ライフサイエンスコーパス: mifepristone

1 ends on the presence of the activator RU486 (mifepristone).

2 nist dexamethasone and the antagonist RU486 (mifepristone).

3 active in the presence of the steroid RU486 (mifepristone).

4 as induced in hepatocytes after injection of mifepristone.

5 n vivo models,4h had potencies comparable to mifepristone.

6 were reversed by the GC receptor antagonist mifepristone.

7 lucocorticoid receptor (GR) antagonists like mifepristone.

8 not be administered strictly 48 hours after mifepristone.

9 pothalamic-pituitary-adrenal axis (HPA) with mifepristone.

10 es and is not inhibited by the GR antagonist mifepristone.

11 by the magnitude of the cortisol response to mifepristone.

12 the progesterone receptor antagonist RU486 [mifepristone (11beta-[p-(dimethylamino)phenyl]-17beta-hy

13 recommended alternative approaches, such as mifepristone, 200 mg orally, followed in 1 to 3 days by

14 0 microg, can be used from 1 to 3 days after mifepristone, 200 mg, for early medical abortion, and ne

15 llowed by subcutaneous injection of vehicle, mifepristone 30 mg/kg, propranolol 10 mg/kg, or both.

16 elative to placebo, individuals who received mifepristone (600 mg daily taken orally for 1 week) exhi

17 Food and Drug Administration specifies mifepristone, 600 mg orally, followed 2 days later by mi

18 ctive of this study was to determine whether mifepristone, a glucocorticoid receptor antagonist, play

19 llowed by truncation of Bid, confirming that Mifepristone activates the TRAIL pathway.

20 at both systemic and intra-CeA (but not BLA) mifepristone administration suppressed yohimbine-induced

21 armacologic treatment with the GR antagonist mifepristone also attenuated disease as effectively as h

22 Chronic treatment with mifepristone also blocked escalated alcohol drinking and

23 endometritis following medical abortion with mifepristone (also known as RU-486) used with misoprosto

24 The stimulation can be eliminated by mifepristone, an antagonist of GR, indicating the involv

25 Mifepristone, an antiprogestin used individually or toge

26 gible patients, 80 were randomly assigned to mifepristone and 84 to placebo.

27 Mifepristone and a prostaglandin have been used successf

28 report the results of a large U.S. study of mifepristone and misoprostol in women with pregnancies o

29 Mifepristone and Tamoxifen induced significant expressio

30 We administered 600 mg of mifepristone and then 400 microg of misoprostol two days

31 a narrow class of antiprogestins, including mifepristone and ulipristal, and whose expression is med

32 Patients received 200 mg of oral mifepristone and were randomly assigned to self-administ

33 ed by the glucocorticoid receptor inhibitor, mifepristone, and a monoclonal antibody against the rece

34 y comparable to known GR antagonists such as mifepristone, and notably, this molecule lowers LDL (-74

35 nd medical therapies including ketoconazole, mifepristone, and pasireotide.

36 To explore the possibility of using mifepristone as a cancer metastasis chemopreventive, we

37 ort further exploration of GR antagonism via mifepristone as a therapeutic strategy for alcoholism.

38 ed the longer-term efficacy of 600 mg/day of mifepristone as an adjunctive treatment, for 1 week, in

39 ts point to a potential therapeutic role for mifepristone as an effective treatment for AD and furthe

40 till in place and bans physicians from using mifepristone based on any new developments in clinical r

41 Systemic mifepristone blocks the reconsolidation of cue-condition

42 fter 24 h and the stimulation was blocked by mifepristone but not spironolactone.

43 s showed that treatment with 1,000 mug/kg of mifepristone consistently switched on cTnT-Q92 expressio

44 cts of misoprostol, which were not shared by mifepristone, correlated with the activation of the G(s)

45 all ligands tested except for bicalutamide, mifepristone, DHT, and R1881 in a competitive binding as

46 Mifepristone did not exert its effect when administered

47 Postreactivation mifepristone did not impair short-term memory.

48 Finally, we show that the GR antagonist mifepristone does not block the expression of EtOH sensi

49 Despite the two-thirds reduction in mifepristone dose, success rates were high: Vietnam 93%,

50 nisolone and the pharmacologic GR antagonist mifepristone each acted directly on primary cultures of

51 erone and glucocorticoid receptor antagonist mifepristone, evident 2 weeks after the cessation of tre

52 medication) principally by a regimen of oral mifepristone followed 24 to 48 hours later by vaginal mi

53 implified medical abortion regimen of 200 mg mifepristone followed by the option of home administrati

54 l timing of misoprostol administration after mifepristone for medical abortion is 2 days, but more fl

55 en returned to the clinic up to 8 days after mifepristone for ultrasonographic evaluation.

56 nd cellular assays further demonstrated that mifepristone had the ability to prevent breast cancer ce

57 tive glucocorticoid receptor (GR) antagonist mifepristone has been approved in the U.S. for the treat

58 The steroidal glucocorticoid antagonist mifepristone has been reported to improve the symptoms o

59 We also tested the use of mifepristone in 56 alcohol-dependent human subjects as p

60 However, Mifepristone in combination with Tamoxifen did not incre

61 inistration of the glucocorticoid antagonist mifepristone in either the nucleus accumbens or ventral

62 their last menstrual period received 200 mg mifepristone in the clinic and then chose whether to tak

63 ed by SWOG was planned to define the role of mifepristone in the treatment of unresectable meningioma

64 ted for in vitro assessment on the basal and mifepristone-induced cell activation levels by FACS anal

65 Inhibition of proteasomal proteases in mifepristone-induced KO-WT, KO-GDP, or KO-GTP MEFs resul

66 Here, we exploited the mifepristone-induced SRC-3 LNCaP prostate cancer cell li

67 Hence, mifepristone induces a novel C-terminal cleavage of APP

68 Taken together, the mifepristone-inducible regulatory system provides a powe

69 by combination of liver-specific expression, mifepristone induction and Cre-loxP recombination to con

70 We also investigated the effects of local mifepristone infusions into the central amygdala (CeA) o

71 Moreover, mifepristone inhibited the expression of focal adhesion

72 oid receptor (GR), whereas the GR antagonist mifepristone inhibits this response.

73 group was tested four hours after the Day 2 mifepristone injection to measure postreactivation short

74 In addition, we infused mifepristone into the basolateral amygdala (BLA) in etha

75 Mifepristone is an oral antiprogestational agent reporte

76 es and demonstrate that brief treatment with mifepristone is associated with a sustained improvement

77 Postreactivation mifepristone may be a promising treatment for PTSD, but

78 Mifepristone may be a valuable pharmacotherapeutic strat

79 The effects of antiprogestin mifepristone (MF) on the growth, progesterone receptor e

80 Administration of the ligand mifepristone (MFP) up-regulated GHRH expression, as show

81 per-dependent adenoviral vector carrying the mifepristone (Mfp)-inducible gene-regulatory system to c

82 low basal cell activation in the absence of mifepristone (MFP).

83 Mifepristone-misoprostol abortion, consisting of oral pi

84 ely tested two simplifications to the French mifepristone-misoprostol regimen in Vietnam and Tunisia.

85 This mifepristone-misoprostol regimen is effective in termina

86 oxin LPS or progesterone receptor antagonist mifepristone more often than current commonly used tocol

87 llet; the glucocorticoid receptor antagonist mifepristone neutralized TA inhibition of angiogenesis.

88 eline responding, we examined the effects of mifepristone on maintained responding and yohimbine-indu

89 Therefore, we investigated the effect of Mifepristone on the tumor necrosis factor alpha-related

90 eA plays an important role in the effects of mifepristone on yohimbine-induced reinstatement of ethan

91 nts were randomly assigned to receive either mifepristone or placebo for 2 years unless disease progr

92 roxyprogesterone acetate, megestrol acetate, mifepristone, pregnanediol, 17alpha-hydroxypregnanolone,

93 parent benefits, because coadministration of mifepristone prevented stress-induced disease ameliorati

94 ment of cells with the GR antagonist RU-486 (Mifepristone) prevented promoter activation by ePi.

95 Postreactivation, but not nonreactivation, mifepristone produced a decrement in the CR that did not

96 the glucocorticoid receptor (GR) antagonist mifepristone reduces alcohol intake in alcohol-dependent

97 of transgene expression using the GeneSwitch mifepristone-regulatable system within the context of an

98 uced CTGF or 3T3 fibroblasts engineered with mifepristone-regulated CTGF were combined with LNCaP hum

99 Mifepristone-regulated gene expression was observed in s

100 ells engineered to express ps20-V5-His under mifepristone regulation showed a 129% increase in microv

101 h-3T3 cells engineered to express lacZ under mifepristone regulation.

102 ng Natural Language Processing (NLP) and 513 mifepristone-related genes were dug out and classified f

103 performed a systems pharmacology analysis of mifepristone-related molecules in the present study.

104 ng concentrations of cyproterone acetate and mifepristone resulted in more complete disruption of the

105 icient mice with the progesterone antagonist mifepristone (RU 486) prevented mammary tumorigenesis.

106 human progesterone receptor (hPR) inhibitor Mifepristone (RU-486) and other hPR ligands, a new class

107 gesterone was abrogated by the PR antagonist mifepristone (RU-486).

108 The glucocorticoid receptor (GR) antagonist mifepristone (RU-486; 10(-6) mol/L) blocked the inhibito

109 Chronic GR antagonism with mifepristone (RU38486) prevented the escalation of alcoh

110 We evaluated the ability of postreactivation mifepristone (RU38486, a glucocorticoid antagonist), alo

111 tment can also mediate NCoR recruitment, but mifepristone (RU486) at nanomolar concentrations is uniq

112 ts of the glucocorticoid receptor antagonist mifepristone (RU486) in the 3xTg-AD mouse model at an ag

113 Mifepristone (RU486), a synthetic steroid compound used

114 and cancer initiation/progression, we used a mifepristone (RU486)-inducible regulatory system to expr

115 e effects were reversed by the GR antagonist mifepristone (RU486).

116 mulated Luc activity, which was abolished by mifepristone (RU486).

117 n, antiglucocorticoid, and antiandrogen drug mifepristone (RU486).

118 ns in fish, and effects of the antiprogestin mifepristone (RU486, an abortive) are unknown.

119 armacological profile with the antiprogestin mifepristone (RU486; Roussel Uclaf SA).

120 ascularization are blocked by TA through the mifepristone-sensitive steroid receptor.

121 In the presence of the antiprogestin mifepristone, this chimeric regulator binds to a target

122 ifically in the liver by a brief exposure of mifepristone to induce permanent genomic recombination m

123 zebrafish liver only by a brief exposure of mifepristone to induce permanent genomic recombination m

124 design a combination treatment of TRAIL and Mifepristone to induce significant apoptosis in prostate

125 confirmed by the activation of caspase-8 in Mifepristone-treated cells.

126 ent phase and 1-week post-treatment phase in mifepristone-treated individuals.

127 In addition, mifepristone treatment also reduced the phosphorylation

128 Mifepristone treatment rescues the pathologically induce

129 Mifepristone treatment was associated with a time-limite

130 Mifepristone was well tolerated and improved liver-funct

131 Long-term administration of mifepristone was well tolerated but had no impact on pat

132 The effects of mifepristone were investigated in 3xTg-AD mice using a c

133 s of human growth hormone in the presence of mifepristone whereas the transgene expression was undete

134 3 could be blocked by the steroid antagonist mifepristone, whereas hydrocortisone and other steroids

135 d molecules, epitiostanol, progesterone, and mifepristone, which decrease ferroportin levels by incre

136 g Administration (FDA)-approved protocol for mifepristone, which is used with misoprostol for medicat

137 ients (30%) were able to complete 2 years of mifepristone without disease progression, adverse effect

138 A fifth group received mifepristone without the CS presentation (nonreactivatio