A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
An estrogen metabolite that acts as a substrate of MRP2 (Km = 75 µM), and through MRP2-mediated transport, functions as a cholestatic agent, decreasing bile flow.
An estrogen metabolite that acts as a substrate of MRP2 (Km = 75 µM), and through MRP2-mediated transport, functions as a cholestatic agent, decreasing bile flow.
A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
An estrogen metabolite that acts as a substrate of MRP2 (Km = 75 µM), and through MRP2-mediated transport, functions as a cholestatic agent, decreasing bile flow.
An estrogen metabolite that acts as a substrate of MRP2 (Km = 75 µM), and through MRP2-mediated transport, functions as a cholestatic agent, decreasing bile flow.
A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
A non-cholestatic regioisomer of E217G that acts as a substrate for MRP2, competing with E217G for MRP2-mediated transport (IC<sub>50</sub> = 14.2 µM).
Ameliorates depression, reduces dopamine-induced neurotoxicity, and attenuates damage in a model of stroke blocks autophagy, reduces inflammation, and inhibits apoptosis in isolated neurons and in brains induces apoptosis in colon cancer cells.
Ameliorates depression, reduces dopamine-induced neurotoxicity, and attenuates damage in a model of stroke blocks autophagy, reduces inflammation, and inhibits apoptosis in isolated neurons and in brains induces apoptosis in colon cancer cells.