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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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1

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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Анотація:
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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2

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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3

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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5

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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6

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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Анотація:
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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8

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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9

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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11

Marangon, Elena, Marco Citterio, Federica Sala, Elena Barisone, Alma Augusta Lippi, Carmelo Rizzari, Andrea Biondi, Maurizio D’Incalci, and Massimo Zucchetti. "Pharmacokinetic profile of imatinib mesylate and N-desmethyl-imatinib (CGP 74588) in children with newly diagnosed Ph+ acute leukemias." Cancer Chemotherapy and Pharmacology 63, no. 3 (June 3, 2008): 563–66. http://dx.doi.org/10.1007/s00280-008-0764-0.

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12

Arellano, Cécile, Peggy Gandia, Thierry Lafont, Rutchanna Jongejan, and Etienne Chatelut. "Determination of unbound fraction of imatinib and N-desmethyl imatinib, validation of an UPLC–MS/MS assay and ultrafiltration method." Journal of Chromatography B 907 (October 2012): 94–100. http://dx.doi.org/10.1016/j.jchromb.2012.09.007.

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13

Gandia, Peggy, Cécile Arellano, Thierry Lafont, Françoise Huguet, Laurence Malard, and Etienne Chatelut. "Should therapeutic drug monitoring of the unbound fraction of imatinib and its main active metabolite N-desmethyl-imatinib be developed?" Cancer Chemotherapy and Pharmacology 71, no. 2 (November 27, 2012): 531–36. http://dx.doi.org/10.1007/s00280-012-2035-3.

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14

Mokosch, Annika S., Stefanie Gerbig, Christoph G. Grevelding, Simone Haeberlein, and Bernhard Spengler. "High-resolution AP-SMALDI MSI as a tool for drug imaging in Schistosoma mansoni." Analytical and Bioanalytical Chemistry 413, no. 10 (March 15, 2021): 2755–66. http://dx.doi.org/10.1007/s00216-021-03230-w.

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Анотація:
AbstractSchistosoma mansoni is a parasitic flatworm causing schistosomiasis, an infectious disease affecting several hundred million people worldwide. Schistosomes live dioeciously, and upon pairing with the male, the female starts massive egg production, which causes pathology. Praziquantel (PZQ) is the only drug used, but it has an inherent risk of resistance development. Therefore, alternatives are needed. In the context of drug repurposing, the cancer drug imatinib was tested, showing high efficacy against S. mansoni in vitro. Besides the gonads, imatinib mainly affected the integrity of the intestine in males and females. In this study, we investigated the potential uptake and distribution of imatinib in adult schistosomes including its distribution kinetics. To this end, we applied for the first time atmospheric-pressure scanning microprobe matrix-assisted laser desorption/ionization mass spectrometry imaging (AP-SMALDI MSI) for drug imaging in paired S. mansoni. Our results indicate that imatinib was present in the esophagus and intestine of the male as early as 20 min after in vitro exposure, suggesting an oral uptake route. After one hour, the drug was also found inside the paired female. The detection of the main metabolite, N-desmethyl imatinib, indicated metabolization of the drug. Additionally, a marker signal for the female ovary was successfully applied to facilitate further conclusions regarding organ tropism of imatinib. Our results demonstrate that AP-SMALDI MSI is a useful method to study the uptake, tissue distribution, and metabolization of imatinib in S. mansoni. The results suggest using AP-SMALDI MSI also for investigating other antiparasitic compounds and their metabolites in schistosomes and other parasites. Graphical abstract
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15

Tan, Ka Liong, Ravindran Ankathil, and Siew Hua Gan. "Method development and validation for the simultaneous determination of imatinib mesylate and N-desmethyl imatinib using rapid resolution high performance liquid chromatography coupled with UV-detection." Journal of Chromatography B 879, no. 30 (November 2011): 3583–91. http://dx.doi.org/10.1016/j.jchromb.2011.09.048.

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16

Bauer, Sebastian, Ralf A. Hilger, Florian Grabellus, James Nagarajah, Mathias Hoiczyk, Annette Reichardt, Marit Ahrens, et al. "Phase I trial of panobinostat (P) and imatinib (IM) in patients with treatment-refractory gastrointestinal stromal tumors (GIST)." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 10032. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.10032.

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10032^ Background: Panobinostat (LBH589; P) is a pan-deacetylase-inhibitor that has preclinical activity in combination with IM in GIST models in vitro and in vivo. Aim of this study was to determine the maximum tolerated dose (MTD) and dose-limiting toxicities (DLT) of escalating doses of P in combination with IM in patients with GIST who have failed IM and sunitinib treatment. Methods: This was a two-center phase I study using a 3+3 design with a prespecified expansion of the MTD cohort. IM was administered at a dose of 400mg qd. Following a 7 day run-in phase, escalating doses of P were added. The starting dose for P was 20 mg given as a three-times-per-week (MWF schedule) oral dose for 3 out of 4 weeks. Doses were increased by 10 mg if no dose limiting toxicities emerged. Blood samples were drawn for PK and biomarker assessments of IM, its main metabolite N-desmethyl-IM, and P using a validated RP-HPLC method. Acetylation of histone A3 was evaluated in peripheral blood mononuclear cells (PBMNC) as pharmacodynamic marker for P activity. Metabolic response using PET (EORTC-PET study criteria) was assessed on day 7 of IM run-in and after 3 weeks of combined treatment with IM and P. Results: In total 12 extensively pretreated (median 5 pretreatments) pts (4 f, 8 m; median age 56 y, 34-75 y) received study treatment at 2 dose levels (DL). 2 dose-limiting toxicities (grade 4 thrombocytopenia) occurred at DL 2 (30 mg). Most common AEs were thrombocytopenia, anemia, fatigue, nausea, emesis, diarrhea, creatinine elevation, abdominal cramping, and weight loss. DL 1 (20mg) was declared MTD, and 5 additional pts were enrolled at DL1. Analysis of P and IM PK revealed mean peak concentration of 14.8 +/- 9.5 ng/ml for P (20 mg). IM plasma concentrations with 400 mg once-daily administration were 2.8 ± 1.1 μg/mL at peak and 1.2 ± 0.4 μg/mL at trough. Histone A3 acetylation was demonstrated in PBMNC from pts treated at DL 1. 11 pts were evaluable for PET response: 1 had mPR, 7 had mSD and 3 had mPD. Longest treatment duration was 17 weeks (median: 6wks). Conclusions: P in combination with IM is moderately tolerated. Evidence of target inhibition at the MTD was associated with limited clinical activity in heavily pretreated pts with GIST.
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17

Darweesh, Ruba S., Tamam El-Elimat, Aref Zayed, Tareq N. Khamis, Wahby M. Babaresh, Tawfiq Arafat, and Ahmed H. Al Sharie. "The effect of grape seed and green tea extracts on the pharmacokinetics of imatinib and its main metabolite, N-desmethyl imatinib, in rats." BMC Pharmacology and Toxicology 21, no. 1 (November 16, 2020). http://dx.doi.org/10.1186/s40360-020-00456-9.

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Abstract Background Imatinib is mainly metabolized by CYP3A4 and to a lesser extent by other isoenzymes, with N-desmethyl imatinib being its major equipotent metabolite. Being a CYP3A4 substrate, imatinib co-administration with CYP3A4 modulators would change its pharmacokinetic profile. The cancer chemoprevention potential and anticancer efficacy of many herbal products such as grape seed (GS) and green tea (GT) extracts had led to an increase in their concomitant use with anticancer agents. GS and GT extracts were demonstrated to be potent inhibitors of CYP3A4. The aim of this study is to investigate the effect of standardized GS and/or GT extracts at two different doses on the pharmacokinetics of imatinib and its metabolite, N-desmethyl imatinib, in SD-rats. Methods Standardized GS and/or GT extracts were administered orally once daily for 21 days, at low (l) and high (h) doses, 50 and 100 mg/kg, respectively, before the administration of a single intragastric dose of imatinib. Plasma samples were collected and analyzed for imatinib and N-desmethyl imatinib concentrations using LC-MS/MS method, then their non-compartmental pharmacokinetic parameters were determined. Results h-GS dose significantly decreased imatinib’s Cmax and the $$ {\mathrm{AUC}}_0^{\infty } $$ AUC 0 ∞ by 61.1 and 72.2%, respectively. Similar effects on N-desmethyl imatinib’s exposure were observed as well, in addition to a significant increase in its clearance by 3.7-fold. l-GT caused a significant decrease in imatinib’s Cmax and $$ {\mathrm{AUC}}_0^{\infty } $$ AUC 0 ∞ by 53.6 and 63.5%, respectively, with more significant effects on N-desmethyl imatinib’s exposure, which exhibited a significant decrease by 79.2 and 81.1%, respectively. h-GT showed similar effects as those of l-GT on the kinetics of imatinib and its metabolite. However, when these extracts were co-administered at low doses, no significant effects were shown on the pharmacokinetics of imatinib and its metabolite. Nevertheless, increasing the dose caused a significant decrease in Cmax of N-desmethyl imatinib by 71.5%. Conclusions These results demonstrated that the pharmacokinetics of imatinib and N-desmethyl imatinib had been significantly affected by GS and/or GT extracts, which could be partially explained by the inhibition of CYP3A-mediated metabolism. However, the involvement of other kinetic pathways such as other isoenzymes, efflux and uptake transporters could be involved and should be characterized. Graphical abstract
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18

Sabri, Alaa, Mervat M. Omran, S. Abdel Azim, Raafat Abdelfattah, Rasha Mahmoud Allam, and Samia A. Shouman. "A Study to Explore the Role of IDH1 (R132) Mutation on Imatinib Toxicity and Effect of ABCG2/OCT1 Expression on N-Desmethyl Imatinib Plasma Level in Egyptian Chronic Myeloid Leukemia Patients." Drug Research, January 11, 2023. http://dx.doi.org/10.1055/a-1924-7746.

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AbstractImatinib mesylate (IM) is the gold standard for treatment of Chronic Myeloid Leukemia (CML). This study aimed to gain more knowledge of the altered PK, pharmacogenetic factors, and gene expression leading to variable IM levels. Fifty patients with chronic phase-CML were enrolled in this study and divided as 25 responders and 25 non-responders (patients are directly recruited after response assessment). HPLC/MS/MS was used to determine trough and peak concentration of imatinib and N-desmethyl imatinib in the blood. PCR-RFLP technique was used to detect IDH1 gene mutation (R132). The median value of IM trough level was significantly higher, the P/T ratio was significantly lower and the α-1-acid glycoprotein (AGP) was significantly higher among responders compared to non-responders (P=0.007, 0.009 and 0.048, respectively). Higher N-desmethyl imatinib peak plasma concentration was observed with low mRNA expression of ABCG2 and OCT1 (P=0.01 and 0.037, respectively). IDH1 R132 gene mutation was associated with a significant increase in toxicities (P=0.028). In conclusion, IM trough level, P/T ratio and AGP was significantly higher in responders. In addition, ABCG2 and OCT1 gene expression may affect the interindividual PK variation. Although a prospective study with a larger patient population is necessary to validate these findings. IDH1 mutation is a predictor of increased toxicity with IM treatment.
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19

Rahimi Kakavandi, Nader, Tayebeh Asadi, Behrouz Jannat, Khosrou Abdi, Mahmoud Ghazi‐Khansari, Hossein Shahali, and Karim Naraki. "Method development for determination of imatinib and its major metabolite, N ‐desmethyl imatinib, in biological and environmental samples by SA–SHS–LPME and HPLC." Biomedical Chromatography 35, no. 7 (February 25, 2021). http://dx.doi.org/10.1002/bmc.5088.

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20

Morawietz, Carolin M., Hicham Houhou, Oliver Puckelwaldt, Laura Hehr, Domenic Dreisbach, Annika Mokosch, Elke Roeb, Martin Roderfeld, Bernhard Spengler, and Simone Haeberlein. "Targeting Kinases in Fasciola hepatica: Anthelminthic Effects and Tissue Distribution of Selected Kinase Inhibitors." Frontiers in Veterinary Science 7 (December 21, 2020). http://dx.doi.org/10.3389/fvets.2020.611270.

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Анотація:
Protein kinases have been discussed as promising druggable targets in various parasitic helminths. New drugs are also needed for control of fascioliasis, a food-borne trematode infection and worldwide spread zoonosis, caused by the liver fluke Fasciola hepatica and related species. In this study, we intended to move protein kinases more into the spotlight of Fasciola drug research and characterized the fasciolicidal activity of two small-molecule inhibitors from human cancer research: the Abelson tyrosine kinase (ABL-TK) inhibitor imatinib and the polo-like 1 (PLK1) inhibitor BI2536. BI2536 reduced viability of 4-week-old immature flukes in vitro, while adult worms showed a blockade of egg production. Together with a significantly higher transcriptional expression of PLK1 in adult compared to immature worms, this argues for a role of PLK1 in fluke reproduction. Both fluke stages expressed ABL1-TK transcripts at similar high levels and were affected by imatinib. To study the uptake kinetic and tissue distribution of imatinib in F. hepatica, we applied matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging (MSI) for the first time in this parasite. Drug imaging revealed the accumulation of imatinib in different fluke tissues from 20 min to 12 h of exposure. Furthermore, we show that imatinib is metabolized to N-desmethyl imatinib by F. hepatica, a bioactive metabolite also found in humans. Besides the vitellarium, gastrodermal tissue showed strong signal intensities. In situ hybridization demonstrated the gastrodermal presence of abl1 transcripts. Finally, we assessed transcriptional changes of physiologically important genes in imatinib-treated flukes. Moderately increased transcript levels of a gene encoding a multidrug resistance protein were detected, which may reflect an attempt to defend against imatinib. Increased expression levels of the cell cycle dependently expressed histone h2b and of two genes encoding superoxide dismutases (SODs) were also observed. In summary, our pilot study demonstrated cross-stage activity of imatinib but not BI2536 against immature and adult F. hepatica in vitro; a fast incorporation of imatinib within minutes, probably via the oral route; and imatinib-induced expression changes of physiologically relevant genes. We conclude that kinases are worth analyzing in more detail to evaluate the potential as therapeutic targets in F. hepatica.
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