ライフサイエンスコーパス: volasertib

1 creased proliferation with the PLK inhibitor volasertib.

2 nts were randomly assigned to receive either volasertib 300 mg by intravenous infusion every 3 weeks

3 ice daily subcutaneously days 1-10 or LDAC + volasertib 350 mg IV days 1 + 15 every 4 weeks.

4 d low-dose cytarabine (LDAC) with or without volasertib, a highly potent and selective inhibitor of p

5 Pharmacologic inhibition of PLK1 with volasertib, a small-molecule ATP-competitive PLK1 inhibi

6 Six patients (11%) receiving volasertib achieved PFS fore more than 1 year, whereas n

7 09 patients receiving treatment, 54 received volasertib and 55 received chemotherapy; demographics we

8 Median PFS was 13.1 weeks and 20.6 weeks for volasertib and chemotherapy (hazard ratio, 1.01; 95% CI,

9 seven (13.0%) and 15 (27.3%) patients in the volasertib and chemotherapy arms, respectively.

10 The 24-week disease control rates for volasertib and chemotherapy were 30.6% (95% CI, 18.0% to

11 ARAC reduces effective doses of volasertib and PD-L1 antibody by 5-fold in a metastatic

12 a nanoparticle co-delivering PLK1 inhibitor (volasertib) and PD-L1 antibody.

13 Responses in the LDAC + volasertib arm were observed across all genetic groups,

14 rvival was significantly prolonged by LDAC + volasertib compared with LDAC (5.6 vs 2.3 months; hazard

15 ound that targeting Plk1 with its inhibitor, volasertib, delayed cyst growth in Pkd1 conditional knoc

16 Patients treated with volasertib experienced more grade 3 and 4 drug-related h

17 Volasertib in combination with the ER antagonist, fulves

18 Volasertib is a potent and selective cell-cycle kinase i

19 LDAC + volasertib led to an increased frequency of adverse even

20 This phase II trial evaluated volasertib or single-agent chemotherapy in patients with

21 ition of PLK2 by the PLK inhibitor, BI 6727 (volasertib), or PLK2 knockdown was proapoptotic in CCA c

22 , transcriptomic changes, and sensitivity to volasertib (PLK1 inhibitor) and barasertib (AukB inhibit

23 expressing resistant cells were sensitive to volasertib (PLK1 inhibitor) and barasertib (AukB inhibit

24 Single-agent volasertib showed antitumor activity in patients with ov

25 L-xL) mRNA levels were markedly reduced upon volasertib treatment in MCF7/LTED cells, while they were

26 blood count recovery) was higher for LDAC + volasertib vs LDAC (31.0% vs 13.3%; odds ratio, 2.91; P

27 diation and the proliferation of MB by using Volasertib (VSB), a Polo-like kinase 1 (PLK1) specific i

28 AEs in patients receiving volasertib were mainly hematologic and manageable.