CCMS Medicine Winter 2017 - 21

www.CHESTERCMS.org

History
We have considerable data that LDL cholesterol causes
atherosclerosis. The bile acid sequestrant cholestyramine was
developed in the late 1900s and the first statin drug, Lovastatin,
was approved by the FDA in 1987.
In February of 2003, Nabil Seidah, at the clinical research
Institute of Montreal, discovered a novel human DNA, the
proprotein convertase, a gene which was located on the short
arm of chromosome 1. Meanwhile, in Paris, Catherine Boileau
had been following families with familial hypercholesterolemia,
a genetic condition that in 90% of cases causes coronary artery
disease, and in 60% of cases leads to early death. These two
researchers got together and published their work linking
mutations in the gene, now identified as PCSK9, to the condition.
Further work was done by Drs. Hobbs and Cohen which
resulted in the approval of Alirocumab (Praluent) in July of 2015
and Evolocumab (Repatha) in August of 2015. A third drug,
Bococizimab, is currently undergoing test trials.

Function
The premise is very simple; low density lipoprotein receptors
(LDL-Rs) in hepatocytes bind to LDL particles and remove them
from circulation. LDL receptors then return to the cell surface
to repeat the process. PCSK9 functions as a binding protein; it
is expressed primarily in hepatocytes and after secretion binds to
the LDL receptors and promotes their degradation by blocking
PCSK9. These drugs result in increased availability of LDL
receptors to remove LDL cholesterol from circulation. In simple
terms, statins block the synthesis and PCSK9 inhibitors increase
clearance of LDL-Cholesterol.

Continued on page 22

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Table of Contents for the Digital Edition of CCMS Medicine Winter 2017

CCMS Medicine Winter 2017 - 1
CCMS Medicine Winter 2017 - 2
CCMS Medicine Winter 2017 - 3
CCMS Medicine Winter 2017 - 4
CCMS Medicine Winter 2017 - 5
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CCMS Medicine Winter 2017 - 8
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CCMS Medicine Winter 2017 - 32
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