Lovastatin-Mevacor: Difference between revisions

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== History/Origin ==
== History/Origin ==


Increasing evidence about the correlation between high cholesterol levels and disease in the 1905’s and 1960’s lead scientists to discover new forms of constraining this link. Many companies researched more about the biosynthetic pathway of cholesterol in order to determine which step is important to slow down the production of cholesterol. Towards the end of the 1970’s, various pharmaceutical companies searched for different alternatives after the discovery of compactin, a potential inhibitor discovered earlier in the decade but was not effective due to its dangerous side effects (caused cancer in dogs). Then in 1979, a statin called mevinolin, isolated from Aspergillus terreus, and another statin called monacolin K, isolated from Monascus ruber, were discovered to be the same compound and were structurally similar to compactin. Later on, this compound was labeled as Lovastatin. Merck Research Laboratories initiated clinical studies using Lovastatin in 1980, until rumors began about Lovastatin being similar to compactin, therefore has the ability to cause cancer and caused research to be shut down. However, it was later  proved by Michael Brown and Joseph Goldstein that the drug can increase cell surface LDL receptors in the liver and decrease LDL levels from a dog’s plasma. With this conclusion, Lovastatin was used in clinical trials using human subjects and produced the same results as shown in the dogs. In 1982, Lovastatin showed success due to its ability to lower LDL levels with individuals suffering from severe hypercholesterolemia. This drug was also beneficial because it did not cause any tumors, nor did it have any serious negative side effects. Lovastatin received FDA approval in 1986, and has lowered the possibility of developing heart diseases or atherosclerosis in millions of individuals suffering from elevated cholesterol levels <ref name= "fourteen"/>
Increasing evidence about the correlation between high cholesterol levels and disease in the 1905’s and 1960’s lead scientists to discover new forms of constraining this link. Many companies researched more about the biosynthetic pathway of cholesterol in order to determine which step is important to slow down the production of cholesterol. Towards the end of the 1970’s, various pharmaceutical companies searched for different alternatives after the discovery of compactin, a potential inhibitor discovered earlier in the decade but was not effective due to its dangerous side effects (caused cancer in dogs). Then in 1979, a statin called mevinolin, isolated from ''Aspergillus terreus'', and another statin called monacolin K, isolated from ''Monascus ruber'', were discovered to be the same compound and were structurally similar to compactin. Later on, this compound was labeled as Lovastatin. Merck Research Laboratories initiated clinical studies using Lovastatin in 1980, until rumors began about Lovastatin being similar to compactin, therefore has the ability to cause cancer and caused research to be shut down. However, it was later  proved by Michael Brown and Joseph Goldstein that the drug can increase cell surface LDL receptors in the liver and decrease LDL levels from a dog’s plasma. With this conclusion, Lovastatin was used in clinical trials using human subjects and produced the same results as shown in the dogs. In 1982, Lovastatin showed success due to its ability to lower LDL levels with individuals suffering from severe hypercholesterolemia. This drug was also beneficial because it did not cause any tumors, nor did it have any serious negative side effects. Lovastatin received FDA approval in 1986, and has lowered the possibility of developing heart diseases or atherosclerosis in millions of individuals suffering from elevated cholesterol levels <ref name= "fourteen"/>


== Function ==
== Function ==

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Sachin Sundar, Michal Harel