Repatha® Delivers Lower LDL-C Levels

Repatha® is a human monoclonal IgG2 directed against human PCSK9. Repatha® binds to PCSK9 and inhibits circulating PCSK9 from binding to the low density lipoprotein (LDL) receptor (LDLR), preventing PCSK9-mediated LDLR degradation and permitting LDLR to recycle back to the liver cell surface. By inhibiting the binding of PCSK9 to LDLR, Repatha® increases the number of LDLRs available to clear LDL from the blood, thereby lowering LDL-C levels.1

Repatha® Mechanism of Action

Repatha® mechanism of action video: 1 of 3

What is PCSK9?

  • PCSK9 is a protein that promotes degradation of LDLRs. This results in fewer LDLRs on the liver cell surface, increasing plasma LDL-C levels2

Repatha® mechanism of action video: 2 of 3

Why Repatha® inhibits PCSK9

  • By inhibiting the binding of PCSK9 to LDLR, Repatha® permits LDLRs to recycle back to the liver cell surface1

  • This in turn increases the number of LDLRs available to clear LDL from the blood, thereby lowering LDL-C levels1

Repatha® mechanism of action video:3 of 3

How Repatha® lowers LDL-C levels

  • Repatha® lowers LDL-C levels by inhibiting PCSK9, increasing the number of LDLRs on the hepatocyte surface, thereby resulting in lower LDL-C plasma concentrations1

PCSK9 Inhibition with Repatha®

PCSK9 levels decrease
LDLR surface expression increase
Plasma LDL-c levels decrease

References: 1. Repatha® (evolocumab) Prescribing Information, Amgen. 2. Qian Y-W, Schmidt RJ, Zhang Y, et al. J Lipid Res. 2007;48:1488-1498.

IMPORTANT SAFETY INFORMATION

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Contraindication: Repatha® is contraindicated in patients with a history of a serious hypersensitivity reaction to Repatha®.

Allergic reactions: Hypersensitivity reactions (e.g. rash, urticaria) have been reported in patients treated with Repatha®, including some that led to discontinuation of therapy. If signs or symptoms of serious allergic reactions occur, discontinue treatment with Repatha®, treat according to the standard of care, and monitor until signs and symptoms resolve.

Adverse Reactions in Primary Hyperlipidemia, including HeFH: The most common adverse reactions (> 5% of Repatha®-treated patients and occurring more frequently than placebo) in clinical trials in primary hyperlipidemia (including HeFH) were: nasopharyngitis, upper respiratory tract infection, influenza, back pain, and injection site reactions.

In a 52-week trial, adverse reactions led to discontinuation of treatment in 2.2% of Repatha®-treated patients and 1% of placebo-treated patients. The most common adverse reaction that led to Repatha® treatment discontinuation and occurred at a rate greater than placebo was myalgia (0.3% versus 0% for Repatha® and placebo, respectively).

From a pool of the 52-week trial and seven 12-week trials: Local injection site reactions occurred in 3.2% and 3.0% of Repatha®-treated and placebo-treated patients, respectively. The most common injection site reactions were erythema, pain, and bruising. The proportions of patients who discontinued treatment due to local injection site reactions in Repatha®-treated patients and placebo-treated patients were 0.1% and 0%, respectively.

Allergic reactions occurred in 5.1% and 4.7% of Repatha®-treated and placebo-treated patients, respectively. The most common allergic reactions were rash (1.0% versus 0.5% for Repatha® and placebo, respectively), eczema (0.4% versus 0.2%), erythema (0.4% versus 0.2%), and urticaria (0.4% versus 0.1%).

Adverse reactions in the Cardiovascular Outcomes trial: The safety profile of Repatha® in this trial was generally consistent with the safety profile described above in the 12- and 52-week controlled trials involving patients with primary hyperlipidemia (including HeFH). Serious adverse events occurred in 24.8% and 24.7% of Repatha®-treated and placebo-treated patients, respectively. Adverse events led to discontinuation of study treatment in 4.4% of patients assigned to Repatha® and 4.2% assigned to placebo. Common adverse reactions (>5% of patients treated with Repatha® and occurring more frequently than placebo) included diabetes mellitus (8.8% Repatha®, 8.2% placebo), nasopharyngitis (7.8% Repatha®, 7.4% placebo), and upper respiratory tract infection (5.1% Repatha®, 4.8% placebo).

Among the 16,676 patients without diabetes mellitus at baseline, the incidence of new-onset diabetes mellitus during the trial was 8.1% in patients assigned to Repatha® compared with 7.7% in those assigned to placebo.

Immunogenicity: Repatha® is a human monoclonal antibody. As with all therapeutic proteins, there is a potential for immunogenicity with Repatha®.

Please see full Prescribing Information.

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What is PCSK9?

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Why Repatha® Inhibits PCSK9

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How Repatha® Lowers LDL-C Levels

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Using the Pushtronex® System

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Using the SureClick® Autoinjector

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