ライフサイエンスコーパス: dinaciclib

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1 As doxorubicin and dinaciclib also reduced BCL-XL, the combinations of BCL-

2 Dinaciclib also significantly sensitized NB cell lines t

3 We found that the CDK inhibitor dinaciclib and HDAC inhibitor panobinostat were the most

4 that the synthetic lethal strategy employing dinaciclib and niraparib was also highly efficacious in

5 palbociclib and multi-CDK inhibitors such as dinaciclib have rejuvenated the field.

6 study demonstrates single agent activity of dinaciclib in relapsed myeloma, with 2 patients achievin

7 expression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.

8 Dinaciclib is a novel potent small molecule inhibitor of

9 K2 and CDK9 activity by small molecules like dinaciclib is a promising strategy and a treatment optio

10 mpetitive inhibitors such as palbociclib and dinaciclib is presented, followed by a compilation of ne

11 ith a clinically relevant experimental drug, dinaciclib, led to potent RALB-dependent antileukemic ef

12 Furthermore, dinaciclib potently suppressed the clonogenic potential

13 tor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for

14 Notably, dinaciclib resensitized TBNC cells, which had acquired r

15 atment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of t

16 Furthermore, dinaciclib revealed in vivo antitumor efficacy in an ort

17 we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-pr

18 ng doxorubicin and CDK9 inhibitors including dinaciclib that synergized with ABT-263 through downregu

19 Administration of dinaciclib to mice bearing MLL-AF9-driven human and mous

20 Dinaciclib was administered on day 1 of a 21-day cycle a

21 atment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse these events and to

22 Using the cyclin-dependent kinase inhibitor dinaciclib, which downregulates MYC expression, we found

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