Relevant bibliographies by topics / P-glycoprotein inhibitors

Academic literature on the topic 'P-glycoprotein inhibitors'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "P-glycoprotein inhibitors"

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Gherbovet, Olga, María Concepción García Alvarez, Jérôme Bignon, and Fanny Roussi. "Original Vinca Derivatives: From P-Glycoprotein Substrates to P-Glycoprotein Inhibitors." Journal of Medicinal Chemistry 59, no. 23 (November 23, 2016): 10774–80. http://dx.doi.org/10.1021/acs.jmedchem.6b00525.

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Chae, Song Wha, Jaeok Lee, Jung Hyun Park, Youngjoo Kwon, Younghwa Na, and Hwa Jeong Lee. "Intestinal P-glycoprotein inhibitors, benzoxanthone analogues." Journal of Pharmacy and Pharmacology 70, no. 2 (December 13, 2017): 234–41. http://dx.doi.org/10.1111/jphp.12832.

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al-Shawi, M. K., I. L. Urbatsch, and A. E. Senior. "Covalent inhibitors of P-glycoprotein ATPase activity." Journal of Biological Chemistry 269, no. 12 (March 1994): 8986–92. http://dx.doi.org/10.1016/s0021-9258(17)37065-5.

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Kono, Yusuke, Iichiro Kawahara, Kohei Shinozaki, Ikuo Nomura, Honoka Marutani, Akira Yamamoto, and Takuya Fujita. "Characterization of P-Glycoprotein Inhibitors for Evaluating the Effect of P-Glycoprotein on the Intestinal Absorption of Drugs." Pharmaceutics 13, no. 3 (March 15, 2021): 388. http://dx.doi.org/10.3390/pharmaceutics13030388.

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For developing oral drugs, it is necessary to predict the oral absorption of new chemical entities accurately. However, it is difficult because of the involvement of efflux transporters, including P-glycoprotein (P-gp), in their absorption process. In this study, we conducted a comparative analysis on the inhibitory activities of seven P-gp inhibitors (cyclosporin A, GF120918, LY335979, XR9576, WK-X-34, VX-710, and OC144-093) to evaluate the effect of P-gp on drug absorption. GF120918, LY335979, and XR9576 significantly decreased the basal-to-apical transport of paclitaxel, a P-gp substrate, across Caco-2 cell monolayers. GF120918 also inhibited the basal-to-apical transport of mitoxantrone, a breast cancer resistance protein (BCRP) substrate, in Caco-2 cells, whereas LY335979 hardly affected the mitoxantrone transport. In addition, the absorption rate of paclitaxel after oral administration in wild-type mice was significantly increased by pretreatment with LY335979, and it was similar to that in mdr1a/1b knockout mice. Moreover, the absorption rate of topotecan, a BCRP substrate, in wild-type mice pretreated with LY335979 was similar to that in mdr1a/1b knockout mice but significantly lower than that in bcrp knockout mice. These results indicate that LY335979 has a selective inhibitory activity for P-gp, and would be useful for evaluating the contribution of P-gp to drug absorption.
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Pleban, Karin, and Gerhard Ecker. "Inhibitors of P-Glycoprotein - Lead Identification and Optimisation." Mini-Reviews in Medicinal Chemistry 5, no. 2 (February 1, 2005): 153–63. http://dx.doi.org/10.2174/1389557053402729.

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Yu, Jun, Peng Zhou, James Asenso, Xiao-Dan Yang, Chun Wang, and Wei Wei. "Advances in plant-based inhibitors of P-glycoprotein." Journal of Enzyme Inhibition and Medicinal Chemistry 31, no. 6 (March 2, 2016): 867–81. http://dx.doi.org/10.3109/14756366.2016.1149476.

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Srivalli, Kale Mohana Raghava, and P. K. Lakshmi. "Overview of P-glycoprotein inhibitors: a rational outlook." Brazilian Journal of Pharmaceutical Sciences 48, no. 3 (September 2012): 353–67. http://dx.doi.org/10.1590/s1984-82502012000300002.

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P-glycoprotein (P-gp), a transmembrane permeability glycoprotein, is a member of ATP binding cassette (ABC) super family that functions specifically as a carrier mediated primary active efflux transporter. It is widely distributed throughout the body and has a diverse range of substrates. Several vital therapeutic agents are substrates to P-gp and their bioavailability is lowered or a resistance is induced because of the protein efflux. Hence P-gp inhibitors were explored for overcoming multidrug resistance and poor bioavailability problems of the therapeutic P-gp substrates. The sensitivity of drug moieties to P-gp and vice versa can be established by various experimental models in silico, in vitro and in vivo. Ever since the discovery of P-gp, the research plethora identified several chemical structures as P-gp inhibitors. The aim of this review was to emphasize on the discovery and development of newer, inert, non-toxic, and more efficient, specifically targeting P-gp inhibitors, like those among the natural herb extracts, pharmaceutical excipients and formulations, and other rational drug moieties. The applications of cellular and molecular biology knowledge, in silico designed structural databases, molecular modeling studies and quantitative structure-activity relationship (QSAR) analyses in the development of novel rational P-gp inhibitors have also been mentioned.
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Chang, Cheng, Praveen M. Bahadduri, James E. Polli, Peter W. Swaan, and Sean Ekins. "Rapid Identification of P-glycoprotein Substrates and Inhibitors." Drug Metabolism and Disposition 34, no. 12 (September 22, 2006): 1976–84. http://dx.doi.org/10.1124/dmd.106.012351.

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Bogman, Katrijn, Anne-Kathrin Peyer, Michael Török, Ernst Küsters, and Jürgen Drewe. "HMG-CoA reductase inhibitors and P-glycoprotein modulation." British Journal of Pharmacology 132, no. 6 (March 2001): 1183–92. http://dx.doi.org/10.1038/sj.bjp.0703920.

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Tarasova, Nadya I., Rishi Seth, Sergey G. Tarasov, Teresa Kosakowska-Cholody, Christine A. Hrycyna, Michael M. Gottesman, and Christopher J. Michejda. "Transmembrane Inhibitors of P-Glycoprotein, an ABC Transporter." Journal of Medicinal Chemistry 48, no. 11 (June 2005): 3768–75. http://dx.doi.org/10.1021/jm049065t.

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Dissertations / Theses on the topic "P-glycoprotein inhibitors"

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Jain, Ritesh Mitra Ashim K. "A novel approach to circumvent P-glycoporotein mediated cellular efflux and permeability enhancement of HIV protease inhibitor saquinavir." Diss., UMK access, 2007.

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Thesis (Ph. D.)--School of Pharmacy. University of Missouri--Kansas City, 2007.
"A dissertation in pharmaceutical science and pharmacology." Advisor: Ashim K. Mitra. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed July 16, 2008. Includes bibliographical references (leaves 231-248). Online version of the print edition.
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Row, Eleanor Catherine. "Design, synthesis and evaluation of coumarin and furanocoumarin compounds as inhibitors of CYP3A4 and P-glycoprotein." Thesis, University of Sheffield, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401162.

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Profit, Louise. "The role of metabolism and P-glycoprotein mediated transport in the disposition of the HIV protease inhibitors." Thesis, University of Liverpool, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366961.

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Edwards, Jeffrey Earl. "THE TRANSPORT AND MODULATION OF HIV PROTEASE INHIBITORS INTO THE RAT CENTRAL NERVOUS SYSTEM AND MILK." UKnowledge, 2004. http://uknowledge.uky.edu/gradschool_diss/468.

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The objective of this dissertation is to study the mechanism by which HIV protease inhibitors enter into the central nervous system (CNS) and breast milk of rats, and what effects MDR modulators have on the distribution and metabolism of HIV protease inhibitors. The transporter P-glycoprotein (P-gp) has been shown to limit the distribution of HIV protease inhibitors into the CNS of rodents. This thesis examined the effects of GF120918, an MDR modulator, on the CNS distribution of amprenavir, an HIV protease inhibitor, in rats. GF120918 significantly increased the unbound CNS concentrations of amprenavir without altering the unbound blood concentrations of amprenavir. The results of these studies show that GF120918 can inhibit P-gp at the blood brain barrier (BBB) to increase the unbound CNS concentration of amprenavir and potentially other HIV protease inhibitors. Many first generation MDR modulators inhibited both P-gp transport and CYP3A metabolism. Therefore, a principal goal of this thesis was to determine if GF120918 could selectively inhibit P-gp transport without inhibiting CYP3A metabolism. Using in vitro (human) and in vivo (rat) studies, GF120918 selectively inhibited P-gp at the BBB without inhibiting CYP3A metabolism. The transporter MRP1 has been shown to both transport HIV protease inhibitors and expressed in the CNS. Studies contained in the thesis have shown that mrp1 is not localized to the BBB of rats, therefore, mrp1 is unlikely to play a significant role in the distribution of HIV protease inhibitors into the CNS of rats. The distribution of nelfinavir, an HIV protease inhibitor, into rat breast milk was studied in the thesis as a first approach in understanding the extent to which HIV protease inhibitors can accumulate into milk. The concentration of nelfinavir in rat milk was approximately half that of plasma. P-gp protein expression was detected in lactating rat mammary tissue. However, GF120918 showed no effect on the distribution of nelfinavir into rat milk suggesting that P-gp does not play a significant role in the distribution of HIV protease inhibitors into milk.
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Patel, Jignesh Mitra Ashim K. "P-glycoprotein mediated efflux and CYP3A4 mediated metabolism of HIV-protease inhibitor, ritonavir, and its interaction with pure herbal constituents." Diss., UMK access, 2004.

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Thesis (Ph. D.)--School of Pharmacy and Dept. of Chemistry. University of Missouri--Kansas City, 2004.
"A dissertation in pharmaceutical science and chemistry." Advisor: Ashim K. Mitra. Typescript. Vita. Description based on contents viewed Feb. 27, 2006; title from "catalog record" of the print edition. Includes bibliographical references (leaves 175-199). Online version of the print edition.
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Woodahl, Erica Lynn. "Genetic variation in the multidrug resistance gene (MDRI) : impact on drug delivery and disposition /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/7950.

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Gashaw, Isabella. "Veränderungen in der Genexpression fremdstoffmetabolisierender Enzyme und Bedeutung genetischer Polymorphismen unter besonderer Berücksichtigung von HIV-Virustatika." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2003. http://dx.doi.org/10.18452/14958.

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Die Therapie der HIV Infektion besteht aus Kombination mehrerer antiretroviraler Substanzen und birgt ein erhöhtes Risiko an Arzneimittelwechselwirkungen. Das bekannte Problem der Virusresistenz kann zudem durch Enzyminduktion begünstigt werden. Das Ziel der vorliegenden Arbeit lag in Untersuchungen zu Einflüssen der Virustatika auf die Expression von Cytochrom P450 Enzymen: 1A1, 1B1, 3A4 sowie der P-Glykoproteins (MDR1) an immortalisierten Zellsystemen. Die Protease Inhibitoren Indinavir, Nelfinavir, Ritonavir und Saquinavir induzierten die Regulation der mRNA Expression über den Aryl-Kohlenwasserstoff-Rezeptor (AhR) und den Pregnan-X-Rezeptor (PXR) dosisabhängig und signifikant. Die Nukleosidischen Reverse Transkriptase Inhibitoren Zalcitabin, Zidovudin und Lamivudin sowie der Nicht-Nukleosidische Inhibitor Nevirapin zeigten induktive Eigenschaften nur für die AhR Zielgene CYP1A1 und CYP1B1. Amprenavir und Efavirenz aktivierten die PXR-Regulation. Die möglichen Auswirkungen der Induktion der untersuchten Gene wurden ausführlich diskutiert. Die molekularen Grundlagen der interindividuell variierenden Aktivität von CYP3A wurden in einer Probandenstudie untersucht. Es wurden die mRNA Expression in den Leukozyten, die Aktivität des Enzyms und einige bekannte Polymorphismen unter Einwirkung von Rifampicin untersucht und diskutiert.
The therapy of HIV infection requires a combination of several antiretroviral substances accompanying risk factors for drug-drug interactions. Moreover, virus resistance can be promoted by enzyme induction caused by antiretroviral drugs. The aim of the study was to investigate the influences of antiretroviral substances on the expression of cytochrome P450 enzymes: 1A1, 1B1, 3A4 and p-glycoprotein (MDR1) using immortalized cell systems. The protease inhibitors indinavir, nelfinavir, ritonavir and saquinavir induced significantly the regulation of mRNA expression through the aryl hydrocarbon receptor (AhR) and the pregnane-x-receptor (PXR) in a concentration-dependent manner. The nucleoside reverse transcriptase inhibitors zalcitabine, zidovudine and lamivudine and the non-nucleoside reverse transcriptase inhibitor nevirapine showed inductive properties only for the AhR target genes CYP1A1 and CYP1B1.Amprenavir and efavirenz activated the PXR target genes. Potentially effects of the described induction are discussed. In a second part of the work, the molecular mechanisms of the individual varying activity of the CYP3A enzyme were investigated applying an in vivo study. CYP3A4 mRNA expression and rifampicin mediated induction in leucocytes were correlated with systemic enzyme activity under induction and known polymorphisms.
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Jovelet, Cécile. "Interactions du vandetanib avec la P-glycoprotéine et passage d'une barrière physiologique : le placenta." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114825.

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La surexpression de protéines d’efflux, et tout particulièrement la P-glycoprotéine, est impliquée dans la multidrug résistance. Dans cette thèse, nous démontrons que le vandetanib, inhibiteur de tyrosine kinase, est à la fois substrat et inhibiteur de la P-glycoprotéine et qu’il est capable de réverser in vitro la résistance à la doxorubicine liée à la surexpression de la P-glycoprotéine.Nous nous sommes également intéressés à l’étude du passage transplacentaire du vandetanib et nous montrons que ce médicament traverse la barrière placentaire
Overexpression of ABC transporters, especially P-glycoprotein, is involved in multidrug resistance. In this study, we demonstrate that vandetanib, a tyrosine kinase inhibitor, is both substrate and inhibitor of P-glycoprotein and is able to reverse in vitro resistance to doxorubicin, linked to overexpression of P-glycoprotein.We also studied the placental transfer of vandetanib and we show that this drug crosses the placenta
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Sonawane, Amit. "Evaluation of novel efflux transport inhibitor for the improvement of drug delivery through epithelial cell monolayer." Thesis, University of Bradford, 2015. http://hdl.handle.net/10454/14424.

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Blood-brain barrier (BBB) is a unique membranous barrier, which segregates brain from the circulating blood. It works as a physical and metabolic barrier between the central nervous system (CNS) and periphery. In mammals, endothelial cells were shown to be of BBB and are characterized by the tight junctions along with efflux system which are responsible for the restriction of movement of molecules within the cells. Efflux system consists of multidrug resistance proteins such as P-glycoprotein (P-gp). P-gp removes substances out back from the brain to the blood before they reach to the brain. So the barrier is impermeable to many compounds such as amino acids, ions, small peptides and proteins, making it the most challenging factor for the development of new drugs for targeting CNS. Curcumin is a bioactive compound that has a number of health promoting benefits such as anti-inflammatory, anticancer, anti-oxidant agent; as well as a role in neurodegenerative diseases, but low oral bioavailability is the major limiting factor. Low water solubility and rapid metabolism are the two important factors responsible for poor bioavailability of curcumin. Galaxolide is a musk compound and previously known for the bioaccumulation of toxic components in the aquatic animals by interference with the activity of multidrug/multixenobiotic resistance efflux transporters (MDR/MXR). The bioavailability of curcumin can be enhanced when administered with galaxolide. This study was carried out to investigate the effect of galaxolide on the permeation of curcumin through the epithelial cell monolayers. MDCKII-MDR1 cell monolayer is used an in vitro blood-brain barrier model while Caco-2 monolayer is used as an in vitro intestinal model, which also expresses the P-glycoprotein. The curcumin and galaxolide were separately solubilised in the DMSO and used in combination to perform permeation study, to determine the effect of galaxolide on curcumin permeation through epithelial cell monolayers. The galaxolide shows an efflux protein inhibition activity and this activity was used to enhance permeation of curcumin through the Caco-2 monolayer. In summary, galaxolide is a novel permeation enhancer molecule, which can be used for the improvement of drug delivery of other bioactive compounds in future.
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Ogunrombi, Modupe Olufunmilayo. "The effect of grapefruit juice, a P-glycoprotein inhibitor, on organic acid and conjugates urinary profile in healthy human subjects / M.O. Ogunrombi." Thesis, North-West University, 2004. http://hdl.handle.net/10394/411.

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P-glycoprotein (p-gp), a member of the superfamily ATP-binding cassette (ABC) is known to be present in the absorptive enterocytes of the gastro-intestinal tract and many other tissues in the body where it acts mainly as a defence mechanism against exogenous assault. Defects in p-gp is speculated to result in the development of diseases as mutations in genes are causes of numerous diseases in the metabolic mosaic that underlies health. Due to the importance of p-gp, particularly in the intestines, mutation of the gene encoding this protein may lead to the presence of unusual compounds, xenobiotics in the body and the urine. It is thought that defective p-gp in the intestine might also lead to the absorption of some metabolites of bacterial origin and residue of digestion which normally would have been refluxed back into the gut by the p-gp. To investigate if defective p-gp may be involved in the manifestation of unusual compounds and organic acids in the urine, inhibition of intestinal p-gp was proposed. Grapefruit juice (GJ), a natural beverage commonly taken by the majority of the populace has been reported to inhibit p-gp activity in the intestine (Spahn-Langguth & Langguth, 2001). Grapefruit juice was administered to healthy subjects in this study and the sugars and organic acids content of the urine sample after administration was analysed and compared with the controls (urine samples taken from the same set of subjects before grapefruit juice administration). These were determined by thin layer chromatography and gas chromatography-mass spectrophotometry respectively. The thin layer chromatography revealed that there was no difference between the concentrations of sugars in the control and samples after the administration of grapefruit juice. This might indicate that the inhibition of p-gp or mutation of the gene encoding p-gp does not result in the presence of sugars in the urine. The analysis of organic acids by gas chromatography-mass spectrophotometry method showed a remarkable difference between the organic acids present in the controls and urine samples after the administration of grapefruit juice as well as their concentrations. The organic acids solely from microbial origin were statistically analysed and the results gave statistically significant increase in these organic acids in the adults. There was no statistically significant increase in the children. In conclusion, this study confirmed that grapefruit juice inhibits p-gp in the intestine and this resulted in the presence of unusual organic acids from microbial origin in the urine of the adults. The presence of some of these organic acids have been indicated in some metabolic disorders and are also known to give rise to toxic effects on brain, liver, muscle and other tissues. There is the need to do more study on p-gp expression in children so that its functional roles and effect of the mutation of the gene encoding this protein can be known.
Thesis (M.Sc. (Pharm.))--North-West University, Potchefstroom Campus, 2004.
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Books on the topic "P-glycoprotein inhibitors"

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Huq, Rokaiya. Energy metabolism in human MCF-7 ADR and ADR-9 breast cancer cells treated with P-glycoprotein inhibitor PSC 833. Sudbury, Ont: Laurentian University, 2000.

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Kankesan, Janarthanan. Studies on the effect of PSC 833, a potent inhibitor of P-glycoprotein function on the development of cancer /cby Janarthanan Kankesan. 2006.

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Book chapters on the topic "P-glycoprotein inhibitors"

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Crowley, Emily, Christopher A. McDevitt, and Richard Callaghan. "Generating Inhibitors of P-Glycoprotein: Where to, Now?" In Methods in Molecular Biology, 405–32. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-416-6_18.

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Wang, Qing, and Tina M. Sauerwald. "Screening for P-Glycoprotein (Pgp) Substrates and Inhibitors." In Methods in Pharmacology and Toxicology, 337–52. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-742-6_20.

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van Triest, B., F. Telleman, H. M. Pinedo, C. L. van der Wilt, and G. J. Peters. "Cross-Resistance to Thymidylate Synthase Inhibitors in P-Glycoprotein and Non-P-Glycoprotein Cell Lines." In Purine and Pyrimidine Metabolism in Man VIII, 189–93. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-2584-4_41.

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Coley, Helen M. "Overcoming Multidrug Resistance in Cancer: Clinical Studies of P-Glycoprotein Inhibitors." In Methods in Molecular Biology, 341–58. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-416-6_15.

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Orlowski, S., J. Nugier, and Eric Ezan. "An Enzymatic Microplate Assay for Testing P-Glycoprotein Substrates and Inhibitors." In Optimization in Drug Discovery, 89–102. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-800-5:089.

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Palmeira, Andreia, Freddy Rodrigues, Emília Sousa, Madalena Pinto, M. Helena Vasconcelos, and Miguel X. Fernandes. "Pharmacophore-Based Screening as a Clue for the Discovery of New P-Glycoprotein Inhibitors." In Advances in Intelligent and Soft Computing, 175–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-13214-8_23.

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Newman, Michael J., Ross Dixon, and Barry Toyonaga. "OC144-093, a Novel P glycoprotein Inhibitor for the Enhancement of Anti-Epileptic Therapy." In Novartis Foundation Symposia, 213–30. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470846356.ch16.

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Guttmann, Oliver P., Ronald Binder, Oliver Gämperli, and Andreas Baumbach. "Antithrombotics for Acute and Chronic Coronary Syndromes." In Manual of Cardiovascular Medicine, 117–24. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198850311.003.0014.

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Thrombus formation involves activation of aggregating platelets as well as the formation of fibrin after activation of the coagulation cascade. Fibrin eventually binds to glycoprotein IIB/IIIA receptors on platelets thereby forming a very solid occlusive clot. There are several molecules interfering with platelet activation: (1) aspirin, which blocks the formation of thromboxane A2; (2) clopidogrel, prasugrel, and ticagrelor which block P2Y12 receptors and their activation by ADP; (3) glycoprotein inhibitors that interfere with glycoprotein IIB/IIIA on platelets, the final common pathway of platelet activation, and finally (4) thrombin inhibitors blocking PAR-1 receptors on platelets. Commonly, after an acute coronary syndrome (ACS) or after percutaneous coronary interventions (PCI) or even bypass surgery, dual antiplatelet therapy (DAPT) is recommended consisting of aspirin plus a P2Y12 inhibitor. The duration of treatment after the acute event is commonly 12 months for those with ACS and 6 months for those with a high bleeding risk. In patients with high ischaemic risk, prolonged DAPT treatment can be considered, but often such patients also have a high bleeding risk. Intravenous platelet inhibitors, such as Reopro, tirofiban, and others, are used mainly during PCI, particularly in patients with ACS. Inhibitors of coagulation cascade, such as factor Xa or factor II inhibitors or vitamin K antagonists are mainly used in patients with ACS and concomitant atrial fibrillation. In these patients, mainly aspirin or in some the P2Y12 inhibitor is skipped for some weeks or months.
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Karthika, Chenmala, and Raman Sureshkumar. "P-Glycoprotein Efflux Transporters and Its Resistance Its Inhibitors and Therapeutic Aspects." In Creatinine - A Comprehensive Update [Working Title]. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.90430.

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Petrovic, Stanko, Slobodan Obradovic, Marijana Petrovic, and Nemanja Rancic. "Platelets in Ulcerative Colitis: From Pathophysiology to Therapy." In Ulcerative Colitis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102041.

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Based on the role of platelets in inflammation and hemostasis it has been assumed that antiplatelet therapy could be beneficial for patients suffering from ulcerative colitis. Platelets present a link between inflammation and coagulation. They have more than 300 active mediators stored in their granules. Upon activation, platelet degranulate and release a lot of microparticles and mediators and interact with other immune and non-immune cells thereby amplifying inflammation. The most important parameters of platelet activation are P-selectin and CD40 ligand expressed on their surface upon activation, and their soluble forms presented in blood. Today, we have potent anti-platelet drugs that can inhibit platelet activation and degranulation, and thereby reduce inflammation. The most important drugs are P2Y12 receptor antagonists such as ticagrelor and clopidogrel and glycoprotein IIbIIIa inhibitors. Ticagrelor is an active drug and besides antiplatelet activity, it has bactericidal activity against Gram-positive strains and Clostridium difficile. Clopidogrel is a prodrug with less anti-inflammatory effect than ticagrelor and no proven bactericidal activity. Glycoprotein IIbIIIa inhibitors are very potent in reducing platelet aggregation but have lower anti-inflammatory potential than ticagrelor and clopidogrel.
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Conference papers on the topic "P-glycoprotein inhibitors"

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Ravula, Ranadheer, Jeffrey Wang, and Ying Huang. "Abstract 1534: Bioassay-guided identification of novel P-glycoprotein inhibitors from traditional Chinese medicines." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1534.

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Mohan, Rishabh, Aleem Gangjee, Ruoli Bai, and Ernest Hamel. "Abstract 4553: Substituted monocyclic pyrimidines as potent tubulin inhibitors that circumvent P-glycoprotein mediated resistance." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4553.

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Atkinson, Caroline, Carole Tactacan, Alvin Kamili, Federica Saletta, Christine Gana, Georgina Eden, Chelsea Mayoh, et al. "Abstract A35: P-Glycoprotein is a resistance mechanism for conventional induction chemotherapy but not ALK inhibitors in high-risk neuroblastoma." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-a35.

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Tripathi, Anushree, and Krishna Misra. "Stilbene analogues as inhibitors of breast cancer Stem cells through P-glycoprotein efflux; A 3D quantitative structure-activity relationship study (Inhibitory activity of stilbenes analogues on breast cancer stem cells)." In 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552134.

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Marongiu, F., M. R. Acca, G. Mulas, M. Conti, G. Sorano, and A. Balestrieri. "FIBRINOPEPTIDE B6 15-42 IN LIVER CIRRHOSIS: A SENSITIVE INDICATOR OF MILD FIBRINOLYSIS ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643063.

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In order to detect even minimal fibrinolysis activation in liver cirrhosis and to investigate whether an increased plasmin activity is related to a mild blood coagulation activation, we measured fibrinopeptide A (FPA) (Mailinckrodt) and fibrinopeptide BB 15-42 (BB 15-42) (IMCO and SORIN Biomedica) in 26 patients (16 men and 10 women, mean age 55.8 ± 13.1 years) with histologically proven liver cirrhosis..Mann-Whitney test, Student’s t test and correlation coefficient r were employed for statistical analysis when appropriate.FPA and BB 15-42 were not normal distributed and thus their levels were exprsessed as median and range.FPA values were significantly different in cirrhotic patients (3.9, 0.9-24.2 ng/ml) from those of the controls (2.5, 0.5-3.9 ng/ml) (p < 0.01).BB 15-42 levels were significantly higher in cirrhotic patients (19.4, 7.1-103.1 ng/ml) than in controls (10.4, 5.1-15.4 ng/ml) (p < 0.01). A posteriori the patients were divided in two subgroups according to whether their FPA levels were high (subgroup 1, n=10, FPA>4.0 ng/ml) or normal (subgroup 2, n=16, FPA < 4.0 ng/ml).In patients with high FPA levels we found higher levels of BB 15-42 (22.2, 9.9-103.1 ng/ml) than in patients with normal FPA (13.6, 7.1-30.7 ng/ml ).Thvis difference was significant (p < 0.02) .There was no relationship between FPA and BB 15-42.Our data indicate that in liver cirrhosis a mild fibrinolysis activation may occur.The role of a chronic intravascular coagulation appears to be significant in this regard.However the impaired clearance of plasminogen activators, the decreased synthesis of fibrinolysis inhibitors and the decreased levels of hystidine rich glycoprotein may be also involved in determining fibrinolysis activation as suggested by the lack of correlation between FPA and BB 15-42.
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Sudakova, E. A., A. V. Shchulkin, Y. V. Abalenikhina, and E. N. Yakusheva. "STUDY OF THE EFFECTS OF NITRIC OXIDE ON FUNCTIONING P - GLYCOPROTEIN." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.230-235.

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The article talks about the effect of nitric oxide (NO) on the functioning of the P-glycoprotein (Pgp) transporter protein in Caco-2 cells. The NO donor is S-nitrosoglutathione (GSNO). When exposed to a specific inhibitor of soluble guanylate cyclase, an increase in the relative amount of Pgp was shown.
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Nedeljković, Nikola V., Vladimir D. Dobričić, Marina Ž. Mijajlović, Gordana P. Radić, Miloš V. Nikolić, Ana S. Stanković, and Zorica B. Vujić. "„IN SILICO“ PREDICTION OF PHARMACOKINETIC PROPERTIES AND DRUGLIKENESS OF NOVEL THIOUREA DERIVATIVES OF NAPROXEN." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.371n.

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Masking the carboxyl group of naproxen with other functional groups may be a promising strategy to decrease its gastrointestinal toxicity. Thiourea moiety has been described as an important pharmacophore in a variety of pharmacologically active compounds, including anti-inflammatory, antiviral, anticancer, hypoglycemic and antimicrobial agents. Our research group has previously designed twenty novel thiourea derivatives of naproxen, containing amino acids (glycine, L-alanine, β-alanine, L-valine and L-phenylalanine – compounds 1,2,3,4 and 5, respectively), their methyl (6–10) and ethyl esters (11–15), as well as aromatic amines (16–20). Pharmacokinetic properties and druglikeness of these compounds were predicted using SwissADME web tool (http://www.swissadme.ch/). Predicted pharmacokinetic properties include potential for gastrointestinal absorption, blood-brain barrier permeability, skin permeability, transport mediated by P-glycoproteins and enzyme inhibitory potential. Druglikeness was evaluated using Lipinski’s, Ghose’s, Veber’s, Egan’s and Muegge’s rules, as well as on the basis of bioavailability score. All tested compounds had high-predicted gastrointestinal absorption and low blood-brain barrier permeability. Also, derivatives 2, 4, 7, 9, 10, 12, 14, 15 and 18 were predicted to be substrates for P-glycoprotein. Derivatives with aromatic amines (16–20) showed inhibitory potential against all tested CYP isoforms. Derivative 19 had the highest, while derivative 13 demonstrated the lowest predicted skin permeability. Finally, derivatives 1–12, except 5 and 10, have druglike structures, since they obey to all imposed rules.
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Prasad Dash, Ranjeet, Bhanuchander Ellendula, and Manish Nivsarkar. "Influence of diabetes progression on intestinal absorption of P-glycoprotein substrate: Implication of epigallocatechin-3-gallate (P-glycoprotein inhibitor) for reducing intestinal drug efflux." In Annual International Conference on Pharmaceutical Sciences and Pharmacology. Global Science & Technology Forum (GSTF), 2013. http://dx.doi.org/10.5176/2345-783x_pharma13.08.

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Abalenikhina, Y. V., A. A. Seidkuliyeva, E. D. Rokunov, D. S. Nemtinov, A. V. Shchulkin, and E. N. Yakusheva. "PARTICIPATION OF NUCLEAR FACTOR OF ERYTHROID ORIGIN-2 IN REGU-LATION P-GLYCOPROTEIN IN MODELING ENDOGENOUS OXIDATIVE STRESS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.251-257.

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The article discusses the mechanisms of regulation of the P-glycoprotein transporter protein (Pgp) in cells of the Caco2 line under conditions of modeling endogenous oxidative stress caused by exposure to DL-butyonine sulfoximine (BSO, a glutathione synthesis inhibitor). Ex-periments have shown that exposure to BSO at concentrations of 10-100 μM leads to a de-crease in the concentration of glutathione, an increase in the amount of Pgp and nuclear factor of erythroid origin 2 (Nrf2). Inhibition of Nrf2 contributed to the normalization of Pgp levels, which proves the participation of the transcription factor in the regulation of the transporter protein under the conditions of modeling endogenous oxidative stress.
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Hatachi, Y., H. Nagai, T. Mio, H. Yasuda, T. Sasaki, M. Asada, M. Mishima, and M. Yamaya. "Inhibitory Effects of Nitroglycerin on Intratumor P-Glycoprotein and Phospholyrated Caveolin-1 in Lewis Lung Carcinoma Bearing Murine Model." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5024.

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