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T-1676427

(CAS: 1000414-39-0)

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AMEDCHEM [email protected]em.com +862168061059 CHINA

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Background Information of T-1676427

T-1676427 is a metabolism of TAK-875. TAK-875 is a G protein-coupled receptor 40 agonist.

Solubility of T-1676427

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Storage Condition of T-1676427

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MSDS Information

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Quality Control and Spectral Data

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Mechanism and Indications

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

Clinical Information

Product Name Sponsor & Collaborators Indications Start Date End Date Phase

Chemical Information

M.Wt Formula CAS No. Synonyms
540.62 C29H32O8S 1000414-39-0

Structure Information of T-1676427

Smiles C(O)(=O)C[[email protected]]1C2=CC=C(OCC3C=CC=C(C4=C(C)C=C(OCCCS(C)(=O)=O)C=C4CO)C=3)C=C2OC1 |&1:4|
InChI InChI=1S/C29H32O8S/c1-19-11-25(35-9-4-10-38(2,33)34)13-22(16-30)29(19)21-6-3-5-20(12-21)17-36-24-7-8-26-23(14-28(31)32)18-37-27(26)15-24/h3,5-8,11-13,15,23,30H,4,9-10,14,16-18H2,1-2H3,(H,31,32)/t23-/m1/s1

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GPR40 Activator 1 1309435-60-6 C31H31NO3S 6
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TUG-770 1402601-82-4 C19H14FNO2 13
GW9508 885101-89-3 C22H21NO3 22
TAK-875 1000413-72-8 C29H32O7S 16
GW-1100 306974-70-9 C27H25FN4O4S 9
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M-I C19H22O5S 0
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AM-6226 C32H36F2O4 0
GPR40 agonist 1 1312788-44-5 C24H20O3 0
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Chemical and Physical Properties

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Reference

[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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