Aoli Wang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Aoli Wang has a total of 44 co-authors. Here are the top co-authors by number of shared publications:
- Qingsong Liu
Chinese Academy of Sciences
2 shared publications - Wenchao Wang
Anhui Province Key Laboratory of Medical Physics and Technology, Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, China
2 shared publications Beilei Wang
Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei 230031, PR China; Hefei Cancer Hospital, Chinese Academy of Sciences, Hefei 230031, PR China; Precision Cancer Medicine Engineering Research Center of Anhui Province, Hefei 230088, PR China
1 shared publication- Beilei Wang
High Magnetic Field Laboratory, Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Mailbox 1110, 350 Shushanhu Road, Hefei, Anhui, 230031, People's Republic of China
1 shared publication - Chen Hu
Hefei Cancer Hospital of CAS, Institute of Health and Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei 230031, P.R. China
1 shared publication - Cheng Chen
Department of Bioinformatics, Precedo Pharmaceuticals Co. Ltd, Hefei, China
1 shared publication
Latest Publications
- 21 August 2025
- Published by Elsevier in Bioorganic Chemistry
- Vol. 164, 108878
Pan-EGFR inhibitor targeting EGFR 19del, L858R/T790M and C797S triple-mutations: Design, synthesis, and pharmacological evaluation
- 21 August 2025
- Published by Elsevier in Bioorganic Chemistry
- Vol. 164, 108878
Pan-EGFR inhibitor targeting EGFR 19del, L858R/T790M and C797S triple-mutations: Design, synthesis, and pharmacological evaluation
- 21 May 2025
- Published by Elsevier in International Immunopharmacology
- Vol. 159, 114839
Repurposing of clinical-stage FLT3 inhibitor HYML-122 as a potent RIPK2 inhibitor for the treatment of inflammatory bowel disease
- 21 May 2025
- Published by Elsevier in International Immunopharmacology
- Vol. 159, 114839
Repurposing of clinical-stage FLT3 inhibitor HYML-122 as a potent RIPK2 inhibitor for the treatment of inflammatory bowel disease
- 23 December 2019
- Published by Springer Nature in Investigational New Drugs
- Vol. 38 (5) , 1272-1281
Discovery of a novel and highly selective CDK9 kinase inhibitor (JSH-009) with potent antitumor efficacy in preclinical acute myeloid leukemia models
Summary Acute myeloid leukemia (AML) is reported to be vulnerable to transcription disruption due to transcriptional addiction. Cyclin-dependent kinase 9 (CDK9), which regulates transcriptional elongation, has attracted extensive attention as a drug target. Although several inhibitors, such as alvocidib and dinaciclib, have shown potent therapeutic effects in clinical trials on AML, the lack of high selectivity for CDK9 and other CDKs has limited their optimal clinical efficacy. Therefore, developing highly selective CDK9 inhibitors is still imperative for the efficacy and safety profile in treating AML. Here, we report a novel highly selective CDK9 inhibitor, JSH-009, which exhibited high potency against CDK9 and displayed great selectivity over 468 kinases/mutants. It also demonstrates impressive in vitro and in vivo antileukemic efficacy in preclinical models of AML, which makes JSH-009 a useful pharmacological tool for elucidating CDK9-mediated transcription and a novel therapeutic candidate for AML.
- 23 December 2019
- Published by Springer Nature in Investigational New Drugs
- Vol. 38 (5) , 1272-1281
Discovery of a novel and highly selective CDK9 kinase inhibitor (JSH-009) with potent antitumor efficacy in preclinical acute myeloid leukemia models
Summary Acute myeloid leukemia (AML) is reported to be vulnerable to transcription disruption due to transcriptional addiction. Cyclin-dependent kinase 9 (CDK9), which regulates transcriptional elongation, has attracted extensive attention as a drug target. Although several inhibitors, such as alvocidib and dinaciclib, have shown potent therapeutic effects in clinical trials on AML, the lack of high selectivity for CDK9 and other CDKs has limited their optimal clinical efficacy. Therefore, developing highly selective CDK9 inhibitors is still imperative for the efficacy and safety profile in treating AML. Here, we report a novel highly selective CDK9 inhibitor, JSH-009, which exhibited high potency against CDK9 and displayed great selectivity over 468 kinases/mutants. It also demonstrates impressive in vitro and in vivo antileukemic efficacy in preclinical models of AML, which makes JSH-009 a useful pharmacological tool for elucidating CDK9-mediated transcription and a novel therapeutic candidate for AML.