Relevant bibliographies by topics / Chloroquine Malaria Drug resistance

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Academic literature on the topic 'Chloroquine Malaria Drug resistance'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Chloroquine Malaria Drug resistance"

1

Skrzypek, Ruth, and Richard Callaghan. "The “pushmi-pullyu” of resistance to chloroquine in malaria." Essays in Biochemistry 61, no. 1 (February 28, 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 implicated resistance mediators are the transporter proteins P-glycoprotein (P-gp) homologue 1 (P-gh1) and Plasmodium falciparum chloroquine-resistance transporter (PfCRT), which reside on the parasite’s digestive vacuole. The presence of PfCRT and P-gh1 on the vacuole membrane is analogous to the two-headed fictional creature known as the “Pushmi-Pullyu”. P-gh1 (Pushmi) increases influx of chloroquine into the vacuole, while PfCRT (Pullmi) causes efflux of chloroquine from the vacuole. This review describes how drug-resistant malarial parasites co-ordinate chloroquine distribution through adaptive mutations to promote their survival in the presence of this cytotoxic drug.
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Yusuf, Yenni. "ANTI-MALARIAL DRUG RESISTANCE." Majalah Kedokteran Andalas 37, no. 1 (May 3, 2015): 64. http://dx.doi.org/10.22338/mka.v37.i1.p64-69.2014.

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AbstrakTujuan studi ini adalah untuk menjelaskan mekanisme resistensi parasit malaria danusaha-usaha yang dapat dilakukan untuk menghadapi munculnya strain parasit yangresisten terhadap artemisinin. Metode yang digunakan adalah studi kepustakaan. ResistensiP.falciparum terhadap obat-obat anti malaria disebabkan oleh perubahan spontan yangterjadi pada beberapa gen seperti P.falciparum multi drug resistance1 (Pfmdr1), P.falciparumchloroquine transporter (Pfcrt), P.falciparum dihydropteroate synthase (Pfdhps), P.falciparumdihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistance-associated proteins(Pfmrp). Penyebaran resistensi tersebut dipengaruhi oleh tingkat transmisi di sebuah wilayah.WHO telah menjalankan usaha untuk menanggulangi penyebaran resistensi tersebut misalnyadengan merekomendasikan penghentian monoterapi artemisinin, dan pemberian anti malariasetelah konfirmasi laboratorium. Selain itu, perlu adanya penggunaan obat kombinasi, produksirejimen dosis tetap, dan pengembangan obat anti malaria baru. Kesimpulan dari hasil studiini ialah munculnya malaria resisten terhadap artemisinin akan menghambat usaha eradikasimalaria karena itu diperlukan usaha-usaha untuk menanggulanginya.AbstractThe objective of this study was to describe the development of anti-malarial drug resistanceof the parasites and the efforts taken to contain the emergence of artemisinin resistant malaria.This was a literature study. The development of resistance to anti-malarial drugs are due tospontaneous changes in certain genes such as of P.falciparum multi drug resistance1 (Pfmdr1),P.falciparum chloroquine resistance transporter (Pfcrt), P.falciparum dihydropteroate synthase(Pfdhps), P.falciparum dihydrofolate reductase (Pfdhfr), and P.falciparum multidrug resistanceassociatedproteins (Pfmrp). The spread of the resistance depends on the transmission ratewithin each area. WHO has established a global plan to contain the spread of this resistance,such as recommendation to withdraw artemisinin-based monotherapies and administrationof treatment after laboratory confirmation. In addition, administration of anti-malarial drugcombination, production of fixed dose regimen and development of new drugs are necessary.The Conclusion is emergence of artemisinin resistant malaria will threaten malaria eradicationthus some efforts are necessarily needed to contain it.Afiliasi penulis: Bagian Parasitologi Fakultas Kedokteran Universitas Hasanudin
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Mixson-Hayden, Tonya, Vidhan Jain, Andrea M. McCollum, Amanda Poe, Avinash C. Nagpal, Aditya P. Dash, Jonathan K. Stiles, Venkatachalam Udhayakumar, and Neeru Singh. "Evidence of Selective Sweeps in Genes Conferring Resistance to Chloroquine and Pyrimethamine in Plasmodium falciparum Isolates in India." Antimicrobial Agents and Chemotherapy 54, no. 3 (December 28, 2009): 997–1006. http://dx.doi.org/10.1128/aac.00846-09.

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ABSTRACT Treatment of Plasmodium falciparum is complicated by the emergence and spread of parasite resistance to many of the first-line drugs used to treat malaria. Antimalarial drug resistance has been associated with specific point mutations in several genes, suggesting that these single nucleotide polymorphisms can be useful in tracking the emergence of drug resistance. In India, P. falciparum infection can manifest itself as asymptomatic, mild, or severe malaria, with or without cerebral involvement. We tested whether chloroquine- and antifolate drug-resistant genotypes would be more commonly associated with cases of cerebral malaria than with cases of mild malaria in the province of Jabalpur, India, by genotyping the dhps, dhfr, pfmdr-1, and pfcrt genes using pyrosequencing, direct sequencing, and real-time PCR. Further, we used microsatellites surrounding the genes to determine the origins and spread of the drug-resistant genotypes in this area. Resistance to chloroquine was essentially fixed, with 95% of the isolates harboring the pfcrt K76T mutation. Resistant genotypes of dhfr, dhps, and pfmdr-1 were found in 94%, 17%, and 77% of the isolates, respectively. Drug-resistant genotypes were equally likely to be associated with cerebral malaria as with mild malaria. We found evidence of a selective sweep in pfcrt and, to a lesser degree, in dhfr, indicating high levels of resistance to chloroquine and evolving resistance to pyrimethamine. Microsatellites surrounding pfcrt indicate that the resistant genotypes (SVMNT) were most similar to those found in Papua New Guinea.
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Shujatullah, Fatima, Haris M. Khan, Abida Khatoon, Parvez A. Khan, and Mohammad Ashfaq. "In Vitro Chloroquine Resistance in Plasmodium falciparum Isolates from Tertiary Care Hospital." Malaria Research and Treatment 2012 (September 24, 2012): 1–4. http://dx.doi.org/10.1155/2012/538481.

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Chloroquine (CQ) has been the mainstay of treatment of malaria for decades. This cost-effective and safe drug has become ineffective for treatment of falciparum malaria in many parts of the world due to development of resistance by the parasite. In addition CQ is not gametocytocidal for P. falciparum and thus cannot block transmission. The extent of problem of chloroquine resistance in P. falciparum is increasing every year. The study was done in period of 2 years. A total of 5653 specimens were examined for malarial infection by employing different diagnostic modalities. Four hundred and thirty-five were found to be positive for P. falciparum by using different diagnostic techniques. All positive specimens were cultured on RPMI 1640 medium; only 108 were found to be culture positive. Sensitivity of isolates to chloroquine was done using Mark III WHO sensitivity plates. The prevalence of malaria infection was found 9.54% in 2010. There were schizont formation at 8 pmol/liter or more of chloroquine concentration in 26 isolates. The emergence of chloroquine (CQ) resistance pattern in Aligarh isolates increases. Antimalarial agents should be used with caution; monotherapies should be avoided.
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Wicht, Kathryn J., Sachel Mok, and David A. Fidock. "Molecular Mechanisms of Drug Resistance in Plasmodium falciparum Malaria." Annual Review of Microbiology 74, no. 1 (September 8, 2020): 431–54. http://dx.doi.org/10.1146/annurev-micro-020518-115546.

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Understanding and controlling the spread of antimalarial resistance, particularly to artemisinin and its partner drugs, is a top priority. Plasmodium falciparum parasites resistant to chloroquine, amodiaquine, or piperaquine harbor mutations in the P. falciparum chloroquine resistance transporter (PfCRT), a transporter resident on the digestive vacuole membrane that in its variant forms can transport these weak-base 4-aminoquinoline drugs out of this acidic organelle, thus preventing these drugs from binding heme and inhibiting its detoxification. The structure of PfCRT, solved by cryogenic electron microscopy, shows mutations surrounding an electronegative central drug-binding cavity where they presumably interact with drugs and natural substrates to control transport. P. falciparum susceptibility to heme-binding antimalarials is also modulated by overexpression or mutations in the digestive vacuole membrane–bound ABC transporter PfMDR1 ( P. falciparum multidrug resistance 1 transporter). Artemisinin resistance is primarily mediated by mutations in P. falciparum Kelch13 protein (K13), a protein involved in multiple intracellular processes including endocytosis of hemoglobin, which is required for parasite growth and artemisinin activation. Combating drug-resistant malaria urgently requires the development of new antimalarial drugs with novel modes of action.
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Summers, Kelly L. "A Structural Chemistry Perspective on the Antimalarial Properties of Thiosemicarbazone Metal Complexes." Mini-Reviews in Medicinal Chemistry 19, no. 7 (March 28, 2019): 569–90. http://dx.doi.org/10.2174/1389557518666181015152657.

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Malaria is a potentially life-threatening disease, affecting approx. 214 million people worldwide. Malaria is caused by a protozoan, Plasmodium falciparum, which is transmitted through the Anopheles mosquito. Malaria treatment is becoming more challenging due to rising resistance against the antimalarial drug, chloroquine. Novel compounds that target aspects of parasite development are being explored in attempts to overcome this wide-spread problem. Anti-malarial drugs target specific aspects of parasite growth and development within the human host. One of the most effective targets is the inhibition of hematin formation, either through inhibition of cysteine proteases or through iron chelation. Metal-thiosemicarbazone (TSC) complexes have been tested for antimalarial efficacy against drug-sensitive and drug-resistant strains of P. falciparum. An array of TSC complexes with numerous transition metals, including ruthenium, palladium, and gold has displayed antiplasmodial activity. Au(I)- and Pd(II)-TSC complexes displayed the greatest potency; 4-amino-7-chloroquine moieties were also found to improve antiplasmodial activity of TSCs. Although promising metal-TSC drug candidates have been tested against laboratory strains of P. falciparum, problems arise when attempting to compare between studies. Future work should strive to completely characterize synthesized metal-TSC structures and assess antiplasmodial potency against several drug-sensitive and drugresistant strains. Future studies need to precisely determine IC50 values for antimalarial drugs, chloroquine and ferroquine, to establish accurate standard values. This will make future comparisons across studies more feasible and potentially help reveal structure-function relationships. Investigations that attempt to link drug structures or properties to antiplasmodial mechanism(s) of action will aid in the design of antimalarial drugs that may combat rising drug resistance.
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Abdulla Mohammed, Walaa Salah, Kyakonye Yasin, N. S. Mahgoub, and Muzamil Mahdi Abdel Hamid. "Cross sectional study to determine chloroquine resistance among Plasmodium falciparum clinical isolates from Khartoum, Sudan." F1000Research 7 (February 20, 2018): 208. http://dx.doi.org/10.12688/f1000research.13273.1.

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Background: Malaria continues to present a global health threat; the World Health Organization (WHO) reported 214 million cases of malaria by the year 2015 with a death rate of 438000. Sudan is endemic to malaria with over 95% of malaria cases due to Plasmodium falciparum. Chloroquine is a well-established drug in the treatment of P. falciparum malaria although its use has declined since its introduction as the drug of choice in treatment of malaria in Sudan. The mechanism of resistance has been attributed to mutations in P. falciparum Chloroquine resistance transporter gene coding for a key food vacuole proteins. In current study we aimed at verifying the genetic cause of resistance to Chloroquine in field isolates of P. falciparum. Methods: Twenty P. falciparum cases were diagnosed from East Nile hospital in Khartoum and recruited in the investigation. Nested PCR was conducted to isolate mutation region in the PfCRT gene and the amplicons were sequenced using Sanger sequencing technique (Macrogen, Soule Korea). Results: 16/20 (80%) of the field isolates contained base pair mutation of codon 76 in the pfcrt gene thus being resistant to chloroquine treatment and only 4/20 (20%) did not contain such mutation. Conclusions: High treatment failures associated with Chloroquine treatment is evident of the high prevalence of mutant strains of P. falciparum field isolates thus suggesting the reduced relevance of Chloroquine as a treatment choice in the management of P. falciparum malaria.
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Maraka, Moureen, Hoseah M. Akala, Asito S. Amolo, Dennis Juma, Duke Omariba, Agnes Cheruiyot, Benjamin Opot, et al. "A seven-year surveillance of epidemiology of malaria reveals travel and gender are the key drivers of dispersion of drug resistant genotypes in Kenya." PeerJ 8 (March 12, 2020): e8082. http://dx.doi.org/10.7717/peerj.8082.

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Malaria drug resistance is a global public health concern. Though parasite mutations have been associated with resistance, other factors could influence the resistance. A robust surveillance system is required to monitor and help contain the resistance. This study established the role of travel and gender in dispersion of chloroquine resistant genotypes in malaria epidemic zones in Kenya. A total of 1,776 individuals presenting with uncomplicated malaria at hospitals selected from four malaria transmission zones in Kenya between 2008 and 2014 were enrolled in a prospective surveillance study assessing the epidemiology of malaria drug resistance patterns. Demographic and clinical information per individual was obtained using a structured questionnaire. Further, 2 mL of blood was collected for malaria diagnosis, parasitemia quantification and molecular analysis. DNA extracted from dried blood spots collected from each of the individuals was genotyped for polymorphisms in Plasmodium falciparum chloroquine transporter gene (Pfcrt 76), Plasmodium falciparum multidrug resistant gene 1 (Pfmdr1 86 and Pfmdr1 184) regions that are putative drug resistance genes using both conventional polymerase chain reaction (PCR) and real-time PCR. The molecular and demographic data was analyzed using Stata version 13 (College Station, TX: StataCorp LP) while mapping of cases at the selected geographic zones was done in QGIS version 2.18. Chloroquine resistant (CQR) genotypes across gender revealed an association with chloroquine resistance by both univariate model (p = 0.027) and by multivariate model (p = 0.025), female as reference group in both models. Prior treatment with antimalarial drugs within the last 6 weeks before enrollment was associated with carriage of CQR genotype by multivariate model (p = 0.034). Further, a significant relationship was observed between travel and CQR carriage both by univariate model (p = 0.001) and multivariate model (p = 0.002). These findings suggest that gender and travel are significantly associated with chloroquine resistance. From a gender perspective, males are more likely to harbor resistant strains than females hence involved in strain dispersion. On the other hand, travel underscores the role of transport network in introducing spread of resistant genotypes, bringing in to focus the need to monitor gene flow and establish strategies to minimize the introduction of resistance strains by controlling malaria among frequent transporters.
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Bushman, Mary, Lindsay Morton, Nancy Duah, Neils Quashie, Benjamin Abuaku, Kwadwo A. Koram, Pedro Rafael Dimbu, et al. "Within-host competition and drug resistance in the human malaria parasite Plasmodium falciparum." Proceedings of the Royal Society B: Biological Sciences 283, no. 1826 (March 16, 2016): 20153038. http://dx.doi.org/10.1098/rspb.2015.3038.

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Infections with the malaria parasite Plasmodium falciparum typically comprise multiple strains, especially in high-transmission areas where infectious mosquito bites occur frequently. However, little is known about the dynamics of mixed-strain infections, particularly whether strains sharing a host compete or grow independently. Competition between drug-sensitive and drug-resistant strains, if it occurs, could be a crucial determinant of the spread of resistance. We analysed 1341 P. falciparum infections in children from Angola, Ghana and Tanzania and found compelling evidence for competition in mixed-strain infections: overall parasite density did not increase with additional strains, and densities of individual chloroquine-sensitive (CQS) and chloroquine-resistant (CQR) strains were reduced in the presence of competitors. We also found that CQR strains exhibited low densities compared with CQS strains (in the absence of chloroquine), which may underlie observed declines of chloroquine resistance in many countries following retirement of chloroquine as a first-line therapy. Our observations support a key role for within-host competition in the evolution of drug-resistant malaria. Malaria control and resistance-management efforts in high-transmission regions may be significantly aided or hindered by the effects of competition in mixed-strain infections. Consideration of within-host dynamics may spur development of novel strategies to minimize resistance while maximizing the benefits of control measures.
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Neto, Zoraima, Marta Machado, Ana Lindeza, Virgílio do Rosário, Marcos L. Gazarini, and Dinora Lopes. "Treatment ofPlasmodium chabaudiParasites with Curcumin in Combination with Antimalarial Drugs: Drug Interactions and Implications on the Ubiquitin/Proteasome System." Journal of Parasitology Research 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/429736.

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Antimalarial drug resistance remains a major obstacle in malaria control. Evidence from Southeast Asia shows that resistance to artemisinin combination therapy (ACT) is inevitable. Ethnopharmacological studies have confirmed the efficacy of curcumin againstPlasmodiumspp. Drug interaction assays between curcumin/piperine/chloroquine and curcumin/piperine/artemisinin combinations and the potential of drug treatment to interfere with the ubiquitin proteasome system (UPS) were analyzed.In vivoefficacy of curcumin was studied in BALB/c mice infected withPlasmodium chabaudiclones resistant to chloroquine and artemisinin, and drug interactions were analyzed by isobolograms. Subtherapeutic doses of curcumin, chloroquine, and artemisinin were administered to mice, and mRNA was collected following treatment for RT-PCR analysis of genes encoding deubiquitylating enzymes (DUBs). Curcumin was found be nontoxic in BALB/c mice. The combination of curcumin/chloroquine/piperine reduced parasitemia to 37% seven days after treatment versus the control group’s 65%, and an additive interaction was revealed. Curcumin/piperine/artemisinin combination did not show a favorable drug interaction in this murine model of malaria. Treatment of mice with subtherapeutic doses of the drugs resulted in a transient increase in genes encoding DUBs indicating UPS interference. If curcumin is to join the arsenal of available antimalarial drugs, future studies exploring suitable drug partners would be of interest.
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Dissertations / Theses on the topic "Chloroquine Malaria Drug resistance"

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Modrzynska, Katarzyna Kinga. "Genetics of drug resistance in malaria : identification of genes conferring chloroquine and artemisinin resistance in rodent malaria parasite Plasmodium chabaudi." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/4888.

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Resistance to antimalarial drugs continues to be a major obstacle in controlling and eradicating malaria. The identification of genetic markers of resistance is vital for disease management but they can be difficult to predict before resistance arises in the field. This thesis describes an alternative approach to gene identification, combining an in vivo experimental evolution model, Linkage Group Selection (LGS) and Solexa genome re-sequencing. Here this model was used to resolve the genetic basis of chloroquine and artemisinin resistance in the rodent malaria parasite Plasmodium chabaudi. AS-30CQ is a parasite with high resistance to chloroquine and resistance to artemisinin. It was crossed with the genetically different drug-sensitive strain AJ. The resulting progeny were selected with drugs and backcrossed to the sensitive parent. Both crosses were treated with increasing concentrations of chloroquine and artemisinin. The frequency of markers from the sensitive parasite were analysed in order to characterize the signatures of drug selection. Three loci involved progressively in chloroquine resistance were identified on chromosomes 11, 3 and 2. One main locus on chromosome 2 was identified with artemisinin selection. The Solexa platform was used to re-sequence the genomes of both AS-30CQ and its sensitive progenitor, AS-sens. The differences between the two genomes were integrated with the LGS data to identify: 1) a strong candidate for the main CQresistance determinant - a putative amino acid transporter on chromosome 11 (aat1) 2) two candidates for high level chloroquine resistance on chromosome 3. and 3) a mutation in ubp1 gene on chromosome 2 that is likely to contribute to the highest level of chloroquine resistance and be main determinant of the artemisinin resistance phenotype. In addition the last section of this thesis describes two otherwise isogenic clones showing low- and high levels of chloroquine resistance were grown competitively to evaluate the effect of these mutations on parasite fitness. The highly resistant strain demonstrated a loss of fitness in relation to its more sensitive progenitor and was outcompeted in untreated and low-treated infections.
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Pokomi, Rostand Fankam. "Selection, synthesis and evaluation of novel drug-like compounds from a library of virtual compounds designed from natural products with antiplasmodial activities." University of the Western Cape, 2020. http://hdl.handle.net/11394/7950.

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Magister Pharmaceuticae - MPharm
Malaria is an infectious disease which continues to kill more than one million people every year and the African continent accounts for most of the malaria death worldwide. New classes of medicine to combat malaria are urgently needed due to the surge in resistance of the Plasmodium falciparum (the parasite that causes malaria in humans) to existing antimalarial drugs. One approach to circumvent the problem of P. falciparum resistance to antimalarial drugs could be the discovery of novel compounds with unique scaffolds and possibly new mechanisms of action. Natural products (NP) provide a wide diversity of compounds with unique scaffolds, as such, a library of virtual compounds (VC) designed from natural products with antiplasmodial activities (NAA) can be a worthy starting point.
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Gunsaru, Bornface. "Simplified Reversed Chloroquines to Overcome Malaria Resistance to Quinoline-based Drugs." PDXScholar, 2010. https://pdxscholar.library.pdx.edu/open_access_etds/400.

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Malaria is a major health problem, mainly in developing countries, and causes an estimated 1 million deaths per year. Plasmodium falciparum is the major type of human malaria parasite, and causes the most infections and deaths. Malaria drugs, like any other drugs, suffer from possible side effects and the potential for emergence of resistance. Chloroquine, which was a very effective drug, has been used since about 1945, but its use is severely limited by resistance, even though it has mild side effects, and is otherwise very efficacious. Research has shown that there are chloroquine reversal agents, molecules that can reinstate antimalarial activity of chloroquine and chloroquine-like drugs; many such reversal agents are composed of two aromatic groups linked to a hydrogen bond acceptor several bonds away. By linking a chloroquine-like molecule to a reversal agent-like molecule, it was hoped that a hybrid molecule could be made with both antimalarial and reversal agent properties. In the Peyton Lab, such hybrid "Reversed Chloroquine" molecules have been synthesized and shown to have better antimalarial activity than chloroquine against the P. falciparum chloroquine-sensitive strain D6, as well as the P. falciparum chloroquine-resistant strains Dd2 and 7G8. The work reported in this manuscript involves simplifying the reversal agent head group of the Reversed Chloroquine molecules, to a single aromatic ring instead of the two rings groups described by others; this modification retained, or even enhanced, the antimalarial activity of the parent Reversed Chloroquine molecules. Of note was compound PL154, which had IC50 values of 0.3 nM and 0.5 nM against chloroquine-sensitive D6 and chloroquine-resistant Dd2. Compound PL106 was made to increase water solubility (a requirement for bioavailability) of the simplified Reversed Chloroquine molecules. Molecular modifications inherent to PL106 were not very detrimental to the antimalarial activity, and PL106 was found to be orally available in mice infected with P. yoelli, with an ED50 value of about 5.5 mg/kg/d. Varying the linker length between the quinoline ring and the protonatable nitrogen, or between the head group and the protonatable nitrogen, did not have adverse effects on the antimalarial activities of the simplified Reversed Chloroquine molecules, in accord with the trends observed for the original design of Reversed Chloroquine molecules as found from previous studies in the Peyton Lab. The simplified Reversed Chloroquine molecules even tolerated aliphatic head groups (rather than the original design which specified aromatic rings), showing that major modifications could be made on the Reversed Chloroquine molecules without major loss in activity. A bisquinoline compound, PL192, was made that contained secondary nitrogens at position 4 of the quinoline ring (PL192 is a modification of piperaquine, a known antimalarial drug that contains tertiary nitrogens at position 4 of the quinoline ring); this compound was more potent than piperaquine which had an IC50 value of 0.7 nM against CQS D6 and an IC50 of 1.5 nM against CQR Dd2, PL192 had IC50 values of 0.63 nM against chloroquine sensitive D6 and 0.02 nM against chloroquine resistant Dd2. Finally, the mechanism of action of these simplified "Reversed Chloroquines" was evaluated; it was found that the simplified "Reversed Chloroquines" behaved like chloroquine in inhibiting β-hematin formation and in heme binding. However, the simplified "Reversed Chloroquines" were found to inhibit chloroquine transport for chloroquine resistant P. falciparum chloroquine resistance transporter expressed in Xenopus oocytes to a lesser extant than the classical reversal agent verapamil. From these studies it was noted that the simplified "Reversed Chloroquines" may not behave as well as classical reversal agents would in restoring chloroquine efficacy, but they are very potent, and so could be a major step in developing drug candidates against malaria.
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Bray, Patrick Gerrard. "Plasmodium falciparum : studies on the mechanism of chloroquine resistance and its reversal." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316597.

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Ursing, Johan. "Plasmodium Falciparum response to chloroquine and artemisinin based combination therapy (Act) in Guinea Bissau." Stockholm : Karolinska institutet, 2009. http://diss.kib.ki.se/2009/978-91-7409-695-8/.

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Liebman, Katherine May. "New 4-Aminoquinoline Compounds to Reverse Drug Resistance in P. falciparum Malaria, and a Survey of Early European Antimalarial Treatments." PDXScholar, 2014. http://pdxscholar.library.pdx.edu/open_access_etds/2114.

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Intermittent fevers caused by Plasmodium parasites have been known for millennia, and have caused untold human suffering. Today, millions of people are afflicted by malaria each year, and hundreds of thousands die. Historically, the most successful synthetic antimalarial drug was chloroquine, as it was safe, inexpensive, and highly efficacious. However, plasmodial resistance to chloroquine now greatly limits its utility. Previously in our laboratories it has been shown that attachment of a "reversal agent moiety" to the side chain of chloroquine can result in the restoration of activity against chloroquine-resistant strains of P. falciparum malaria. In the first part of the work presented here, a study has been made of the importance of the quinoline ring substitution pattern to the activity of such reversed chloroquines. The compounds presented here include those bearing a substituent in the 2-, 5, 6-, 7-, and/or 8- position, and include those with chloro, bromo, iodo, fluoro, nitro, trifluoromethyl, methyl, and methoxy substituents. For reversed chloroquines, 2-, 5-, and 8- substituents have been found to decrease in vitro antiplasmodial activity against P. falciparum relative to 7-chloro substitution, whereas 6- and 7- substituted compounds with various substituents have in many cases similar activity to that of 7-chloro substituted compounds. Little difference has been observed between 6- and 7- substitution, or between chlorine and a methyl group in position 6. In most cases these effects on activity are directionally similar to those observed for chloroquine analogs without an attached reversal agent, but the magnitude of the effect is generally smaller, suggesting that the activities of reversed chloroquines are less affected by modifications to the quinoline ring system than is true for chloroquine analogs without an attached reversal agent. The second portion of this work presents an asymmetrical bis-quinoline (PL241) that is highly active against P. falciparum malaria, with an IC50 of less than 0.1 nM for all strains tested. Mechanistic studies have been performed in which the substitution patterns of the two quinoline rings of PL241 are modified in ways that indicate that either ring system is equally capable of participating in the antimalarial activity of these compounds. The excellent in vitro antiplasmodial activity of PL241 makes this a compound of great interest for further development as a potential antimalarial drug. In the third part of this work, a survey has been made of antimalarial treatments recommended in the European medical literature from the time of Pliny the Elder (active in the first century A.D.) through the advent of modern malaria chemotherapy in the early twentieth century. In the fifteen primary sources utilized in this study, 251 distinct substances - primarily plants - were identified as having likely been used in the treatment of malaria. Of the 38 substances that were described in three or more sources, at least fifteen have been examined by other workers for antiplasmodial activity; in many cases, they were found to have antiplasmodial activity in vitro or in vivo. However, the majority of the phytotherapies for malaria identified in this project have not yet been tested against Plasmodium species, and may provide valuable leads in the search for new compounds active against drug-resistant malaria.
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Marijani, Theresia. "Modelling drug resistance in malaria." Thesis, Stellenbosch : University of Stellenbosch, 2009. http://hdl.handle.net/10019.1/4063.

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Ng, Anna. "Taste-masked and controlled-release formulations of chloroquine." Thesis, University College London (University of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267929.

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Tesfaselassie, Elias Sibhatu. "Antimalarial Drug Discovery using Triazoles to Overcome Chloroquine Resistance." PDXScholar, 2015. https://pdxscholar.library.pdx.edu/open_access_etds/2506.

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Malaria is considered as one of the most prevalent and debilitating diseases affecting humans. Plasmodium falciparum is the most virulent form of the parasite which developed resistance to several antimalarial drugs. Chloroquine is one of the most successful antimalarials developed that is safe, effective, and cheap. However, its use has been limited due to the emergence of drug resistance. Click chemistry, particularly, the copper(I)-catalyzed reaction between azides and alkynes has shown to have a cutting-edge advantage in medicinal chemistry by its reliability, selectivity and biocompatibility. Triazole-based antimalarials were synthesized via copper(I)-catalyzed alkyne-azide cycloaddition reaction by modifying the aliphatic chains terminal of chloroquine. The compounds synthesized contain triazole ring directly connected to an aromatic ring or via a piperazine linker. When tested for their in vitro antimalarial activity against D6, Dd2 and 7G8 strains of P. falciparum, 12 out of 28 compounds showed better activity against chloroquine resistant strains. Particularly, PL403 and PL448 exhibited potent activity than chloroquine against CQ-resistant strains Dd2 and 7G8, with IC50 values of 12.8 & 14.5 nM, and 15.2 & 11 nM respectively. The efficiency of synthesizing several triazole-based antimalarials have proven click chemistry to be fast and efficient reaction. Generally, para-substitutions and di-substitutions with electron-withdrawing groups were found to be beneficial for having better antimalarial activity for these group of click compounds. Moreover, the incorporation of piperazine linker has brought an enhanced antimalarial activity.
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Abrahem, Abrahem F. "Mechanisms of drug resistance in malaria." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0033/MQ50704.pdf.

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Books on the topic "Chloroquine Malaria Drug resistance"

1

Peters, Wallace. Chemotherapy and drug resistance in malaria. 2nd ed. London: Academic Press, 1987.

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Arora, Gunjan, Andaleeb Sajid, and Vipin Chandra Kalia, eds. Drug Resistance in Bacteria, Fungi, Malaria, and Cancer. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3.

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Arrow, Kenneth Joseph, Hellen Gelband, and Claire Panosian. Saving lives, buying time: Economics of malaria drugs in an age of resistance. Edited by Institute of Medicine (U.S.). Committee on the Economics of Antimalarial Drugs and NetLibrary Inc. Washington, D.C: National Academies Press, 2004.

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Mazonde, Isaac Ncube. Malaria epidemiological case study: An assessment of the attitudes of the risk population towards curative chloroquin tablets in Ngamiland, North West Botswana. Gaborone: National Institute of Development Research and Documentation, University of Botswana, 1988.

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Staines, Henry M. Treatment and Prevention of Malaria: Antimalarial Drug Chemistry, Action and Use. Basel: Springer Basel, 2012.

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Kalia, Vipin Chandra, Gunjan Arora, and Andaleeb Sajid. Drug Resistance in Bacteria, Fungi, Malaria, and Cancer. Springer, 2018.

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Rosenthal, MD Philip J. Antimalarial Chemotherapy: Mechanisms of Action, Resistance, and New Directions in Drug Discovery. Humana Press, 2010.

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(Editor), Kenneth J. Arrow, Claire B. Panosian (Editor), and Hellen Gelband (Editor), eds. Saving Lives, Buying Time: Economics of Malaria Drugs in an Age of Resistance. National Academy Press, 2004.

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Rosenthal, Philip J. Antimalarial Chemotherapy: Mechanisms of Action, Resistance, and New Directions in Drug Discovery. Humana Press, 2014.

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Antimalarial Chemotherapy: Mechanisms of Action, Resistance, and New Directions in Drug Discovery (Infectious Disease). Humana Press, 2001.

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Book chapters on the topic "Chloroquine Malaria Drug resistance"

1

Martiney, James A., Angel S. Ferrer, Anthony Cerami, Sergey Dzekunov, and Paul Roepe. "Chloroquine Uptake, Altered Partitioning and the Basis of Drug Resistance: Evidence for Chloride-Dependent Ionic Regulation." In Novartis Foundation Symposium 226 - Transport and Trafficking in the Malaria-Infected Erythrocyte, 265–80. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470515730.ch18.

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Shah, Naman K., and Neena Valecha. "Antimalarial drug resistance." In Advances in Malaria Research, 383–407. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118493816.ch14.

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Kumar, Santosh C. M. "Drug Resistance in Malaria." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 429–47. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_19.

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Upadhyay, Santosh K., Ramesh C. Rai, Rekha Gehtori, Ashutosh Paliwal, Poonam Gautam, and Penny Joshi. "Drug Resistance in Cancer." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 449–73. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_20.

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Cheah, Phaik Yeong, Michael Parker, and Nicholas P. J. Day. "Ethics and Antimalarial Drug Resistance." In Ethics and Drug Resistance: Collective Responsibility for Global Public Health, 55–73. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-27874-8_4.

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Abstract There has been impressive progress in malaria control and treatment over the past two decades. One of the most important factors in the decline of malaria-related mortality has been the development and deployment of highly effective treatment in the form of artemisinin-based combination therapies (ACTs). However, recent reports suggest that these gains stand the risk of being reversed due to the emergence of ACT resistance in the Greater Mekong Subregion and the threat of this resistance spreading to Africa, where the majority of the world’s malaria cases occur, with catastrophic consequences. This chapter provides an overview of strategies proposed by malaria experts to tackle artemisinin-resistant malaria, and some of the most important practical ethical issues presented by each of these interventions. The proposed strategies include mass antimalarial drug administrations in selected populations, and mandatory screening of possibly infected individuals prior to entering an area free of artemisinin-resistant malaria. We discuss ethical issues such as tensions between the wishes of individuals versus the broader goal of malaria elimination, and the risks of harm to interventional populations, and conclude by proposing a set of recommendations.
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Uhlemann, Anne-Catrin, Yongyuth Yuthavong, and David A. Fidock. "Mechanisms of Antimalarial Drug Action and Resistance." In Molecular Approaches to Malaria, 427–61. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817558.ch23.

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Arora, Gunjan, Ankur Kulshreshtha, Kriti Arora, Puneet Talwar, Rishi Raj, Gurpreet Grewal, Andaleeb Sajid, and Ritushree Kukreti. "Emerging Themes in Drug Resistance." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 1–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_1.

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Arora, Gunjan, Richa Misra, and Andaleeb Sajid. "Synthetic Solutions to Drug Resistance." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 595–608. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_26.

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Ray, Shilpa, Susmita Das, and Mrutyunjay Suar. "Molecular Mechanism of Drug Resistance." In Drug Resistance in Bacteria, Fungi, Malaria, and Cancer, 47–110. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-48683-3_3.

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Bassat, Quique, and Pedro L. Alonso. "Drug Resistance in Malaria in Developing Countries." In Antimicrobial Resistance in Developing Countries, 95–116. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-89370-9_7.

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Conference papers on the topic "Chloroquine Malaria Drug resistance"

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Fatumo, Segun, Ezekiel Adebiyi, Gunnar Schramm, Roland Eils, and Rainer Konig. "An in silico Approach to Detect Efficient Malaria Drug Targets to Combat the Malaria Resistance Problem." In 2009 International Association of Computer Science and Information Technology - Spring Conference. IEEE, 2009. http://dx.doi.org/10.1109/iacsit-sc.2009.128.

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Konieczna, I., L. Lechowicz, M. Chrzanowska, M. Chyb, S. Cholewa, D. Grzegorczyk, J. Ciura, and J. Gaweda. "AB1319 Drug resistance in bacteria isolated from urine of rheumatoid arthritispatients and induction of resistance by chloroquine." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5607.

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Sultan, Ali A., Devendra Bansal, Fahmi Y. Khan, Musaed Al Samawi, Praveen Kumar Bharti, Pradyumna Kumar Mohapatra, Jagdeesh Mahanta, Rakesh Sehgal, and Neeru Singh. "Point Mutation in Chloroquine Resistance-Associated Genes (Pfcrt and Pfmdr-1) in Imported Cases of Malaria in Qatar." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbpp2721.

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Reports on the topic "Chloroquine Malaria Drug resistance"

1

Gunsaru, Bornface. Simplified Reversed Chloroquines to Overcome Malaria Resistance to Quinoline-based Drugs. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.400.

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Tesfaselassie, Elias. Antimalarial Drug Discovery using Triazoles to Overcome Chloroquine Resistance. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2503.

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Liebman, Katherine. New 4-Aminoquinoline Compounds to Reverse Drug Resistance in P. falciparum Malaria, and a Survey of Early European Antimalarial Treatments. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.2112.

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