ライフサイエンスコーパス: pirfenidone

1 and CD8 proliferation index were reduced by pirfenidone.

2 conventional therapy were treated with oral pirfenidone.

3 nses was equal or superior to nintedanib and pirfenidone.

4 the activation of the necroptosis pathway by pirfenidone.

5 senicapoc, compared to the FDA-approved drug pirfenidone.

6 p38gamma-specific pharmacological inhibitor pirfenidone.

7 inically useful TGF-beta signaling inhibitor pirfenidone.

8 MHC-mismatched tracheal allografts received pirfenidone (0.5%) in pulverized food according to diffe

9 Mean change in percentage FVC in the pirfenidone 1197 mg/day group was intermediate to that i

10 e assigned to pirfenidone 2403 mg/day, 87 to pirfenidone 1197 mg/day, and 174 to placebo.

11 in a 2:1:2 ratio to pirfenidone 2403 mg/day, pirfenidone 1197 mg/day, or placebo; in study 006, patie

12 ed the study, the mean eGFR increased in the pirfenidone 1200-mg/d group (+3.3 +/- 8.5 ml/min per 1.7

13 pirfenidone 2400-mg/d group, and none in the pirfenidone 1200-mg/d group during the study (P = 0.25).

14 tion were enrolled in the study and received Pirfenidone (1200 mg/day) for 24 months.

15 trial), including all patients randomized to pirfenidone 2,403 mg/d (n = 623) or placebo (n = 624).

16 hemodialysis in the placebo group, 1 in the pirfenidone 2400-mg/d group, and none in the pirfenidone

17 The dropout rate was high (11 of 25) in the pirfenidone 2400-mg/d group, and the change in eGFR was

18 mg/day group was intermediate to that in the pirfenidone 2403 mg/day and placebo groups.

19 change at week 72 was -8.0% (SD 16.5) in the pirfenidone 2403 mg/day group and -12.4% (18.5) in the p

20 Patients in the pirfenidone 2403 mg/day group had higher incidences of n

21 ibrosis (12 [3%] vs 25 [7%]) occurred in the pirfenidone 2403 mg/day groups than in the placebo group

22 06, patients were assigned in a 1:1 ratio to pirfenidone 2403 mg/day or placebo.

23 dy 004, 174 of 435 patients were assigned to pirfenidone 2403 mg/day, 87 to pirfenidone 1197 mg/day,

24 dy 006, 171 of 344 patients were assigned to pirfenidone 2403 mg/day, and 173 to placebo.

25 , patients were assigned in a 2:1:2 ratio to pirfenidone 2403 mg/day, pirfenidone 1197 mg/day, or pla

26 ic pulmonary fibrosis to receive either oral pirfenidone (2403 mg per day) or placebo for 52 weeks.

27 Randomisation was stratified by dose of pirfenidone (2403 mg/day [the maximum dose] or <2403 mg/

28 Pirfenidone [5-methyl-1-phenyl-2-(1H)-pyridone] down-reg

29 In addition, pre-treatment with pirfenidone, a drug presently used to inhibit TGF-beta s

30 We evaluated pirfenidone, a Food and Drug Administration (FDA)-approv

31 Pirfenidone, a new, investigational antifibrotic agent,

32 allograft model, we evaluated the effect of pirfenidone, a novel antifibrotic agent, on the developm

33 sults of a phase 2 study that suggested that pirfenidone, a novel antifibrotic and anti-inflammatory

34 Pirfenidone alone showed a small but significant (P<0.05

35 Pirfenidone also inhibits production of tumor necrosis f

36 specific p38gamma pharmacological inhibitor pirfenidone also suppresses pro-inflammatory cytokine ex

37 -cell receptor (TCR) activation, and whether pirfenidone alters regulatory T cells (CD4CD25) suppress

38 We first evaluated whether pirfenidone alters T-cell proliferation and cytokine rel

39 We previously showed that pirfenidone, an anti-fibrotic agent, reduces lung allogr

40 Pre-treatment of aged macrophages with pirfenidone, an anti-fibrotic drug with antioxidant and

41 Whether pirfenidone, an oral antifibrotic agent without hemodyna

42 Pirfenidone, an oral antifibrotic agent, has been shown

43 Pirfenidone, an oral antifibrotic drug that is often use

44 In two of three phase 3 trials, pirfenidone, an oral antifibrotic therapy, reduced disea

45 research into the safety and efficacy of (a) pirfenidone and (b) the combination of pirfenidone plus

46 ly enhanced the anti-proliferative effect of pirfenidone and favorably modulated TGFbeta-induced cell

47 Objectives: We used pooled data from pirfenidone and IFNy-1b trials to explore the associatio

48 strategies include the anti-fibrotic agents pirfenidone and interferon-gamma.

49 ogeneic response, whereas the combination of pirfenidone and low dose rapamycin had more remarkable e

50 w insights into the anti-fibrotic actions of pirfenidone and nintedanib and identifies novel targets

51 Pirfenidone and Nintedanib are the only currently-approv

52 Currently, pirfenidone and nintedanib are the only FDA-approved dru

53 ffectiveness of the antifibrotic medications pirfenidone and nintedanib in patients with idiopathic p

54 g the effect of the antifibrotic medications pirfenidone and nintedanib on clinically important outco

55 hic pulmonary fibrosis have established that pirfenidone and nintedanib prevent about 50% of the decl

56 t findings were annotated as associated with pirfenidone and nintedanib treatment in silico via Corem

57 ed (FDR-p = 0.04) with genes associated with pirfenidone and nintedanib treatment.

58 C), serum LOXL2 (sLOXL2) concentrations, and pirfenidone and nintedanib use, were randomly assigned (

59 Questions about pirfenidone and nintedanib were informed by systematic r

60 tive results of recently completed trials of pirfenidone and nintedanib, and results that will come f

61 IPF is currently treated with pirfenidone and nintedanib, compounds which slow the rat

62 Food and Drug Administration-approved drugs, pirfenidone and nintedanib, only slow disease progressio

63 aking studies that confirmed that two drugs, pirfenidone and nintedanib, slowed disease progression,

64 to those of FDA-approved anti-fibrosis drugs pirfenidone and nintedanib.

65 le, and SGRQ scores were similar between the pirfenidone and placebo groups at week 24.

66 on-free survival were identified between the pirfenidone and placebo groups, irrespective of the defi

67 even patients were randomized to each of the pirfenidone and placebo groups.

68 The model predicted how pirfenidone and Src inhibitor WH-4-023 reduce actin fila

69 l-cause mortality between patients receiving pirfenidone and those on nintedanib (HR, 1.14; 95% CI, 0

70 stantially alter the tolerability profile of pirfenidone, and is unlikely to be beneficial in IPF.

71 tudies demonstrated the potential utility of pirfenidone as a therapeutic against septic shock and th

72 se findings support further investigation of pirfenidone as an effective treatment for patients with

73 ing induced animals received a daily dose of pirfenidone (as a standard anti-fibrotic drug) (300 mg/k

74 Pirfenidone, as compared with placebo, reduced disease p

75 - 4.8 ml/min per 1.73 m(2); P = 0.026 versus pirfenidone at 1200 mg/d).

76 domly assigned 26 subjects to placebo, 26 to pirfenidone at 1200 mg/d, and 25 to pirfenidone at 2400

77 o, 26 to pirfenidone at 1200 mg/d, and 25 to pirfenidone at 2400 mg/d.

78 with IPF aged 40-80 years and established on pirfenidone (at least 1602 mg/day for 8 weeks or longer)

79 r IIP-PH, IPF-PH, and IIP-PH with nintedanib/pirfenidone background therapy), but not in patients wit

80 5) of mice receiving a continuous regimen of pirfenidone beginning on day 5 after transplantation had

81 F from the placebo groups of three trials of pirfenidone (CAPACITY 004, CAPACITY 006, and ASCEND) wer

82 te the antifibrotic efficacy of esomeprazole/pirfenidone combination.

83 RT alone and was also associated with higher pirfenidone concentrations.

84 meostasis and emphasize the possibility that pirfenidone could be employed as a novel therapeutic reg

85 were randomly assigned (1:1) to 2403 mg oral pirfenidone daily or placebo using a central validated i

86 Pirfenidone dampened splenic germinal center B-cell and

87 In vivo administration of pirfenidone decreased superoxide formation, increased he

88 Anti-fibrosis treatment using pirfenidone disrupts the polarization and mechanical act

89 y suggest that addition of acetylcysteine to pirfenidone does not substantially alter the tolerabilit

90 t (0.6%, -3.5 to 4.7); however, a consistent pirfenidone effect was apparent until week 48 (p=0.005)

91 Additionally, pirfenidone effects on alloantigen-induced T-cell prolif

92 Mice on a continuous daily regimen of pirfenidone failed to develop evidence of chronic allogr

93 F and myocardial fibrosis, administration of pirfenidone for 52 weeks reduced myocardial fibrosis.

94 II randomized, placebo-controlled studies of pirfenidone for IPF (the two CAPACITY [Clinical Studies

95 First-line therapy includes nintedanib or pirfenidone for IPF and mycophenolate mofetil for ILD du

96 Pirfenidone for two years benefits CHC patients and impr

97 In these experiments, pirfenidone given 2 to 4.25 h after SEB resulted in 80 t

98 Lco from baseline was -0.7% (SD 7.1) for the pirfenidone group and -2.5% (8.8) for the placebo group,

99 6MWD from baseline was -2.0 m (68.1) for the pirfenidone group and -26.7 m (79.3) for the placebo gro

100 in FVC at week 72 was -9.0% (SD 19.6) in the pirfenidone group and -9.6% (19.1) in the placebo group,

101 reported in 120 (94%) of 127 patients in the pirfenidone group and 101 (81%) of 124 patients in the p

102 s occurred in 12 (18%) of 67 patients in the pirfenidone group and 11 (16%) of 67 patients in the con

103 Twelve patients (26%) in the pirfenidone group and 14 patients (30%) in the placebo g

104 ts were reported in 18 (14%) patients in the pirfenidone group and 20 (16%) patients in the placebo g

105 levant and significant risk reduction in the pirfenidone group compared with the placebo group.

106 At week 24, the pirfenidone group showed an 8.0% improvement from baseli

107 lated adverse events were more common in the pirfenidone group than in the placebo group but rarely l

108 lity outcomes was significantly lower in the pirfenidone group than in the placebo group in the poole

109 was -87.7 mL (Q1-Q3 -338.1 to 148.6) in the pirfenidone group versus -157.1 mL (-370.9 to 70.1) in t

110 gastrointestinal disorders (60 [47%] in the pirfenidone group vs 32 [26%] in the placebo group), fat

111 d pneumonia (four [6%] of 67 patients in the pirfenidone group vs eight [12%] of 67 patients in the c

112 p), and rash (two [3%] of 67 patients in the pirfenidone group vs none in the control group).

113 ared with the placebo group, patients in the pirfenidone group were less likely to have a decline in

114 The most common adverse events in the pirfenidone group were nausea, insomnia and rash.

115 In the pirfenidone group, as compared with the placebo group, t

116 III IPF clinical trials, patients receiving pirfenidone had a lower risk of nonelective respiratory-

117 tor-beta production by purified T cells, and pirfenidone had no effect on the suppressive properties

118 The data show pirfenidone has a favourable benefit risk profile and re

119 In this study, we tested the hypothesis that pirfenidone has immune modulating activities and evaluat

120 factor, connective tissue growth factor, and pirfenidone have shown promising results in preclinical

121 standard-of-care (SOC) drugs, nintedanib and pirfenidone, have senolytic properties.

122 In vitro chemotaxis assays demonstrated that pirfenidone impaired macrophage migration to monocyte ch

123 Pirfenidone in combination with glucocorticoids provides

124 ne versus placebo-Clinical Studies Assessing Pirfenidone in Idiopathic Pulmonary Fibrosis: Research o

125 h analysis of three large, phase 3 trials of pirfenidone in IPF.

126 the two CAPACITY [Clinical Studies Assessing Pirfenidone in IPF: Research of Efficacy and Safety Outc

127 We evaluated the efficacy and safety of pirfenidone in patients with grade 2 or grade 3 radiatio

128 The favorable effects of pirfenidone in patients with HFpEF will need to be confi

129 tolerability of acetylcysteine combined with pirfenidone in patients with IPF.

130 e aimed to assess the efficacy and safety of pirfenidone in patients with progressive fibrosing uncla

131 cy of saracatinib relative to nintedanib and pirfenidone in three preclinical models: 1) in vitro in

132 y of the PPI esomeprazole when combined with pirfenidone in vitro and in vivo.

133 Furthermore, pirfenidone increased transcript levels of FN1 and COL1A

134 Moreover, in senescent IPF cells, pirfenidone induced mixed lineage kinase domain-like pse

135 s to assess whether two-years treatment with Pirfenidone influences necroinflammation, fibrosis and s

136 Additionally, pirfenidone inhibited TCR-induced production of multiple

137 Pirfenidone inhibits the mechanical activation of macrop

138 These findings suggest that pirfenidone is a candidate drug to be evaluated for prev

139 Taken together, our data suggest that pirfenidone is a potential therapeutic agent to ameliora

140 In conclusion, these results suggest that pirfenidone is a promising agent for individuals with ov

141 Pirfenidone is a promising new treatment for IPF that is

142 e a delay of onset or abrogation of OAD when pirfenidone is administered in the early posttransplanta

143 Pirfenidone is an oral antifibrotic agent that benefits

144 f IPF and other fibrotic lung diseases where pirfenidone is prescribed.

145 l benefit from addition of acetylcysteine to pirfenidone is unlikely, with the possibility of a harmf

146 Mice receiving pirfenidone limited to the early posttransplantation per

147 Pirfenidone may be an important new agent in transplanta

148 tion in response to TGFbeta in comparison to pirfenidone monotherapy.

149 1 patients received concomitant IPF therapy (pirfenidone n=55 or nintedanib n=29).

150 s by IL-1B blockade (n = 19) or antifibrotic pirfenidone (n = 18) reduced CCR2(+) macrophage accumula

151 o placebo in the CAPACITY studies evaluating pirfenidone (n = 347) or the INSPIRE study evaluating in

152 ts were randomly assigned to receive 2403 mg pirfenidone (n=127) or placebo (n=126) and were included

153 the synthesis of many drug analogues such as pirfenidone, naproxen, ibuprofen, geraniol, umbelliferon

154 daily in addition to local standard of care (pirfenidone, nintedanib, or neither) for at least 52 wee

155 The effect of pirfenidone on death after hospitalization is uncertain.

156 e sought to confirm the beneficial effect of pirfenidone on disease progression in such patients.

157 ne versus placebo to determine the effect of pirfenidone on mortality outcomes over 120 weeks.

158 PF receiving standard of care treatment with pirfenidone or nintedanib or in those not receiving stan

159 ebo, with or without background IPF therapy (pirfenidone or nintedanib), in an approximately 3:1 rati

160 r greater, were randomly assigned to receive pirfenidone or placebo for 52 weeks.

161 nary fibrosis were randomly assigned to oral pirfenidone or placebo for a minimum of 72 weeks in 110

162 Of interest, pirfenidone (Pf), an FDA approved anti-fibrotic drug to

163 Pirfenidone (PFD) is an antifibrotic agent with benefici

164 valuate the effects of the antifibrotic drug pirfenidone (PFD) on arrhythmogenic atrial remodeling in

165 Recent preclinical studies suggested that pirfenidone (PFD) prevents fibrosis in various diseases,

166 In addition, the antifibrotic molecule pirfenidone (PFD) was shown to ameliorate fibrosis in th

167 tial of targeting the TGF-beta pathway using Pirfenidone (PFD), a TGF-beta inhibitor, either alone or

168 In this study, we showed that pirfenidone (PFD), an anti-lung fibrosis drug, inhibited

169 erated random number table to receive either pirfenidone plus glucocorticoids or glucocorticoids alon

170 f (a) pirfenidone and (b) the combination of pirfenidone plus mycophenolate; and 3) suggests the use

171 Treatment with the antifibrotic drug pirfenidone preserved TZ architecture and was associated

172 mma or treatment with the p38gamma inhibitor pirfenidone protects against the chemically induced form

173 pared with those of the drugs nintedanib and pirfenidone, recently approved for IPF.

174 In study 004, pirfenidone reduced decline in FVC (p=0.001).

175 In comparison to placebo, pirfenidone reduced myocardial extracellular volume (bet

176 rther, treatment with the anti-fibrotic drug pirfenidone reduced pulmonary fibrosis in this model.

177 n peripheral blood lymphocytes revealed that pirfenidone reduced SEB-induced cytokine levels 50 to 80

178 Pirfenidone reduced the decline in the 6-minute walk dis

179 ular mechanisms by which esomeprazole and/or pirfenidone regulate lung fibrosis.

180 study of cells treated with esomeprazole or pirfenidone revealed that the drugs target several extra

181 Pirfenidone's ability to reduce cytokine expression in t

182 ic inhibition or antifibrotic treatment with pirfenidone significantly diminished RV fibrosis progres

183 ploidentical model of sclerodermatous cGVHD, pirfenidone significantly reduced macrophages in the ski

184 -approved antifibrotic drugs, nintedanib and pirfenidone, slow the rate of decline in lung function,

185 Antifibrotic therapy with nintedanib or pirfenidone slows annual FVC decline by approximately 44

186 ally targeting collagen family members while pirfenidone targets the keratins.

187 site spirometry was lower in patients given pirfenidone than placebo (treatment difference 95.3 mL [

188 he approved treatment options nintedanib and pirfenidone, the medical need for a safe and well-tolera

189 differences in the pooled analysis favouring pirfenidone therapy compared with placebo for treatment-

190 everal analytic approaches demonstrated that pirfenidone therapy is associated with a reduction in th

191 everal analytic approaches demonstrated that pirfenidone therapy is associated with a reduction in th

192 razole enhances the antifibrotic efficacy of pirfenidone through complementary molecular mechanisms.

193 al durations 72-120 weeks) and Assessment of Pirfenidone to Confirm Efficacy and Safety in Idiopathic

194 tcomes] trials and the ASCEND [Assessment of Pirfenidone to Confirm Efficacy and Safety in Idiopathic

195 also known as N-acetylcysteine) is used with pirfenidone to treat idiopathic pulmonary fibrosis (IPF)

196 Pirfenidone treatment beginning one month post-transplan

197 rosing unclassifiable ILD could benefit from pirfenidone treatment, which has an acceptable safety an

198 eters were not significantly suppressed with pirfenidone treatment.

199 and death after hospitalization with use of pirfenidone versus placebo over 52 weeks using data deri

200 yses and meta-analyses of clinical trials of pirfenidone versus placebo to determine the effect of pi

201 he three global randomised phase 3 trials of pirfenidone versus placebo-Clinical Studies Assessing Pi

202 se data and data from two Japanese trials of pirfenidone versus placebo-Shionogi Phase 2 (SP2) and Sh

203 hospitalized for any reason, treatment with pirfenidone was associated with lower risk of death afte

204 Pirfenidone was associated with lower risk of respirator

205 Pirfenidone was found to inhibit the responder frequency

206 Pirfenidone was given orally three times daily at doses

207 for nintedanib, and additional research into pirfenidone was recommended.

208 rials, the between-group difference favoring pirfenidone was significant for death from any cause (P=

209 Background antifibrotic treatment (pirfenidone) was allowed.

210 , CDH11, and TNS1) have been associated with pirfenidone, while five genes (CLINT1, CADM1, MTDH, SYDE

211 Combining pirfenidone with an ART regimen was associated with grea