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Repatha Offers Additional LDL-C Reduction in a Convenient Dosage Form

Michael R. Page, PharmD, RPh
Richard Mullvain, RPh, BCPS (AQC), CCCC, a cardiovascular clinical pharmacist and expert in cardiovascular care at the Essentia Health Heart & Vascular Center in Duluth, Minnesota, delivered a focused clinical review on the topic of the PCSK9 inhibitor Repatha (evolocumab), and its impact on low-density lipoprotein cholesterol (LDL-C).
At a Science & Innovation Theater held at the Academy of Managed Care Pharmacy (AMCP) Annual Meeting 2017 in Denver Colorado, Richard Mullvain, RPh, BCPS (AQC), CCCC, a cardiovascular clinical pharmacist and expert in cardiovascular care at the Essentia Health Heart & Vascular Center in Duluth, Minnesota, delivered a focused clinical review on the topic of the proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor Repatha (evolocumab).1
Mullvain discussed the definition of clinical atherosclerotic cardiovascular disease (ASCVD), which includes coronary heart disease (ie, acute coronary syndrome, history of myocardial infarction, stable or unstable angina, coronary or other arterial revascularization), peripheral arterial disease, and stroke or transient ischemic attack, according to guidelines published jointly in 2013 by the American College of Cardiology and the American Heart Association.1,2
Regarding the mechanistic characteristics of Repatha, Mullvain discussed the importance of PCSK9 in the body, and the therapeutic effect of inhibiting this endogenous protein. In the body, PCSK9 mediates the degradation of low-density lipoprotein receptors (LDLRs). Normally, LDLRs clear circulating low-density lipoprotein cholesterol (LDL-C) from the systemic circulation. By inhibiting PCSK9, Repatha facilitates LDLR recycling to the surface of liver cells, increasing the number of LDLRs available to clear circulating LDL-C.1,3
From the standpoint of pharmacokinetic and pharmacodynamic characteristics, Repatha is a human monoclonal IgG2 antibody. Within 4 hours of administration, Repatha exerts maximum suppression of PCSK9 levels, with no clinically meaningful drug-drug interactions with high-intensity statin therapy. Drug-drug interaction studies with Repatha in combination with medications other than statins have not been performed.1,3
Based on pharmacokinetic data, age, patient-specific factors such as gender, race, and kidney function do not significantly affect the disposition of Repatha. Repatha is a large protein that is not metabolized by the liver or excreted by the kidneys. Rather, it is eliminated mainly through binding to its pharmacologic target (PCSK9). Additionally, because it is a large protein, Repatha is not expected to cross the blood-brain barrier.1,3
In 4 clinical trials, Repatha has been shown to induce significant reductions in LDL-C levels in multiple patient populations, including patients with heterozygous familial hypercholesterolemia, homozygous familial hypercholesterolemia, or clinical ASCVD. These 4 studies include LAPLACE-2, which was a randomized double-blind study of patients with clinical ASCVD receiving statin therapy, DESCARTES, a 52-week safety and efficacy study, as well as RUTHERFORD-2 and TESLA, which evaluated Repatha in patients with familial hypercholesterolemia.1,4-7
In LAPLACE-2, patients with clinical ASCVD who required additional LDL-C reduction were randomized to receive statin therapy with any of 3 common regimens: atorvastatin 80 mg daily, rosuvastatin 40 mg daily, or simvastatin 40 mg daily. During a 4-week LDL-C stabilization period, patients received statins alone. After 4 weeks, 296 patients were randomized to receive either Repatha or a placebo (via subcutaneous injection) plus statin therapy. After 12 weeks of treatment, patients were evaluated on a primary end point of the mean percent change from baseline in LDL-C at week 12, and secondary end points of the percentage of patients achieving in LDL-C less than 70 mg/dL, and the percent change from baseline in other lipid parameters.1,4
Patients receiving subcutaneous injections of Repatha every 2 weeks plus statin (n = 147) achieved LDL-C reductions up to 77% greater than those achieved with placebo. Specifically, patients receiving atorvastatin 80 mg plus placebo achieved a 1% reduction in LDL-C from baseline, while patients receiving Repatha achieved a 64% reduction over the same period of time (a 63 percentage point difference). For patients receiving rosuvastatin 40 mg, a 2% increase in LDL-C was observed compared with a 65% reduction in LDL-C among patients receiving Repatha (a 66 percentage point difference). Finally, in patients receiving simvastatin 40 mg daily, a 13% increase in LDL-C was observed, versus a 64% reduction in LDL-C with Repatha (a 77 percentage-point difference).1,4
In terms of the percentage of patients achieving an LDL-C level less than 70 mg/dL at week 12, 90% of patients receiving Repatha with atorvastatin 80 mg, 88% of patients receiving Repatha with rosuvastatin 40 mg, and 87% of patients receiving Repatha with simvastatin 40 mg achieved this target.1,4

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