ライフサイエンスコーパス: pirfenidone

1 p38gamma-specific pharmacological inhibitor pirfenidone.

2 conventional therapy were treated with oral pirfenidone.

3 inically useful TGF-beta signaling inhibitor pirfenidone.

4 and CD8 proliferation index were reduced by pirfenidone.

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

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

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

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

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

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

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

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

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

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

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

16 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

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

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

19 06, patients were assigned in a 1:1 ratio to pirfenidone 2403 mg/day or placebo.

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

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

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

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

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

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

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

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

28 Pirfenidone, a new, investigational antifibrotic agent,

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

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

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

32 Pirfenidone also inhibits production of tumor necrosis f

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

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

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

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

37 Pirfenidone, an oral antifibrotic agent, has been shown

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

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

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

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

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

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

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

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

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

47 Pirfenidone, as compared with placebo, reduced disease p

48 - 4.8 ml/min per 1.73 m(2); P = 0.026 versus pirfenidone at 1200 mg/d).

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

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

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

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

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

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

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

56 Pirfenidone dampened splenic germinal center B-cell and

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

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

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

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

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

62 Pirfenidone for two years benefits CHC patients and impr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Additionally, pirfenidone inhibited TCR-induced production of multiple

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

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

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

84 Pirfenidone is a promising new treatment for IPF that is

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

86 Pirfenidone is an oral antifibrotic agent that benefits

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

88 Mice receiving pirfenidone limited to the early posttransplantation per

89 Pirfenidone may be an important new agent in transplanta

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

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

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

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

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

95 Pirfenidone (PFD) is an antifibrotic agent with benefici

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

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

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

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

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

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

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

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

104 Pirfenidone's ability to reduce cytokine expression in t

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

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

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

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

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

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

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

112 Pirfenidone treatment beginning one month post-transplan

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

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

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

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

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

118 Pirfenidone was associated with lower risk of respirator

119 Pirfenidone was found to inhibit the responder frequency

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

121 Combining pirfenidone with an ART regimen was associated with grea