It is CC1=CC(=CC(=C1C2=CC=CC(=C2)COC3=CC4=C(C=C3)[C@@H](CO4)CC(=O)O)C)OCCCS(=O)(=O)C.
What is EC number of Tak875？
805-621-8
What is exact mass of Tak875？
524.18687453
What is molecular formula of Tak875？
C29H32O7S
TAK-875 Induces Hepatotoxicity Through Generation of Reactive Oxygen Species in A GPR40-Dependent Manner
Kim M J, et al. Biomolecules & Therapeutics, 2018, 26(6), 599.
TAK-875 is a G protein-coupled receptor 40 (GPR40) agonist that significantly improves hyperglycemia. However, hepatotoxicity of TAK-875 led to the early termination of its development. The direct hepatotoxicity of TAK-875 can be assessed through in vitro 2D and 3D HepG2 culture models. TAK-875 reduces the viability of human hepatoma cell line HepG2 2D and 3D cultures in a concentration (>50 μM) and time-dependent manner, both corresponding to ROS production. Cell processing steps · Cells were treated with varying concentrations of TAK-875, APAP, or DMSO (final 0.5%) in culture medium for 24 h. · The control group was treated with only 0.5% DMSO. Fibroblasts were seeded into 6-well plates at a density of 1.5×10 5 /well, while HepG2 cells were seeded into 96-well plates at a density of 1.0×10 4 /well. · For ROS assay, each cell line was seeded in 6-well plates at 1.5 × 10 5 /well.
TAK-875 Improves Cognitive Deficits and Reduces Beta-Amyloid Production in Mice
Liu C, et al. Psychopharmacology, 2021, 238(8), 2133-2146.
TAK-875 is a G protein-coupled receptor 40 (GPR40) agonist. GPR40 is expressed in brain and peripheral cells and is related to cognitive functions such as spatial orientation, memory and learning. Research suggests that GPR40 may be a potential therapeutic target for AD. TAK-875, as a GPR40 agonist, has the potential to become a drug for Alzheimer's disease (AD). The activation of GPR40 by TAK-875 can effectively rescue cognitive deficits in APPswe/PS1dE9 mice. These effects may be mediated by the regulation of PLC/PKC/ADAM10 signaling pathway, which promoted APP non-amyloidogenic processing pathway and reduced Aβ production. Experiment content · Fifty APPswe/PS1dE9 mice and 10 wild-type littermates were randomly divided into 6 groups for experiments with different administration methods. · The TAK-875, GW1100, and normal saline (NS) were administered intracerebroventricularly once per day for 7 consecutive days through an intracerebroventricular administration system. · The infusion volume for each medication every day was 5 μl, but in GW1100 + TAK-H group, to exclude interference factor from infusion volume, the infusion volume for each drug was 2.5 μl. · In addition, the mice in GW1100 + TAK-H group were initially treated with GW1100, and then with TAK-875 30 min later.
Related Research
Mechanism Investigation of TAK-875 As GPR40 Agonist
Original Article: TAK-875 Mitigates β-Cell Lipotoxicity-Induced Metaflammation Damage through Inhibiting the TLR4-NF-κB Pathway
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Kim M J, et al. Biomolecules & Therapeutics, 2018, 26(6), 599.
Liu C, et al. Psychopharmacology, 2021, 238(8), 2133-2146.
