Comparative Metabolism of Radiolabeled Muraglitazar in Animals and Humans by Quantitative and Qualitative Metabolite Profiling
Muraglitazar (Pargluva), a dual α/γ peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering effects in animal models and in patients with diabetes. This study describes the in vivo and in vitro comparative metabolism of [ 14 C]muraglitazar in rats, dogs, m...
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Published in | Drug metabolism and disposition Vol. 35; no. 1; pp. 150 - 167 |
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Main Authors | , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Bethesda, MD
American Society for Pharmacology and Experimental Therapeutics
01.01.2007
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Abstract | Muraglitazar (Pargluva), a dual α/γ peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering
effects in animal models and in patients with diabetes. This study describes the in vivo and in vitro comparative metabolism
of [ 14 C]muraglitazar in rats, dogs, monkeys, and humans by quantitative and qualitative metabolite profiling. Metabolite identification
and quantification methods used in these studies included liquid chromatography/mass spectrometry (LC/MS), LC/tandem MS, LC/radiodetection,
LC/UV, and a newly described mass defect filtering technique in conjunction with high resolution MS. After oral administration
of [ 14 C]muraglitazar, absorption was rapid in all species, reaching a concentration peak for parent and total radioactivity in plasma
within 1 h. The most abundant component in plasma at all times in all species was the parent drug, and no metabolite was present
in greater than 2.5% of the muraglitazar concentrations at 1 h postdose in rats, dogs, and humans. All metabolites observed
in human plasma were also present in rats, dogs, or monkeys. Urinary excretion of radioactivity was low (<5% of the dose)
in all intact species, and the primary route of elimination was via biliary excretion in rats, monkeys, and humans. Based
on recovered doses in urine and bile, muraglitazar showed a very good absorption in rats, monkeys, and humans. The major drug-related
components in bile of rats, monkeys, and humans were glucuronides of muraglitazar and its oxidative metabolites. The parent
compound was a minor component in bile, suggesting extensive metabolism of the drug. In contrast, the parent drug and oxidative
metabolites were the major components in feces, and no glucuronide conjugates were found, suggesting that glucuronide metabolites
were excreted in bile and hydrolyzed in the gastrointestinal tract. The metabolites of muraglitazar resulted from both glucuronidation
and oxidation. The metabolites in general had greatly reduced activity as PPARα/γ activators relative to muraglitazar. In
conclusion, muraglitazar was rapidly absorbed, extensively metabolized through glucuronidation and oxidation, and mainly eliminated
in the feces via biliary excretion of glucuronide metabolites in all species studied. Disposition and metabolic pathways were
qualitatively similar in rats, dogs, monkeys, and humans. |
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AbstractList | Muraglitazar (Pargluva), a dual alpha/gamma peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering effects in animal models and in patients with diabetes. This study describes the in vivo and in vitro comparative metabolism of [(14)C]muraglitazar in rats, dogs, monkeys, and humans by quantitative and qualitative metabolite profiling. Metabolite identification and quantification methods used in these studies included liquid chromatography/mass spectrometry (LC/MS), LC/tandem MS, LC/radiodetection, LC/UV, and a newly described mass defect filtering technique in conjunction with high resolution MS. After oral administration of [(14)C]muraglitazar, absorption was rapid in all species, reaching a concentration peak for parent and total radioactivity in plasma within 1 h. The most abundant component in plasma at all times in all species was the parent drug, and no metabolite was present in greater than 2.5% of the muraglitazar concentrations at 1 h postdose in rats, dogs, and humans. All metabolites observed in human plasma were also present in rats, dogs, or monkeys. Urinary excretion of radioactivity was low (<5% of the dose) in all intact species, and the primary route of elimination was via biliary excretion in rats, monkeys, and humans. Based on recovered doses in urine and bile, muraglitazar showed a very good absorption in rats, monkeys, and humans. The major drug-related components in bile of rats, monkeys, and humans were glucuronides of muraglitazar and its oxidative metabolites. The parent compound was a minor component in bile, suggesting extensive metabolism of the drug. In contrast, the parent drug and oxidative metabolites were the major components in feces, and no glucuronide conjugates were found, suggesting that glucuronide metabolites were excreted in bile and hydrolyzed in the gastrointestinal tract. The metabolites of muraglitazar resulted from both glucuronidation and oxidation. The metabolites in general had greatly reduced activity as PPARalpha/gamma activators relative to muraglitazar. In conclusion, muraglitazar was rapidly absorbed, extensively metabolized through glucuronidation and oxidation, and mainly eliminated in the feces via biliary excretion of glucuronide metabolites in all species studied. Disposition and metabolic pathways were qualitatively similar in rats, dogs, monkeys, and humans. Muraglitazar (Pargluva), a dual α/γ peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering effects in animal models and in patients with diabetes. This study describes the in vivo and in vitro comparative metabolism of [ 14 C]muraglitazar in rats, dogs, monkeys, and humans by quantitative and qualitative metabolite profiling. Metabolite identification and quantification methods used in these studies included liquid chromatography/mass spectrometry (LC/MS), LC/tandem MS, LC/radiodetection, LC/UV, and a newly described mass defect filtering technique in conjunction with high resolution MS. After oral administration of [ 14 C]muraglitazar, absorption was rapid in all species, reaching a concentration peak for parent and total radioactivity in plasma within 1 h. The most abundant component in plasma at all times in all species was the parent drug, and no metabolite was present in greater than 2.5% of the muraglitazar concentrations at 1 h postdose in rats, dogs, and humans. All metabolites observed in human plasma were also present in rats, dogs, or monkeys. Urinary excretion of radioactivity was low (<5% of the dose) in all intact species, and the primary route of elimination was via biliary excretion in rats, monkeys, and humans. Based on recovered doses in urine and bile, muraglitazar showed a very good absorption in rats, monkeys, and humans. The major drug-related components in bile of rats, monkeys, and humans were glucuronides of muraglitazar and its oxidative metabolites. The parent compound was a minor component in bile, suggesting extensive metabolism of the drug. In contrast, the parent drug and oxidative metabolites were the major components in feces, and no glucuronide conjugates were found, suggesting that glucuronide metabolites were excreted in bile and hydrolyzed in the gastrointestinal tract. The metabolites of muraglitazar resulted from both glucuronidation and oxidation. The metabolites in general had greatly reduced activity as PPARα/γ activators relative to muraglitazar. In conclusion, muraglitazar was rapidly absorbed, extensively metabolized through glucuronidation and oxidation, and mainly eliminated in the feces via biliary excretion of glucuronide metabolites in all species studied. Disposition and metabolic pathways were qualitatively similar in rats, dogs, monkeys, and humans. Muraglitazar (Pargluva), a dual alpha/gamma peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering effects in animal models and in patients with diabetes. This study describes the in vivo and in vitro comparative metabolism of [(14)C]muraglitazar in rats, dogs, monkeys, and humans by quantitative and qualitative metabolite profiling. Metabolite identification and quantification methods used in these studies included liquid chromatography/mass spectrometry (LC/MS), LC/tandem MS, LC/radiodetection, LC/UV, and a newly described mass defect filtering technique in conjunction with high resolution MS. After oral administration of [(14)C]muraglitazar, absorption was rapid in all species, reaching a concentration peak for parent and total radioactivity in plasma within 1 h. The most abundant component in plasma at all times in all species was the parent drug, and no metabolite was present in greater than 2.5% of the muraglitazar concentrations at 1 h postdose in rats, dogs, and humans. All metabolites observed in human plasma were also present in rats, dogs, or monkeys. Urinary excretion of radioactivity was low (<5% of the dose) in all intact species, and the primary route of elimination was via biliary excretion in rats, monkeys, and humans. Based on recovered doses in urine and bile, muraglitazar showed a very good absorption in rats, monkeys, and humans. The major drug-related components in bile of rats, monkeys, and humans were glucuronides of muraglitazar and its oxidative metabolites. The parent compound was a minor component in bile, suggesting extensive metabolism of the drug. In contrast, the parent drug and oxidative metabolites were the major components in feces, and no glucuronide conjugates were found, suggesting that glucuronide metabolites were excreted in bile and hydrolyzed in the gastrointestinal tract. The metabolites of muraglitazar resulted from both glucuronidation and oxidation. The metabolites in general had greatly reduced activity as PPARalpha/gamma activators relative to muraglitazar. In conclusion, muraglitazar was rapidly absorbed, extensively metabolized through glucuronidation and oxidation, and mainly eliminated in the feces via biliary excretion of glucuronide metabolites in all species studied. Disposition and metabolic pathways were qualitatively similar in rats, dogs, monkeys, and humans. |
Author | Wen Chyi Shyu Nirmala Raghavan Ming Yao Wenying Li Haiying Zhang Gamini Chandrasena W. Griffith Humphreys Mingshe Zhu Suresh Yeola Donglu Zhang Lifei Wang Narayanan Hariharan Samuel Bonacorsi Litao Zhang Peter T. Cheng James Mitroka Vinayak Hosagrahara |
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Cites_doi | 10.1124/dmd.105.007856 10.1111/j.1742-1241.2000.tb11914.x 10.1124/dmd.105.007153 10.1592/phco.22.17.1527.34128 10.2337/dc05-1146 10.1201/b14095 10.1124/dmd.105.007617 10.1021/jm0496436 10.2165/00003495-199040020-00007 10.2165/00003495-200060020-00009 10.2337/diabetes.55.01.06.db05-0648 10.2165/00003495-199957060-00007 10.1083/jcb.43.3.506 10.1146/annurev.med.52.1.239 10.1002/jms.521 |
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References | 2019091113233803000_35.1.150.1 (2019091113233803000_35.1.150.10) 2000; 54 (2019091113233803000_35.1.150.5) 1993; 10 2019091113233803000_35.1.150.11 2019091113233803000_35.1.150.12 (2019091113233803000_35.1.150.4) 2000; 2 2019091113233803000_35.1.150.13 2019091113233803000_35.1.150.14 2019091113233803000_35.1.150.15 2019091113233803000_35.1.150.16 2019091113233803000_35.1.150.2 2019091113233803000_35.1.150.17 2019091113233803000_35.1.150.3 2019091113233803000_35.1.150.18 (2019091113233803000_35.1.150.6) 2001; 88 2019091113233803000_35.1.150.7 2019091113233803000_35.1.150.8 2019091113233803000_35.1.150.9 |
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Snippet | Muraglitazar (Pargluva), a dual α/γ peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering
effects in animal... Muraglitazar (Pargluva), a dual alpha/gamma peroxisome proliferator-activated receptor (PPAR) activator, has both glucose- and lipid-lowering effects in animal... |
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Title | Comparative Metabolism of Radiolabeled Muraglitazar in Animals and Humans by Quantitative and Qualitative Metabolite Profiling |
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