101 Feb 2025BIOORGANIC & MEDICINAL CHEMISTRY LETTERS
Discovery of a selective and potent inhibitor of c-Jun N-terminal kinase 1 with anti-pulmonary fibrosis effect
Article
Author: Yuan, Yaxia ; Liu, Jinfeng ; Huang, Weiwei ; Chen, Xiabin ; Ren, Shuhua ; Huang, Yi ; 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.
01 Dec 2024Molecular diversity
Identification of potential JNK3 inhibitors through virtual screening, molecular docking and molecular dynamics simulation as therapeutics for Alzheimer’s disease
Article
Author: 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.
10 Oct 2024JOURNAL OF MEDICINAL CHEMISTRY
Structure Optimization of c-Jun N-terminal Kinase 1 Inhibitors for Treating Idiopathic Pulmonary Fibrosis
Article
Author: Qian, Hewen ; Yuan, Yaxia ; Huang, Weiwei ; Ren, Shuhua ; Chen, Xiabin ; Ding, Yuanqing ; Hou, Shurong ; Ma, Lei ; Liu, Fengling ; Chi, Man ; Huang, Yi ; 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
News (Medical) associated with CC-9000113 Jan 2025
Phase 2Phase 1License out/in
25 May 2023
26 Jan 2017
100 Deals associated with CC-90001
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R&D Status
10 top R&D records. to view more data
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| Indication | Highest Phase | Country/Location | Organization | Date |
|---|---|---|---|---|
| Fibrosis, Liver | Phase 2 | United States | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Japan | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Australia | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Canada | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | France | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Germany | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Poland | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | Spain | 14 Aug 2019 | |
| Fibrosis, Liver | Phase 2 | United Kingdom | 14 Aug 2019 | |
| Liver Cirrhosis | Phase 2 | United States | 14 Aug 2019 |
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Clinical Result
Clinical Result
Indication
Phase
Evaluation
View All Results
NCT03142191 (Pubmed) Manual  | Phase 2 | 112 | sbgjuxyhqz(qvtrqjgmzu) = rvnfzvgibw gewewfsoxv (xdpnsddjta ) | Positive | 14 Mar 2024 | ||
sbgjuxyhqz(qvtrqjgmzu) = waaxmpsbnm gewewfsoxv (xdpnsddjta ) | |||||||
NCT02510937 (ERS2017) Manual | Phase 1 | 16 | (100mg) | czqfwxumjy(vqgxogsjyy) = The most common AEs were GI in nature (all mild to moderate). oihhzncteh (oyqxllazhr ) | Positive | 06 Dec 2017 | |
(200/400mg) |
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