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1 on the progression of IPF and the effect of nintedanib.
2 ced by TGFbeta antibody or the anti-fibrotic nintedanib.
3 first acute exacerbation (hazard ratio with nintedanib, 1.15; 95% CI, 0.54 to 2.42; P=0.67); in INPU
4 by intravenous infusion on day 1 plus either nintedanib 200 mg orally twice daily or matching placebo
5 six cycles of pemetrexed and cisplatin plus nintedanib (200 mg twice daily) or placebo followed by n
6 most frequent grade >/= 3 adverse event (AE; nintedanib 43.2% v placebo 12.2%); rates of febrile neut
8 retion were compared with those of the drugs nintedanib and pirfenidone, recently approved for IPF.
9 re was no significant difference between the nintedanib and placebo groups in the time to the first a
10 arrhea, with rates of 61.5% and 18.6% in the nintedanib and placebo groups, respectively, in INPULSIS
11 recently completed trials of pirfenidone and nintedanib, and results that will come from ongoing tria
12 CK inhibitors, such as dasatinib, bosutinib, nintedanib, and WH-4-023, are able to induce cell death
13 ed the efficacy and safety of docetaxel plus nintedanib as second-line therapy for non-small-cell lun
17 cal and clinical research and development of nintedanib from the initial drug discovery process to th
18 f first-line treatment in the docetaxel plus nintedanib group (206 patients) compared with those in t
20 istology (322 patients in the docetaxel plus nintedanib group and 336 in the docetaxel plus placebo g
21 significantly improved in the docetaxel plus nintedanib group compared with the docetaxel plus placeb
22 that were more common in the docetaxel plus nintedanib group than in the docetaxel plus placebo grou
25 idence from phase III studies has shown that nintedanib has significant efficacy in the treatment of
27 oward improved overall survival also favored nintedanib (HR, 0.77; 95% CI, 0.46 to 1.29; P = .319).
28 could participate in the INPULSIS trials of nintedanib if they had honeycombing and/or traction bron
32 al designed to assess efficacy and safety of nintedanib plus chemotherapy as first-line treatment of
34 (200 mg twice daily) or placebo followed by nintedanib plus placebo monotherapy until progression.
35 brosis have established that pirfenidone and nintedanib prevent about 50% of the decline in forced vi
36 patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consiste
37 at confirmed that two drugs, pirfenidone and nintedanib, slowed disease progression, leading to a his
40 in a similar way, and responded similarly to nintedanib, to that of patients with honeycombing on HRC
41 valuate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patie
42 rial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and
43 (sLOXL2) concentrations, and pirfenidone and nintedanib use, were randomly assigned (1:1) to inject 1
44 .70; 95% CI, 0.40 to 1.21; P = .197; median [nintedanib v placebo], 20.6 months v 15.2 months) and me
46 8; P<0.001) in INPULSIS-1 and -113.6 ml with nintedanib versus -207.3 ml with placebo (difference, 93
47 ual rate of change in FVC was -114.7 ml with nintedanib versus -239.9 ml with placebo (difference, 12
48 ion were reported in 6.8% of those receiving nintedanib versus 17.1% of those in the placebo group.
49 LSIS-2, there was a significant benefit with nintedanib versus placebo (hazard ratio, 0.38; 95% CI, 0
50 placebo was -225.7 and -221.0 ml/yr, and the nintedanib versus placebo difference in the adjusted ann
51 events were sepsis (five with docetaxel plus nintedanib vs one with docetaxel plus placebo), pneumoni
52 s was six; the median treatment duration for nintedanib was 7.8 months and 5.3 months for placebo.
53 stent with a slowing of disease progression; nintedanib was frequently associated with diarrhea, whic
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