ライフサイエンスコーパス: artemisinin

1 $10 to $100/kg (cannabidiol), and >$100/kg (artemisinin).

2 derives its importance from the antimalarial artemisinin.

3 reased tolerance of Plasmodium falciparum to artemisinin.

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

5 hoto-oxidation of dihydroartemisinic acid to artemisinin.

6 e storage of phytotoxic compounds, including artemisinin.

7 emendous clinical impact of the antimalarial artemisinin.

8 parasite that shows moderate sensitivity to artemisinin.

9 es of regenerated gl plantlets biosynthesize artemisinin.

10 gence of Plasmodium falciparum resistance to artemisinins.

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

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

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

14 n, which is required for parasite growth and artemisinin activation.

15 r gamma-aminobutyric acid (GABA), define how artemisinins also interfere presynaptically with GABAerg

16 falciparum malaria, including in areas with artemisinin and ACT partner-drug resistance.

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

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

19 ith tolerance to cellular stresses caused by artemisinin and environmental factors.

20 Artemisinin and its derivatives (ART) are crucial first-

21 Artemisinin and its derivatives (ARTs) are frontline ant

22 ence indicates that endoperoxides, including artemisinin and its derivatives, possess antileishmanial

23 of antimalarial resistance, particularly to artemisinin and its partner drugs, is a top priority.

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

25 not be ruled out due to its effect on both, artemisinin and lignin.

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

27 re threatened by the emergence and spread of artemisinin and partner drug resistance in Plasmodium fa

28 Artemisinin and partner-drug resistance in Plasmodium fa

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

30 Semisynthetic artemisinins and other bioactive peroxides are best know

31 Because the frequency of resistance to artemisinins and piperaquine is increasing in Southeast

32 nce: chloroquine, sulfadoxine-pyrimethamine, artemisinin, and piperaquine.

33 s implicate the mitochondrion as a target of artemisinins, and treatment of wild-type parasites with

34 red their infections, including 9 of 10 with artemisinin- and piperaquine-resistant infections.

35 (2019) demonstrate that artemisinin antimalarial drugs bind to gephyrin at the s

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

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

38 When artemisinins are combined with a single partner drug, al

39 Artemisinins are effective against a variety of parasite

40 with those of two first-line malaria drugs, artemisinin (ART) and chloroquine (CQ), lowering the IC(

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

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

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

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

45 Artemisinin (ART)-class drugs are activated in vivo by n

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

47 The compounds presented include artemisinin (ART, 1), parthenolide (PTL, 2), thapsigargi

48 these two types of GT-free materials produce artemisinin, artemisinic acid, and arteannuin B.

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

50 efore and after introduction of a universal, artemisinin-based antimalarial treatment strategy for al

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

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

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

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

55 Artemisinin-based combination therapies (ACTs) have been

56 Artemisinin-based combination therapies (ACTs) have demo

57 25mg/kg) primaquine (PQ) in combination with artemisinin-based combination therapies (ACTs) in areas

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

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

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

61 parasitaemia after treatment with different artemisinin-based combination therapies (ACTs).

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

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

64 Triple artemisinin-based combination therapies (TACTs), which c

65 Artemisinin-based combination therapies are the first li

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

67 with a single partner drug, all recommended artemisinin-based combination therapies have shown reduc

68 Seven years after the policy change to artemisinin-based combination therapies in 2005, the pfc

69 However, emergence of resistance to artemisinin-based combination therapies in Africa would

70 Triple artemisinin-based combination therapies, combining artem

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

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

73 Resistance to artemisinin-based combination therapies, the standard tr

74 tes acquire resistance to current first-line artemisinin-based combination therapies.

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

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

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

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

79 Artemisinin-based combination therapy (ACT) forms the fi

80 Artemisinin-based combination therapy (ACT) is recommend

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

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

83 policy of universal radical cure, combining artemisinin-based combination therapy (ACT) with a hypno

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

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

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

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

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

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

90 entified; however, none were associated with artemisinin-based combination therapy resistance.

91 e (delayed P. falciparum clearance following artemisinin-based combination therapy), is widespread ac

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

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

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

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

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

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

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

99 Pitting rate was high (55.8%) with artemisinin-based combinations, but <10% with the nonart

100 Artemisinin-based therapies are the only effective treat

101 doption of a universal policy of efficacious artemisinin-based therapy for malaria infections due to

102 eading to a revision of the current dogma of artemisinin biosynthesis in A. annua but also may expedi

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

104 employed all the above approaches to examine artemisinin biosynthesis in the reported A. annua glandl

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

106 nated inbred A. annua plants can express the artemisinin biosynthetic pathway.

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

108 ty for Aa547, which may have implications in artemisinin catabolism as well as lignification in A. an

109 le diversity, which may have implications in artemisinin catabolism as well as lignification.

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

111 ubsample, with being seen at a facility with Artemisinin Combination Therapies (ACTs) in stock (adjus

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

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

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

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

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

117 sistance in Plasmodium falciparum malaria to artemisinin combination therapies in the Greater Mekong

118 We show here that the two commonly used artemisinin combination therapies of artesunate plus amo

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

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

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

122 efficacy, safety, and tolerability of triple artemisinin combination therapies.

123 doxine-pyrimethamine (ASSP) is the frontline artemisinin combination therapy (ACT) in India.

124 Ws) were trained to treat malaria cases with artemisinin combination therapy after testing with a rap

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

126 antimalarial treatment policy was changed to artemisinin combination therapy for uncomplicated malari

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

128 t of preexisting immunity on the efficacy of artemisinin combination therapy must be examined to moni

129 t of preexisting immunity on the efficacy of artemisinin combination therapy regimens in a malaria-ho

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

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

132 the use of insecticide-treated bed nets and artemisinin combination therapy, the threat of drug resi

133 nrolled in a multinational clinical trial of artemisinin combination therapy.

134 th parenteral artesunate followed by an oral artemisinin-combination therapy.

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

136 Surprisingly, the artemisinin component typically makes a negligible contr

137 s treated with antimalarial drugs lacking an artemisinin component, as well as the absence of posttre

138 r, Aa547 expression was related inversely to artemisinin content and directly to total lignin content

139 se relationship between Aa547 expression and artemisinin content.

140 For example, global artemisinin demand could be met with fewer than 10 biore

141 Treatment with an artemisinin derivative decreased mortality compared with

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

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

144 me 12 with candidate resistance loci against artemisinin derivatives was evident in Ghana and Malawi.

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

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

147 m Kelch13 (K13) protein confer resistance to artemisinin derivatives, the current front-line antimala

148 ic features that overcome the liabilities of artemisinin derivatives.

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

150 Random, irrational, subtherapeutic artemisinin doses and self-medication with ACT along wit

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

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

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

154 emical entities with very potent, similar to artemisinins, fast-killing potency against asexual blood

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

156 Artemisinin has paved the way for the current malaria tr

157 However, the yield fluctuation of artemisinin has remained an unsolved problem in meeting

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

159 The antimalarial artemisinins have also been implicated in the regulation

160 Artemisinins have also shown anti-inflammatory effects,

161 Artemisinins have revolutionized the treatment of Plasmo

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

163 dular trichome (GT)-specific biosynthesis of artemisinin in all currently used Artemisia annua cultiv

164 approaches for high and stable production of artemisinin in the future.

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

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

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

168 Our data provide a comprehensive picture of artemisinin-induced effects on inhibitory signaling in t

169 ing rings from malaria-infected patients and artemisinin-induced quiescent parasites.

170 theses of chlorolissoclimide, nigelladine A, artemisinin, ingenol, hippolachnin A, communesin A, and

171 The antimalarial agents artemisinins inhibit cytomegalovirus (CMV) in vitro and

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

173 Artemisinin is highly effective against drug-resistant m

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

175 One of the attractive properties of artemisinins is their extremely fast-killing capability,

176 The -O-O- linkage in artemisinin makes peroxidases relevant to its metabolism

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

178 547 showed greater binding affinity for post-artemisinin metabolite, deoxyartemisinin, as compared to

179 bolite, deoxyartemisinin, as compared to pre-artemisinin metabolites (dihydroartemisinic hydroperoxid

180 Binding of artesunate, an artemisinin monomer, to vimentin prevents virus-induced

181 alarial at all, and nearly 10% received oral artemisinin monotherapy, which is not recommended becaus

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

183 = 0%, p = 0.228), in the risk of stillbirth (artemisinins, n = 10/654; quinine, n = 11/615; aHR = 0.2

184 high-value compounds (i.e., cannabidiol and artemisinin) offer net economic benefits at accumulation

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

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

187 At present, resistance to artemisinins or key partner drugs included in combinatio

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

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

190 pared with other antimalarial drugs with the artemisinin pharmacophore.

191 he long rain in 2016, two rounds of MDA with artemisinin/piperaquine (Artequick) and low-dose primaqu

192 by Aa547 showed higher expression in the low-artemisinin plant stage whereas Aa528 and Aa540 showed h

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

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

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

196 Artemisinin reduction assay also indicated inverse relat

197 olecular mechanisms of target recognition by artemisinins remain poorly characterized.

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

199 Artemisinin resistance (delayed P. falciparum clearance

200 1-13, the prevalence of molecular markers of artemisinin resistance (kelch13 Cys580Tyr mutations) and

201 valence of molecular markers associated with artemisinin resistance (kelch13 mutations, in particular

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

203 the repertoire of mutations associated with artemisinin resistance and suggest that the mitochondrio

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

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

206 Artemisinin resistance can be tracked using the K13 mole

207 large-scale multisite projects: the Tracking Artemisinin Resistance Collaboration II (TRAC2) and the

208 insecticide-treated bed nets in the Myanmar artemisinin resistance containment (MARC) zones using mu

209 ant further investigation for involvement in artemisinin resistance evolution.

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

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

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

213 Artemisinin resistance in falciparum malaria is associat

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

215 reat posed to treatment of severe malaria by artemisinin resistance in parasite early ring stages.

216 Suspected artemisinin resistance in Plasmodium falciparum can be e

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

218 udies have identified several mechanisms for artemisinin resistance in Plasmodium falciparum, includi

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

220 the de novo emergence of Pfkelch13-mediated artemisinin resistance in Rwanda, potentially compromisi

221 The emergence of artemisinin resistance in the malaria parasite Plasmodiu

222 iting confirmed that this mutation can drive artemisinin resistance in vitro.

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

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

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

226 the Lao People's Democratic Republic, where artemisinin resistance is prevalent.

227 Artemisinin resistance is primarily mediated by mutation

228 Artemisinin resistance is rapidly spreading in Southeast

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

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

231 lations carried out on PfK13 R539T and C580Y artemisinin resistance mutant structures revealed some l

232 d the structural alterations associated with artemisinin resistance mutations remain unknown.

233 Artemisinin resistance observed in Southeast Asia threat

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

235 This emerging artemisinin resistance threatens to undermine the effect

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

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

238 eller domain, mutations in which can mediate artemisinin resistance(5,6), in pretreatment samples col

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

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

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

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

243 ia over a 1-year period in areas affected by artemisinin resistance.

244 w parasite age affects parasite clearance in artemisinin resistance.

245 involved in a pathway recently implicated in artemisinin resistance.

246 hromosome 10 that may epistatically modulate artemisinin resistance.

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

248 parasites conferred high levels of in vitro artemisinin resistance.

249 be incorporated in individual assessments of artemisinin resistance.

250 e clearance will improve characterization of artemisinin resistance.

251 asite clearance half-life on parasite age in artemisinin resistant infections is consistent with ring

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 The current epidemic of artemisinin resistant Plasmodium falciparum in Southeast

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

257 The majority of artemisinin-resistant isolates also had increased plasme

258 Identification of artemisinin-resistant isolates in India together with ne

259 ation guideline, these 15 isolates were true artemisinin-resistant isolates.

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

261 ite invoked a strong possibility of emerging artemisinin-resistant malaria parasites.

262 mar is a premalaria elimination country with artemisinin-resistant malaria.

263 single-nucleotide polymorphism associated to artemisinin-resistant malaria.

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

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

266 o diversify antimalarial therapy in areas of artemisinin-resistant P. falciparum in Viet Nam.

267 apies (ACTs) in areas of low transmission or artemisinin-resistant P. falciparum, several single-site

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

269 nhibits ring-stage survival of wild-type and artemisinin-resistant parasites harboring the PfKelch13:

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

271 eater sharing of larger IBD segments between artemisinin-resistant parasites versus sensitive parasit

272 nation therapy that retains activity against artemisinin-resistant parasites.

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

274 In the Greater Mekong Subregion, where artemisinin-resistant Plasmodium falciparum is now wides

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

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

277 28 and Aa540 showed higher expression in the artemisinin-rich plant stage.

278 Assessing artemisinin safety requires weighing the risks of malari

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

280 A formal synthesis of artemisinin starting from amorphadiene is described.

281 f the parasite life cycle and synergize with artemisinins, suggesting that Pf20S inhibitors have pote

282 To broadly explore artemisinin susceptibility in apicomplexan parasites, we

283 intermediate filament protein vimentin as an artemisinin target, validated by detailed biochemical an

284 artemether and artesunate are derivatives of artemisinin, the beneficial anti-Ebola virus (EBOV) effe

285 For the past decade in Southeast Asia, artemisinins, the core component of first-line antimalar

286 Artemisinins, the most effective antimalarials available

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

288 1 (c.144T>G) , highlighting the potential of artemisinin to prevent sensory loss in CLRN1 (c.144T>G)

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

290 Artemisinin treatment also effectively restored hair cel

291 Except for the effects of artemisinin treatment and transfusion, causal interpreta

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

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

294 The relationship between artemisinin treatments (artesunate, dihydroartemisinin,

295 Maximum binding affinity for artemisinin was shown by Aa547.

296 Using a biotin-labeled artemisinin, we identified the intermediate filament pro

297 of GRASP55 mRNA, or on exposure to the drug artemisinin (which activates GCUSP), the localization of

298 Artemisinins, which are derived from plants, are subject

299 Partially overlapping binding of artemisinins with the substrate pyridoxal inhibits PLP b

300 sinin-based combination therapies, combining artemisinins with two currently available partner drugs,