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Academic literature on the topic 'Artemisinin, Syk Inhibitor, Artemisinin resistance'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Artemisinin, Syk Inhibitor, Artemisinin resistance"

1

Tsamesidis, Ioannis, Karine Reybier, Giuseppe Marchetti, Maria Carmina Pau, Patrizia Virdis, Claudio Fozza, Francoise Nepveu, Philip S. Low, Francesco Michelangelo Turrini, and Antonella Pantaleo. "Syk Kinase Inhibitors Synergize with Artemisinins by Enhancing Oxidative Stress in Plasmodium falciparum-Parasitized Erythrocytes." Antioxidants 9, no. 8 (August 14, 2020): 753. http://dx.doi.org/10.3390/antiox9080753.

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Although artemisinin-based combination therapies (ACTs) treat Plasmodium falciparum malaria effectively throughout most of the world, the recent expansion of ACT-resistant strains in some countries of the Greater Mekong Subregion (GMS) further increased the interest in improving the effectiveness of treatment and counteracting resistance. Recognizing that (1) partially denatured hemoglobin containing reactive iron (hemichromes) is generated in parasitized red blood cells (pRBC) by oxidative stress, (2) redox-active hemichromes have the potential to enhance oxidative stress triggered by the parasite and the activation of artemisinin to its pharmaceutically active form, and (3) Syk kinase inhibitors block the release of membrane microparticles containing hemichromes, we hypothesized that increasing hemichrome content in parasitized erythrocytes through the inhibition of Syk kinase might trigger a virtuous cycle involving the activation of artemisinin, the enhancement of oxidative stress elicited by activated artemisinin, and a further increase in hemichrome production. We demonstrate here that artemisinin indeed augments oxidative stress within parasitized RBCs and that Syk kinase inhibitors further increase iron-dependent oxidative stress, synergizing with artemisinin in killing the parasite. We then demonstrate that Syk kinase inhibitors achieve this oxidative enhancement by preventing parasite-induced release of erythrocyte-derived microparticles containing redox-active hemichromes. We also observe that Syk kinase inhibitors do not promote oxidative toxicity to healthy RBCs as they do not produce appreciable amounts of hemichromes. Since some Syk kinase inhibitors can be taken daily with minimal side effects, we propose that Syk kinase inhibitors could evidently contribute to the potentiation of ACTs.
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2

Marchetti, Giuseppe, Alessandro Dessì, Roberto Dallocchio, Ioannis Tsamesidis, Maria Carmina Pau, Francesco Michelangelo Turrini, and Antonella Pantaleo. "Syk Inhibitors: New Computational Insights into Their Intraerythrocytic Action in Plasmodium falciparum Malaria." International Journal of Molecular Sciences 21, no. 19 (September 23, 2020): 7009. http://dx.doi.org/10.3390/ijms21197009.

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Resistance to antimalarial drugs has spread rapidly over the past few decades. The WHO recommends artemisinin-based combination therapies for the treatment of uncomplicated malaria, but unfortunately these approaches are losing their efficacy in large areas of Southeast Asia. In 2016, artemisinin resistance was confirmed in 5 countries of the Greater Mekong subregion. We focused our study on Syk inhibitors as antimalarial drugs. The Syk protein is present in human erythrocytes, and the membrane of protein band 3 is its major target following activation by oxidant stress. Tyr phosphorylation of band 3 occurs during P. falciparum growth, leading to the release of microparticles containing hemicromes and structural weakening of the host cell membrane, simplifying merozoite reinfection. Syk inhibitors block these events by interacting with the Syk protein’s catalytic site. We performed in vitro proteomics and in silico studies and compared the results. In vitro studies were based on treatment of the parasite’s cellular cultures with different concentrations of Syk inhibitors, while proteomics studies were focused on the Tyr phosphorylation of band 3 by Syk protein with the same concentrations of drugs. In silico studies were based on different molecular modeling approaches in order to analyze and optimize the ligand–protein interactions and obtain the highest efficacy in vitro. In the presence of Syk inhibitors, we observed a marked decrease of band 3 Tyr phosphorylation according to the increase of the drug’s concentration. Our studies could be useful for the structural optimization of these compounds and for the design of novel Syk inhibitors in the future.
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3

Kimata-Ariga, Yoko, and Rena Morihisa. "Effect of Artemisinin on the Redox System of NADPH/FNR/Ferredoxin from Malaria Parasites." Antioxidants 11, no. 2 (January 29, 2022): 273. http://dx.doi.org/10.3390/antiox11020273.

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FNR and ferredoxin constitute a redox cascade, which provides reducing power in the plastid of malaria parasites. Recently, mutation of ferredoxin (D97Y) was reported to be strongly related to the parasite’s resistance to the front-line antimalarial drug artemisinin. In order to gain insight into the mechanism for the resistance, we studied the effect of dihydroartemisinin (DHA), the active compound of artemisinin, on the redox cascade of NADPH/FNR/ferredoxin in in vitro reconstituted systems. DHA partially inhibited the diaphorase activity of FNR by decreasing the affinity of FNR for NADPH. The activity of the electron transfer from FNR to wild-type or D97Y mutant ferredoxin was not significantly affected by DHA. An in silico docking analysis indicated possible binding of DHA molecule in the binding cavity of 2′5′ADP, a competitive inhibitor for NADPH, on FNR. We previously showed that the D97Y mutant of ferredoxin binds to FNR more strongly than wild-type ferredoxin, and ferredoxin and FNR are generally known to be involved in the oxidative stress response. Thus, these results suggest that ferredoxin is not a direct target of artemisinin, but its mutation may be involved in the protective response against the oxidative stress caused by artemisinin.
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4

Pratama, Mohammad Rizki Fadhil, and Tutus Gusdinar. "BETWEEN ARTEMISININ AND DERIVATIVES WITH NEURAMINIDASE: A DOCKING STUDY INSIGHT." Asian Journal of Pharmaceutical and Clinical Research 10, no. 8 (August 1, 2017): 304. http://dx.doi.org/10.22159/ajpcr.2017.v10i8.18667.

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Objectives: This study aims to find the relationship between artemisinins and neuraminidase (NA) with molecular docking study and also to determine the most potent NA inhibitor from artemisinin and derivatives.Methods: All ligands were sketched and optimized using Gaussian 03W with Hartree-Fock method basis sets 6-311G. Molecular docking was performed using AutoDock 4.2.3 toward NA in complexes with oseltamivir as co-crystal ligand. The main parameters used were the free energy of binding (ΔG) and dissociation constant (Ki) as affinity marker.Results: Artesunate provided most negative free ΔG and lowest Ki toward NA with −9.55 kcal/mol and 100.66 nM, respectively. Artesunate shows higher affinity than oseltamivir with interactions between artesunate and amino acids at position 246 had important influences on artesunate affinity toward NA from H5N1.Conclusion: In silico molecular docking results indicated that artesunate could be considered as NA inhibitor and should be potential to be developed as anti-influenza particularly to H5N1 with oseltamivir resistance.
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5

von Bredow, Lukas, Thomas Martin Schäfer, Julian Hogenkamp, Maik Tretbar, Daniel Stopper, Fabian B. Kraft, Julian Schliehe-Diecks, et al. "Synthesis, Antiplasmodial, and Antileukemia Activity of Dihydroartemisinin–HDAC Inhibitor Hybrids as Multitarget Drugs." Pharmaceuticals 15, no. 3 (March 9, 2022): 333. http://dx.doi.org/10.3390/ph15030333.

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Artemisinin-based combination therapies (ACTs) are the gold standard for the treatment of malaria, but the efficacy is threatened by the development of parasite resistance. Histone deacetylase inhibitors (HDACis) are an emerging new class of potential antiplasmodial drugs. In this work, we present the design, synthesis, and biological evaluation of a mini library of dihydroartemisinin–HDACi hybrid molecules. The screening of the hybrid molecules for their activity against selected human HDAC isoforms, asexual blood stage P. falciparum parasites, and a panel of leukemia cell lines delivered important structure–activity relationships. All synthesized compounds demonstrated potent activity against the 3D7 and Dd2 line of P. falciparum with IC50 values in the single-digit nanomolar range. Furthermore, the hybrid (α)-7c displayed improved activity against artemisinin-resistant parasites compared to dihydroartemisinin. The screening of the compounds against five cell lines from different leukemia entities revealed that all hydroxamate-based hybrids (7a–e) and the ortho-aminoanilide 8 exceeded the antiproliferative activity of dihydroartemisinin in four out of five cell lines. Taken together, this series of hybrid molecules represents an excellent starting point toward the development of antimalarial and antileukemia drug leads.
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6

Lee, Dong-Hwan, Md Hasanuzzaman, Daeho Kwon, Hye-Young Choi, So Myoung Kim, Dong Jin Kim, Dong Ju Kang, et al. "10-Phenyltriazoyl Artemisinin is a Novel P-glycoprotein Inhibitor that Suppresses the Overexpression and Function of P-glycoprotein." Current Pharmaceutical Design 24, no. 46 (April 26, 2019): 5590–97. http://dx.doi.org/10.2174/1381612825666190222155700.

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Background: The effect of drugs on ATP-binding cassette transporters, especially permeabilityglycoprotein (P-gp), is an important consideration during new anti-cancer drug development. Objective: In this context, the effects of a newly synthesized artemisinin derivative, 10-(4-phenyl-1H-1,2,3- triazol)-artemisinin (5a), were evaluated on P-gp expression and function. Methods: Reverse transcript polymerase chain reaction and immunoblotting techniques were used to determine the effect of 5a on P-gp expression in LS174T cells. In addition, the ability of 5a to work as either a substrate or an inhibitor of P-gp was investigated through different methods. Results: The results revealed that 5a acts as a novel P-gp inhibitor that dually suppresses the overexpression and function of P-glycoprotein. Co-treatment of LS174T cell line, human colon adenocarcinoma cell line, with 5a and paclitaxel recovered the anticancer effect of paclitaxel by controlling the acquired drug resistance pathway. The overexpression of P-gp induced by rifampin and paclitaxel in a colorectal cell line was suppressed by 5a which could be a novel inhibitory substrate inhibiting the transport of paclitaxel by P-gp. Conclusion: The results revealed that 5a can be classified as a type B P-gp inhibitor (with both substrate and inhibitor activities) with an additional function of suppressing P-gp overexpression. The results might be clinically useful in the development of anticancer drugs against cancers with multidrug resistance.
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7

Kirkman, Laura A., Wenhu Zhan, Joseph Visone, Alexis Dziedziech, Pradeep K. Singh, Hao Fan, Xinran Tong, et al. "Antimalarial proteasome inhibitor reveals collateral sensitivity from intersubunit interactions and fitness cost of resistance." Proceedings of the National Academy of Sciences 115, no. 29 (July 2, 2018): E6863—E6870. http://dx.doi.org/10.1073/pnas.1806109115.

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We describe noncovalent, reversible asparagine ethylenediamine (AsnEDA) inhibitors of the Plasmodium falciparum proteasome (Pf20S) β5 subunit that spare all active subunits of human constitutive and immuno-proteasomes. The compounds are active against erythrocytic, sexual, and liver-stage parasites, against parasites resistant to current antimalarials, and against P. falciparum strains from patients in Africa. The β5 inhibitors synergize with a β2 inhibitor in vitro and in mice and with artemisinin. P. falciparum selected for resistance to an AsnEDA β5 inhibitor surprisingly harbored a point mutation in the noncatalytic β6 subunit. The β6 mutant was resistant to the species-selective Pf20S β5 inhibitor but remained sensitive to the species-nonselective β5 inhibitors bortezomib and carfilzomib. Moreover, resistance to the Pf20S β5 inhibitor was accompanied by increased sensitivity to a Pf20S β2 inhibitor. Finally, the β5 inhibitor-resistant mutant had a fitness cost that was exacerbated by irradiation. Thus, used in combination, multistage-active inhibitors of the Pf20S β5 and β2 subunits afford synergistic antimalarial activity with a potential to delay the emergence of resistance to artemisinins and each other.
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8

Pulcini, Serena, Henry M. Staines, Jon K. Pittman, Ksenija Slavic, Christian Doerig, Jean Halbert, Rita Tewari, et al. "Expression in Yeast Links Field Polymorphisms in PfATP6 to in Vitro Artemisinin Resistance and Identifies New Inhibitor Classes." Journal of Infectious Diseases 208, no. 3 (April 18, 2013): 468–78. http://dx.doi.org/10.1093/infdis/jit171.

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9

Mustière, Romain, Patrice Vanelle, and Nicolas Primas. "Plasmodial Kinase Inhibitors Targeting Malaria: Recent Developments." Molecules 25, no. 24 (December 15, 2020): 5949. http://dx.doi.org/10.3390/molecules25245949.

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Recent progress in reducing malaria cases and ensuing deaths is threatened by factors like mutations that induce resistance to artemisinin derivatives. Multiple drugs are currently in clinical trials for malaria treatment, including some with novel mechanisms of action. One of these, MMV390048, is a plasmodial kinase inhibitor. This review lists the recently developed molecules which target plasmodial kinases. A systematic review of the literature was performed using CAPLUS and MEDLINE databases from 2005 to 2020. It covers a total of 60 articles and describes about one hundred compounds targeting 22 plasmodial kinases. This work highlights the strong potential of compounds targeting plasmodial kinases for future drug therapies. However, the majority of the Plasmodium kinome remains to be explored.
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10

Bao, Changlei, Qian He, Hui Wang, Yanan Sun, Yahang Xu, Yan Pan, Yadan Hu, et al. "Artemisinin and Its Derivate Alleviate Pulmonary Hypertension and Vasoconstriction in Rodent Models." Oxidative Medicine and Cellular Longevity 2022 (June 17, 2022): 1–21. http://dx.doi.org/10.1155/2022/2782429.

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Background. Pulmonary arterial hypertension (PAH) is a complex pulmonary vasculature disease characterized by progressive obliteration of small pulmonary arteries and persistent increase in pulmonary vascular resistance, resulting in right heart failure and death if left untreated. Artemisinin (ARS) and its derivatives, which are common antimalarial drugs, have been found to possess a broad range of biological effects. Here, we sought to determine the therapeutic benefit and mechanism of ARS and its derivatives treatment in experimental pulmonary hypertension (PH) models. Methods. Isolated perfused/ventilated lung and isometric tension measurements in arteries were performed to test pulmonary vasoconstriction and relaxation. Monocrotaline (MCT) and hypoxia+Su5416 (SuHx) were administered to rats to induce severe PH. Evaluation methods of ARS treatment and its derivatives in animal models include echocardiography, hemodynamics measurement, and histological staining. In vitro, the effect of these drugs on proliferation, viability, and hypoxia-inducible factor 1α (HIF1α) was examined in human pulmonary arterial smooth muscle cells (hPASMCs). Results. ARS treatment attenuated pulmonary vasoconstriction induced by high K+ solution or alveolar hypoxia, decreased pulmonary artery (PA) basal vascular tension, improved acetylcholine- (ACh-) induced endothelial-dependent relaxation, increased endothelial nitric oxide (NO) synthase (eNOS) activity and NO levels, and decreased levels of NAD(P)H oxidase subunits (NOX2 and NOX4) expression, NAD(P)H oxidase activity, and reactive oxygen species (ROS) levels of pulmonary arteries (PAs) in MCT-PH rats. NOS inhibitor, L-NAME, abrogated the effects of ARS on PA constriction and relaxation. Furthermore, chronic application of both ARS and its derivative dihydroartemisinin (DHA) attenuated right ventricular systolic pressure (RVSP), Fulton index (right ventricular hypertrophy), and vascular remodeling of PAs in the two rat PH models. In addition, DHA inhibited proliferation and migration of hypoxia-induced PASMCs. Conclusions. In conclusion, these results indicate that treatment with ARS or DHA can inhibit PA vasoconstriction, PASMC proliferation and migration, and vascular remodeling, as well as improve PA endothelium-dependent relaxation, and eventually attenuate the development and progression of PH. These effects might be achieved by decreasing NAD(P)H oxidase generated ROS production and increasing eNOS activation to release NO in PAs. ARS and its derivatives might have the potential to be novel drugs for the treatment of PH.
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