Relevant bibliographies by topics / N-desmethyl imatinib

Academic literature on the topic 'N-desmethyl imatinib'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "N-desmethyl imatinib"

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Wang, Zhe, Li Wang, Meng-ming Xia, Wei Sun, Cheng-ke Huang, Xiao Cui, Guo-xin Hu, Qing-quan Lian, and Zeng-shou Wang. "Pharmacokinetics Interaction between Imatinib and Genistein in Rats." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/368976.

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The objective of this work was to investigate the effect of orally administered genistein on the pharmacokinetics of imatinib and N-desmethyl imatinib in rats. Twenty-five healthy male SD (Sprague-Dawley) rats were randomly divided into five groups: A group (control group), B group (multiple dose of 100 mg/kg genistein for consecutive 15 days), C group (multiple dose of 50 mg/kg genistein for consecutive 15 days), D group (a single dose of 100 mg/kg genistein), and E group (a single dose of 50 mg/kg genistein). A single dose of imatinib is administered orally 30 min after administration of genistein (100 mg/kg or 50 mg/kg). The pharmacokinetic parameters of imatinib and N-desmethyl imatinib were calculated by DAS 3.0 software. The multiple dose of 100 mg/kg or 50 mg/kg genistein significantly (P<0.05) decreased theAUC0-tandCmaxof imatinib.AUC0-tand theCmaxof N-desmethyl imatinib were also increased, but without any significant difference. However, the single dose of 100 mg/kg or 50 mg/kg genistein has no effect on the pharmacokinetics of imatinib and N-desmethyl imatinib. Those results indicated that multiple dose of genistein (100 mg/kg or 50 mg/kg) induces the metabolism of imatinib, while single dose of genistein has no effect.
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Liu, Xian-yun, Tao Xu, Wan-shu Li, Jun Luo, Pei-wu Geng, Li Wang, Meng-ming Xia, Meng-chun Chen, Lei Yu, and Guo-xin Hu. "The Effect of Apigenin on Pharmacokinetics of Imatinib and Its Metabolite N-Desmethyl Imatinib in Rats." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/789184.

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The purpose of this study was to determine the effect of apigenin on the pharmacokinetics of imatinib and N-desmethyl imatinib in rats. Healthy male SD rats were randomly divided into four groups: A group (the control group), B group (the long-term administration of 165 mg/kg apigenin for 15 days), C group (a single dose of 165 mg/kg apigenin), and D group (a single dose of 252 mg/kg apigenin). The serum concentrations of imatinib and N-desmethyl imatinib were measured by HPLC, and pharmacokinetic parameters were calculated using DAS 3.0 software. The parameters ofAUC(0-t),AUC(0−∞),Tmax,Vz/F, andCLz/Ffor imatinib in group B were different from those in group A (P<0.05). Besides,MRT(0−t)andMRT(0−∞)in groups C and D differed distinctly from those in group A as well. The parameters ofAUC(0-t)andCmaxfor N-desmethyl imatinib in group C were significantly lower than those in group A (P<0.05); however, compared with groups B and D, the magnitude of effect was modest. Those results indicated that apigenin in the short-term study inhibited the metabolism of imatinib and its metabolite N-desmethyl imatinib, while in the long-term study the metabolism could be accelerated.
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Bornhäuser, Martin, Stefan Pursche, Malte Bonin, Jens Freiberg-Richter, Andreas Jenke, Thomas Illmer, Gerhard Ehninger, and Eberhard Schleyer. "Elimination of Imatinib Mesylate and Its Metabolite N-Desmethyl-Imatinib." Journal of Clinical Oncology 23, no. 16 (June 1, 2005): 3855–56. http://dx.doi.org/10.1200/jco.2005.05.246.

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4

Schleyer, E., O. G. Ottmann, T. Illmer, S. Pursche, T. Leopold, M. Bonin, J. Freiberg-Richter, et al. "Pharmacokinetics of Imatinib and its Main Metabolite N-desmethyl-imatinib." TumorDiagnostik & Therapie 25, no. 04 (August 2004): 192–96. http://dx.doi.org/10.1055/s-2004-813484.

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Khan, Muhammad Suleman, Daniel T. Barratt, and Andrew A. Somogyi. "Impact ofCYP2C8*3polymorphism onin vitrometabolism of imatinib to N-desmethyl imatinib." Xenobiotica 46, no. 3 (July 10, 2015): 278–87. http://dx.doi.org/10.3109/00498254.2015.1060649.

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Zhang, Y., S. Qiang, Z. Yu, W. Zhang, Z. Xu, L. Yang, A. Wen, and T. Hang. "LC-MS-MS Determination of Imatinib and N-Desmethyl Imatinib in Human Plasma." Journal of Chromatographic Science 52, no. 4 (April 10, 2013): 344–50. http://dx.doi.org/10.1093/chromsci/bmt037.

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7

Rao, Zhi, Bo-xia Li, Yong-Wen Jin, Wen-Kou, Yan-rong Ma, Guo-qiang Zhang, Fan Zhang, Yan Zhou, and Xin-an Wu. "Simultaneous Determination of Imatinib and N-Desmethyl Imatinib in Rat Plasma and Tissues Using LC-MS/MS." Current Pharmaceutical Analysis 15, no. 2 (January 4, 2019): 121–29. http://dx.doi.org/10.2174/1573412913666170821124952.

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Background: Imatinib (IM) is a chemotherapy medication metabolized by CYP3A4 to Ndesmethyl imatinib (NDI), which shows similar pharmacologic activity to the parent drug. Although methods for determination of IM and/or NDI have been developed extensively, only few observations have been addressed to simultaneously determine IM and NDI in biological tissues such as liver, kidney, heart, brain and bone marrow. Methods: A validated LC-MS/MS method was developed for the quantitative determination of imatinib (IM) and N-desmethyl imatinib (NDI) from rat plasma, bone marrow, brain, heart, liver and kidney. The plasma samples were prepared by protein precipitation, and then the separation of the analytes was achieved using an Agilent Zorbax Eclipse Plus C18 column (4.6 × 100 mm, 3.5 µm) with gradient elution running water (A) and methanol (B). Mass spectrometric detection was achieved by a triplequadrupole mass spectrometer equipped with an electrospray source interface in positive ionization mode. Results: This method was used to investigate the pharmacokinetics and the tissue distributions in rats following oral administration of 25 mg/kg of IM. The pharmacokinetic profiles suggested that IM and NDI are disappeared faster in rats than human, and the tissue distribution results showed that IM and NDI had good tissue penetration and distribution, except for the brain. This is the first report about the large penetrations of IM and NDI in rat bone marrow. Conclusion: The method demonstrated good sensitivity, accuracy, precision and recovery in assays of IM and NDI in rats. The described assay was successfully applied for the evaluation of pharmacokinetics and distribution in the brain, heart, liver, kidney and bone marrow of IM and NDI after a single oral administration of IM to rats.
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Mlejnek, Petr, Petr Dolezel, Edgar Faber, and Petr Kosztyu. "Interactions of N-desmethyl imatinib, an active metabolite of imatinib, with P-glycoprotein in human leukemia cells." Annals of Hematology 90, no. 7 (January 12, 2011): 837–42. http://dx.doi.org/10.1007/s00277-010-1142-7.

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Solassol, I., F. Bressolle, L. Philibert, V. Charasson, C. Astre, and F. Pinguet. "Liquid Chromatography‐Electrospray Mass Spectrometry Determination of Imatinib and Its Main Metabolite, N‐Desmethyl‐Imatinib in Human Plasma." Journal of Liquid Chromatography & Related Technologies 29, no. 20 (December 2006): 2957–74. http://dx.doi.org/10.1080/10826070600981058.

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10

Zhang, Mei, Grant A. Moore, Liam J. Fernyhough, Murray L. Barclay, and Evan J. Begg. "Determination of imatinib and its active metabolite N-desmethyl imatinib in human plasma by liquid chromatography/tandem mass spectrometry." Analytical and Bioanalytical Chemistry 404, no. 6-7 (August 3, 2012): 2091–96. http://dx.doi.org/10.1007/s00216-012-6284-0.

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Dissertations / Theses on the topic "N-desmethyl imatinib"

1

Khan, Muhammad Suleman. "Impact of CYP2C8 single nucleotide polymorphisms on in-vitro metabolism of imatinib to N-desmethyl imatinib." Thesis, 2015. http://hdl.handle.net/2440/105021.

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Imatinib is a first line therapy for the treatment of chronic myeloid leukaemia (CML). Treatment with imatinib must be continuous and indefinite for most patients to maintain disease control. Despite excellent efficacy and tolerability, up to 50% of CML patients discontinue imatinib due to lack of efficacy and adverse events. Imatinib is metabolised to its main metabolite N-desmethyl imatinib by CYP3A4 and CYP2C8. In vitro human liver microsome (HLM) studies indicate imatinib autoinhibition of CYP3A4-mediated metabolism, suggesting a more significant role for CYP2C8 upon chronic dosing. CYP2C8 is polymorphic and functional effects of the major CYP2C8 polymorphisms CYP2C8*3 and CYP2C8*4 on N-desmethyl imatinib formation are unknown. It was hypothesised that CYP2C8*3 and CYP2C8*4 genetic polymorphisms will decrease imatinib metabolism to N-desmethyl imatinib in HLM. Therefore the aim of this study was to examine the impact of CYP2C8*3 and CYP2C8*4 on N-demethylation of imatinib in HLMs genotyped for CYP2C8*1/*1 (n=5), CYP2C8*1/*3 (n=4), CYP2C8*1/*4 (n=2), in CYP2C8*3/*3 pooled HLM, and in expressed CYP2C8 and CYP3A4 enzymes. Effects of CYP-selective chemical and antibody inhibitors on N-demethylation were also determined. A single enzyme Michaelis-Menten model with substrate inhibition best fitted wild-type CYP2C8*1/*1 HLM kinetic data (median ± SD K𝚒 = 139 ± 61 μM). Three of four CYP2C8*1/*3 HLMs showed single enzyme but no substrate inhibition kinetics. Binding affinity (K𝚖) was approximately 2-fold higher in CYP2C8*1/*3 HLMs as compared to CYP2C8*1/*1 (median ± SD K𝚖 = 6 ± 2 vs 11 ± 2 μM, p=0.04). Intrinsic clearance (Cl𝚒𝚗𝚝) was higher in CYP2C8*1/*3 HLMs compared to CYP2C8*1/*1 (median ± SD Cl𝚒𝚗𝚝 = 19 ± 8 vs 13 ± 2 μl/min/mg, p = 0.25). CYP2C8*3/*3 (pooled HLM) showed highest binding affinity (K𝚖 = 3.6 μM) and weak autoinhibition (K𝚒 = 449 μM) kinetics. N-desmethyl imatinib formation was below the limit of quantification in one CYP2C8*1/*4 HLM, whereas the other CYP2C8*1/*4 HLM showed lower intrinsic clearance (Cl𝚒𝚗𝚝 = 7 vs 11 ± 2 μl/min/mg) due to 2-fold lower catalytic activity (V𝚖𝚊𝚡) compared to the wild-type (V𝚖𝚊𝚡 = 73 vs 140 ± 31 pmol/min/mg). A single enzyme model with substrate inhibition best fitted expressed CYP2C8 kinetic data (K𝚒 = 149 μM). Expressed CYP3A4 showed two site enzyme kinetics with no evidence of autoinhibition. CYP2C8 inhibitors reduced N-demethylation in HLM by 47-75%, compared to 0-30% for CYP3A4 inhibitors. Two unidentified peaks M1 and M2 were found in expressed CYP3A4, whereas they were absent in expressed CYP2C8. These results indicate that CYP2C8*3 may enhance CYP2C8 activity by influencing autoinhibition, and that in vitro the metabolism and autoinhibition of imatinib N-demethylation appears mainly mediated by CYP2C8 and not CYP3A4. CYP2C8*4 appears a reduced functional allele for imatinib N-demethylation.
Thesis (M.Phil.) (Research by Publication) -- University of Adelaide, School of Medicine, 2015.
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