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1  animals treated with the oral iron chelator deferiprone.
2 a in CEP mice treated at the highest dose of deferiprone.
3 r Parkin-independent mitophagy stimulated by deferiprone.
4 al sensing of anti-HIV replication drug i.e. deferiprone.
5 were coordinately affected by ciclopirox and deferiprone.
6 can be inhibited by the drugs ciclopirox and deferiprone.
7 to detect any potential protective effect of deferiprone.
8  intravenous deferoxamine, augmented by oral deferiprone.
9 proved brain distribution when compared with deferiprone.
10  and effectiveness of long-term therapy with deferiprone.
11  with placebo (change in hippocampal QSM for deferiprone, -0.36 ppb [95% CI, -0.76 to 0.04 ppb]; for
12 placebo (change in NTB composite z score for deferiprone, -0.80 [95% CI, -0.98 to -0.62]; for placebo
13 in photosensitivity in CEP mice treated with deferiprone (1 or 3 mg/mL in drinking water) for 26 week
14 treated with the orally active iron chelator deferiprone (1,2 dimethyl-3-hydroxypyrid-4-one, L1) at a
15 2 early onset PD patients, were administered deferiprone, 10 or 15 mg/kg BID or placebo, for 6 months
16               These trial findings show that deferiprone 15 mg/kg twice a day decreased hippocampal Q
17                                              Deferiprone 15 mg/kg twice a day or placebo administered
18       Seventy-two patients were treated with deferiprone 20, 40, or 60mg/kg/day or placebo, divided i
19 given vehicle; (II) Def group, rats received deferiprone (200 mg/kg orally once daily for 10 days); (
20 .p.; and (IV) Cis + Def group, rats received deferiprone (200 mg/kg orally once daily for 10 days, ra
21                               One patient on deferiprone 20mg/kg/day experienced reversible neutropen
22  that, in patients with less severe disease, deferiprone 20mg/kg/day may reduce disease progression,
23 h less severe disease suggested a benefit of deferiprone 20mg/kg/day on ICARS, FARS, kinetic function
24 analogues of catechol (benzene-1,2-diol) and deferiprone (3-hydroxy-1,2-dimethyl-4(1H)-pyridone), TRE
25  (2:1) to receive an oral solution of either deferiprone (30 mg/kg per day divided into two equal dos
26 ing the effectiveness of the studied dose of deferiprone, 47 patients discontinued therapy, whereas 1
27 al oral placebo (deferoxamine group) or oral deferiprone 75 mg/kg per day (combined group).
28 ned 1:1 to receive orally administered daily deferiprone (75-100 mg/kg per day) or daily deferasirox
29  are no randomised clinical trials comparing deferiprone, a less expensive iron chelator, with defera
30 mic treatment of Plp1 mutant Jimpy mice with deferiprone, a small molecule iron chelator, reduced oli
31 metabolomics on mammalian cells treated with deferiprone, a therapeutic iron chelator that stimulates
32                                      Whereas deferiprone acts synergistically with the zinc chelator
33      They treated CEP mice for 26 weeks with deferiprone (an iron chelator) and report that it revers
34 ediated by oxidative stress and inhibited by deferiprone, an iron chelator.
35 iologic assessment of European outcomes with deferiprone, an oral alternative chelator available for
36  were enrolled; 186 were assigned to receive deferiprone and 186 to receive placebo.
37 ian follow-up was 379 days (IQR 294-392) for deferiprone and 381 days (350-392) for deferasirox.
38 lly-used chelators, namely, desferrioxamine, deferiprone and deferasirox and compared them with exper
39  and clinically unachievable concentrations, deferiprone and deferasirox significantly reduced the ca
40  nature of its structure, DFO is larger than deferiprone and is thus less able to access some intrace
41 emoval from Tf/2N by 3-hydroxypyridin-4-one (deferiprone) and nitrilotriacetic acid (NTA) are essenti
42 nically applied medications desferrioxamine, deferiprone, and deferasirox.
43                              Deferasirox and deferiprone are the only two oral chelators used in adul
44 demonstrated an acceptable safety profile of deferiprone at 20mg/kg/day for the treatment of patients
45 re assigned (in a 1:1 ratio) to receive oral deferiprone at a dose of 15 mg per kilogram of body weig
46  hippocampal volume loss was not affected by deferiprone, but exploratory analysis of other brain reg
47       The only alternative treatment is oral deferiprone, but its long-term efficacy on myocardial ir
48 esults concluded that rapping cisplatin with deferiprone can mitigate neurotoxicity induced by cispla
49        We assessed whether the iron chelator deferiprone can reduce brain iron and slow disease progr
50 rly research suggests that the iron chelator deferiprone can reduce nigrostriatal iron content in per
51 gnetic resonance imaging (MRI) suggests that deferiprone can unload myocardial iron faster than defer
52 and mortality in Italian subjects exposed to deferiprone compared with deferoxamine.
53 S2, we evaluated whether iron chelation with deferiprone could decrease ALAS2 expression and subseque
54 xamine (DFO) and the hydroxypiridinone (HPO) deferiprone (CP20) chelate iron as well as other metals.
55 in comparison to simple dialkyl HPOs such as Deferiprone (CP20) which cause up to 70% inhibition.
56                       The QSM confirmed that deferiprone decreased iron in the hippocampus compared w
57 herapy with one of the three iron chelators (deferiprone, deferasirox, or deferoxamine).
58  with mean scores of 4.1 points [0.2] in the deferiprone-deferiprone group and of 4.7 points [0.3] in
59 m cardiomyocytes exceeded that obtained with deferiprone, desferrioxamine, or deferasirox at similar
60 oxidase (HRP), via glutaraldehyde (Glu), for deferiprone detection using impedimetric technique.
61                                              Deferiprone (DFP) is a hydroxypyridinone-derived iron ch
62  of each of the 3 drugs, deferoxamine (DFO), deferiprone (DFP), and deferasirox (DFX), including thei
63 retinal protection by the oral iron chelator deferiprone (DFP).
64 nistration of the FDA-approved iron chelator deferiprone evidenced significant reductions in tumor si
65   For both Tf/2N and Tf-FeN, iron removal by deferiprone follows simple saturation kinetics, while ir
66 iron content in 17 patients who had received deferiprone for 24 to 48 months ranged from 5.9 to 41.2
67                Twenty-six patients continued deferiprone for a mean of 39.4 months (range, 12 to 49).
68           When the patients who had received deferiprone for longer than 3 years were considered sepa
69 e included, with 53 randomly assigned to the deferiprone group (mean [SD] age, 73.0 [8.0] years; 29 m
70 e patients, 88 were randomly assigned to the deferiprone group (n=58) or placebo group (n=30) between
71  therapy in 22.0% of the participants in the deferiprone group and 2.7% of those in the placebo group
72 , 76 patients completed the study (49 in the deferiprone group and 27 in the placebo group).
73 PDRS total score at baseline was 34.3 in the deferiprone group and 33.2 in the placebo group and incr
74 e 193 patients in the safety analysis in the deferiprone group and two (1%) cases of reversible renal
75                                          The deferiprone group had significantly less myocardial iron
76 ntion-to-treat analysis, participants in the deferiprone group showed accelerated cognitive decline o
77 ial iron (T2* <20 ms) was less common in the deferiprone group than in the desferrioxamine controls (
78 ostriatal iron content decreased more in the deferiprone group than in the placebo group.
79 ent groups: 183 (95%) of 193 patients in the deferiprone group versus 192 (97%) of 197 patients in th
80  of 2.48 points (SE 0.63) in patients in the deferiprone group versus 3.99 points (0.82) for patients
81 were 4.6 points (SE 0.3) for patients in the deferiprone group versus 4.7 points (0.4) for those in t
82 n in the desferrioxamine controls versus the deferiprone group was 5.5 (95% CI 1.2-28.8).
83 of neutropenia (4 participants [7.5%] in the deferiprone group) was higher than in similar studies (1
84 om the placebo group and 20 [37.7%] from the deferiprone group).
85 h was seen in 12 (21%) of 58 patients in the deferiprone group, but was not seen in any patients in t
86 group and of 4.7 points [0.3] in the placebo-deferiprone group.
87 ly assigned to a treatment group (194 to the deferiprone group; 199 to the deferasirox group).
88            Patients receiving 20mg/kg/day of deferiprone had no significant change in FARS, similar t
89                       The oral iron chelator deferiprone has been demonstrated to remove myocardial i
90         Two new oral agents, deferasirox and deferiprone, have become available in the last 8 years.
91 s at the time of change from deferoxamine to deferiprone in either the intention-to-treat analysis or
92 assess safety, tolerability, and efficacy of deferiprone in Friedreich ataxia (FRDA).
93  regions revealed increased volume loss with deferiprone in frontal areas.
94 ar of therapy, and led to discontinuation of deferiprone in only one patient in years 2 to 4.
95 spective study of the safety and efficacy of deferiprone in patients with thalassemia major, we have
96 orinated compounds have clear advantage over deferiprone in that they are metabolized more slowly.
97  PINK1-dependent mitophagy without affecting deferiprone-induced mitophagy.
98 ice or in vitro loading with zinc, abrogated deferiprone-induced murine thymocyte apoptosis.
99         Bidentate hydroxypyridinones such as deferiprone interact with intracellular zinc pools in a
100 early AD, suggesting that lowering iron with deferiprone is detrimental to patients with AD.
101                                         Oral deferiprone is more effective than desferrioxamine in re
102 s study evaluated whether the iron chelator, deferiprone, is well tolerated, able to chelate iron fro
103                     Thus, the iron chelators deferiprone (L1) and deferoxamine (Dfx), which are alrea
104 hobiology, we administered the iron chelator deferiprone (L1) intraperitoneally to beta-thalassemic m
105 hepatic iron depletion: iron chelation using deferiprone (L1) versus iron-deficient diets.
106 bility of the nano Au sensor is to determine deferiprone level in spiked urine and serum samples.
107                               Treatment with deferiprone of UROS-deficient erythroid cell lines and p
108 lation treatments in paediatric populations, deferiprone offers a valuable treatment option for this
109 r the beneficial effect of the iron chelator deferiprone on iron overload.
110  as well as treatment with the iron chelator deferiprone, preserves vision and attenuates retinal gan
111 amine, combination treatment with additional deferiprone reduced myocardial iron and improved the eje
112 posure of murine thymocytes to either DFO or deferiprone resulted in significant reductions in the la
113  In the extension study, patients continuing deferiprone retained a similar rate of disease progressi
114          Embracing the cisplatin dosage with deferiprone reversed cisplatin-induced neuropathy, in wh
115 ession in patients switching from placebo to deferiprone seemed to slow (4.4 points [1.1] vs 1.4 poin
116 eatment of NZB/W mice with the iron chelator deferiprone significantly delayed the onset of albuminur
117 ic oxide and iron chelators deferoxamine and deferiprone significantly inhibited pregnenolone product
118                    This report presents that Deferiprone, the only clinically used 3-hydroxypyridin-4
119                                              Deferiprone therapy was well tolerated and was associate
120 tion and mood were not adversely affected by deferiprone therapy.
121                               The ability of deferiprone to preferentially access zinc pools was also
122                            Although 30 mg/kg deferiprone treated patients showed a trend for improvem
123                                              Deferiprone-treated patients receiving 20 or 40mg/kg/day
124 itin levels in the 26 patients who continued deferiprone treatment were significantly lower than in t
125  function in 15 patients receiving long-term deferiprone treatment with 30 matched thalassaemia major
126 er of these events was considered related to deferiprone use.
127 s aged >10 years) to show non-inferiority of deferiprone versus deferasirox in the per-protocol popul
128                           Non-inferiority of deferiprone versus deferasirox was established (treatmen
129      We aimed to show the non-inferiority of deferiprone versus deferasirox.
130 controlled trials shows superior efficacy of deferiprone versus deferoxamine, the superiority of comb
131 th dopaminergic medications was not planned, deferiprone was associated with worse scores in measures
132 h transfusion-dependent haemoglobinopathies, deferiprone was effective and safe in inducing control o
133         On the other hand, iron chelation by deferiprone was not associated with changes in postbleac
134                                              Deferiprone was well tolerated and adverse events were s
135                                              Deferiprone was well tolerated at 20mg/kg/day, whereas m
136                                              Deferiprone was well tolerated, achieved target engageme
137         The main serious adverse events with deferiprone were agranulocytosis in 2 participants and n
138 helators, such as EDTA, desferrioxamine, and deferiprone, were found to cause the nanoshells to degra
139 (iron-binding equivalents), as compared with deferiprone which caused 40% inhibition of the enzyme ac
140  be modulated by drugs such as ciclopirox or deferiprone, which might be repositioned to control canc
141  nano Au sensor exhibited a good response to deferiprone with a wide linear range (0.005-1000microM)
142 us deferoxamine, the superiority of combined deferiprone with deferoxamine versus deferoxamine alone,
143 ccess in 69 [55.2%] of 125 patients assigned deferiprone with primary composite efficacy endpoint dat
144 8 months, in which all participants received deferiprone with the same regimen as the main study.

 
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