ライフサイエンスコーパス: atovaquone

1 ttenuates the chemotoxicity of plumbagin and atovaquone.

2 the NKA inhibitory activity of plumbagin and atovaquone.

3 that are resistant to the anti-malarial drug atovaquone.

4 intaining little to no cross-resistance with atovaquone.

5 sensitivity of the cytochrome bc1 complex to atovaquone.

6 ve either enhanced or reduced sensitivity to atovaquone.

7 ty of the bovine bc1 complex (Ki = 80 nm) to atovaquone.

8 erential sensitivity of these two species to atovaquone.

9 e bc(1) complexes resistant to inhibition by atovaquone.

10 new antimalarial agents: 5-fluoroorotate and atovaquone.

11 line and a broad spectrum antiparasitic drug atovaquone.

12 arasite cytochrome b predicted resistance to atovaquone.

13 ubstantially mitigated cross-resistance with atovaquone.

14 nvestigated the hypoxia modifying effects of atovaquone.

15 or this study we focus on the anti-malarial, atovaquone.

16 an endochin-like quinolone (ELQ) prodrug and atovaquone.

17 fected patients receiving treatment doses of atovaquone.

18 to established antimalarials chloroquine and atovaquone.

19 ng clinical isolates harboring resistance to atovaquone.

20 cross-resistance with the antimalarial drug atovaquone.

21 , dihydroartemisinin (1.5 nM [1.0-2.0]), and atovaquone (0.3 nM [0.2-0.4]).

22 developed in 122 of 536 patients assigned to atovaquone (15.7 cases per 100 person-years), as compare

23 mg twice daily (BID) for 14 days followed by atovaquone 1500 mg BID for 14 days, or vice-versa, with

24 open-label, randomized trial comparing daily atovaquone (1500-mg suspension) with daily dapsone (100

25 0 subjects receiving EFV in combination with atovaquone 750 mg BID achieved an atovaquone C avg>18.5

26 ggest that the currently recommended dose of atovaquone 750 mg BID for treatment of mild to moderate

27 of 10 subjects receiving EFV-based cART plus atovaquone 750 mg BID had an atovaquone C avg>15 microg/

28 Subjects were randomly assigned to atovaquone 750 mg twice daily (BID) for 14 days followed

29 The subjects were assigned to receive either atovaquone (750 mg every 12 hours) and azithromycin (500

30 Atovaquone, a 2-hydroxynaphthoquinone, is a competitive

31 al. (2019) report that mosquitoes exposed to atovaquone, a known antimalarial, are resistant to infec

32 roximately 200 fold) than that observed with atovaquone, a licensed bc(1)-specific antimalarial drug.

33 n the Cambodian Cam3.II line was reversed by atovaquone, a mitochondrial electron transport chain inh

34 t parasites with different concentrations of atovaquone, a mitochondrial inhibitor, the recovery of d

35 Resistance to atovaquone, a second-line agent, may also be developing.

36 Atovaquone, a ubiquinone analogue, targets C. felis cyto

37 r show that a combination of tafenoquine and atovaquone achieves cure with no recrudescence in both m

38 sistent with oxidative stress, we found that atovaquone activated endoplasmic reticulum (ER) stress,

39 etermine the pharmacokinetics of aerosolized atovaquone (administered with and without a synthetic su

40 Atovaquone also downregulated both OXPHOS and glycolysis

41 is study, we addressed the antiviral role of atovaquone, an FDA Pregnancy Category C drug and pyrimid

42 Atovaquone, an FDA-approved oxidative phosphorylation (O

43 llowing dose regimens: (1) 250 milligrams of atovaquone and 100 milligrams of proguanil (250/100 mill

44 milligrams on day -7, (4) 500 milligrams of atovaquone and 200 milligrams of proguanil (500/200 mill

45 igrams) on day -7 or, (5) 1000 milligrams of atovaquone and 400 milligrams of proguanil (1000/400 mil

46 with this protocol, such as the antimalarial Atovaquone and antitheilerial Parvaquone, thus evidencin

47 Treatment combining atovaquone and azithromycin (A&A) has been associated wi

48 that infects domestic cats, is treated with atovaquone and azithromycin (A&A).

49 therapy in 65 percent of those who received atovaquone and azithromycin and 73 percent of those who

50 or the treatment of babesiosis, a regimen of atovaquone and azithromycin is as effective as a regimen

51 We describe the emergence of atovaquone and azithromycin resistance associated with m

52 The most common adverse effects with atovaquone and azithromycin were diarrhea and rash (each

53 d by 15 percent of the subjects who received atovaquone and azithromycin, as compared with 72 percent

54 In vitro response to atovaquone and cytochrome b sequence of clinical isolate

55 nnot tolerate trimethoprim-sulfamethoxazole, atovaquone and dapsone are similarly effective for the p

56 Our study provides a novel function for atovaquone and highlights that the rediscovery of pregna

57 ith chloroquine resistance, a combination of atovaquone and proguanil or quinine plus tetracycline or

58 d ELQ-468) that alone or in combination with atovaquone are highly efficacious against B. duncani and

59 These findings establish atovaquone as a novel, clinically accessible STAT3 inhib

60 Six cases were receiving atovaquone as a prophylaxis.

61 ation because of adverse events was 3.78 for atovaquone as compared with dapsone (95 percent confiden

62 potency equal to that of orally administered atovaquone at 10 mg/kg.

63 l antimalarial agents acquired resistance to atovaquone at high frequency, but not to 5-fluoroorotate

64 The antitoxoplasmosis drug atovaquone, at a very low concentration (0.03 microM), t

65 Impressively, a combination of ELQ-334 and atovaquone, at doses as low as 5.0 mg/kg each, resulted

66 FDA-approved prophylactic antimalarial drug atovaquone (ATO) recently was repurposed as an antitumor

67 The FDA-approved antimalarial drug atovaquone (ATO), a mitochondrial complex III inhibitor,

68 ceiving EFV-based cART had 47% and 44% lower atovaquone AUCtau than subjects not receiving cART at at

69 dose by aerosol, mean peak concentrations of atovaquone averaged 52 microg/mL in plasma and 31 microg

70 purposing an FDA-approved antimalarial drug, atovaquone (AVO).

71 abesiosis consists of two drug combinations, atovaquone + azithromycin or quinine + clindamycin.

72 st drugs commonly used for treatment such as atovaquone, azithromycin, and clindamycin.

73 Other agents included atovaquone, azithromycin, and/or clindamycin.

74 Mosquito exposure to atovaquone before, or shortly after, P. falciparum infec

75 of the changes in cytochrome b structure and atovaquone binding with the mutated bc(1) complexes prov

76 of the amino acid side-chains may determine atovaquone-binding affinity, and thereby selective toxic

77 e, including amino acid substitutions in the atovaquone-binding regions of cytochrome b (cytb) and th

78 ovide the first molecular description of how atovaquone binds to the bc1 complex and explain the diff

79 These results indicate that atovaquone binds to the ubiquinol oxidation pocket of th

80 Here, we show that atovaquone blocks this domain movement by locking the ir

81 based cART plus atovaquone 750 mg BID had an atovaquone C avg>15 microg/mL, which has previously been

82 ation with atovaquone 750 mg BID achieved an atovaquone C avg>18.5 microg/mL, a concentration that ha

83 que metabolic signatures were also found for atovaquone, chloroquine, proguanil, cycloguanil and meth

84 We observed that only atovaquone collapsed DeltaPsim and inhibited parasite re

85 strate superior efficacy of tafenoquine plus atovaquone combination over current therapies for the tr

86 ge for future clinical evaluation of ELQ and atovaquone combination therapy for treatment of human ba

87 in 33% of isolates from patients exposed to atovaquone, compared with 6% from those who were not (P=

88 e identified TTFA (complex II inhibitor) and Atovaquone (complex III inhibitor), which robustly block

89 Taken together, these studies suggest that atovaquone could be a broad-spectrum antiviral drug and

90 ructural basis for the selective toxicity of atovaquone could help in designing drugs against infecti

91 human placental tissue model, we found that atovaquone could limit ZIKV infection in a dose-dependen

92 azole, with second-line therapies, including atovaquone, dapsone, and pentamide.

93 me b, the sensitivity of the yeast enzyme to atovaquone decreased (Ki = 100 nm) with no loss in activ

94 hat oxidative stress caused by plumbagin and atovaquone degrades NKA, resulting in the inability to m

95 Our findings demonstrate that atovaquone disrupts cellular homeostasis and metabolism,

96 e AUCtau than subjects not receiving cART at atovaquone doses of 750 mg BID and 1500 mg BID, respecti

97 In addition, atovaquone eradicates hypoxia in FaDu, HCT116 and H1299

98 Atovaquone exposure (area under the curve) during liver

99 re common in patients with AIDS and PCP with atovaquone exposure, but the clinical significance of th

100 posure were matched with 45 patients with no atovaquone exposure.

101 carinii pneumonia (PCP) are associated with atovaquone exposure.

102 ng on the reduction of cross-resistance with atovaquone for activity against the clinical isolates W2

103 c stem cell transplantation, extended use of atovaquone for Pneumocystis prophylaxis was associated w

104 nous pyrimidine nucleosides, indicating that atovaquone functions through the inhibition of the pyrim

105 Furthermore, atovaquone had no effect on mammalian DeltaPsim.

106 or FDA-approved small molecule drugs (e.g., atovaquone, hydroxyurea).

107 the field, greatly enhancing the utility of atovaquone in malaria control.

108 Resistance to atovaquone in the field is associated with point mutatio

109 f oxidative stress-mediated by plumbagin and atovaquone in the inhibition of NKA activity.

110 ant) and to evaluate the efficacy of inhaled atovaquone in the prevention and treatment of Pneumocyst

111 val of rats with PCP and, when combined with atovaquone, increased plasma and lung concentrations of

112 In these enzymes, the IC(50) for atovaquone increases from 25 nm for the enzyme from wild

113 tch clamping demonstrates that plumbagin and atovaquone inhibit outward and the inward current flowin

114 We confirm that plumbagin and atovaquone inhibit the proliferation of three human (OVC

115 , we show that the common antiparasitic drug atovaquone inhibits arbovirus replication through intrac

116 In malaria parasites, atovaquone inhibits mitochondrial electron transport at

117 Atovaquone inhibits respiration in target organisms by s

118 utinely achieved clinically in human plasma, atovaquone inhibits STAT3 phosphorylation, the expressio

119 Atovaquone inhibits the bc1 complex competitively with a

120 Atovaquone is a substituted 2-hydroxynaphthoquinone that

121 Atovaquone is a substituted hydroxynaphthoquinone that i

122 Atovaquone is a substituted hydroxynaphthoquinone that i

123 Atovaquone is a ubiquinone analogue, and decreases the O

124 Atovaquone is an anti-malarial drug used in combination

125 Atovaquone is an antiparasitic drug that selectively inh

126 However, among those not receiving dapsone, atovaquone is better tolerated and may be the preferred

127 t a 7- to 10-day course of azithromycin plus atovaquone is effective for mild babesiosis.

128 Atovaquone is not a kinase inhibitor but instead rapidly

129 to a commonly used antimalarial medication, atovaquone, is apparently unable to spread.

130 A computed energy-minimized structure for atovaquone liganded to the yeast bc1 complex suggests th

131 se-dependent manner, providing evidence that atovaquone may function as an antiviral in humans.

132 oelii; these mutants exhibited resistance to atovaquone-mediated collapse of mitochondrial membrane p

133 expression signature of STAT3, we discovered atovaquone (Mepron), an antimicrobial approved by the US

134 Atovaquone (Mepron, 566c80) is an effective agent agains

135 onokiol, Mito-magnolol, Mito-metformin, Mito-atovaquone, Mito-hydroxyurea) accumulate in tumor cell m

136 lysis of recrudescent parasites after ELQ or atovaquone monotherapy identified genetic substitutions

137 Long-acting injectable medications, such as atovaquone, offer the prospect of a "chemical vaccine" f

138 ach to characterize the molecular effects of atovaquone on EOC cells.

139 rial endpoint used to evaluate the action of atovaquone on tumour hypoxia in patients with NSCLC was

140 nanoluciferase decreased upon treatment with atovaquone or LHVS, two compounds that are known to comp

141 roviral therapy (cART) impacted steady-state atovaquone plasma concentrations in human immunodeficien

142 A promising alternative treatment is atovaquone plus azithromycin.

143 Atovaquone pressure selects parasites with mutations in

144 artesunate-amodiaquine (2.9%) and artesunate-atovaquone-proguanil (1.0%) groups.

145 An additional group received daily atovaquone-proguanil (250-100 mg) for 9 days, starting 1

146 (cohort 1A), six participants received daily atovaquone-proguanil 1 day before CHMI (cohort 1B), and

147 oral regimen only (95 AL, 162 mefloquine, 36 atovaquone-proguanil [AP], and 17 others), and 87 were a

148 M265 1 day before CHMI and six of six in the atovaquone-proguanil cohort were protected, whereas plac

149 Indonesia or Papua New Guinea, in which case atovaquone-proguanil is best, with mefloquine or quinine

150 uine, chloroquine, chloroquine-proguanil) or atovaquone-proguanil on the incubation period.

151 sed combination therapies are not available, atovaquone-proguanil or quinine plus clindamycin is used

152 Single-dose atovaquone-proguanil provides effective malaria chemopro

153 re observed after artesunate-amodiaquine and atovaquone-proguanil therapies, respectively.

154 ble-blind trial to establish the efficacy of atovaquone-proguanil to prevent malaria with the goal of

155 iaquine, atovaquone-proguanil, or artesunate-atovaquone-proguanil treatment groups and followed for 2

156 Artesunate-atovaquone-proguanil was a highly effective alternative

157 Atovaquone-proguanil was characterized by a slow blood s

158 Artesunate-atovaquone-proguanil was not associated with any failure

159 yed symptom onset after 60 days, while using atovaquone-proguanil was not.

160 istance, few alternative non-ACTs, including atovaquone-proguanil, are currently available.

161 randomly assigned to artesunate-amodiaquine, atovaquone-proguanil, or artesunate-atovaquone-proguanil

162 Allocation to DSM265, atovaquone-proguanil, or placebo was randomised by an in

163 However, the proportion of atovaquone-proguanil-treated patients with positive smea

164 onartemisinin drugs quinine, mefloquine, and atovaquone-proguanil.

165 es, tafenoquine was used in combination with atovaquone-proguanil.

166 also resistant to the synergistic effects of atovaquone/ proguanil combination.

167 ee holidays." The standard treatment dose of atovaquone/proguanil (250 mg/100 mg, 4 tablets/day for 3

168 old to evaluate the effects of chloroquine, atovaquone/proguanil (Malarone), and doxycycline on the

169 tolerability, and acceptability of the 3-day atovaquone/proguanil schedule for malarial chemoprophyla

170 The 3-day atovaquone/proguanil schedule had an impressively high c

171 All participants received atovaquone/proguanil treatment if blood-stage infection

172 Atovaquone/proguanil was the most commonly prescribed an

173 nrolled and prescribed the 3-day schedule of atovaquone/proguanil, completed at least 1 day before de

174 ochrome b genes from 2 of 4 patients who had atovaquone prophylaxis failure contained mutations resul

175 Fifteen patients with previous atovaquone prophylaxis or treatment exposure were matche

176 nce of PCP was significantly associated with atovaquone prophylaxis.

177 Atovaquone rapidly decreases the OCR by more than 80% in

178 dertaking clinical studies to assess whether atovaquone reduces tumour hypoxia in patients, thereby i

179 Atovaquone represents a class of antimicrobial agents wi

180 f this class to overcome parasite Q(o)-based atovaquone resistance and provides critical structural i

181 Based on our malaria atovaquone resistance data, a series of cytochrome b mut

182 Laboratory studies have indicated that atovaquone resistance disadvantages parasites in mosquit

183 To assess the possibility that atovaquone resistance might be developing, the genes for

184 o-lethal fitness cost of clinically relevant atovaquone resistance to P. falciparum in the mosquito s

185 To better understand the molecular basis of atovaquone resistance, we have introduced seven of the m

186 viding direct proof that the mutation causes atovaquone resistance.

187 ative explanation for the molecular basis of atovaquone resistance.

188 e and cytochrome b sequence did not indicate atovaquone resistance.

189 cular and biochemical characterization of an atovaquone-resistant field isolate, TM902CB.

190 To that end, we derived nine independent atovaquone-resistant malaria parasite lines by suboptima

191 have introduced seven of the mutations from atovaquone-resistant P. jirovecii into the cytochrome b

192 Here we generate atovaquone-resistant parasites that differ from wild typ

193 imalarial drugs artesunate, chloroquine, and atovaquone, resulting in accelerated parasite clearance

194 These results highlight atovaquone's potential to activate immune responses, off

195 ects animals from lethal infection caused by atovaquone-sensitive and -resistant B. duncani strains.

196 levels of expression, compared with the 3D7 (atovaquone-sensitive) control strain in bc(1) and cytoch

197 This suggests that atovaquone, shown to inhibit mitochondrial electron tran

198 of P(f)-type Complex III inhibitors such as atovaquone, stigmatellin, and UHDBT.

199 Atovaquone targets parasite cytochrome b.

200 parasites rendered the complex resistant to atovaquone, thereby providing direct proof that the muta

201 The administration of oral atovaquone to mice inhibited tumor growth and prolonged

202 not recover NKA activity in the plumbagin or atovaquone treated SKOV-3 and OVCAR-3 cells.

203 tion factor A (TFAM), in the supernatants of atovaquone-treated cells, indicating the release of immu

204 ts revealed enhanced NK cell activity toward atovaquone-treated cells.

205 in was upregulated on the plasma membrane of atovaquone-treated EOC cells.

206 The recent, growing failure of atovaquone treatment and increased mortality of patients

207 The failure of atovaquone treatment and mortality of patients with mala

208 cytochrome b, a modification associated with atovaquone treatment failure in humans.

209 These effects were also observed with atovaquone treatment of primary blasts isolated from pat

210 Cohort 1 (n = 14) received atovaquone treatment, while cohort 2 (n = 15) did not.

211 se of reactive oxygen species resulting from atovaquone treatment.

212 ases per 100 person-years; relative risk for atovaquone vs. dapsone, 0.85; 95 percent confidence inte

213 We found that atovaquone was able to inhibit ZIKV and chikungunya viru

214 When atovaquone was combined with surfactant, mean peak conce

215 Atovaquone was shown to inhibit the respiratory chain of

216 50% growth inhibition, while the IC(50) for atovaquone (which does not inhibit FPPS) remained the sa

217 shift of the inhibitory constant (K(i)) for atovaquone with a concomitant reduction in the V(max) of

218 ogates to model the molecular interaction of atovaquone with human and resistant pathogen enzymes.

219 We have examined the interaction of atovaquone with the bc1 complex isolated from Saccharomy