ライフサイエンスコーパス: deferoxamine

1 nyl-p-phenylenediamine and the iron chelator deferoxamine.

2 ted with the iron chelators 2-2-dipyridyl or deferoxamine.

3 ct of SNP in HEK293 cells is also blocked by deferoxamine.

4 of the methacholine response associated with deferoxamine.

5 modulated during intravenous chelation with deferoxamine.

6 tration than the nonlipophilic iron chelator deferoxamine.

7 vely than the nonlipid soluble iron chelator deferoxamine.

8 the inhibitor of hydroxyl radical formation, deferoxamine.

9 e, and the equivalence of deferasirox versus deferoxamine.

10 rent doses of deferasirox and the comparator deferoxamine.

11 reduced promoter inducibility by hypoxia and deferoxamine.

12 ance chelation monotherapy with subcutaneous deferoxamine.

13 ubjects exposed to deferiprone compared with deferoxamine.

14 prove hepatic iron in thalassemia as well as deferoxamine.

15 ccurred in the presence of the iron chelator deferoxamine.

16 prone can unload myocardial iron faster than deferoxamine.

17 diomyocytes treatment with the iron chelator deferoxamine.

18 pared to a value of 11.5 for the siderophore deferoxamine.

19 Deferoxamine mesylate and starch-deferoxamine (1 mM) prevented bafilomycin-induced calcei

20 The iron chelator, deferoxamine (1 mM), and the endogenous.OH scavenger, as

21 hibition of S-nitrosocysteine decay, whereas deferoxamine (100 microM) was ineffective.

22 onds at 1 year (Gmeans ratio, 1.12) and with deferoxamine (11.6 milliseconds to 12.3 milliseconds; Gm

23 plus apamin, whereas endothelial denudation, deferoxamine, 1H-(1,2,4)-oxadiazole-[4,3-a]quinoxalin-1-

24 e presence of catalase, hypoxia (8% oxygen), deferoxamine, 3-aminobenzamide [an inhibitor of poly(ADP

25 s comparable between deferasirox (35.4%) and deferoxamine (30.8%).

26 arget dose 40 mg/kg per day) vs subcutaneous deferoxamine (50-60 mg/kg per day for 5-7 days/week) for

27 we examined the effects of the iron chelator deferoxamine (500 mg intra-arterially over 1 hour) on va

28 he antioxidants vitamin C (10 micromol/L) or deferoxamine (500 micromol/L) restored LV relaxant respo

29 igs were also treated with an iron chelator, deferoxamine, (50mg/kg, i.m.) or vehicle and killed at d

30 s, at which time either 67Ga-DF-folate, 67Ga-deferoxamine (67Ga-DF) or 67Ga-citrate was administered

31 lmost completely inhibited by treatment with deferoxamine, a cell-permeable iron chelator.

32 are powerful iron chelators comparable with deferoxamine, a clinically useful iron-chelating agent.

33 n this report, we investigate the ability of deferoxamine, a scavenger of free iron, the hydroxyl rad

34 Deferoxamine, a very high affinity chelator having log b

35 Administration of deferoxamine abrogated methylglyoxal conjugation, normal

36 Deferoxamine accounted for 71% of chelation-related char

37 d pigmentary retinopathy following high-dose deferoxamine administration.

38 emoval of iron was completely effected using deferoxamine, after which iron could be rebound to the l

39 nomycin D, and the G1/S cell cycle inhibitor deferoxamine, all promote survival after trophic factor

40 nsfusions, iron overload, noncompliance, and deferoxamine allergy.

41 enotypes by the cell-permeable iron chelator deferoxamine allowed the conclusion that increased level

42 ombined deferiprone with deferoxamine versus deferoxamine alone, and the equivalence of deferasirox v

43 Deferoxamine, alpha-tocopherol, and dimethylsulfoxide ea

44 Cobalt and deferoxamine also increased MKP-1 mRNA levels, suggestin

45 (89)Zr was complexed with deferoxamine (also known as desferrioxamine B, desferoxa

46 nase C alpha and its suppression by EGCG and deferoxamine (an iron chelator), a possible mechanism in

47 lopurinol (a xanthine oxidase inhibitor), or deferoxamine (an iron chelator), suggesting that ROS may

48 r), Me2SO (a hydroxyl radical scavenger), or deferoxamine (an iron chelator).

49 4.7 macrophage cells treated with hypoxia or deferoxamine, an iron chelator mimicking hypoxia.

50 tyl cysteine, a glutathione precursor, or by deferoxamine, an iron chelator.

51 animals were treated with either vehicle or deferoxamine, an iron chelator.

52 flow-induced vasodilatation was restored by deferoxamine, an iron chelator.

53 Deferoxamine, an iron sequestrating antioxidant, prevent

54 The antioxidants, deferoxamine and alpha-tocopherol, effectively prevented

55 Hypoxic mimetics, such as deferoxamine and dimethyloxalylglycine, were also found

56 py was repressed, but were hypersensitive to deferoxamine and displayed a growth defect similar to th

57 The reducing agents deferoxamine and dithiothreitol reversed the ECA inhibit

58 Deferoxamine and iron may modulate CD47 expression.

59 l neurons is suppressed by the G1/S blockers deferoxamine and mimosine, as well as by the CDK-inhibit

60 Trastuzumab was conjugated with deferoxamine and radiolabeled with (89)Zr.

61 Pertuzumab was conjugated with deferoxamine and radiolabeled with (89)Zr.

62 ease in susceptibility to the iron-chelators deferoxamine and salicylhydroxamic acid.

63 ic protoporphyria) or with the iron chelator deferoxamine and the porphyrin precursor 5-aminolevulini

64 H(2)O(2) were prevented by the iron chelator deferoxamine and the vitamin E analog Trolox, suggesting

65 r currently used is deferasirox, followed by deferoxamine and then combination therapies.

66 the trial with continuation of subcutaneous deferoxamine and were randomized to receive additional o

67 se, dimethyl thiourea, superoxide dismutase, deferoxamine, and dimethyl sulfoxide significantly inhib

68 The reducing agents, dithionite, deferoxamine, and dithiothreitol, reversed and exogenous

69 tramethylchroman-2-carboxylic acid (Trolox), deferoxamine, and U-74389G.

70 Deferoxamine appears capable of binding to gadolinium io

71 lowed by 8 mg/kg/hr for 90 mins or 100 mg/kg deferoxamine at -15 mins or vehicle.

72 the G1/S blockers mimosine, ciclopirox, and deferoxamine at concentrations that correlate with their

73 nterrupted infusion of high-dose intravenous deferoxamine, augmented by oral deferiprone.

74 ynthesis, namely, 4,6-dioxoheptanoic acid or deferoxamine; (b) This increased stability of 5-aminolev

75 ent with antioxidants (ascorbate, Trolox, or deferoxamine), but was prevented by the NMDA receptor an

76 n be blocked by the peroxynitrite scavenger, deferoxamine, but not by dithiothreitol, which triggers

77 ke of Fe was stimulated two- to threefold by deferoxamine, but this increment could be abolished by c

78 The (89)Zr-p-isothiocyanatobenzyl-deferoxamine-CD3 PET probe was assessed in a murine tumo

79 Among 330 patients who had received deferoxamine chelation therapy, 224 (68%) reported no co

80 per patient decade for patients who require deferoxamine chelation.

81 at pharmacological activators of HIF-1 (e.g. deferoxamine, cobalt chloride) could also protect cultur

82 son to the standard chelation monotherapy of deferoxamine, combination treatment with additional defe

83 in C and by -8.9+/-2.2 ms in the presence of deferoxamine compared with -0.8+/-2.2 ms in the absence

84 chelatable iron, 16%, p < 0.01 (59Fe in the deferoxamine-containing medium), and decreased 59Fe in f

85 )I via an iodination reagent or coupled with deferoxamine (Df) and complexed with (89)Zr.

86 aluate the whole-body distribution of (89)Zr-deferoxamine (Df)-pembrolizumab in two rodent models (mi

87 ophene) (PEDOT) into which an iron chelator, deferoxamine (DFA), has been doped during the polymeriza

88 Both deferoxamine (DFO) and ethylenediaminetetraacetic acid (

89 Deferoxamine (DFO) has shown therapeutic promise for the

90 ive phase 2 study, evaluated combination DFX-deferoxamine (DFO) in patients with severe transfusional

91 (Fc) and iron chelating moieties composed of deferoxamine (DFO) into the final gel scaffold in revers

92 Deferoxamine (DFO) is a high-affinity Fe (III) chelator

93 Experimental studies suggest that deferoxamine (DFO) limits the generation of reactive oxy

94 parative purposes, we have also administered deferoxamine (DFO) PO and sc in aqueous solution at a do

95 on by giving equimolar amounts of NaHBED and deferoxamine (DFO) to Cebus apella monkeys as either a s

96 ddition, administration of the iron chelator deferoxamine (DFO) to mice prior to administration of to

97 Deferoxamine (DFO), an antioxidant and iron chelator kno

98 ) containing the FDA-approved small molecule deferoxamine (DFO), an iron chelator that increases HIF-

99 s developed to measure simultaneously NTBPI, deferoxamine (DFO), and its major metabolite.

100 arize the properties of each of the 3 drugs, deferoxamine (DFO), deferiprone (DFP), and deferasirox (

101 solution, PS conjugated to the iron chelator deferoxamine (DFO), or lactated Ringer's solution alone

102 d by subcutaneous (SC) injection of HBED and deferoxamine (DFO), the reference chelator, in rodents a

103 uced following addition of the iron chelator deferoxamine (DFO).

104 e complex structure of the widely used drug, deferoxamine (DFO).

105 x (DFX; Exjade, Novartis) is not inferior to deferoxamine (DFO; Desferal, Novartis) for the removal o

106 This study examined the role of deferoxamine (DFX) in brain injury and HT in a rat model

107 but 3 mg/kg Desmethyl tirilazad or 100 mg/kg deferoxamine does not.

108 and iron availability through treatment with deferoxamine dramatically increased Zygomycetes pathogen

109 ite dramatic gains in life expectancy in the deferoxamine era for patients with transfusion-dependent

110 The ability of a 67Ga-labeled deferoxamine-folate conjugate (67Ga-DF-folate) to target

111 noninferiority of deferasirox compared with deferoxamine for myocardial iron removal.

112 e combined treatment group compared with the deferoxamine group in myocardial T2* (ratio of change in

113 ndomized to receive additional oral placebo (deferoxamine group) or oral deferiprone 75 mg/kg per day

114 In normal volunteers, deferoxamine had no effect on the response to methacholi

115 t iron/hydrogen peroxide-induced DNA damage; deferoxamine had no effect.

116 Although this alternative to parenteral deferoxamine has been a major advance for patients with

117 For three decades, deferoxamine has been the only approved iron chelator.

118 s maintained on the parenteral iron chelator deferoxamine have myocardial iron loading.

119 diet supplement or with hydroxyethyl starch deferoxamine (HES-DFO) by weekly intravenous injections

120 Deferoxamine improved nitric oxide-mediated, endothelium

121 Deferoxamine improved the blood flow response to methach

122 Neither desmethyl tirilazad nor deferoxamine improves pathologic results.

123 These results indicate that deferoxamine improves spatial memory performance, possib

124 as observed with infected cells treated with deferoxamine in comparison to growth under iron-replete

125 ption of the cSHMT gene is also inhibited by deferoxamine in MCF-7 cells, indicating that mimosine in

126 type was to treatment with the Fe3+ chelator deferoxamine, indicating that it is defective for intrac

127 pounds were found to inhibit hypoxia but not deferoxamine-induced HIF-1alpha protein stabilization.

128 Subjects were admitted for 4 assessments: deferoxamine infusion and urinary iron measurement to as

129 Deferoxamine infusion decreased serum iron levels (P<0.0

130 ional iron overload have depended on nightly deferoxamine infusions for iron chelation.

131 strated that the iron chelators mimosine and deferoxamine inhibit DNA replication in mammalian cells,

132 Desmethyl tirilazad (20 mg/kg) and 100 mg/kg deferoxamine inhibit lipid peroxidation.

133 The antioxidants tempol, ebselen, and deferoxamine inhibited CO-induced O2*- production and co

134 t has been proposed that in combination with deferoxamine it may have additional effect.

135 Other siderophores (pyoverdine, ferrichrome, deferoxamine) likewise inhibited ROS and NETs in neutrop

136 ation of the bacteria with the iron chelator deferoxamine markedly inhibited the magnitude of .OH spi

137 ing the intracellular iron-chelating reagent deferoxamine mesylate (Desferal).

138 Both hypoxia-mimetic deferoxamine mesylate (DFO) and TGF-beta1 inhibited adip

139 compared to those of three metal chelators; deferoxamine mesylate (DFO), 1,10-phenanthroline (o-phen

140 e to increase the nose-to-brain transport of deferoxamine mesylate (DFO), a neuroprotector unable to

141 generation, we studied if an iron chelator, deferoxamine mesylate (DFO), alone or in combination wit

142 The use of deferoxamine mesylate (DFO), an iron chelator, to treat

143 bital infusion of PP-IX or the iron chelator deferoxamine mesylate (DFO), with the first committed he

144 p53 in response to hypoxia mimetics such as deferoxamine mesylate and CoCl(2), regardless of their H

145 hat the structurally distinct iron chelators deferoxamine mesylate and mimosine prevent apoptosis ind

146 Deferoxamine mesylate and starch-deferoxamine (1 mM) pre

147 bined exposure to 1A10 and the iron chelator deferoxamine mesylate has synergistic antiproliferative

148 Moreover, upmodulation by deferoxamine mesylate implicates huntingtin as an iron-r

149 n or the membrane-impermeable iron chelator, deferoxamine mesylate salt, was able to increase MT2 lev

150 8-fold more susceptible to the iron chelator deferoxamine mesylate than hRRM2, although the iron cont

151 increased to 7.4, antioxidants (allopurinol, deferoxamine mesylate, and glutathione), vasodilators (a

152 lyzing a commercially available siderophore, deferoxamine mesylate, in both the free ligand and Fe-bo

153 tional activity of stabilized p53 induced by deferoxamine mesylate, which mimics hypoxia, in normal c

154 1 activity and HIF-1alpha protein induced by deferoxamine mesylate.

155 duced by treatment with the hypoxia mimetic, deferoxamine mesylate.

156 ; and (3) G1 blockers, such as rapamycin and deferoxamine, mimicked the anti-proliferative effects of

157 with antioxidants (dithiothreitol, trolox or deferoxamine, nitric oxide synthase inhibitor (N(G)-mono

158 superoxide dismutase (O(2)(.) scavenger) or deferoxamine (OH. inhibitor).

159 ndosteal endothelium with the small molecule deferoxamine or a genetic approach rescues HSCs loss, pr

160 tivity was pharmacologically inhibited using deferoxamine or dimethyloxaloylglycine, and also when th

161 ts from astrocytoma cells exposed to iron or deferoxamine over different time intervals.

162 stablishing noninferiority of deferasirox vs deferoxamine (P = .057 for superiority of deferasirox).

163 Deferoxamine pretreatment also diminishes gadd153 induct

164 Chelation of the iron with deferoxamine prevented this process as did melatonin whi

165 neal epithelial cells with the iron chelator deferoxamine prevents the appearance of nuclear ferritin

166 In diabetic mice, deferoxamine promoted neovascularization and enhanced wo

167 s with the iron chelators phenanthroline and deferoxamine protected them from candidal injury, even t

168 In addition, systemic treatment of deferoxamine reduced ICH-induced LCN2 upregulation (p<0.

169 Deferoxamine reduces free radicals by chelating iron and

170 elated retinal hemorrhagic lesions in utero, deferoxamine-related decreases in vision, ocular allergy

171 The iron chelator deferoxamine rescued FRDA fibroblasts more than controls

172 or catalase, or the chelation of nickel with deferoxamine, resulted in inhibition of NFAT activation.

173 inhibitor) or the chelation of vanadate with deferoxamine, resulted in inhibition of NFAT activation.

174 inhibitor), or the chelation of vanadate by deferoxamine, resulted in inhibition of p53 activation a

175 Deferoxamine retinopathy primarily targets the RPE-Bruch

176 Unconjugated 67Ga-deferoxamine showed no tumor affinity.

177 markedly by the HIF-1 activators hypoxia or deferoxamine, suggesting that it could operate in a nega

178 hows superior efficacy of deferiprone versus deferoxamine, the superiority of combined deferiprone wi

179 ctions in LIC after 1 year of deferasirox or deferoxamine therapy correlated with transfusional iron

180 Patients who underwent deferoxamine therapy had a significant reduction of GLC

181 y from the values at the time of change from deferoxamine to deferiprone in either the intention-to-t

182 everal oral iron chelators and variations of deferoxamine to prolong the half-life have been develope

183 eased vision following high-dose intravenous deferoxamine to treat systemic iron overload.

184 on of antioxidants 2-methyl aminochroman and deferoxamine to UW solution inhibited necrotic cell deat

185 However, deferoxamine-treated animals showed significant improvem

186 aining electron-dense particles, whereas ALA+deferoxamine treatment resulted in higher PP-IX in the c

187 eral white and gray matter in pigs which had deferoxamine treatment.

188 the superiority of combined deferiprone with deferoxamine versus deferoxamine alone, and the equivale

189 induction of NDRG1 expression by hypoxia and deferoxamine was diminished by RNA interference knockdow

190 ement conferring inducibility by hypoxia and deferoxamine was localized to an early growth response 1

191 Deferoxamine was used to inhibit depolymerization during

192 h as diethylenetriamine pentaacetic acid and deferoxamine, we reveal that a unique histidine at posit

193 hanolamine with encapsulated glutathione and deferoxamine, were prepared and labeled with 99mTc and 1

194 Deferoxamine, which chelates iron, interacts with free h

195 ffect can be reversed with the iron chelator deferoxamine, which results in hypoxia-inducible factor