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HMG-CoA reductase inhibitors, the statins, block the rate-limiting enzyme of cholesterol biosynthesis. 3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase converts HMG-CoA into mevalonate, the precursor of sterols and isoprenoids. The first inhibitors of this step, ML-236A, ML-236B and ML-236C, were isolated from Penicillium citrinum in 1976. Crystal structures reported in 2001 showed that statins occupy the HMG-CoA binding site and block substrate access. Lovastatin, simvastatin and pravastatin sodium are fungal statins or close derivatives. Atorvastatin calcium, rosuvastatin calcium, fluvastatin sodium and pitavastatin calcium are fully synthetic statins. Researchers use them to study cholesterol synthesis, protein prenylation and lipid-dependent signaling in cells.
QH536 is a potent degrader of HMGCR, exhibiting an EC50 of 0.22 μM. This compound is notable for not causing cholesterol accumulation in cells, thereby mitigating potential side effects. QH536 demonstrates anti-inflammatory properties and has applications in research related to cardiovascular disease and nonalcoholic steatohepatitis.
