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Journal articles on the topic 'Chloroquine resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

de Bruijn, M. H. L. "Chloroquine resistance." Parasitology Today 5, no. 10 (1989): 326. http://dx.doi.org/10.1016/0169-4758(89)90125-7.

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Edaye, Sonia, Dagobert Tazoo, D. Scott Bohle, and Elias Georges. "3-Halo Chloroquine Derivatives Overcome Plasmodium falciparum Chloroquine Resistance Transporter-Mediated Drug Resistance in P. falciparum." Antimicrobial Agents and Chemotherapy 59, no. 12 (2015): 7891–93. http://dx.doi.org/10.1128/aac.01139-15.

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ABSTRACTPolymorphism in thePlasmodium falciparumchloroquine resistance transporter (PfCRT) was shown to cause chloroquine resistance. In this report, we examined the antimalarial potential of novel 3-halo chloroquine derivatives (3-chloro, 3-bromo, and 3-iodo) against chloroquine-susceptible and -resistantP. falciparum. All three derivatives inhibited the proliferation ofP. falciparum; with 3-iodo chloroquine being most effective. Moreover, 3-iodo chloroquine was highly effective at potentiating and reversing chloroquine toxicity of drug-susceptible and -resistantP. falciparum.

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3

Chen, Nanhua, Dennis E. Kyle, Cielo Pasay, et al. "pfcrt Allelic Types with Two Novel Amino Acid Mutations in Chloroquine-Resistant Plasmodium falciparum Isolates from the Philippines." Antimicrobial Agents and Chemotherapy 47, no. 11 (2003): 3500–3505. http://dx.doi.org/10.1128/aac.47.11.3500-3505.2003.

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ABSTRACT Mutations in the pfcrt and pfmdr1 genes have been associated with chloroquine resistance in Plasmodium falciparum. Ten and five mutations, respectively, have been identified in these genes from chloroquine-resistant parasites worldwide. Mutation patterns in pfcrt revealed that chloroquine resistance evolved independently in southeast Asia, South America, and Papua New Guinea. However, the evolution of chloroquine resistance in the rest of the Pacific region is unclear. In this study, we examined sequence polymorphisms in these genes in isolates from Morong, Philippines, and compared t

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4

Lim, Pharath, Sophy Chy, Frédéric Ariey, et al. "pfcrt Polymorphism and Chloroquine Resistance in Plasmodium falciparum Strains Isolated in Cambodia." Antimicrobial Agents and Chemotherapy 47, no. 1 (2003): 87–94. http://dx.doi.org/10.1128/aac.47.1.87-94.2003.

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ABSTRACT Plasmodium falciparum chloroquine resistance was first detected in Cambodia in the early sixties. Treatment with chloroquine was abandoned 20 years ago. In vitro chloroquine sensitivity monitoring indicates that all eastern Cambodian isolates were sensitive to chloroquine, whereas most isolates collected from western provinces displayed reduced susceptibility to chloroquine. This indicates that the rate of chloroquine resistance remains high and stable in this region in the absence of chloroquine pressure. Characterization of codons 72 to 78 and 218 to 220 of pfcrt revealed six distin

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5

Shafik, Sarah Heckmatt, Sashika Natasha Richards, Ben Corry, and Rowena Elizabeth Martin. "Mechanistic basis for multidrug resistance and collateral drug sensitivity conferred to the malaria parasite by polymorphisms in PfMDR1 and PfCRT." PLOS Biology 20, no. 5 (2022): e3001616. http://dx.doi.org/10.1371/journal.pbio.3001616.

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Polymorphisms in the Plasmodium falciparum multidrug resistance protein 1 (pfmdr1) gene and the Plasmodium falciparum chloroquine resistance transporter (pfcrt) gene alter the malaria parasite’s susceptibility to most of the current antimalarial drugs. However, the precise mechanisms by which PfMDR1 contributes to multidrug resistance have not yet been fully elucidated, nor is it understood why polymorphisms in pfmdr1 and pfcrt that cause chloroquine resistance simultaneously increase the parasite’s susceptibility to lumefantrine and mefloquine—a phenomenon known as collateral drug sensitivity

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6

Lehane, Adele M., and Kiaran Kirk. "Chloroquine Resistance-Conferring Mutations in pfcrt Give Rise to a Chloroquine-Associated H+ Leak from the Malaria Parasite's Digestive Vacuole." Antimicrobial Agents and Chemotherapy 52, no. 12 (2008): 4374–80. http://dx.doi.org/10.1128/aac.00666-08.

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ABSTRACT Chloroquine resistance in the malaria parasite Plasmodium falciparum is conferred by mutations in the P. falciparum chloroquine resistance transporter (PfCRT). PfCRT localizes to the membrane of the parasite's internal digestive vacuole, an acidic organelle in which chloroquine accumulates to high concentrations and exerts its toxic effect. Mutations in PfCRT are thought to reduce chloroquine accumulation in this organelle. How they do so is the subject of ongoing debate. Recently we have shown that in the presence of chloroquine there is an increased leak of H+ from the digestive vac

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7

Ridley, Robert G. "Malaria: Dissecting chloroquine resistance." Current Biology 8, no. 10 (1998): R346—R349. http://dx.doi.org/10.1016/s0960-9822(98)70218-0.

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8

Adagu, I. S., W. N. Ogala, D. J. Carucci, M. T. Duraisingh, and D. C. Warhurst. "Field chloroquine-resistance determinants." Annals of Tropical Medicine & Parasitology 91, sup1 (1997): S107—S111. http://dx.doi.org/10.1080/00034983.1997.11813248.

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9

ADAGU, I. S. "Field chloroquine resistance determinants." Annals of Tropical Medicine And Parasitology 91, no. 2 (1997): 107–12. http://dx.doi.org/10.1080/00034989761391.

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10

Ridley, R. G., W. Hofheinz, H. Matile, et al. "4-aminoquinoline analogs of chloroquine with shortened side chains retain activity against chloroquine-resistant Plasmodium falciparum." Antimicrobial Agents and Chemotherapy 40, no. 8 (1996): 1846–54. http://dx.doi.org/10.1128/aac.40.8.1846.

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We have synthesized several 4-aminoquinolines with shortened side chains that retain activity against chloroquine-resistant isolates of Plasmodium falciparum malaria (W. Hofheinz, C. Jaquet, and S. Jolidon, European patent 94116281.0, June 1995). We report here an assessment of the activities of four selected compounds containing ethyl, propyl, and isopropyl side chains. Reasonable in vitro activity (50% inhibitory concentration, < 100 nM) against chloroquine-resistant P. falciparum strains was consistently observed, and the compounds performed well in a variety of plasmodium berghei animal

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11

Millet, Julie, Marylin Torrentino-Madamet, Sandrine Alibert, et al. "Dihydroethanoanthracene Derivatives as In Vitro Malarial Chloroquine Resistance Reversal Agents." Antimicrobial Agents and Chemotherapy 48, no. 7 (2004): 2753–56. http://dx.doi.org/10.1128/aac.48.7.2753-2756.2004.

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ABSTRACT The ability of four 9,10-dihydroethanoanthracene derivatives (BG920, BG932, BG958, and BG996), as well as verapamil and promethazine, to reverse chloroquine resistance was assessed against 24 chloroquine-resistant and 10 chloroquine-susceptible strains of Plasmodium falciparum from different countries. The 9,10-dihydroethanoanthracene derivatives clearly increase chloroquine susceptibility only in chloroquine-resistant isolates.

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DAILY, J. P., C. ROBERTS, S. M. THOMAS, et al. "Prevalence of Plasmodium falciparum pfcrt polymorphisms and in vitro chloroquine sensitivity in Senegal." Parasitology 126, no. 5 (2003): 401–5. http://dx.doi.org/10.1017/s0031182003002981.

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Mutations in pfcrt K76T are associated with chloroquine resistance in Plasmodium falciparum. Previous studies of K76T mutations in Senegal reported the association of T76 with in vitro-resistant isolates, but this mutation was also prevalent in chloroquine-sensitive isolates. This suggests involvement of additional genetic loci in modulating chloroquine resistance. Additional pfcrt polymorphisms at codons A220S, Q271E, N326S and R371I have been found in chloroquine-resistant isolates. We wanted to test if sequential acquisition of mutations at these codons leads to in vitro chloroquine resista

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13

van Schalkwyk, Donelly A., Jason C. Walden, and Peter J. Smith. "Reversal of Chloroquine Resistance inPlasmodium falciparum Using Combinations of Chemosensitizers." Antimicrobial Agents and Chemotherapy 45, no. 11 (2001): 3171–74. http://dx.doi.org/10.1128/aac.45.11.3171-3174.2001.

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ABSTRACT Research into chloroquine resistance reversal in Plasmodium falciparum has revealed a widespread range of functionally and structurally diverse chemosensitizers. However, nearly all of these chemosensitizers reverse resistance optimally only at concentrations that are toxic to humans. Verapamil, desipramine, and trifluoperazine were shown to potentiate chloroquine accumulation in a chloroquine-resistant (CQr) strain of P. falciparum, while progesterone, ivermectin, and cyclosporin A were not shown to potentiate chloroquine accumulation. The simultaneous use of two or even three of the

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14

Martin, R. E., R. V. Marchetti, A. I. Cowan, S. M. Howitt, S. Broer, and K. Kirk. "Chloroquine Transport via the Malaria Parasite's Chloroquine Resistance Transporter." Science 325, no. 5948 (2009): 1680–82. http://dx.doi.org/10.1126/science.1175667.

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15

Crandall, Ian, Jeffrey Charuk, and Kevin C. Kain. "Nonylphenolethoxylates as Malarial Chloroquine Resistance Reversal Agents." Antimicrobial Agents and Chemotherapy 44, no. 9 (2000): 2431–34. http://dx.doi.org/10.1128/aac.44.9.2431-2434.2000.

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ABSTRACT Malaria-associated morbidity and mortality are increasing because of widespread resistance to one of the safest and least expensive antimalarials, chloroquine. The availability of an inexpensive agent that is capable of reversing chloroquine resistance would have a major impact on malaria treatment worldwide. The interaction of nonylphenolethoxylates (NPEs, commercially available synthetic surfactants) with drug-resistant Plasmodium falciparum was examined to determine if NPEs inhibited the growth of the parasites and if NPEs could sensitize resistant parasites to chloroquine. NPEs in

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Amin, Md Nurul, Mahmuda Yasmin, Marufa Zerin Akhtar, and Chowdhury Rafiqul Ahsan. "Molecular Pattern of Anti-malarial Drug Resistance of Plasmodium falciparum in Bangladeshi Troops Working in Endemic Areas of Bangladesh and Africa." Bangladesh Journal of Microbiology 37, no. 1 (2020): 1–6. http://dx.doi.org/10.3329/bjm.v37i1.51202.

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Members of Bangladesh Armed Forces work in two different malaria endemic area, Chittagong Hill Tracts (CHT) in Bangladesh and Sub-Saharan countries in Africa. This under-recognized group remained unexplored for long in respect to drug resistant falciparum malaria they usually suffer from. In this study, a total of 252 ‘dried blood samples on filter paper’ were collected between November 2014 and February 2016, from Plasmodium falciparum positive Bangladeshi troops working in Chittagong Hill Tracts (CHT), Bangladesh and five Sub Saharan African Countries namely, Central African Republic (CAR),

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17

Skrzypek, Ruth, and Richard Callaghan. "The “pushmi-pullyu” of resistance to chloroquine in malaria." Essays in Biochemistry 61, no. 1 (2017): 167–75. http://dx.doi.org/10.1042/ebc20160060.

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Malarial infection continues to impart devastating health problems in the developing world. Treatment of malaria has involved chemotherapy since 168 BC, with the most prevalent and successful forms using plant alkaloids. Perhaps the greatest treatment success against malaria was by chloroquine, a synthetic derivative of the quinines found in the Cinchona tree bark. Chloroquine is able to kill parasites by interfering with haem metabolism in the parasite’s digestive vacuole. The widespread use of chloroquine predictably resulted in the development of drug-resistant malaria and the most highly i

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18

Ibraheem, Zaid O., Roslaini Abd Majid, Hasidah Mohd Sidek, et al. "In Vitro Antiplasmodium and Chloroquine Resistance Reversal Effects of Andrographolide." Evidence-Based Complementary and Alternative Medicine 2019 (December 13, 2019): 1–16. http://dx.doi.org/10.1155/2019/7967980.

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The emergence of drug-resistant strains of Plasmodium falciparum is the worst catastrophe that has ever confronted the dedicated efforts to eradicate malaria. This urged for searching other alternatives or sensitizers that reverse chloroquine resistance. In this experiment, the potential of andrographolide to inhibit plasmodial growth and reverse CQ resistance was tested in vitro using the SYBRE green-1-based drug sensitivity assay and isobologram technique, respectively. Its safety level toward mammalian cells was screened as well against Vero cells and RBCs using MTT-based drug sensitivity a

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19

Alecrim, Maria das Graças C., Wilson Alecrim, and Vanize Macêdo. "Plasmodium vivax resistance to chloroquine (R2) and mefloquine (R3) in Brazilian Amazon region." Revista da Sociedade Brasileira de Medicina Tropical 32, no. 1 (1999): 67–68. http://dx.doi.org/10.1590/s0037-86821999000100013.

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We report for the first time a patient with malaria due to Plasmodium vivax who showed R2 resistance to chloroquine and R3 resistance to mefloquine in the Brazilian Amazon region based on WHO clinical criteria for diagnosis of malaria resistance. Failure was observed with unsupervised oral chloroquine, chloroquine under rigorous supervision and mefloquine in the same scheme. Finally, the patient was cured with oral artesunate.

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&NA;. "pfcrt mutations confer chloroquine resistance." Inpharma Weekly &NA;, no. 1362 (2002): 15. http://dx.doi.org/10.2165/00128413-200213620-00031.

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21

Airede, Abdulkareem I. "Congenital malaria with chloroquine resistance." Annals of Tropical Paediatrics 11, no. 3 (1991): 267–69. http://dx.doi.org/10.1080/02724936.1991.11747512.

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22

Collignon, P. "Chloroquine Resistance in Plasmodium vlvax." Journal of Infectious Diseases 164, no. 1 (1991): 222–23. http://dx.doi.org/10.1093/infdis/164.1.222.

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23

Rieckmann, K. H., D. R. Davis, and D. C. Hutton. "PLASMODIUM VIVAX RESISTANCE TO CHLOROQUINE?" Lancet 334, no. 8673 (1989): 1183–84. http://dx.doi.org/10.1016/s0140-6736(89)91792-3.

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24

Baird, J. Kevin. "Chloroquine Resistance in Plasmodium vivax." Antimicrobial Agents and Chemotherapy 48, no. 11 (2004): 4075–83. http://dx.doi.org/10.1128/aac.48.11.4075-4083.2004.

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25

Frean, John. "Pfmdr1 gene and chloroquine resistance." Transactions of the Royal Society of Tropical Medicine and Hygiene 92, no. 1 (1998): 123. http://dx.doi.org/10.1016/s0035-9203(98)90986-5.

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Basco, Leonardo K., Pascal Ringwald, Auguste Bilongo Manéné, and Jacques Chandenier. "False chloroquine resistance in Africa." Lancet 350, no. 9072 (1997): 224. http://dx.doi.org/10.1016/s0140-6736(05)62397-5.

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27

Lehane, Adele M., Donelly A. van Schalkwyk, Stephanie G. Valderramos, David A. Fidock, and Kiaran Kirk. "Differential Drug Efflux or Accumulation Does Not Explain Variation in the Chloroquine Response of Plasmodium falciparum Strains Expressing the Same Isoform of Mutant PfCRT." Antimicrobial Agents and Chemotherapy 55, no. 5 (2011): 2310–18. http://dx.doi.org/10.1128/aac.01167-10.

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ABSTRACTMutant forms of thePlasmodium falciparumchloroquine resistance transporter (PfCRT) mediate chloroquine resistance by effluxing the drug from the parasite's digestive vacuole, the acidic organelle in which chloroquine exerts its parasiticidal effect. However, different parasites bearing the same mutant form of PfCRT can vary substantially in their chloroquine susceptibility. Here, we have investigated the biochemical basis for the difference in chloroquine response among transfectant parasite lines having different genetic backgrounds but bearing the same mutant form of PfCRT. Despite s

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Krogstad, D., I. Gluzman, D. Kyle, et al. "Efflux of chloroquine from Plasmodium falciparum: mechanism of chloroquine resistance." Science 238, no. 4831 (1987): 1283–85. http://dx.doi.org/10.1126/science.3317830.

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Ekong, R. M., K. J. H. Robson, D. A. Baker, and D. C. Warhurst. "Transcripts of the multidrug resistance genes in chloroquine-sensitive and chloroquine-resistant Plasmodium falciparum." Parasitology 106, no. 2 (1993): 107–15. http://dx.doi.org/10.1017/s0031182000074904.

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SUMMARYHomologues of the mammalian multidrug resistance gene have been identified in isolates and clones of Plasmodium falciparum and designated pfmdr1 and pfmdr2. Mutations in pfmdr1 have been associated with chloroquine resistance but confirmation could not be obtained in a genetic cross. We have examined the copy number and expression of pfmdr1 and pfmdr2 in chloroquine-sensitive and -resistant P. falciparum and have found no relationship between the copy number of either gene and chloroquine resistance. However, a marked correlation was seen between levels of mRNA transcribed for each gene

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30

Hunt, P. "Chloroquine resistance in Plasmodium chabaudi: are chloroquine-resistance transporter (crt) and multi-drug resistance (mdr1) orthologues involved?" Molecular and Biochemical Parasitology 133, no. 1 (2004): 27–35. http://dx.doi.org/10.1016/j.molbiopara.2003.08.010.

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FRANCO, YESENIA L., CHRISTINE KHAN, and SIHEM AIT-OUDHIA. "Pharmacodynamic Modeling Identifies Synergistic Interaction Between Chloroquine and Trastuzumab in Refractory HER2- positive Breast Cancer Cells." Cancer Diagnosis & Prognosis 3, no. 2 (2023): 175–82. http://dx.doi.org/10.21873/cdp.10198.

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Background/Aim: Despite improvements in HER2-positive breast cancer (BC) patients’ outcomes with trastuzumab, the occurrence of intrinsic or acquired resistance presents a clinical challenge. Here, we quantitatively assess the combinatorial effects of chloroquine, an autophagy inhibitor, with trastuzumab on JIMT-1 cells, a HER2-positive BC cell-line primarily resistant to trastuzumab. Materials and Methods: The temporal changes in JIMT-1 cellular viability were assessed using the CCK-8 kit, where JIMT-1 cells were exposed for 72-h to trastuzumab (0.007-17.19 μM) or chloroquine (5-50 μM) as sin

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Ehrhardt, Stephan, Teunis A. Eggelte, Sarah Kaiser, et al. "Large-Scale Surveillance of Plasmodium falciparum crt(K76T) in Northern Ghana." Antimicrobial Agents and Chemotherapy 51, no. 9 (2007): 3407–9. http://dx.doi.org/10.1128/aac.00179-07.

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ABSTRACT Surveillance of Plasmodium falciparum crt(K76T) [Pfcrt(K76T)], a resistance marker of chloroquine and, limitedly, amodiaquine, in >4,000 children in northern Ghana revealed a prevalence of 79%. Pfcrt(K76T) was heterogeneously distributed and associated with chloroquine use, low parasitemia, and the dry season. Widespread chloroquine resistance challenges the regional life span of amodiaquine as a partner drug in artemisinin combination therapy.

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33

Evlakhov, V. I., I. Z. Poyassov, and T. P. Berezina. "The Impact of T- and L-Type Calcium Channels Blockers on Pulmonary Microhemodynamics in Experimental Model of Pulmonary Thromboembolism." Российский физиологический журнал им И М Сеченова 109, no. 5 (2023): 643–55. http://dx.doi.org/10.31857/s0869813923050035.

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In acute experiments on isolated perfused rabbit’s Сhinchilla lungs changes of pulmonary microhemodynamics were studied in case of pulmonary embolization in the comparison group and after pretreatment with ethosuximide, mibefradil, chloroquine and nifedipine. In response to administration of T-type Ca2+-channel blockers ethosuximide and mibefradil, pulmonary artery pressure, precapillary and pulmonary vascular resistance decreased approximately to the same extent, postcapillary resistance did not change. After pretreatment with chloroquine pulmonary artery pressure, precapillary and pulmonary

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Nzila, Alexis, Eddy Mberu, Pat Bray, et al. "Chemosensitization of Plasmodium falciparum by Probenecid In Vitro." Antimicrobial Agents and Chemotherapy 47, no. 7 (2003): 2108–12. http://dx.doi.org/10.1128/aac.47.7.2108-2112.2003.

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ABSTRACT Resistance to drugs can result from changes in drug transport, and this resistance can sometimes be overcome by a second drug that modifies the transport mechanisms of the cell. This strategy has been exploited to partly reverse resistance to chloroquine in Plasmodium falciparum. Studies with human tumor cells have shown that probenecid can reverse resistance to the antifolate methotrexate, but the potential for reversal of antifolate resistance has not been studied in P. falciparum. In the present study we tested the ability of probenecid to reverse antifolate resistance in P. falcip

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35

Domarle, O., G. Blampain, H. Agnaniet, et al. "In Vitro Antimalarial Activity of a New Organometallic Analog, Ferrocene-Chloroquine." Antimicrobial Agents and Chemotherapy 42, no. 3 (1998): 540–44. http://dx.doi.org/10.1128/aac.42.3.540.

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ABSTRACT The in vitro activities of new organometallic chloroquine analogs, based on 4-amino-quinoleine compounds bound to a molecule of ferrocene, were evaluated against chloroquine-susceptible, chloroquine-intermediate, and chloroquine-resistant, culture-adaptedPlasmodium falciparum lineages by a proliferation test. One of the ferrocene analogs totally restored the activity of chloroquine against chloroquine-resistant parasites. This compound, associated with tartaric acid for better solubility, was highly effective. The role of the ferrocene in reversing chloroquine resistance is discussed,

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Warring, Sally D., Zhicheng Dou, Vern B. Carruthers, Geoffrey I. McFadden, and Giel G. van Dooren. "Characterization of the Chloroquine Resistance Transporter Homologue in Toxoplasma gondii." Eukaryotic Cell 13, no. 11 (2014): 1360–70. http://dx.doi.org/10.1128/ec.00027-14.

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ABSTRACT Mutations in the Plasmodium falciparum chloroquine resistance transporter ( Pf CRT) protein confer resistance to the antimalarial drug chloroquine. Pf CRT localizes to the parasite digestive vacuole, the site of chloroquine action, where it mediates resistance by transporting chloroquine out of the digestive vacuole. Pf CRT belongs to a family of transporter proteins called the chloroquine resistance transporter family. CRT family proteins are found throughout the Apicomplexa, in some protists, and in plants. Despite the importance of Pf CRT in drug resistance, little is known about t

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Cowman, A. F., S. Karcz, D. Galatis, and J. G. Culvenor. "A P-glycoprotein homologue of Plasmodium falciparum is localized on the digestive vacuole." Journal of Cell Biology 113, no. 5 (1991): 1033–42. http://dx.doi.org/10.1083/jcb.113.5.1033.

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Resistance to chloroquine in Plasmodium falciparum bears a striking similarity to the multi-drug resistance (MDR) phenotype of mammalian tumor cells which is mediated by overexpression of P-glycoprotein. We show here that the P. falciparum homologue of the P-glycoprotein (Pgh1) is a 160,000-D protein that is expressed throughout the asexual erythrocytic life cycle of the parasite. Quantitative immunoblotting analysis has shown that the protein is expressed at approximately equal levels in chloroquine resistant and sensitive isolates suggesting that overexpression of Pgh1 is not essential for c

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Soniran, Olajoju T., Olufunmilayo A. Idowu, and Segun S. Ogundapo. "Factors associated with high prevalence of PfCRT K76T mutation in Plasmodium falciparum isolates in a rural and urban community of Ogun State, Nigeria." MalariaWorld Journal 8, no. 13 (2017): 1–6. https://doi.org/10.5281/zenodo.10777256.

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<strong>Background.</strong> Antimalarial drug-resistant <em>Plasmodium falciparum</em> strains have been a major obstacle to the global efforts of controlling and eliminating malaria. The hope of reintroducing chloroquine for the treatment of uncomplicated malaria follows recent reports on decreases in the prevalence of chloroquine-resistant <em>P. falciparum</em> in several countries and recently, its total disappearance in Malawi and Zambia. In Nigeria, the discontinued use of chloroquine for malaria treatment was officially announced in 2005. A few available reports have shown a persistent

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Emerson, Lyndal R., Martin E. Nau, Rodger K. Martin, Dennis E. Kyle, Maryanne Vahey, and Dyann F. Wirth. "Relationship between Chloroquine Toxicity and Iron Acquisition in Saccharomyces cerevisiae." Antimicrobial Agents and Chemotherapy 46, no. 3 (2002): 787–96. http://dx.doi.org/10.1128/aac.46.3.787-796.2002.

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ABSTRACT Chloroquine is one of the most effective antimalarials, but resistance to it is becoming widespread. However, we do not fully understand either the drug's mode of action or the mechanism of resistance. In an effort to expand our understanding of the mechanism of action and resistance associated with chloroquine, we used Saccharomyces cerevisiae as a model eukaryotic system. To aid in the discovery of potential drug targets we applied the transcriptional profiling method to identify genes transcriptionally responsive to chloroquine treatment in S. cerevisiae. Among the genes that were

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K.A., Obaniyi, Sunday O.J., Said R.O., Luka J., and Salau-Deen B.M. "CROSS-RESISTANCE BETWEEN SULFADOXINE-PYRIMETHAMINE AND OTHER ANTIMALARIAL DRUGS: A STUDY OF PREGNANT WOMEN IN ILORIN KWARA STATE NIGERIA." International Journal of Advanced Research 13, no. 03 (2025): 1107–15. https://doi.org/10.21474/ijar01/20657.

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Antimalarial resistance remains a serious problem in malaria-endemic regions, particularly in pregnant women, who are likely to suffer from complications. The research evaluates the resistance to commonly employed antimalarial medications-Chloroquine, Artesunate, and Arthether-among pregnant women in Ilorin, Nigeria, at different trimesters and during delivery. Cross-sectional study was conducted among 253 pregnant women presenting at antenatal clinics within Ilorin, Kwara State. Venous blood from study participants in different pregnancy stages (first trimester, second trimester, third trimes

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Guantai, Eric, and Kelly Chibale. "Chloroquine Resistance: Proposed Mechanisms and Countermeasures." Current Drug Delivery 7, no. 4 (2010): 312–23. http://dx.doi.org/10.2174/156720110793360577.

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42

&NA;. "Unravelling the mechanism of chloroquine resistance." Inpharma Weekly &NA;, no. 1121 (1998): 4. http://dx.doi.org/10.2165/00128413-199811210-00004.

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&NA;. "Reversing chloroquine resistance 'a realistic possibility'." Inpharma Weekly &NA;, no. 1281 (2001): 2. http://dx.doi.org/10.2165/00128413-200112810-00001.

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Waters, Andrew P. "Chloroquine resistance—discovering the missing link?" Nature Medicine 4, no. 1 (1998): 23–24. http://dx.doi.org/10.1038/nm0198-023.

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Krogstad, D. J., P. H. Schlesinger, and B. L. Herwaldt. "Antimalarial agents: mechanism of chloroquine resistance." Antimicrobial Agents and Chemotherapy 32, no. 6 (1988): 799–801. http://dx.doi.org/10.1128/aac.32.6.799.

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Warhurst, D. C. "Mechanism of chloroquine resistance in malaria." Parasitology Today 4, no. 8 (1988): 211–13. http://dx.doi.org/10.1016/0169-4758(88)90160-3.

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Krungkrai, J. "Mechanisms of chloroquine action and resistance." Chulalongkorn Medical Journal 38, no. 6 (1994): 307–14. http://dx.doi.org/10.58837/chula.cmj.38.6.2.

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Frappier, F., A. Jossang, J. Soudon, et al. "Bisbenzylisoquinolines as modulators of chloroquine resistance in Plasmodium falciparum and multidrug resistance in tumor cells." Antimicrobial Agents and Chemotherapy 40, no. 6 (1996): 1476–81. http://dx.doi.org/10.1128/aac.40.6.1476.

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Abstract:

Ten naturally occurring bisbenzylisoquinolines (BBIQ) and two dihydro derivatives belonging to five BBIQ subgroups were evaluated in vitro for their ability to inhibit Plasmodium falciparum growth and, in drug combination, to reverse the resistance to chloroquine of strain FcB1. The same alkaloids were also assessed in vitro for their potentiating activity against vinblastine with the multidrug-resistant clone CCRF-CEM/VLB, established from lymphoblastic acute leukemia. Three of the BBIQ tested had 50% inhibitory concentrations of less than 1 microM. The most potent antimalarial agent was cocs

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Subramony, Hariharan, Noppadon Tangpukdee, Srivicha Krudsood, Kittiyod Poovorawan, Sant Muangnoicharoen, and Polrat Wilairatana. "Evaluation of Efficacy of Chloroquine for Plasmodium Vivax Infection Using Parasite Clearance Times: A 10-Year Study and Systematic Review." Annals of the Academy of Medicine, Singapore 45, no. 7 (2016): 303–14. http://dx.doi.org/10.47102/annals-acadmedsg.v45n7p303.

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Abstract:

Introduction: Chloroquine, in combination with primaquine, is used as the firstline treatment for uncomplicated P. vivax malaria in Thailand. In view of the declining efficacy of chloroquine in many P. vivax endemic areas, the possibility of emergence of chloroquine-resistant P. vivax in Thailand is a concern. The aim of this study was to assess the trends in therapeutic efficacy of chloroquine and primaquine for the treatment of uncomplicated P. vivax malaria and to assess the utility of parasite clearance times as a measure of efficacy. Materials and Methods: This study consisted of: 1) revi

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Heymann, David L., Richard W. Steketee, Jack J. Wirima, Deborah A. McFarland, Charles O. Khoromana, and Carlos C. Campbell. "Antenatal chloroquine chemoprophylaxis in Malawi: chloroquine resistance, compliance, protective efficacy and cost." Transactions of the Royal Society of Tropical Medicine and Hygiene 84, no. 4 (1990): 496–98. http://dx.doi.org/10.1016/0035-9203(90)90011-3.

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