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1 ithout the cyclin-dependent kinase inhibitor palbociclib.
2 oading schedule and may be administered with palbociclib.
3 the literature describing the development of palbociclib.
4 cer cells to the FDA-approved CDK4 inhibitor palbociclib.
5 d responses to the CDK4/6-specific inhibitor palbociclib.
6 inuous oral letrozole 2.5 mg daily plus oral palbociclib 125 mg, given once daily for 3 weeks followe
7 e-based randomisation system to receive oral palbociclib (125 mg daily for 3 weeks followed by a week
8 ase 2 study demonstrated that treatment with palbociclib (200 mg daily for 14 days every 21 days) res
11 ined with ATP-competitive inhibitors such as palbociclib and dinaciclib is presented, followed by a c
12 clinical relevance, combined treatment with palbociclib and FLT3 inhibitors results in synergistic c
13 e combination of the CDK4 and CDK6 inhibitor palbociclib and fulvestrant was associated with signific
15 cell-cycle and OCT2-targeting activities of palbociclib and LEE011, combined with their potential fo
16 educed toxicity of CDK4/6 inhibitors such as palbociclib and multi-CDK inhibitors such as dinaciclib
18 ncer cells activate autophagy in response to palbociclib, and that the combination of autophagy and C
19 e used the PubMed search terms "PD0332991," "palbociclib," and "CDK4/6 inhibitor" to find all publish
20 GSK2334470 in combination with ribociclib or palbociclib, another CDK4/6 inhibitor, synergistically i
21 tivation, suggesting that inhibitors such as palbociclib are likely to provide therapeutic benefit in
25 ostat (pan-histone deacetylase inhibitor) or palbociclib (CDK4/6 inhibitor) or ABT-199 (BCL2 antagoni
26 his today is the use of the CDK4/6 inhibitor palbociclib combined with aromatase inhibitors for the t
27 AI and in baseline plasma from the PALOMA3 (Palbociclib Combined With Fulvestrant in Hormone Recepto
28 at, when targeted using the CDK4/6 inhibitor palbociclib, defines overlap and divergence of adjuvant
29 While CDK4/6 inhibitors are FDA approved (palbociclib) for treating advanced estrogen receptor-pos
30 incorporated sites of action of four drugs (palbociclib, gemcitabine, paclitaxel and actinomycin D)
31 ts had occurred (145 in the fulvestrant plus palbociclib group and 114 in the fulvestrant plus placeb
32 atients (13%) of 345 in the fulvestrant plus palbociclib group and 30 (17%) of 172 patients in the fu
33 73%) of 345 patients in the fulvestrant plus palbociclib group and 38 (22%) of 172 patients in the fu
34 hs (95% CI 9.2-11.0) in the fulvestrant plus palbociclib group and 4.6 months (3.5-5.6) in the fulves
35 utropenia (223 [65%] in the fulvestrant plus palbociclib group and one [1%] in the fulvestrant plus p
36 rly- and late-phase clinical trials in which palbociclib has been investigated in a broad array of tu
38 er, coadministration of the CDK4/6 inhibitor palbociclib in combination with H3B-6527 could effective
39 e aimed to assess the safety and efficacy of palbociclib in combination with letrozole as first-line
40 lvestrant plus placebo with fulvestrant plus palbociclib in patients with progression after receiving
41 inistration-approved CDK4/6 kinase inhibitor palbociclib induces apoptosis of FLT3-ITD leukemic cells
45 CDK4/6 pathway by small-molecule inhibitors palbociclib (PD-0332991) and ribociclib (LEE011) resulte
48 12, we randomly assigned 165 patients, 84 to palbociclib plus letrozole and 81 to letrozole alone.
49 and 26.1 months (11.2-not estimable) for the palbociclib plus letrozole group (HR 0.299, 0.156-0.572;
50 le group and 20.2 months (13.8-27.5) for the palbociclib plus letrozole group (HR 0.488, 95% CI 0.319
51 le group and 18.1 months (13.1-27.5) for the palbociclib plus letrozole group (HR 0.508, 0.303-0.853;
52 ow-up 29.6 months [95% CI 27.9-36.0] for the palbociclib plus letrozole group and 27.9 months [25.5-3
53 ion-free survival events had occurred in the palbociclib plus letrozole group and 59 in the letrozole
55 s reported in 45 (54%) of 83 patients in the palbociclib plus letrozole group versus one (1%) of 77 p
56 hat occurred in more than one patient in the palbociclib plus letrozole group were pulmonary embolism
59 , including compounds that target CDK4/CDK6 (palbociclib, ribociclib, and abemaciclib), aurora kinase
61 rafenib-resistant tumors remain sensitive to palbociclib, suggesting that initial treatment with vemu
62 in-dependent kinase 4/6 inhibitor, PD0332991/palbociclib, that mimics the endogenous effect of p16(IN
63 f patients most suitable for the addition of palbociclib to endocrine therapy after tumour recurrence
67 tients with advanced WD/DDLS, treatment with palbociclib was associated with a favorable PFS and occa
69 tegy A was 31.6 QALMs versus strategy C when palbociclib was included in strategy C; similarly, strat
70 tegy A was 31.6 QALMs versus strategy C when palbociclib was included in strategy C; similarly, strat
71 rgetable and the selective CDK4/6 inhibitor, palbociclib, was recently FDA approved for the treatment
73 itial treatment with vemurafenib followed by palbociclib with or without mTOR inhibitors might provid
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