Relevant bibliographies by topics / Antimalarials Dihydropteroate Synthase

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Academic literature on the topic 'Antimalarials Dihydropteroate Synthase'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Antimalarials Dihydropteroate Synthase"

1

Khim, Nimol, Christiane Bouchier, Marie-Thérèse Ekala, et al. "Countrywide Survey Shows Very High Prevalence of Plasmodium falciparum Multilocus Resistance Genotypes in Cambodia." Antimicrobial Agents and Chemotherapy 49, no. 8 (2005): 3147–52. http://dx.doi.org/10.1128/aac.49.8.3147-3152.2005.

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ABSTRACT Cambodia is located in an area of resistance to multiple antimalarials and has been the first country to implement the systematic use of an artesunate-mefloquine combination as first-line treatment for Plasmodium falciparum malaria. Little is known, however, about the prevalence of resistance mutations within the natural parasite populations, impeding rational drug policy in this context. Using direct sequencing of PCR products, we have analyzed sequence polymorphism of the dihydrofolate reductase-thymidylate synthase, dihydropteroate synthetase, and multidrug resistance 1 genes in a
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2

Nduati, Eunice, Sonya Hunt, Eddy M. Kamau, and Alexis Nzila. "2,4-Diaminopteridine-Based Compounds as Precursors for De Novo Synthesis of Antifolates: a Novel Class of Antimalarials." Antimicrobial Agents and Chemotherapy 49, no. 9 (2005): 3652–57. http://dx.doi.org/10.1128/aac.49.9.3652-3657.2005.

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ABSTRACT We have tested the hypothesis that 2,4-diamino-6-hydroxymethyl-pteridine (DAP), 2,4-diaminopteroic acid (DAPA), and 2,4 diamino-N10-methyl-pteroic acid (DAMPA) could be converted into aminopterin (from DAP and DAPA) and methotrexate (from DAMPA), both of which are potent inhibitors of dihydrofolate reductase, a proven drug target for Plasmodium falciparum. DAP, DAPA, and DAMPA inhibited parasite growth in the micromolar range; DAMPA was the most active, with 50% inhibitory concentrations in vitro of 446 ng/ml against the antifolate-sensitive strain and 812 ng/ml against the highly res
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3

Chotpatiwetchkul, Warot, Kanokthip Boonyarattanakalin, Duangkamol Gleeson, and M. Paul Gleeson. "Exploring the catalytic mechanism of dihydropteroate synthase: elucidating the differences between the substrate and inhibitor." Organic & Biomolecular Chemistry 15, no. 26 (2017): 5593–601. http://dx.doi.org/10.1039/c7ob01272a.

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QM/MM calculations are reported that help elucidate the reaction mechanism of DHPS, a validated antimicrobial and antimalarial target that has become increasingly compromised due to disease resistance.
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Lucchi, Naomi W., Sheila Akinyi Okoth, Franklin Komino, et al. "Increasing Prevalence of a Novel Triple-Mutant Dihydropteroate Synthase Genotype in Plasmodium falciparum in Western Kenya." Antimicrobial Agents and Chemotherapy 59, no. 7 (2015): 3995–4002. http://dx.doi.org/10.1128/aac.04961-14.

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ABSTRACTThe molecular basis of sulfadoxine-pyrimethamine (SP) resistance lies in a combination of single-nucleotide polymorphisms (SNPs) in two genes coding forPlasmodium falciparumdihydrofolate reductase (Pfdhfr) andP. falciparumdihydropteroate synthase (Pfdhps), targeted by pyrimethamine and sulfadoxine, respectively. The continued use of SP for intermittent preventive treatment in pregnant women in many African countries, despite SP's discontinuation as a first-line antimalarial treatment option due to high levels of drug resistance, may further increase the prevalence of SP-resistant paras
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5

Winstanley, P. A., E. K. Mberu, I. S. Szwandt, A. M. Breckenridge, and W. M. Watkins. "In vitro activities of novel antifolate drug combinations against Plasmodium falciparum and human granulocyte CFUs." Antimicrobial Agents and Chemotherapy 39, no. 4 (1995): 948–52. http://dx.doi.org/10.1128/aac.39.4.948.

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The potency of antimalarial dihydrofolate reductase inhibitors, alone and in synergistic combination with dihydropteroate synthetase inhibitors, against the Kenyan K39 strain of Plasmodium falciparum (pyrimethamine resistant) and against normal replicating human bone marrow cells in in vitro culture has been studied. Therapeutic indices and rank order of synergistic potency were derived. Trimethoprim, pyrimethamine, and the quinazolines WR159412 and WR158122 had the smallest therapeutic indices (1.39, 4.38, 2.56, and 90.0, respectively), while the three triazines clociguanil, WR99210, and chlo
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Abugri, James, Felix Ansah, Kwaku P. Asante, Comfort N. Opoku, Lucas A. Amenga-Etego, and Gordon A. Awandare. "Prevalence of chloroquine and antifolate drug resistance alleles in Plasmodium falciparum clinical isolates from three areas in Ghana." AAS Open Research 1 (December 3, 2018): 1. http://dx.doi.org/10.12688/aasopenres.12825.2.

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Background: The emergence and spread of resistance in Plasmodium falciparum to chloroquine (CQ) necessitated the change from CQ to artemisinin-based combination therapies (ACTs) as first-line drug for the management of uncomplicated malaria in Ghana in 2005. Sulphadoxine-pyrimethamine (SP) which was the second line antimalarial drug in Ghana, was now adopted for intermittent preventive treatment of malaria in pregnancy (IPTp). Methods: To examine the prevalence of molecular markers associated with CQ and antifolate drug resistance in Ghana, we employed restriction fragment length polymorphism
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7

Talawanich, Yuwadee, Sumalee Kamchonwongpaisan, Worachart Sirawaraporn, and Yongyuth Yuthavong. "Use of bacterial surrogates as a tool to explore antimalarial drug interaction: Synergism between inhibitors of malarial dihydrofolate reductase and dihydropteroate synthase." Acta Tropica 149 (September 2015): 64–69. http://dx.doi.org/10.1016/j.actatropica.2015.05.011.

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8

Pearce, Richard J., Chris Drakeley, Daniel Chandramohan, Frank Mosha, and Cally Roper. "Molecular Determination of Point Mutation Haplotypes in the Dihydrofolate Reductase and Dihydropteroate Synthase of Plasmodium falciparum in Three Districts of Northern Tanzania." Antimicrobial Agents and Chemotherapy 47, no. 4 (2003): 1347–54. http://dx.doi.org/10.1128/aac.47.4.1347-1354.2003.

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ABSTRACT The antimalarial combination of sulfadoxine and pyrimethamine (SP) was introduced as first-line treatment for uncomplicated malaria in Tanzania during 2001 following 18 years of second-line use. The genetic determinants of in vitro resistance to the two drugs individually are shown to be point mutations at seven sites in the dihydrofolate reductase gene (dhfr) conferring resistance to pyrimethamine and five sites in the dihydropteroate synthase (dhps) gene conferring resistance to sulfadoxine. Different combinations of mutations within each gene confer differing degrees of insensitivi
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9

Karema, Corine, Mallika Imwong, Caterina I. Fanello, et al. "Molecular Correlates of High-Level Antifolate Resistance in Rwandan Children with Plasmodium falciparum Malaria." Antimicrobial Agents and Chemotherapy 54, no. 1 (2009): 477–83. http://dx.doi.org/10.1128/aac.00498-09.

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ABSTRACT Antifolate drugs have an important role in the treatment of malaria. Polymorphisms in the genes encoding the dihydrofolate reductase and dihydropteroate synthetase enzymes cause resistance to the antifol and sulfa drugs, respectively. Rwanda has the highest levels of antimalarial drug resistance in Africa. We correlated the efficacy of chlorproguanil-dapsone plus artesunate (CPG-DDS+A) and amodiaquine plus sulfadoxine-pyrimethamine (AQ+SP) in children with uncomplicated malaria caused by Plasmodium falciparum parasites with p fdhfr and p fdhps mutations, which are known to confer redu
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10

Lumb, Vanshika, Manoj K. Das, Neeru Singh, Vas Dev, Wajihullah Khan, and Yagya D. Sharma. "Multiple Origins of Plasmodium falciparum Dihydropteroate Synthetase Mutant Alleles Associated with Sulfadoxine Resistance in India." Antimicrobial Agents and Chemotherapy 55, no. 6 (2011): 2813–17. http://dx.doi.org/10.1128/aac.01151-10.

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ABSTRACTWith the spread of chloroquine (CQ)-resistant malaria in India, sulfadoxine-pyrimethamine (SP) alone or in combination with artesunate is used as an alternative antimalarial drug. Due to continuous drug pressure, thePlasmodium falciparumparasite is exhibiting resistance to antifolates because of mutations in candidate genes dihydrofolate reductase (dhfr) and dihydropteroate synthetase (dhps). Our earlier study on flanking microsatellite markers ofdhfrmutant alleles from India had shown a single origin of the pyrimethamine resistance and some minor haplotypes which shared haplotypes wit
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Dissertations / Theses on the topic "Antimalarials Dihydropteroate Synthase"

1

Baca, Arthur Martin. "Crystal structure of dihydropteroate synthase from Mycobacterium tuberculosis /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/8079.

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