Thus, these highly proliferable cells are far less sensitive to drugs interfering with mitochondrial energy production. Drugs which lead to strong mitochondrial toxicity in vivo might not have any effect on cell viability of such cells.
Overlooking mitochondrial toxicity early in preclinical studies can cause high costs for development without any chance for commercialisation.
Two well-known examples withdrawn from the market due to undetected drug-induced mitochondrial toxicity are troglitazone (Daiichi Sankyo Co., withdrawn from the market in 2000, see Masubuchi et al., 2006), and cerivastatin (Bayer AG, withdrawn from the market in 2001, see Kaufmann et al., 2006).
There is a long list of drugs failing in later-stages of the drug development due to undiscovered mitochondrial toxicity and the list of these drugs goes on and on. Although it remains one of the primary reasons for late-stage drug attrition, mitochondrial toxicity is still not addressed by most preclinical screens.
Pharmacelsus solved the critical challenge of undiscovered mitochondrial toxicity and established a state-of-the-art multi-tiered mitochondrial toxicity screening enabling early hazard identification of pharmaceuticals.
Download the free white paper highlighting how to screen for mitochondrial toxicity and introducing the new screening tool Mitoscreen at Pharmacelsus.
Services available at Pharmacelsus: ADME & in vitro Pharmacology, Target Finding & Biological Profiling, in vivo Pharmacology & PK, Bioanalytics, Target-Based Bioassays.
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