Page:Amgen Inc. v. Sanofi.pdf/8

4 receptors, and ligands] can also be involved in inflammatory disorders, uncontrolled cell growth, or other biological pathways that may be associated with disease.” Id., at 8.

One part of this effort has focused on the creation of antibodies to treat patients with high LDL cholesterol. A silent killer, LDL cholesterol can contribute to the formation of plaque in the arteries that may lead to cardiovascular disease, heart attacks, and strokes. For many people with high LDL cholesterol, drugs called statins offer an effective treatment. For others, statins do not work well or come with unwelcome side effects. In those cases, a relatively new antibody-based treatment known as a PCSK9 inhibitor may be appropriate. See Amgen Inc. v. Sanofi, 872 F. 3d 1367, 1371 (CA Fed. 2017).

PCSK9 is a naturally occurring protein that binds to and degrades LDL receptors. That can pose a problem because the body produces LDL receptors to perform the beneficial function of extracting LDL cholesterol from the bloodstream. See ibid. Scientists have understood this much for some time. But it wasn’t until fairly recently that they began exploring how antibodies might be used to inhibit PCSK9 from binding to and degrading LDL receptors as a way to treat patients with high LDL cholesterol.

In the mid-2000s, a number of pharmaceutical companies began looking into the possibility of making antibodies to target PCSK9. See Brief for Respondents 7; Brief for Arnold Ventures et al. as Amici Curiae 17–20. More precisely, they sought to create antibodies that could bind to a particular region of PCSK9 called the “sweet spot.” See Brief for Petitioners 10–11. The sweet spot is a sequence of 15 amino acids out of PCSK9’s 692 total amino acids. Id., at 11. By binding to the sweet spot, scientists found, an antibody could prevent PCSK9 from binding to and degrading LDL receptors. See id., at 10–11; Amgen, 872 F. 3d, at 1371.

Eventually, Amgen developed a PCSK9-inhibiting drug