Yvonne Will

TL;DR: To increase detection of drug-induced mitochondrial effects in a preclinical cell-based assay, HepG2 cells were forced to rely on mitochondrial oxidative phosphorylation rather than glycolysis by substituting galactose for glucose in the growth media.

TL;DR: It is demonstrated that ERβ is localized to mitochondria, suggesting a role for mitochondrial ERβ in estrogen effects on this important organelle.

TL;DR: A thorough analysis of properties for 119 marketed CNS drugs and a set of 108 Pfizer CNS candidates focused on understanding the relationships between physicochemical properties, in vitro ADME attributes, primary pharmacology binding efficiencies, and in vitro safety data.

TL;DR: Assays for mitochondrial function, cell models that better report mitochondrial impairment, and new animal models that more faithfully reflect clinical manifestations of mitochondrial dysfunction are discussed in the context of how such data can reduce late stage attrition of drug candidates and can yield safer drugs in the future.

TL;DR: Data indicate that biguanide-induced lactic acidosis can be attributed to acceleration of glycolysis in response to mitochondrial impairment, and the desired clinical outcome, viz., decreased blood glucose, could be due to increased glucose uptake and Glycolytic flux in Response to drug-induced mitochondrial dysfunction.