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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 e/ZnS shells and surface functionalized with penicillamine.
5 4-benzyl-2-oxazolidinones and in the case of penicillamine.
6 sodium nitroprusside and S-nitroso-N-acetyl-penicillamine.
7 ds include DOPA, amphetamine, ephedrine, and penicillamine.
8 failed previous therapy with gold salts and penicillamine.
9 e reacting species is observed with DOPA and penicillamine.
10 ), a cyclized N-protected derivative of D(-)-penicillamine.
11 stability and is inhibited by isoleucine and penicillamine.
12 amine treatment versus 12 receiving low-dose penicillamine.
13 on induced by minocycline, sulfasalazine, or penicillamine.
14 obtained by modification of the amino acid D-penicillamine.
15 icenter trial of high-dose versus low-dose D-penicillamine.
16 MG had recently been provoked by the drug D-penicillamine.
17 (SNP), 1 mmol/L, and S-nitroso-N-acetyl-D-L-penicillamine, 0.1 mmol/L, significantly increased basal
18 imilarly, the NO donor S-nitroso-N-acetyl-dl-penicillamine (1-1000 microm) down-regulated the express
19 hibitors (27 [16.4%]), statins (22 [13.3%]), penicillamine (10 [6.1%]), and tumor necrosis factor inh
20 NO-releasing compounds S-nitroso-N-acetyl-penicillamine (10(-4) mol/L, -34+/-5%) and nitroglycerin
23 er previously reported candidate drugs: 2 to penicillamine, 2 to allopurinol, and 1 to sulfasalazine.
24 n of cyclic and topological constraints with penicillamines, 2 (Tyr-cyclo[d-Pen-Gly-Phe-Pen]-Pro-Leu-
25 rosocaptopril, glucose-S-nitroso-N-acetyl-dl-penicillamine-2, and the S-nitroso tripeptide acetyl-Phe
26 onsumption in response to S-nitroso-N-acetyl-penicillamine (-35+/-7%) or nitroglycerin (-16+/-5%) was
27 e rifle PM) with and without the Cu chelator penicillamine, (4) water-soluble components of the rifle
29 th AI and addition of S-nitroso-N-acetyl-d,l-penicillamine (a NO donor) but was not significantly inc
33 small number of case reports also implicate penicillamine and minocycline as agents capable of induc
36 The NO donor SNAP (S-nitroso-N-acetyl-DL-penicillamine) and a soluble guanylyl cyclase agonist (Y
37 s, including H(2)S, 7a-thiospironolactone, L-penicillamine, and captopril, in a time- and concentrati
38 nous nephropathy associated with gold salts, penicillamine, and mercury and use these historical stud
39 g 0.1% (wt/wt) aminoguanidine, pyridoxamine, penicillamine, and nucleophilic compounds NC-I and NC-II
40 onnitrosylated parent molecules, N-acetyl-DL-penicillamine, and reduced gluthatione were without effe
41 ggested that minocycline, sulfasalazine, and penicillamine are associated with antineutrophil cytopla
43 ion of pyrogallol and S-nitroso-N-acetyl-D,L-penicillamine, as well as hydrogen peroxide induced a ti
44 and measure transpersulfidation from a bulky penicillamine-based persulfide to a cysteine-based thiol
45 steine differs from the antiarthritis drug D-penicillamine by only two methyl groups on the beta-carb
46 of a series of FSDs (N-acetyl-L-cysteine, D-penicillamine, captopril, L-cysteine, or reduced glutath
48 3 RCTs examining high-dose versus low-dose D-penicillamine (D-Pen Trial), recombinant human relaxin v
49 cancer therapy with a novel combination of D-penicillamine (D-pen) and Idarubicin (Ida) in a syntheti
52 e treated mice with a copper chelator, D-(-)-penicillamine (D-PEN), starting immediately following in
54 ne and the therapeutic agents penicillamine, penicillamine disulfide, N-acetylcysteine, and captopril
57 PBC who had received ineffective therapy (D-penicillamine [DPCA] or placebo) for 5.6 +/- 0.07 years
58 PAECs) with the NO donor, S-nitroso-N-acetyl-penicillamine, dramatically inhibited killing of PAEC ta
59 delta-opioid ligand [2-D-penicillamine, 5-D-penicillamine]enkephalin (DPDPE) had no effect on these
61 eceiving placebo; and 3) a 104-week trial of penicillamine for early systemic sclerosis, with 15 unde
62 ize MitoSNO, mitochondria-selective N-acetyl-penicillamine, had no effect on either mtH(2)O(2) genera
63 ine have teratogenic effects in animals, and penicillamine has known teratogenic effects in humans.
67 peptides were equally or more effective than penicillamine in trapping AcH in a cell-free system.
68 rug (Thalidomide) and false negative drug (D-penicillamine) in the conventional mouse embryonic stem
72 d suggest that the conversion of cysteine to penicillamine may partly suppress MeHg formation in cyst
75 amine thiyl radical (S-NAP) from N-acetyl-DL-penicillamine (NAP) and sulfate anion radical (SO3-) fro
76 itrosoglutathione and S-nitroso-N-acetyl-d,l-penicillamine), nitric oxide, oxidized GSH, and hydrogen
78 he nitric oxide donors S-nitroso-N-acetyl-DL-penicillamine or diethyltriamine nitric oxide complex, w
79 utathione, either with S-nitroso-N-acetyl-dl-penicillamine or with S-nitroso-L-cysteine indicate that
80 rs, sodium nitroprusside, S-nitroso-N-acetyl-penicillamine, or 3-morpholinosydnonimine, increased hem
82 itroso-acetyl-DL-penicillamine, S-nitroso-DL-penicillamine, or S-nitroso-glutathione) decreased, in a
83 C3H mice, and in response to Cu chelation by penicillamine (PCA) and dietary supplementation of the m
85 ve since cysteine was largely metabolized to penicillamine (PEN) over time at a rate that increased w
86 hylcysteine (Ecy), Thr, Met, D-Cys, Ser, and penicillamine (Pen) produced progressively less efficien
88 , and homocystine and the therapeutic agents penicillamine, penicillamine disulfide, N-acetylcysteine
89 of a series of N-terminal dipeptides of D(-)-penicillamine, prepared from the synthon 3-formyl-2,2,5,
90 E-selectin expression by S-nitroso-N-acetyl-penicillamine pretreatment and thiol deprivation was ass
92 g; administration of a NO donor, S-nitroso-N-penicillamine, reduced oocyst and infection scores; and
93 oncentration of the NO donor S-nitroso-amino-penicillamine reduces the number of viral particles in a
94 he NO-generating compound S-nitroso-L-acetyl penicillamine resulted in a significant decrease in vira
96 e S-nitroso compounds, S-nitroso-N-acetyl-dl-penicillamine, S-nitrosoglutathione, S-nitrosocaptopril,
98 tivity, since GSNO and S-nitroso-N-acetyl-dl-penicillamine significantly and reversibly reduced total
100 eatment with the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) (1 mmol/L for 90 minutes), followed
101 treated with the NO donor S-nitroso-N-acetyl penicillamine (SNAP) at concentrations ranging from 0.3
102 TG or another NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) at doses relevant to the human mode
103 ANP and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) caused concentration-dependent decr
105 osydnonimine (SIN-1), and S-nitroso-N-acetyl-penicillamine (SNAP) on the resting activity (RA) of aff
106 usly by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure
107 ication of the NO-mimetic S-nitroso-N-acetyl-penicillamine (SNAP) or intracellular perfusion with cGM
108 80% in the presence of S-nitroso-N-acetyl-DL-penicillamine (SNAP) or sodium nitroprusside (SNP).
109 mol/L KCl to the NO donor S-nitroso-N-acetyl-penicillamine (SNAP) or to NO is markedly suppressed by
111 ocytes to the NO donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) resulted in a rapid shift in cellul
113 as from a solid NO donor, S-nitroso-N-acetyl penicillamine (SNAP) stored within "coffee pod" style re
115 es for NO, the NO donor S-nitroso-N-acetyl-D-penicillamine (SNAP) was encapsulated within poly(lactic
116 osure to the NO donors S-nitroso-N-acetyl-dl-penicillamine (SNAP), 3-morpholinosydnonimine (SIN-1), o
120 dition to the cultures of S-nitroso-N-acetyl-penicillamine (SNAP), an NO donor, as well as by additio
121 opyridine, SK&F 96365 and S-nitroso-N-acetyl-penicillamine (SNAP), but was decreased by amiloride and
122 e effects of an NO donor, S-nitroso-N-acetyl penicillamine (SNAP), in buffer-perfused Langendorff hea
123 lication of the NO donor, S-nitroso-N-acetyl-penicillamine (SNAP), reproducibly increased the frequen
124 antly more resistant to S-nitro-N-acetyl-d,l-penicillamine (SNAP), sodium nitroprusside (SNP), and hy
130 reated with nitric oxide donors, S-nitroso-N-penicillamine (SNAP, 25 muM) or diethylenetriamine-NONO
131 he NO-releasing drug S-nitrosyl-N-acetyl-D,L-penicillamine (SNAP; 0-0.5 mM) inhibited dimerization of
132 enerate nitric oxide (S-nitroso-N-acetyl-D,L-penicillamine [SNAP] or (Z)-1-[2-(2-aminoethyl)-N-(2-amm
133 le or nitric oxide donor (S-nitroso-N-acetyl-penicillamine [SNAP] or PAPA NONOATE, 3-[2-Hydroxy-2-nit
134 [SIN-1], 3 mmol/L) or NO (S-nitroso-N-acetyl penicillamine [SNAP]; 3 mmol/L) were analyzed for DNA st
135 ium nitroprusside (SNP) and S-nitroso-acetyl-penicillamine stimulated bile flow and increased both HC
136 otoxin RgIA using a combination of selective penicillamine substitutions together with natural and no
137 copper chelators diethyldithiocarbamate and penicillamine than was catalysis by wild-type CuZnSOD.
138 he nitric oxide donor S-nitroso-N-acetyl-D,L-penicillamine that were restored by administration of su
140 e numerous reports of such patients stopping penicillamine therapy to protect their fetus from terato
141 iol-vinylsulfone (SV), thiol-acetamide (SA), penicillamine-thiol-maleimide (PM) or penicillamine-thio
143 cal (GS) from glutathione (GSH), N-acetyl-DL-penicillamine thiyl radical (S-NAP) from N-acetyl-DL-pen
145 emic sclerosis, with 15 undergoing high-dose penicillamine treatment versus 12 receiving low-dose pen
146 hese defects did not seem to be secondary to penicillamine use, cholestasis, or poor hepatocellular s
147 nine, methyl alpha-glucopyranoside, glucose, penicillamine, valinol, phenylalanine, and tryptophan fr
149 ium nitroprusside (SNP) and S-nitroso-acetyl-penicillamine were markedly reduced in endotoxemic IPRL
150 ng molecules, L-cysteine, glutathione, and D-penicillamine, were studied separately, and it was found
152 dified through a single terminal Cys or Pen (penicillamine) with a PEG chain of average length of 2,