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Background Information of M-I

M-I is a metabolism of TAK-875. TAK-875 is a G protein-coupled receptor 40 agonist.

Solubility of M-I

Solubility Sources

Storage Condition of M-I

Storage Condition Sources

MSDS Information

MSDS Sources

Quality Control and Spectral Data

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Mechanism and Indications

Signaling Pathways GPCR/G Protein
Target GPR40
Research Area Metabolic Disease

Clinical Information

Product Name Sponsor & Collaborators Indications Start Date End Date Phase

Chemical Information

M.Wt Formula CAS No. Synonyms
362.44 C19H22O5S

Structure Information of M-I

Smiles C1(C2=C(C)C=C(OCCCS(C)(=O)=O)C=C2C)=CC=CC(C(O)=O)=C1
InChI InChI=1S/C19H22O5S/c1-13-10-17(24-8-5-9-25(3,22)23)11-14(2)18(13)15-6-4-7-16(12-15)19(20)21/h4,6-7,10-12H,5,8-9H2,1-3H3,(H,20,21)

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T-1676427 1000414-39-0 C29H32O8S 0
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Chemical and Physical Properties

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[1].Kogame A, et al. Disposition and metabolism of the G protein-coupled receptor 40 agonist TAK-875 (fasiglifam) in rats, dogs, and humans. Xenobiotica. 2018 Mar 20:1-41.
1. The absorption, distribution, metabolism and excretion of fasiglifam were investigated in rats, dogs, and humans. 2. The absolute oral bioavailability of fasiglifam was high in all species (> 76.0%). 3. After oral administration of [14C]fasiglifam, the administered radioactivity was quantitatively recovered and the major route of excretion of radioactivity was via feces in all species. 4. Fasiglifam was a major component in the plasma and feces in all species. Its oxidative metabolite (M-I) was observed as a minor metabolite in rat and human plasma (< 10% of plasma radioactivity). In human plasma, hydroxylated fasiglifam (T-1676427), the glucuronide of fasiglifam (fasiglifam-G), and the glucuronide of M-I were detected as additional minor metabolites (< 2% of plasma radioactivity). None of these metabolites were specific to humans. Fasiglifam-G was the major components in the rat and dog bile. 5. In vitro cytochrome P450 (CYP) and uridine diphosphate glucuronosyltransferase (UGT) reaction phenotyping indicated that oxidation (to form M-I and T-1676427) and glucuronidation of fasiglifam are mainly mediated by CYP3A4/5 and UGT1A3, respectively. 6. Fasiglifam and fasiglifam-G are substrates of BCRP and Mrp2/MRP2, respectively. 7. Glucuronidation of fasiglifam-G was found to be the predominant elimination pathway of fasiglifam in all species tested, including humans.

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