1610408-97-3
Chemical Structure
Enitociclib
Synonym(s): (+)-BAY-1251152; (+)-VIP152; (S)-Enitociclib
- CAS No.: 1610408-97-3
- Formula:C19H18F2N4O2S
- Molecular Weight:404.43
IUPAC Name: (R)-((2-((5-fluoro-4-(4-fluoro-2-methoxyphenyl)pyridin-2-yl)amino)pyridin-4-yl)methyl)(imino)(methyl)-l6-sulfanone
InChIKey: YZCUMZWULWOUMD-NDEPHWFRSA-N
SMILES: COC1=C(C2=C(F)C=NC(NC3=CC(C[S@@](=O)(C)=N)=CC=N3)=C2)C=CC(F)=C1
Biological Activity:
Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma[1][2][3][4].
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Enitociclib | 99.89% | Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma. |
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Enitociclib (Standard) | ≥98% | Enitociclib (Standard) is the analytical standard of Enitociclib (HY-103019). This product is intended for research and analytical applications. Enitociclib ((+)-BAY-1251152; (+)-VIP152) is a selective CDK9 inhibitor (IC50=3 nM) that inhibits transcriptional elongation by blocking Ser2/Ser5 phosphorylation of RNA polymerase II. Enitociclib specifically depletes key short-lived proteins such as c-MYC, MCL-1 and induces tumor cell apoptosis. Enitociclib also interferes with the production of enhancer RNAs (eRNA) and enhancer-promoter interactions, and downregulates oncogene expression at the epigenetic level. Enitociclib exerts synergistic effects with agents including Bortezomib (HY-10227), Lenalidomide (HY-A0003), Pomalidomide (HY-10984), Venetoclax (HY-15531) and Paclitaxel (HY-B0015), and even reverses paclitaxel resistance. Enitociclib serves as a vital research tool for various malignancies such as double-hit diffuse large B-cell lymphoma, multiple myeloma and pancreatic ductal adenocarcinoma. | ||||||||||||||||||||
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References
- [1]. Frigault MM, et al. Enitociclib, a Selective CDK9 Inhibitor, Induces Complete Regression of MYC+ Lymphoma by Downregulation of RNA Polymerase II Mediated Transcription. Cancer Res Commun. 2023;3(11):2268-2279. [Content Brief]
- [2]. Jiang V, et al. The CDK9 inhibitor enitociclib overcomes resistance to BTK inhibition and CAR-T therapy in mantle cell lymphoma. Biomark Res. 2024;12(1):62. Published 2024 Jun 18. [Content Brief]
- [3]. Tran S, et al. Enitociclib, a selective CDK9 inhibitor: in vitro and in vivo preclinical studies in multiple myeloma. Blood Neoplasia. 2024;2(1):100050. Published 2024 Oct 24. [Content Brief]
- [4]. Hamdan FH, et al. Interactive enhancer hubs (iHUBs) mediate transcriptional reprogramming and adaptive resistance in pancreatic cancer. Gut. 2023;72(6):1174-1185. [Content Brief]
