ライフサイエンスコーパス: artemisinin

1 hoto-oxidation of dihydroartemisinic acid to artemisinin.

2 e storage of phytotoxic compounds, including artemisinin.

3 7' varieties, produce more arteannuin B than artemisinin.

4 re is no consensus on biochemical targets of artemisinin.

5 fundamental to the metabolic engineering of artemisinin.

6 R pathways mitigate protein damage caused by artemisinin.

7 pregabalin, memantine, and the antimalarial artemisinin.

8 f arteannuin B as a new precursor source for artemisinin.

9 d light, and the output is pure, crystalline artemisinin.

10 gence of Plasmodium falciparum resistance to artemisinins.

11 by parasites with reduced responsiveness to artemisinins.

12 ith an antiparasitic profile comparable with artemisinin (1), with no cross-resistance in a resistant

13 al anomalies was similar for first-trimester artemisinin (1.5% [95% CI 0.6%-3.5%]) and quinine exposu

14 tabolites including 22 sesquiterpenes (e.g., artemisinin), 26 monoterpenes, two triterpenes, one dite

15 Artemisinin, a sesquiterpene lactone produced by Artemis

16 tion fingerprint with that generated from an artemisinin ABPP equivalent confirms a highly conserved

17 inst drug resistance in comparison with pure artemisinin (AN).

18 ulating gametocytes is needed in areas where artemisinin and ACT resistance is prevalent.

19 zymatic conversion steps are central to both artemisinin and arteannuin X biosynthesis.

20 Artemisinin and its derivatives (ARTs) are frontline ant

21 in the network may improve the production of artemisinin and its precursors.

22 To meet the growing demand for artemisinin and make it accessible to the poorest, an in

23 cilitate low-cost production and delivery of artemisinin and other drugs through metabolic engineerin

24 inin-piperaquine failures are caused by both artemisinin and piperaquine resistance, and commonly occ

25 ated with clinical or in vitro resistance to artemisinin, and many African mutations appear to be neu

26 sk of miscarriage associated with the use of artemisinins anytime during the first trimester (n = 37/

27 nce that the final steps in the synthesis of artemisinin are nonenzymatic in vivo.

28 ovide biochemical and cellular evidence that artemisinins are potent inhibitors of Plasmodium falcipa

29 Artemisinins are the cornerstone of anti-malarial drugs.

30 The recent emergence of resistance to artemisinin (ART) and its partner drugs in ART-based com

31 dium falciparum relies almost exclusively on artemisinin (ART) combination therapies (ACTs) in endemi

32 asites that have decreased susceptibility to artemisinin (ART) derivatives and ACT partner drugs, res

33 The artemisinin (ART)-based antimalarials have contributed s

34 Artemisinin (ART)-based combination therapies are the mo

35 Experimental evidence suggests that when an artemisinin (ART)-sensitive (K13 wild-type) Plasmodium f

36 the content of dihydroartemisinic aldehyde, artemisinin, artemisinic acid and arteannuin B content o

37 affected the activity of this pathway toward artemisinin, artemisinic acid, and arteannuin b but also

38 Thus, reports that resistance to artemisinins (ARTs) has emerged, and that the prevalence

39 3 days of artemisinin as part of an artemisinin combination therap

40 meric structures, which combine two units of artemisinin, as lead compounds of interest.

41 the recent and rapid decline in efficacy of artemisinin-based combination (MAS3) on the Thailand-Mya

42 Artemisinin-based combination therapies (ACTs) are recom

43 Artemisinin-based combination therapies (ACTs) are the f

44 Artemisinin-based combination therapies (ACTs) are the m

45 Artemisinin-based combination therapies (ACTs) are the m

46 The worldwide use of artemisinin-based combination therapies (ACTs) has contr

47 Artemisinin-based combination therapies (ACTs) have been

48 o trials comparing its efficacy with that of artemisinin-based combination therapies (ACTs) in Latin

49 The global adoption of artemisinin-based combination therapies (ACTs) in the ea

50 adhering to this recommendation to restrict artemisinin-based combination therapies (ACTs) to positi

51 timalarial chemotherapy, globally reliant on artemisinin-based combination therapies (ACTs), is threa

52 r' drug from another class, and are known as artemisinin-based combination therapies (ACTs).

53 by the emergence and spread of resistance to artemisinin-based combination therapies (ACTs).

54 Prolonged courses of artemisinin-based combination therapies are currently ef

55 In western Cambodia, where artemisinin-based combination therapies are failing, the

56 Artemisinin-based combination therapies are the first li

57 Accumulating evidence of the safety of artemisinin-based combination therapies for the treatmen

58 ne and wide availability of highly effective artemisinin-based combination therapies, it is time to r

59 threatens the long-term clinical utility of artemisinin-based combination therapies, the cornerstone

60 ecting man, have been reduced in part due to artemisinin-based combination therapies.

61 hat this might relate to the introduction of artemisinin-based combination therapies.

62 The efficacy of artemisinin-based combination therapy (ACT) and rectal a

63 tests, and treat positive malaria cases with artemisinin-based combination therapy (ACT) and those wh

64 The efficacy of artemisinin-based combination therapy (ACT) for Plasmodi

65 Artemisinin-based combination therapy (ACT) has become t

66 Artemisinin-based combination therapy (ACT) is the first

67 nosis and treat confirmed malaria using oral artemisinin-based combination therapy (ACT) or rectal ar

68 Administration of artemisinin-based combination therapy (ACT) to infant an

69 the current malaria treatment, the so-called Artemisinin-based Combination Therapy (ACT).

70 T-positive children able to swallow received artemisinin-based combination therapy (Coartem).

71 ic assessment of the therapeutic efficacy of artemisinin-based combination therapy are warranted.

72 laced sulfadoxine-pyrimethamine (SP) with an artemisinin-based combination therapy as the first-line

73 as also associated with a modest increase in artemisinin-based combination therapy coverage (3.56 per

74 and supports a unified treatment policy for artemisinin-based combination therapy for all Plasmodium

75 The combination of MB with an artemisinin-based combination therapy has been confirmed

76 outheast Asia threatens the continued use of artemisinin-based combination therapy in endemic countri

77 commendations to use rapid diagnostic tests, artemisinin-based combination therapy, and rectal artesu

78 c study in Uganda of the most widely adopted artemisinin-based combination therapy, artemether-lumefa

79 ingle low doses of primaquine, when added to artemisinin-based combination therapy, might prevent tra

80 partner drug used in the leading first-line artemisinin-based combination therapy.

81 days, followed by a standard 3-day course of artemisinin-based combination therapy.

82 raquine (DP) is an effective, well tolerated artemisinin-based combination therapy.

83 Quinine or alternative artemisinin-based combination treatment (ACT) is the rec

84 e the costs of preventive malaria treatment (artemisinin-based combination treatment [ACT]) for all c

85 to pyronaridine-artesunate as an alternative artemisinin-based combination treatment for malaria in s

86 Artemisinin-based therapies are the only effective treat

87 omoter variation, DBR2 expression levels and artemisinin biosynthesis capabilities are discussed and

88 gene-terpene network that is associated with artemisinin biosynthesis in self-pollinated (SP) Artemis

89 rted the oral delivery of a non-protein drug artemisinin biosynthesized ( approximately 0.8 mg/g dry

90 evealed that the consequence of blocking the artemisinin biosynthetic pathway is the redirection of s

91 e for a series of oxidation reactions in the artemisinin biosynthetic pathway.

92 split dosing should be incorporated into all artemisinin combination regimen designs.

93 Artemisinin combination therapies (ACTs) are used worldw

94 The efficacy of CQ and alternative artemisinin combination therapies (ACTs) for vivax malar

95 western Kenya pre- and post- introduction of artemisinin combination therapies (ACTs) were genotyped

96 um malaria were randomized to receive 1 of 3 artemisinin combination therapies (ACTs) with or without

97 lciparum threatens to reduce the efficacy of artemisinin combination therapies (ACTs), thus compromis

98 (LLINs), indoor residual spraying (IRS), and artemisinin combination therapies (ACTs).

99 nin (or its semisynthetic analogs), known as artemisinin combination therapies (ACTs).

100 measures: early case management with quality artemisinin combination therapies (avoiding artesunate m

101 Unfortunately, more recent remedies such as artemisinin combination therapies have been rendered les

102 ug resistance, causing high failure rates of artemisinin combination therapies in some areas.

103 ion, emerging resistance to partner drugs in artemisinin combination therapies seriously threatens gl

104 nt front-line antimalarial treatments, ACTs (artemisinin combination therapies), the discovery of nov

105 um malaria depends greatly on treatment with artemisinin combination therapies.

106 needed in the face of emerging resistance to artemisinin combination therapies.

107 n-piperaquine has been adopted as first-line artemisinin combination therapy (ACT) for multidrug-resi

108 ne, the partner drug in the local first-line artemisinin combination therapy (ACT).

109 Molecular markers that predict failure of artemisinin combination therapy are urgently needed to m

110 Artemisinin combination therapy effectively clears asexu

111 ata of early treatment failures with an oral artemisinin combination therapy in a pre-artemisinin res

112 3 days of artemisinin as part of an artemisinin combination therapy regimen might be insuffi

113 The benefits of 3-d artemisinin combination therapy regimens to treat malari

114 t of these efforts has been the promotion of Artemisinin Combination Therapy, but despite these effor

115 o first-line antimalarial therapy, including artemisinin combination therapy, chloroquine, and sulfad

116 alongside mass treatment strategies with an artemisinin combination therapy, has been suggested as a

117 artemisinin, is a component of a widely used artemisinin combination therapy.

118 rmation regarding the safety and efficacy of artemisinin combination treatments for malaria in pregna

119 The efficacy of artemisinin-combination therapy (ACT) continues to be ex

120 compound that could replace the fast-acting artemisinin component and harbor additional gametocytoci

121 Surprisingly, the artemisinin component typically makes a negligible contr

122 associated with first-line treatment with an artemisinin derivative compared with quinine.

123 rasite clearance in patients treated with an artemisinin derivative or an ACT.

124 ty data in human pregnancies, have prevented artemisinin derivatives from being recommended for malar

125 ong first-trimester pregnancies treated with artemisinin derivatives versus quinine or no antimalaria

126 d onset of action and potent activity of the artemisinin derivatives while exhibiting greatly improve

127 Upon short-term exposure (4 h), artemisinin derivatives, quinine and mefloquine impacted

128 parasite clearance rate after treatment with artemisinin derivatives.

129 ic features that overcome the liabilities of artemisinin derivatives.

130 ts recent developments on different types of artemisinin-derived dimers and their structural and func

131 ant malaria DNA, which confers resistance to artemisinin drugs, was also demonstrated.

132 loss in a sensitivity analysis restricted to artemisinin exposures during the embryo sensitive period

133 tress pathways associated with resistance of artemisinin family anti-malarials, we observe growth inh

134 B (g g(-1) , dry weight, dw) and 0.17-0.25% artemisinin (g g(-1) , dw), the levels of which were sig

135 Youyou Tu for her work on the development of artemisinin has been universally welcomed by the Interna

136 py, but despite these efforts, resistance to artemisinin has begun to emerge.

137 Artemisinin has paved the way for the current malaria tr

138 Recent reports that resistance has arisen to artemisinins has caused considerable concern.

139 cribed as 'The discoveries of Avermectin and Artemisinin have revolutionized therapy for patients suf

140 m falciparum parasites that are resistant to artemisinins have been detected in Southeast Asia.

141 Resistance to artemisinins, however, has emerged in Southeast Asia.

142 ore effective than a comparable dose of pure artemisinin in a rodent malaria model.

143 role in the biosynthesis of the antimalarial artemisinin in Artemisia annua.

144 hat WP overcomes existing resistance to pure artemisinin in the rodent malaria Plasmodium yoelii.

145 rican allele, was found to be susceptible to artemisinin in vitro on a ring-stage survival assay.

146 proaches half the concentration observed for artemisinin in wild-type plants, demonstrating high-flux

147 elling exercises, that twice daily dosing of artemisinins increases malaria parasite killing and so c

148 Artemisinin-induced dormancy is a proposed mechanism for

149 In nonimmune populations, artemisinin-induced P. falciparum clearance is related t

150 Antimalarial immunity correlates with fast artemisinin-induced parasite clearance and low pitting r

151 thway for artemisinic acid, the precursor of artemisinin, into the high-biomass crop tobacco.

152 Artemisinin is an important antimalarial drug, but, at p

153 Artemisinin is highly effective against drug-resistant m

154 The primary cost of artemisinin is the very expensive process used to extrac

155 n resistance by quantifying the contribution artemisinins make to the overall therapeutic capacity of

156 lumefantrine and mefloquine, and the active artemisinin metabolite dihydroartemisinin.

157 age in first-line falciparum treatments with artemisinin (n=183) versus quinine (n=842; HR 0.78 [95%

158 = 0%, p = 0.228), in the risk of stillbirth (artemisinins, n = 10/654; quinine, n = 11/615; aHR = 0.2

159 Artemisinin-NO-donor hybrid compounds show promise as po

160 ining identified 47 genes that mapped to the artemisinin, non-amorphadiene sesquiterpene, monoterpene

161 ls (n = 40) with monotherapy arms containing artemisinin or a derivative (76 arms).

162 the flow of artemisinic aldehyde into either artemisinin or arteannuin B, we determined the content o

163 The use of artemisinin or other endoperoxides in combination with o

164 in kelch13 and other loci that contribute to artemisinin or partner drug resistance.

165 of malaria are combination drugs containing artemisinin (or its semisynthetic analogs), known as art

166 um falciparum-infected patients treated with artemisinins, parasitemia declines through so-called pit

167 nal enzymes known to affect flux through the artemisinin pathway.

168 pared with other antimalarial drugs with the artemisinin pharmacophore.

169 nt antimalarial drugs are combinations of an artemisinin plus a 'partner' drug from another class, an

170 The high artemisinin producers (HAPs), which includes the '2/39',

171 more artemisinin than arteannuin B; the low artemisinin producers (LAPs), which include the 'Meise',

172 e quinine, extracted from cinchona bark, and artemisinin (qinghao), extracted from Artemisia annua in

173 hole intact plant cells bioencapsulating the artemisinin reduced the parasitemia levels in challenged

174 riod of a rapid increase in the emergence of artemisinin resistance (2001-2014).

175 K13 mutations conferring moderate artemisinin resistance (notably E252Q) predominated init

176 We explored the relation between artemisinin resistance and dihydroartemisinin-piperaquin

177 sensitivity tests and molecular markers for artemisinin resistance and for contextualising the 'day

178 ese data present PI3P as the key mediator of artemisinin resistance and the sole PfPI3K as an importa

179 The underlying mechanisms associated with artemisinin resistance are poorly understood, and the im

180 Throughout, we examine artemisinin resistance as an example to emphasize challe

181 We investigate the likely impact of artemisinin resistance by quantifying the contribution a

182 Artemisinin resistance can be tracked using the K13 mole

183 tantial benefits in reduction of pressure on artemisinin resistance evolution, delaying its emergence

184 ant further investigation for involvement in artemisinin resistance evolution.

185 Artemisinin resistance extends across much of Myanmar.

186 The molecular epidemiology of these artemisinin resistance genotypes in African parasite pop

187 smodium falciparum infections worldwide, but artemisinin resistance has risen rapidly in Southeast As

188 Elevated PI3P induced artemisinin resistance in absence of PfKelch13 mutations

189 Data suggests genetic signature of artemisinin resistance in Africa might be different from

190 efforts to reduce the emergence or spread of artemisinin resistance in African parasite populations.

191 We find PI3P levels to be predictive of artemisinin resistance in both clinical and engineered l

192 sts that the PfKelch13 mutations that confer artemisinin resistance in falciparum malaria have multip

193 declining malaria transmission and emerging artemisinin resistance in northwestern Thailand.

194 Although polymorphisms associated with artemisinin resistance in P. falciparum in Southeast Asi

195 om parasite clinical isolates that displayed artemisinin resistance in patients and in vitro, and use

196 Suspected artemisinin resistance in Plasmodium falciparum can be e

197 Artemisinin resistance in Plasmodium falciparum has emer

198 anopheline mosquitoes, and the emergence of artemisinin resistance in Plasmodium falciparum in south

199 K13 gene mutations are a primary marker of artemisinin resistance in Plasmodium falciparum malaria

200 Artemisinin resistance in Plasmodium falciparum threaten

201 Artemisinin resistance in Plasmodium falciparum threaten

202 r failures of monotherapy and is linked with artemisinin resistance in Plasmodium falciparum.

203 d by PK4 kinase activity plays a key role in artemisinin resistance in recrudescent malaria infection

204 The emergence of artemisinin resistance in Southeast Asia imperils effort

205 Emergence of artemisinin resistance in southeast Asia poses a serious

206 y been shown to be important determinants of artemisinin resistance in Southeast Asia.

207 arasite populations that are associated with artemisinin resistance in Southeast Asian parasites.

208 large-scale surveillance efforts to contain artemisinin resistance in the Greater Mekong Subregion a

209 s, further suggesting their role in emerging artemisinin resistance in the Greater Mekong Subregion.

210 The emergence of artemisinin resistance in the malaria parasite Plasmodiu

211 The high prevalence of artemisinin resistance in this recent malaria outbreak s

212 m patients with acute malaria and found that artemisinin resistance is associated with increased expr

213 In Preah Vihear, where artemisinin resistance is emerging, ten (16%) of 63 pati

214 In Pursat, where artemisinin resistance is entrenched, 37 (46%) of 81 pat

215 ransmission and immunity on the emergence of artemisinin resistance is important particularly as incr

216 In the Greater Mekong subregion (GMS), artemisinin resistance is increasingly compounded by par

217 Artemisinin resistance is rapidly spreading in Southeast

218 s had recrudescence and in Ratanakiri, where artemisinin resistance is rare, one (2%) of 60 patients

219 PfKelch13 mutations associated with artemisinin resistance lead to decreased abundance of Pf

220 Artemisinin resistance observed in Southeast Asia threat

221 ions are that public health surveillance for artemisinin resistance should not rely on kelch13 data a

222 K13 appears to be a major determinant of artemisinin resistance throughout Southeast Asia.

223 and implemented comprehensively if spread of artemisinin resistance to other regions is to be avoided

224 Artemisinin resistance to P. falciparum, which is now pr

225 No evidence of artemisinin resistance was found outside Southeast Asia

226 ain polymorphisms previously associated with artemisinin resistance were not identified.

227 Mutations in the Kelch13 marker for artemisinin resistance were present in 93% of samples, m

228 K13 mutations linked to artemisinin resistance were uncommon and did not increas

229 rasite clearance distributions in an area of artemisinin resistance with the aim refining the in vivo

230 modium falciparum K13 mutations (a marker of artemisinin resistance) in reducing treatment efficacy r

231 To monitor the spread of artemisinin resistance, a molecular marker is urgently n

232 transformed approaches to the monitoring of artemisinin resistance, allowing introduction of molecul

233 3 mutations were tested for association with artemisinin resistance, and extended haplotypes on chrom

234 relationship between parasite clearance and artemisinin resistance, as well as the predictive value

235 ain-carrying protein K13 are associated with artemisinin resistance, but the underlying molecular mec

236 Despite the emergence of artemisinin resistance, few alternative non-ACTs, includ

237 f the kelch protein K13 gene associated with artemisinin resistance, implying mutants in this gene ma

238 ress made in defining the molecular basis of artemisinin resistance, which has identified a primary r

239 h13 propeller gene mutations associated with artemisinin resistance--a non-synonymous Cys580Tyr subst

240 ed prior to 2004, preceding the emergence of artemisinin resistance-associated genotypes and phenotyp

241 both parasite clearance time (PCt(1/2)) and artemisinin resistance-associated kelch13 genotypes over

242 are now tracking the emergence and spread of artemisinin resistance.

243 hromosome 10 that may epistatically modulate artemisinin resistance.

244 cal boundaries and population frequencies of artemisinin resistance.

245 porter) also showed strong associations with artemisinin resistance.

246 rum Kelch13 (PfKelch13), a primary marker of artemisinin resistance.

247 a useful adjunct in tracking and containing artemisinin resistance.

248 vealed parasite genetic loci associated with artemisinin resistance.

249 ller mutations are important determinants of artemisinin resistance.

250 involved in a pathway recently implicated in artemisinin resistance.

251 Artemisinin resistant falciparum malaria is an increasin

252 y enhance and restore drug effectiveness" in artemisinin resistant P. falciparum malaria infections.

253 ral artemisinin combination therapy in a pre-artemisinin resistant P. falciparum Thai isolate in this

254 However, artemisinin resistant parasites have recently emerged in

255 l in tracking the emergence and/or spread of artemisinin resistant parasites.

256 The current epidemic of artemisinin resistant Plasmodium falciparum in Southeast

257 hemical differences between PfKelch13-mutant artemisinin-resistant and -sensitive strains of P. falci

258 Artemisinin-resistant falciparum malaria has emerged in

259 f-life provided a predicted likelihood of an artemisinin-resistant infection which depends on the pop

260 ue of 10% predicts the potential presence of artemisinin-resistant infections in most but not all sce

261 We show that contemporary artemisinin-resistant isolates from Cambodia develop and

262 As part of studies on the epidemiology of artemisinin-resistant malaria between Jan 1, 2008, and D

263 ogens into plantation areas, most worryingly artemisinin-resistant malaria parasites.

264 ATION: Our results suggest that the dominant artemisinin-resistant P falciparum C580Y lineage probabl

265 We aimed to assess the spread of artemisinin-resistant P falciparum in Myanmar by determi

266 The emergence and spread of fit artemisinin-resistant P falciparum parasite lineages, wh

267 This mechanism may mitigate the emergence of artemisinin-resistant P. falciparum in Africa.

268 mmunological conditions for the expansion of artemisinin-resistant P. falciparum.

269 Artemisinin-resistant parasites also exhibit decelerated

270 outside of the kelch13 locus associated with artemisinin-resistant parasites may yield new molecular

271 These findings suggest that artemisinin-resistant parasites remain in a state of dec

272 The ability of artemisinin-resistant parasites to infect such highly di

273 opeller sequencing to identify and eliminate artemisinin-resistant parasites.

274 support a widespread selective sweep for an artemisinin-resistant phenotype, the impact of these mut

275 uence the emergence of Plasmodium falciparum artemisinin-resistant phenotypes and genotypes over time

276 The emergence of artemisinin-resistant Plasmodium falciparum in Southeast

277 As the prevalence of artemisinin-resistant Plasmodium falciparum malaria incr

278 Artemisinin-resistant Plasmodium falciparum parasites ar

279 from hemoglobin (HBalpha and HBbeta) in the artemisinin-resistant strains.

280 uyou Tu for the discovery of avermectins and artemisinin, respectively, therapies that revolutionized

281 ess to important industrial compounds (e.g., artemisinin, resveratrol, vanillin).

282 Assessing artemisinin safety requires weighing the risks of malari

283 Of the tested secondary plant metabolites, artemisinin, scoparone, lactucin and esculetin all induc

284 w doses of this beta2-selective inhibitor in artemisinin-sensitive and -resistant parasites.

285 phenotype, the impact of these mutations on artemisinin susceptibility is unknown and will require f

286 ngqing' and 'Anamed' varieties, produce more artemisinin than arteannuin B; the low artemisinin produ

287 study of Plasmodium falciparum resistance to artemisinin, the frontline antimalarial drug.

288 Artemisinins, the most effective antimalarials available

289 al burden of malaria, emerging resistance to artemisinin threatens these gains.

290 ia chemotherapy progressing from quinine and artemisinin to ozonide-based compounds.

291 ce and combinatorial stimulation by low-dose artemisinin to photoactivate PPIX to produce cytotoxic r

292 ient and appropriate foods for administering artemisinin to those infected with malaria.

293 ug resistant Plasmodium falciparum including artemisinin-tolerant parasites highlights the need for n

294 No genetic similarities were found to artemisinin-tolerant parasites recently described in Cam

295 relate with parasite clearance half-lives in artemisinin-treated patients.

296 Compared to quinine, artemisinin treatment in the first trimester was not ass

297 ss the effect of first-trimester malaria and artemisinin treatment on miscarriage and major congenita

298 The relationship between artemisinin treatments (artesunate, dihydroartemisinin,

299 hibit no or minimal change in sensitivity to artemisinins, when compared with parental strains.

300 Artemisinins, which are derived from plants, are subject