ライフサイエンスコーパス: nintedanib

1 nintedanib and 43 [14%] patients initiating nintedanib).

2 ent exposure-years in patients who initiated nintedanib).

3 n the selective poor response of SCC-TAFs to nintedanib.

4 on the progression of IPF and the effect of nintedanib.

5 ent exposure-years in patients who initiated nintedanib.

6 ost participants with diarrhea also received nintedanib.

7 approved anti-fibrosis drugs pirfenidone and nintedanib.

8 bility of drug-induced lung injury caused by nintedanib.

9 dependently isolated cell lines resistant to nintedanib.

10 ent exposure-years in patients who initiated nintedanib.

11 L881V) revealed that it remains sensitive to nintedanib.

12 ent exposure-years in patients who initiated nintedanib.

13 ced by TGFbeta antibody or the anti-fibrotic nintedanib.

14 first acute exacerbation (hazard ratio with nintedanib, 1.15; 95% CI, 0.54 to 2.42; P=0.67); in INPU

15 t the end of an INPULSIS trial could receive nintedanib 100 mg twice daily or 150 mg twice daily in I

16 Patients receiving nintedanib 100 mg twice daily or placebo at the end of a

17 eudo-random number generator to receive oral nintedanib 150 mg twice a day or placebo for 12 weeks in

18 ebo at the end of an INPULSIS trial received nintedanib 150 mg twice daily in INPULSIS-ON.

19 Patients receiving nintedanib 150 mg twice daily or placebo at the end of a

20 Patients received oral nintedanib (150 mg or 200 mg twice daily for 12 weeks) o

21 by intravenous infusion on day 1 plus either nintedanib 200 mg orally twice daily or matching placebo

22 ) plus cisplatin (75 mg/m(2)) on day 1, then nintedanib (200 mg twice daily) or matched placebo on da

23 six cycles of pemetrexed and cisplatin plus nintedanib (200 mg twice daily) or placebo followed by n

24 most frequent grade >/= 3 adverse event (AE; nintedanib 43.2% v placebo 12.2%); rates of febrile neut

25 ent exposure-years in patients who continued nintedanib, 71.2 events per 100 patient exposure-years i

26 Nintedanib, a tyrosine kinase inhibitor, has been shown

27 Our study identified nintedanib, a US Food and Drug Administration-approved a

28 signed, in a 1:1 ratio, to receive 150 mg of nintedanib, administered orally twice daily, or placebo.

29 The efficacy and safety of nintedanib, an intracellular tyrosine kinase inhibitor,

30 y to nintedanib, RET(L881V) was resistant to nintedanib analogs lacking a phenyl group.

31 ent exposure-years in patients who continued nintedanib and 0.7 events per 100 patient exposure-years

32 s were reported in eight (7%) patients given nintedanib and 18 (8%) patients given placebo.

33 ent exposure-years in patients who continued nintedanib and 2.4 events per 100 patient exposure-years

34 e double-blind period, 116 patients received nintedanib and 230 patients received placebo.

35 20 (5%) of 430 patients who continued nintedanib and 31 (10%) of 304 patients who initiated ni

36 onary fibrosis (51 [12%] patients continuing nintedanib and 43 [14%] patients initiating nintedanib).

37 in 53 (93%) of 57 participants who received nintedanib and 50 (79%) of 63 patients in the placebo gr

38 ent exposure-years in patients who continued nintedanib and 6.7 events per 100 patient exposure-years

39 randomly assigned to receive docetaxel plus nintedanib and 659 to receive docetaxel plus placebo.

40 contacts with a methyl group and aniline in nintedanib and blocks water access to two oxygen atoms o

41 Furthermore, nintedanib and bufalin combined therapy relieved the tum

42 nthesis of eight kinase inhibitors including Nintedanib and Hesperadin in yields exceeding 76%.

43 the anti-fibrotic actions of pirfenidone and nintedanib and identifies novel targets for future mecha

44 fibrotic efficacy of saracatinib relative to nintedanib and pirfenidone in three preclinical models:

45 nt whether the standard-of-care (SOC) drugs, nintedanib and pirfenidone, have senolytic properties.

46 retion were compared with those of the drugs nintedanib and pirfenidone, recently approved for IPF.

47 Administration-approved antifibrotic drugs, nintedanib and pirfenidone, slow the rate of decline in

48 Despite the approved treatment options nintedanib and pirfenidone, the medical need for a safe

49 ibrogenic responses was equal or superior to nintedanib and pirfenidone.

50 re was no significant difference between the nintedanib and placebo groups in the time to the first a

51 arrhea, with rates of 61.5% and 18.6% in the nintedanib and placebo groups, respectively, in INPULSIS

52 Nintedanib and possibly perfinidone can be considered in

53 ts, possibly due to enhanced Bcl-2 levels by nintedanib and the activation of the necroptosis pathway

54 o resistance of RET mutants against the TKIs nintedanib and vandetanib.

55 phamide, (b) rituximab, (c) tocilizumab, (d) nintedanib, and (e) the combination of nintedanib plus m

56 A conditional recommendation was made for nintedanib, and additional research into pirfenidone was

57 SYDE1, and MCTS1) have been associated with nintedanib, and MYDGF has been implicated with treatment

58 ptor-like kinase 5 (Alk5) inhibitor (Alk5i), nintedanib, and obeticholic acid therapy limited fibroge

59 recently completed trials of pirfenidone and nintedanib, and results that will come from ongoing tria

60 CK inhibitors, such as dasatinib, bosutinib, nintedanib, and WH-4-023, are able to induce cell death

61 Pirfenidone and Nintedanib are the only currently-approved drugs to trea

62 Currently, pirfenidone and nintedanib are the only FDA-approved drugs for the treat

63 The antifibrotic drugs, such as nintedanib, are indicated for the treatment of IPF and P

64 Our results suggest nintedanib as a new drug candidate for KIT D816V-targete

65 ed the efficacy and safety of docetaxel plus nintedanib as second-line therapy for non-small-cell lun

66 nitiated nintedanib permanently discontinued nintedanib because of diarrhoea.

67 Light-triggered release of nintedanib (BIBF 1120), a small molecule angiogenesis in

68 Nintedanib (BIBF1120) is a potent, oral, small-molecule

69 Molecular docking studies show that nintedanib binds to the adenosine triphosphate binding p

70 n vivo in BMP9/10ib mouse ECs, sirolimus and nintedanib blocked the overactivation of mTOR and VEGFR2

71 The RET-nintedanib co-crystal structure disclosed that Leu-730 i

72 ay co-crystal structure of RET kinase domain-nintedanib complex to 1.87 angstrom resolution and a RET

73 PF is currently treated with pirfenidone and nintedanib, compounds which slow the rate of disease pro

74 and the receptor tyrosine kinase inhibitor, nintedanib, could synergistically fully block, but also

75 n mice, as well as synergistically increased nintedanib efficacy.

76 Conversely, nintedanib enhanced B cell lymphoma 2 expression in sene

77 he greatest perturbing activity was shown by nintedanib, followed by imatinib, dasatinib, and acetylc

78 double-blind fashion, followed by open-label nintedanib for 40 weeks.

79 A 74-year-old man was treated with nintedanib for idiopathic pulmonary fibrosis (IPF).

80 ospray technology to co-delivery bufalin and nintedanib for tumor-targeted combination therapy.

81 Nintedanib (formerly known as BIBF 1120) is an intracell

82 cal and clinical research and development of nintedanib from the initial drug discovery process to th

83 f first-line treatment in the docetaxel plus nintedanib group (206 patients) compared with those in t

84 -free survival was not different between the nintedanib group (median 6.8 months [95% CI 6.1-7.0]) an

85 , 347 patients were randomly assigned to the nintedanib group (n=116) or to the placebo group (n=231)

86 and 458 were randomly assigned to either the nintedanib group (n=229) or the placebo group (n=229).

87 eek 12 was -2.57 x 10(-3) ng/mL/month in the nintedanib group and -1.90 x 10(-3) ng/mL/month in the p

88 hange in FVC over 12 weeks was 5.9 mL in the nintedanib group and -70.2 mL in the placebo group (diff

89 f change in FVC was -52.4 ml per year in the nintedanib group and -93.3 ml per year in the placebo gr

90 as reached in 21 (37%) of 57 patients in the nintedanib group and 20 (32%) of 63 in the placebo group

91 35 patients in the docetaxel plus nintedanib group and 25 in the docetaxel plus placebo gr

92 istology (322 patients in the docetaxel plus nintedanib group and 336 in the docetaxel plus placebo g

93 lated serious adverse events occurred in the nintedanib group and 43 occurred in the placebo group.

94 duration was 5.3 months (IQR 2.8-7.3) in the nintedanib group and 5.1 months (2.7-7.8) in the placebo

95 ts were reported in 99 (44%) patients in the nintedanib group and 89 (39%) patients in the placebo gr

96 was reported in 75.7% of the patients in the nintedanib group and in 31.6% of those in the placebo gr

97 oea was reported in two (2%) patients in the nintedanib group and two (1%) patients in the placebo gr

98 significantly improved in the docetaxel plus nintedanib group compared with the docetaxel plus placeb

99 that were more common in the docetaxel plus nintedanib group than in the docetaxel plus placebo grou

100 tes of febrile neutropenia were low (4.5% in nintedanib group v 0% in placebo group).

101 bolic events (17 [30%] of 57 patients in the nintedanib group vs 13 [21%] of 63 patients in the place

102 ment groups was neutropenia (73 [32%] in the nintedanib group vs 54 [24%] in the placebo group).

103 decreased neutrophil count (22 [39%] in the nintedanib group vs seven [11%] in the placebo group [5.

104 The most frequent adverse event in the nintedanib groups was diarrhea, with rates of 61.5% and

105 These findings suggest that nintedanib has a manageable safety and tolerability prof

106 idence from phase III studies has shown that nintedanib has significant efficacy in the treatment of

107 Primary PFS favored nintedanib (hazard ratio [HR], 0.56; 95% CI, 0.34 to 0.9

108 Thirty-six days after starting to take nintedanib, he admitted to our hospital due to respirato

109 oward improved overall survival also favored nintedanib (HR, 0.77; 95% CI, 0.46 to 1.29; P = .319).

110 patients receiving pirfenidone and those on nintedanib (HR, 1.14; 95% CI, 0.79-1.65; P = 0.471).

111 could participate in the INPULSIS trials of nintedanib if they had honeycombing and/or traction bron

112 b in 2D and to oxaliplatin, selumitinib, and nintedanib in 3D cell culture.

113 dian exposure time for patients treated with nintedanib in both the INPULSIS and INPULSIS-ON trials w

114 Nintedanib in combination with docetaxel is an effective

115 430 (59%) patients had received nintedanib in INPULSIS and continued nintedanib in INPUL

116 The safety profile of nintedanib in INPULSIS-ON was consistent with that obser

117 eceived nintedanib in INPULSIS and continued nintedanib in INPULSIS-ON, and 304 (41%) had received pl

118 d received placebo in INPULSIS and initiated nintedanib in INPULSIS-ON.

119 n patients who received at least one dose of nintedanib in INPULSIS-ON.

120 assess the long-term efficacy and safety of nintedanib in INPULSIS-ON.

121 iguingly, a trial with the antifibrotic drug nintedanib in non-small cell lung cancer reported clinic

122 hange in CRPM is not a marker of response to nintedanib in patients with idiopathic pulmonary fibrosi

123 ise the long-term safety and tolerability of nintedanib in patients with idiopathic pulmonary fibrosi

124 the antifibrotic medications pirfenidone and nintedanib in patients with idiopathic pulmonary fibrosi

125 al to investigate the efficacy and safety of nintedanib in patients with ILD associated with systemic

126 SMAD3 in SCC-TAFs in the clinical failure of nintedanib in SCC and supports that patients with ADC ma

127 n an INPULSIS trial could receive open-label nintedanib in the extension trial, INPULSIS-ON.

128 ibrotic phenotype and antitumor responses to nintedanib in vitro and in vivo.

129 thout background IPF therapy (pirfenidone or nintedanib), in an approximately 3:1 ratio in each bexot

130 Nintedanib increased caspase-3 activity in the presence

131 Likewise, we reported that nintedanib inhibited the tumor-promoting fibrotic phenot

132 ronic disease, and early antifibrotic agent (nintedanib) intervention modified early disease severity

133 Nintedanib is a RET TKI that inhibits the vandetanib-res

134 Nintedanib is an oral angiokinase inhibitor used as seco

135 Repurposing of sirolimus plus nintedanib might provide therapeutic benefit in patients

136 concomitant IPF therapy (pirfenidone n=55 or nintedanib n=29).

137 uited and were randomly allocated to receive nintedanib (n=57) or placebo (n=63).

138 The adverse-event profile of nintedanib observed in this trial was similar to that ob

139 the antifibrotic medications pirfenidone and nintedanib on clinically important outcomes such as mort

140 opathic pulmonary fibrosis and the effect of nintedanib on these biomarkers.

141 ministration-approved drugs, pirfenidone and nintedanib, only slow disease progression.

142 brosis or diet-induced steatohepatitis given nintedanib or aspirin and clopidogrel down-regulated the

143 Administration of nintedanib or aspirin and clopidogrel to mice with chron

144 andard of care treatment with pirfenidone or nintedanib or in those not receiving standard of care tr

145 First-line therapy includes nintedanib or pirfenidone for IPF and mycophenolate mofe

146 Antifibrotic therapy with nintedanib or pirfenidone slows annual FVC decline by ap

147 gemcitabine and cisplatin chemotherapy with nintedanib or placebo in locally advanced muscle-invasiv

148 y of pemetrexed plus cisplatin combined with nintedanib or placebo in unresectable malignant pleural

149 isease progression after six cycles received nintedanib or placebo maintenance on days 1-21 of each c

150 Patients were randomly assigned (1:1) to nintedanib or placebo using permuted blocks with random

151 randomly assigned in a 3:2 ratio to receive nintedanib or placebo.

152 f 576 patients received at least one dose of nintedanib or placebo; 51.9% had diffuse cutaneous syste

153 orally given the multiple tyrosine inhibitor nintedanib or vehicle (controls); liver tissues were col

154 tion to local standard of care (pirfenidone, nintedanib, or neither) for at least 52 weeks.

155 with idiopathic pulmonary fibrosis could use nintedanib over the long-term to slow disease progressio

156 b and 31 (10%) of 304 patients who initiated nintedanib permanently discontinued nintedanib because o

157 exclusively revealed highest activities for Nintedanib (pIC50 5.90 uM).

158 215-0.8] for IIP-PH, IPF-PH, and IIP-PH with nintedanib/pirfenidone background therapy), but not in p

159 al designed to assess efficacy and safety of nintedanib plus chemotherapy as first-line treatment of

160 tober 2015, 38 patients received second-line nintedanib plus docetaxel.

161 , (d) nintedanib, and (e) the combination of nintedanib plus mycophenolate.

162 (200 mg twice daily) or placebo followed by nintedanib plus placebo monotherapy until progression.

163 brosis have established that pirfenidone and nintedanib prevent about 50% of the decline in forced vi

164 Sirolimus plus nintedanib prevented vascular pathology in the oral muco

165 he piperazine, anilino, and phenyl groups of nintedanib, providing a structural basis for explaining

166 patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consiste

167 Mechanistically, the reduced fibrosis and nintedanib response of SCC-TAFs was associated with incr

168 Comparisons of RET-nintedanib, RET(G810A), and RET-vandetanib crystal struc

169 L881V mutation did not affect sensitivity to nintedanib, RET(L881V) was resistant to nintedanib analo

170 placebo for 12 weeks followed by open-label nintedanib, rising concentrations of CRPM over 12 weeks

171 Nintedanib selectively reduced the viability of iPSC-der

172 at confirmed that two drugs, pirfenidone and nintedanib, slowed disease progression, leading to a his

173 Nintedanib targets proangiogenic and pro-fibrotic pathwa

174 Nintedanib targets VEGF receptors 1-3, PDGF receptors al

175 s, including diarrhea, were more common with nintedanib than with placebo.

176 annual rate of decline in FVC was lower with nintedanib than with placebo; no clinical benefit of nin

177 The addition of nintedanib to chemotherapy was safe but did not improve

178 We investigated the effect of adding nintedanib to neoadjuvant chemotherapy on response and s

179 Conclusion Addition of nintedanib to pemetrexed plus cisplatin resulted in PFS

180 ural protein (Nsp) 3, avanafil to Nsp15, and nintedanib to the nucleocapsid protein involved in packa

181 in a similar way, and responded similarly to nintedanib, to that of patients with honeycombing on HRC

182 xpression and synergistically interacts with nintedanib treatment in IPF fibroblasts.

183 annotated as associated with pirfenidone and nintedanib treatment in silico via Coremine.

184 ) with genes associated with pirfenidone and nintedanib treatment.

185 valuate the efficacy and safety of 150 mg of nintedanib twice daily as compared with placebo in patie

186 rial suggested that treatment with 150 mg of nintedanib twice daily reduced lung-function decline and

187 (sLOXL2) concentrations, and pirfenidone and nintedanib use, were randomly assigned (1:1) to inject 1

188 .70; 95% CI, 0.40 to 1.21; P = .197; median [nintedanib v placebo], 20.6 months v 15.2 months) and me

189 .49; 95% CI, 0.30 to 0.82; P = .006; median [nintedanib v placebo], 9.7 v 5.7 months).

190 8; P<0.001) in INPULSIS-1 and -113.6 ml with nintedanib versus -207.3 ml with placebo (difference, 93

191 ual rate of change in FVC was -114.7 ml with nintedanib versus -239.9 ml with placebo (difference, 12

192 ion were reported in 6.8% of those receiving nintedanib versus 17.1% of those in the placebo group.

193 LSIS-2, there was a significant benefit with nintedanib versus placebo (hazard ratio, 0.38; 95% CI, 0

194 placebo was -225.7 and -221.0 ml/yr, and the nintedanib versus placebo difference in the adjusted ann

195 and preserved lung function, treatment with nintedanib versus placebo for 12 weeks did not affect th

196 events were sepsis (five with docetaxel plus nintedanib vs one with docetaxel plus placebo), pneumoni

197 s was six; the median treatment duration for nintedanib was 7.8 months and 5.3 months for placebo.

198 Nintedanib was also active on primary samples of KIT D81

199 lung injury due to nintedanib was suspected, nintedanib was discontinued.

200 quently drug lymphocyte stimulation test for nintedanib was found to be positive.

201 stent with a slowing of disease progression; nintedanib was frequently associated with diarrhea, whic

202 ib than with placebo; no clinical benefit of nintedanib was observed for other manifestations of syst

203 equently led to permanent discontinuation of nintedanib was progression of idiopathic pulmonary fibro

204 Because lung injury due to nintedanib was suspected, nintedanib was discontinued.

205 Questions about pirfenidone and nintedanib were informed by systematic reviews and answe

206 d substantial stability for Fluphenazine and Nintedanib with Sirt2.