90564-26-4Relevant academic research and scientific papers
Highly Selective Inhibition of Tyrosine Kinase 2 (TYK2) for the Treatment of Autoimmune Diseases: Discovery of the Allosteric Inhibitor BMS-986165
Wrobleski, Stephen T.,Moslin, Ryan,Lin, Shuqun,Zhang, Yanlei,Spergel, Steven,Kempson, James,Tokarski, John S.,Strnad, Joann,Zupa-Fernandez, Adriana,Cheng, Lihong,Shuster, David,Gillooly, Kathleen,Yang, Xiaoxia,Heimrich, Elizabeth,McIntyre, Kim W.,Chaudhry, Charu,Khan, Javed,Ruzanov, Max,Tredup, Jeffrey,Mulligan, Dawn,Xie, Dianlin,Sun, Huadong,Huang, Christine,D'Arienzo, Celia,Aranibar, Nelly,Chiney, Manoj,Chimalakonda, Anjaneya,Pitts, William J.,Lombardo, Louis,Carter, Percy H.,Burke, James R.,Weinstein, David S.
, p. 8973 - 8995 (2019)
Small molecule JAK inhibitors have emerged as a major therapeutic advancement in treating autoimmune diseases. The discovery of isoform selective JAK inhibitors that traditionally target the catalytically active site of this kinase family has been a formi
COMPOUNDS AND METHODS FOR INHIBITING VIRAL REPLICATION AND METHODS OF TREATING AND PREVENTING FLAVIVIRAL INFECTIONS
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, (2022/02/05)
The present disclosure relates to a compound of formula (I) or a pharmaceutically acceptable salt thereof. The present disclosure further relates to methods of inhibiting viral replication including contacting one or more cells that have been infected wit
Compound used as CDK7 kinase inhibitor and application thereof
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Paragraph 0216; 0220-0221, (2021/04/17)
The invention relates to a compound used as a CDK7 kinase inhibitor and application thereof. Specifically, the compound disclosed by the invention has a structure shown as a formula I, and the definitions of all groups and substituents are as described in the specification. The compounds of the present invention are useful as inhibitors of cyclin-dependent kinase 7 (CDK7) for the treatment or prevention of proliferative diseases such as cancer, especially for modulating and treating diseases associated with abnormal activity of cyclin-dependent kinase 7 (CDK7).
HETEROCYCLIC COMPOUNDS FOR INHIBITING TYK2 ACTIVITIES
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Page/Page column 12-13, (2021/09/17)
Provided are Compounds 1-8, and their pharmaceutically acceptable salts or prodrugs thereof. Compounds 1-8 are selective binders to TYK2's JH2 and they exhibit significant inhibitory effects on the physiological function of TYK2 and they have excellent in vivo pharmacokinetic properties. Compounds 1-5 and 7 have several deuterium substitutions on methyl to improve pharmacokinetic (PK) properties.
JMX0207, a Niclosamide Derivative with Improved Pharmacokinetics, Suppresses Zika Virus Infection Both in Vitro and in Vivo
Butler, David,Chen, Haiying,D'Brant, Lianna,Fan, Xiaoyu,Hu, Saiyang,Koetzner, Cheri A.,Kramer, Laura D.,Kuo, Lili,Lang, Yuekun,Li, Hongmin,Li, Zhong,Rugenstein, Natasha,Samrat, Subodh Kumar,Tharappel, Anil M.,Trudeau, Nicole,Xu, Jimin,Zhang, Jing,Zhang, Qing-Yu,Zhou, Jia
, p. 2616 - 2628 (2020/11/09)
Flaviviruses causes significant human disease. Recent outbreaks of the Zika virus highlight the need to develop effective therapies for this class of viruses. Previously we identified niclosamide as a broad-spectrum inhibitor for flaviviruses by targeting
TYK2 INHIBITORS AND USES THEREOF
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Paragraph 00424, (2020/06/10)
Described herein are compounds that are useful in treating a TYK2-mediated disorder. In some embodiments, the TYK2-mediated disorder is an autoimmune disorder, an inflammatory disorder, a proliferative disorder, an endocrine disorder, a neurological disorder, or a disorder associated with transplantation.
AMIDE-SUBSTITUTED HETEROCYCLIC COMPOUNDS FOR THE TREATMENT OF CONDITIONS RELATED TO THE MODULATION OF IL-12, IL-23 AND/OR IFN-ALPHA
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Page/Page column 94, (2020/05/29)
Compounds having the following formula I: or a stereoisomer or pharmaceutically-acceptable salt thereof, where R1, R2, R3, R4, and R5 are as defined herein, are useful in the modulation of IL-12, IL-2
COMPOUND AS ACC INHIBITOR AND USE THEREOF
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Paragraph 0329; 0330, (2020/06/15)
Disclosed are a class of compounds which are inhibitors of acetyl-CoA carboxylase (ACC) and the use thereof. In particular, provided are compounds as shown in formula I or isomers, pharmaceutically acceptable salts, solvates, crystals or prodrugs thereof, and methods for preparing the same, and pharmaceutical compositions comprising the compounds and the use of the compounds or compositions for treating and/or preventing diseases associated with ACC expression, such as fibrotic diseases, metabolic diseases, cancers or tissue hyperplasia diseases. The compound has a good inhibitory activity against ACC and shows good promise to be a therapeutic drug for fibrotic diseases, metabolic diseases, cancers or tissue hyperplasia diseases.
Drug Design Targeting T-Cell Factor-Driven Epithelial-Mesenchymal Transition as a Therapeutic Strategy for Colorectal Cancer
Abraham, Adedoyin D.,Esquer, Hector,Zhou, Qiong,Tomlinson, Nicholas,Hamill, Brayden D.,Abbott, Joshua M.,Li, Linfeng,Pike, Laura A.,Rinaldetti, Sébastien,Ramirez, Dominique A.,Lunghofer, Paul J.,Gomez, Jose D.,Schaack, Jerome,Nemkov, Travis,D'Alessandro, Angelo,Hansen, Kirk C.,Gustafson, Daniel L.,Messersmith, Wells A.,Labarbera, Daniel V.
supporting information, p. 10182 - 10203 (2019/11/29)
Metastasis is the cause of 90% of mortality in cancer patients. For metastatic colorectal cancer (mCRC), the standard-of-care drug therapies only palliate the symptoms but are ineffective, evidenced by a low survival rate of ~11%. T-cell factor (TCF) transcription is a major driving force in CRC, and we have characterized it to be a master regulator of epithelial-mesenchymal transition (EMT). EMT transforms relatively benign epithelial tumor cells into quasi-mesenchymal or mesenchymal cells that possess cancer stem cell properties, promoting multidrug resistance and metastasis. We have identified topoisomerase IIα (TOP2A) as a DNA-binding factor required for TCF-transcription. Herein, we describe the design, synthesis, biological evaluation, and in vitro and in vivo pharmacokinetic analysis of TOP2A ATP-competitive inhibitors that prevent TCF-transcription and modulate or reverse EMT in mCRC. Unlike TOP2A poisons, ATP-competitive inhibitors do not damage DNA, potentially limiting adverse effects. This work demonstrates a new therapeutic strategy targeting TOP2A for the treatment of mCRC and potentially other types of cancers.
