Senexin B | CDK8/19 inhibitor

Senexin B chemical structure

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Senexin B (1449228-40-3) is a potent inhibitor of cyclin-dependent kinases 8 and 19.1 It suppressed tumor growth and augmented the effects of fulvestrant in ER-positive breast cancer xenografts. KD50s: CDK8 = 59 nM, CDK19 = 23 nM.2 Senexin B also showed synergistic effects with lapatinib and trastuzumab in a panel of HER2+ breast cancer cell lines. Senexin B and ALK5 inhibitor SB431542 afforded generation of pancreatic islet cells from pluripotent stem cells without any mutagenic effects.4 Combination treatment of Senexin B and Imatinib intensified apoptotic cell death in chronic myelogenous leukemia cells and prevented quiescence-mediated escape from apoptosis.5

References/Citations:

  1. McDermott et al. (2017), Inhibition of CDK8 mediator kinase suppresses estrogen dependent transcription and the growth of estrogen receptor positive breast cancer; Oncotarget 8 12558
  2. Chen et al. (2019); Systemic Toxicity Reported for CDK8/19 Inhibitors CCT251921 and MSC2530818 In Not Due to Target Inhibition, Cells, 8 1413
  3. Ding et al. (2022); Inhibition of CDK8/19 Mediator kinase potentiates HER2-targeting drugs and bypasses resistance to these agents in vitro and in vivo, Proc. Natl. Acad. Sci. USA, 119 e2201073119
  4. Sakuma et al. (2023); CDK8/19 inhibition plays an important role in pancreatic ß-cell induction from human iPSCs, Stem Cell Res. Ther., 14 1
  5. Khamidullina et al. (2025); CDK8/19 inhibition attenuates G1 arrest induced by BCR-ABL antagonists and accelerates death of chronic myelogenous leukemia cells, Cell Death Discov., 11 62
1449228-40-3, BCD-115, CDK19 inhibitor, CDK8 inhibitor, CDK8/19 inhibitor, Senexin B, Senexin B supplier
Alternate Name:
BCD-115

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Senexin B (1449228-40-3) is a potent inhibitor of cyclin-dependent kinases 8 and 19.1 It suppressed tumor growth and augmented the effects of fulvestrant in ER-positive breast cancer xenografts. KD50s: CDK8 = 59 nM, CDK19 = 23 nM.2 Senexin B also showed synergistic effects with lapatinib and trastuzumab in a panel of HER2+ breast cancer cell lines. Senexin B and ALK5 inhibitor SB431542 afforded generation of pancreatic islet cells from pluripotent stem cells without any mutagenic effects.4 Combination treatment of Senexin B and Imatinib intensified apoptotic cell death in chronic myelogenous leukemia cells and prevented quiescence-mediated escape from apoptosis.5

References/Citations:

  1. McDermott et al. (2017), Inhibition of CDK8 mediator kinase suppresses estrogen dependent transcription and the growth of estrogen receptor positive breast cancer; Oncotarget 8 12558
  2. Chen et al. (2019); Systemic Toxicity Reported for CDK8/19 Inhibitors CCT251921 and MSC2530818 In Not Due to Target Inhibition, Cells, 8 1413
  3. Ding et al. (2022); Inhibition of CDK8/19 Mediator kinase potentiates HER2-targeting drugs and bypasses resistance to these agents in vitro and in vivo, Proc. Natl. Acad. Sci. USA, 119 e2201073119
  4. Sakuma et al. (2023); CDK8/19 inhibition plays an important role in pancreatic ß-cell induction from human iPSCs, Stem Cell Res. Ther., 14 1
  5. Khamidullina et al. (2025); CDK8/19 inhibition attenuates G1 arrest induced by BCR-ABL antagonists and accelerates death of chronic myelogenous leukemia cells, Cell Death Discov., 11 62