ライフサイエンスコーパス: penicillamine

1 ution was feasible using a complexing agent (penicillamine).

2 -year time period in patients treated with D-penicillamine.

3 nitrosoglutathione and S-nitroso-N-acetyl-DL-penicillamine.

4 4-benzyl-2-oxazolidinones and in the case of penicillamine.

5 sodium nitroprusside and S-nitroso-N-acetyl-penicillamine.

6 ds include DOPA, amphetamine, ephedrine, and penicillamine.

7 failed previous therapy with gold salts and penicillamine.

8 e reacting species is observed with DOPA and penicillamine.

9 ), a cyclized N-protected derivative of D(-)-penicillamine.

10 stability and is inhibited by isoleucine and penicillamine.

11 amine treatment versus 12 receiving low-dose penicillamine.

12 on induced by minocycline, sulfasalazine, or penicillamine.

13 obtained by modification of the amino acid D-penicillamine.

14 icenter trial of high-dose versus low-dose D-penicillamine.

15 MG had recently been provoked by the drug D-penicillamine.

16 (SNP), 1 mmol/L, and S-nitroso-N-acetyl-D-L-penicillamine, 0.1 mmol/L, significantly increased basal

17 imilarly, the NO donor S-nitroso-N-acetyl-dl-penicillamine (1-1000 microm) down-regulated the express

18 NO-releasing compounds S-nitroso-N-acetyl-penicillamine (10(-4) mol/L, -34+/-5%) and nitroglycerin

19 D-Penicillamine(2,5)-enkephalin (DPDPE) is a potent opioid

20 oid receptor agonists, deltorphin II, and [D-penicillamine(2,5)]-enkephalin.

21 er previously reported candidate drugs: 2 to penicillamine, 2 to allopurinol, and 1 to sulfasalazine.

22 n of cyclic and topological constraints with penicillamines, 2 (Tyr-cyclo[d-Pen-Gly-Phe-Pen]-Pro-Leu-

23 rosocaptopril, glucose-S-nitroso-N-acetyl-dl-penicillamine-2, and the S-nitroso tripeptide acetyl-Phe

24 onsumption in response to S-nitroso-N-acetyl-penicillamine (-35+/-7%) or nitroglycerin (-16+/-5%) was

25 By contrast the delta-opioid ligand [2-D-penicillamine, 5-D-penicillamine]enkephalin (DPDPE) had

26 th AI and addition of S-nitroso-N-acetyl-d,l-penicillamine (a NO donor) but was not significantly inc

27 Penicillamine (adjusted IRR 2.51, 95% CI 1.29-4.89, P =

28 ed model was verified by exposing worms to D-penicillamine and menadione.

29 small number of case reports also implicate penicillamine and minocycline as agents capable of induc

30 Penicillamine and trientine have teratogenic effects in

31 Food and Drug Administration, which includes penicillamine and trientine.

32 The NO donor SNAP (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (Y

33 g 0.1% (wt/wt) aminoguanidine, pyridoxamine, penicillamine, and nucleophilic compounds NC-I and NC-II

34 onnitrosylated parent molecules, N-acetyl-DL-penicillamine, and reduced gluthatione were without effe

35 ggested that minocycline, sulfasalazine, and penicillamine are associated with antineutrophil cytopla

36 articles was achieved with the assistance of penicillamine as a complexation ligand.

37 ion of pyrogallol and S-nitroso-N-acetyl-D,L-penicillamine, as well as hydrogen peroxide induced a ti

38 steine differs from the antiarthritis drug D-penicillamine by only two methyl groups on the beta-carb

39 of a series of FSDs (N-acetyl-L-cysteine, D-penicillamine, captopril, L-cysteine, or reduced glutath

40 nds tightly to the active site zinc, while D-penicillamine catalyzes metal removal.

41 3 RCTs examining high-dose versus low-dose D-penicillamine (D-Pen Trial), recombinant human relaxin v

42 cancer therapy with a novel combination of D-penicillamine (D-pen) and Idarubicin (Ida) in a syntheti

43 The antiarthritis drug D-penicillamine (D-PEN) catalyzes zinc(II) transfer from c

44 ts and subjects previously reported in the D-penicillamine (D-Pen) trial.

45 e treated mice with a copper chelator, D-(-)-penicillamine (D-PEN), starting immediately following in

46 In contrast, the antiarthritis drug D-penicillamine, D-PEN, which differs from D-Cys only by t

47 ne and the therapeutic agents penicillamine, penicillamine disulfide, N-acetylcysteine, and captopril

48 -doped quantum dots (Qdots) decorated with D-penicillamine (DPA-MnQdots).

49 olled clinical trial in which therapy with D-penicillamine (DPCA) was shown to be ineffective.

50 PBC who had received ineffective therapy (D-penicillamine [DPCA] or placebo) for 5.6 +/- 0.07 years

51 PAECs) with the NO donor, S-nitroso-N-acetyl-penicillamine, dramatically inhibited killing of PAEC ta

52 delta-opioid ligand [2-D-penicillamine, 5-D-penicillamine]enkephalin (DPDPE) had no effect on these

53 eceiving placebo; and 3) a 104-week trial of penicillamine for early systemic sclerosis, with 15 unde

54 ine have teratogenic effects in animals, and penicillamine has known teratogenic effects in humans.

55 icacy, whereas the results of therapy with D-penicillamine have been disappointing.

56 Penicillamine, if given before the terminal clinical sta

57 ticipated in the High-Dose Versus Low-Dose D-Penicillamine in Early Diffuse SSc trial.

58 peptides were equally or more effective than penicillamine in trapping AcH in a cell-free system.

59 rug (Thalidomide) and false negative drug (D-penicillamine) in the conventional mouse embryonic stem

60 The NO donor S-nitroso-N-acetyl-DL-penicillamine inhibited caspase-1 activity in cells as w

61 m the TG the NO donor, S-nitroso-N-acetyl-dl-penicillamine, inhibited M-current.

62 and provides insight into the mechanism of D-penicillamine inhibition.

63 fasalazine, auranofin, intramuscular gold, D-penicillamine, methotrexate, and/or azathioprine).

64 ometric detection of cysteine, homocysteine, penicillamine, N-acetylcysteine, and glutathione.

65 amine thiyl radical (S-NAP) from N-acetyl-DL-penicillamine (NAP) and sulfate anion radical (SO3-) fro

66 The effects of other drugs, including D-penicillamine, nonsteroidal antiinflammatory drugs (NSAI

67 he nitric oxide donors S-nitroso-N-acetyl-DL-penicillamine or diethyltriamine nitric oxide complex, w

68 utathione, either with S-nitroso-N-acetyl-dl-penicillamine or with S-nitroso-L-cysteine indicate that

69 rs, sodium nitroprusside, S-nitroso-N-acetyl-penicillamine, or 3-morpholinosydnonimine, increased hem

70 -cysteine, glutathione, dimercaptosuccinate, penicillamine, or gamma-glutamylcysteine.

71 itroso-acetyl-DL-penicillamine, S-nitroso-DL-penicillamine, or S-nitroso-glutathione) decreased, in a

72 C3H mice, and in response to Cu chelation by penicillamine (PCA) and dietary supplementation of the m

73 hylcysteine (Ecy), Thr, Met, D-Cys, Ser, and penicillamine (Pen) produced progressively less efficien

74 iol antioxidants N-acetyl cysteine (NAC) and penicillamine (PEN), respectively.

75 , and homocystine and the therapeutic agents penicillamine, penicillamine disulfide, N-acetylcysteine

76 of a series of N-terminal dipeptides of D(-)-penicillamine, prepared from the synthon 3-formyl-2,2,5,

77 E-selectin expression by S-nitroso-N-acetyl-penicillamine pretreatment and thiol deprivation was ass

78 D-penicillamine protected against advanced glycation end p

79 g; administration of a NO donor, S-nitroso-N-penicillamine, reduced oocyst and infection scores; and

80 oncentration of the NO donor S-nitroso-amino-penicillamine reduces the number of viral particles in a

81 he NO-generating compound S-nitroso-L-acetyl penicillamine resulted in a significant decrease in vira

82 NO donors (S-nitroso-acetyl-DL-penicillamine, S-nitroso-DL-penicillamine, or S-nitroso-

83 e S-nitroso compounds, S-nitroso-N-acetyl-dl-penicillamine, S-nitrosoglutathione, S-nitrosocaptopril,

84 Penicillamine should be used early and adverse prognosti

85 tivity, since GSNO and S-nitroso-N-acetyl-dl-penicillamine significantly and reversibly reduced total

86 dium nitroprusside (SNP) or S-nitroso-acetyl penicillamine (SNAP) (0.25 to 1 mmol/L).

87 eatment with the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) (1 mmol/L for 90 minutes), followed

88 treated with the NO donor S-nitroso-N-acetyl penicillamine (SNAP) at concentrations ranging from 0.3

89 TG or another NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) at doses relevant to the human mode

90 ANP and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) caused concentration-dependent decr

91 whereas the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) decreased it.

92 osydnonimine (SIN-1), and S-nitroso-N-acetyl-penicillamine (SNAP) on the resting activity (RA) of aff

93 usly by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure

94 ication of the NO-mimetic S-nitroso-N-acetyl-penicillamine (SNAP) or intracellular perfusion with cGM

95 80% in the presence of S-nitroso-N-acetyl-DL-penicillamine (SNAP) or sodium nitroprusside (SNP).

96 mol/L KCl to the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) or to NO is markedly suppressed by

97 The NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) rapidly reduced N-type currents whe

98 ocytes to the NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) resulted in a rapid shift in cellul

99 ulated DC to the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) resulted in DC apoptosis.

100 es for NO, the NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was encapsulated within poly(lactic

101 osure to the NO donors S-nitroso-N-acetyl-dl-penicillamine (SNAP), 3-morpholinosydnonimine (SIN-1), o

102 S-Nitroso-N-acetyl-D, L-penicillamine (SNAP), a nitric oxide (NO) donor, and des

103 S-nitroso-N-acetyl-D,L-penicillamine (SNAP), a NO donor, was added after remova

104 S-Nitroso-N-acetyl-D,L-penicillamine (SNAP), a pharmacological NO donor, did no

105 dition to the cultures of S-nitroso-N-acetyl-penicillamine (SNAP), an NO donor, as well as by additio

106 opyridine, SK&F 96365 and S-nitroso-N-acetyl-penicillamine (SNAP), but was decreased by amiloride and

107 e effects of an NO donor, S-nitroso-N-acetyl penicillamine (SNAP), in buffer-perfused Langendorff hea

108 lication of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), reproducibly increased the frequen

109 antly more resistant to S-nitro-N-acetyl-d,l-penicillamine (SNAP), sodium nitroprusside (SNP), and hy

110 concentrations of NO donor S-nitroso acetyl penicillamine (SNAP).

111 nitroso-L-glutathione (GSNO) and S-nitroso-N-penicillamine (SNAP).

112 eatment with the NO donor S-nitroso-N-acetyl penicillamine (SNAP).

113 The NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP, 0.1 to 1 mmol/L) oxidized the mitoc

114 In contrast, S-nitroso-N-acetyl-penicillamine (SNAP, 10(-4) mol/L), which releases NO sp

115 reated with nitric oxide donors, S-nitroso-N-penicillamine (SNAP, 25 muM) or diethylenetriamine-NONO

116 he NO-releasing drug S-nitrosyl-N-acetyl-D,L-penicillamine (SNAP; 0-0.5 mM) inhibited dimerization of

117 enerate nitric oxide (S-nitroso-N-acetyl-D,L-penicillamine [SNAP] or (Z)-1-[2-(2-aminoethyl)-N-(2-amm

118 le or nitric oxide donor (S-nitroso-N-acetyl-penicillamine [SNAP] or PAPA NONOATE, 3-[2-Hydroxy-2-nit

119 [SIN-1], 3 mmol/L) or NO (S-nitroso-N-acetyl penicillamine [SNAP]; 3 mmol/L) were analyzed for DNA st

120 ium nitroprusside (SNP) and S-nitroso-acetyl-penicillamine stimulated bile flow and increased both HC

121 copper chelators diethyldithiocarbamate and penicillamine than was catalysis by wild-type CuZnSOD.

122 he nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine that were restored by administration of su

123 Antecedent D-penicillamine therapy may have been protective against t

124 e numerous reports of such patients stopping penicillamine therapy to protect their fetus from terato

125 iol-vinylsulfone (SV), thiol-acetamide (SA), penicillamine-thiol-maleimide (PM) or penicillamine-thio

126 (SA), penicillamine-thiol-maleimide (PM) or penicillamine-thiol-thiol (PS).

127 cal (GS) from glutathione (GSH), N-acetyl-DL-penicillamine thiyl radical (S-NAP) from N-acetyl-DL-pen

128 emic sclerosis, with 15 undergoing high-dose penicillamine treatment versus 12 receiving low-dose pen

129 hese defects did not seem to be secondary to penicillamine use, cholestasis, or poor hepatocellular s

130 nine, methyl alpha-glucopyranoside, glucose, penicillamine, valinol, phenylalanine, and tryptophan fr

131 The duration of the use of D-penicillamine was significantly associated with improved

132 ium nitroprusside (SNP) and S-nitroso-acetyl-penicillamine were markedly reduced in endotoxemic IPRL

133 Similarly, d-penicillamine, which inhibits lysyl oxidase enzymatic ac

134 dified through a single terminal Cys or Pen (penicillamine) with a PEG chain of average length of 2,

135 The SNAP analog N-acetyl-DL-penicillamine (xSNAP; with no NO moiety) had no effect.