"... maybe people should be able to have their statin...with their drinking water."
Dr. John Reckless, consultant endocrinologist
With the knowledge that high cholesterol (blood fat) increases a person's risk of suffering a heart attack (or stroke), the quest was on to discover drugs that could be used to lower cholesterol. In 1959 scientists working at the Max Planck Institute in Heidelberg, Germany, identified the HMG-CoA reductase enzyme as a major contributor to production of internal cholesterol. The discovery inspired scientists worldwide to start searching for drugs to inhibit the enzyme and thereby reduce levels of cholesterol.
By 1976 Japanese researcher Akira Endo, from Sankyo, isolated the first inhibitor (Compactin, ML- 236B) of HMG-CoA reductase enzyme from the fungus Penicillium citrinium. Endo had chosen to begin his search in molds and fungi for the sole reason that this was his own particular area of expertise. In 1979 Carl Hoffman and colleagues working for Merck & Co. in the United States isolated MK-733 (later to be named Simvastatin) from a strain of the fungus Aspergillus terreus. But in 1980 clinical trials with Compactin were discontinued after rumors it caused cancers in dogs, and further setbacks to the drug followed.
In July 1982 the Federal Drug Administration (FDA) allowed Merck special permission to give Simvastatin to patients with severely high cholesterol. Simvastatin produced dramatic results with very few side effects and was approved by the FDA in September 1987.
