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Statins play a pivotal role in establishing the linear relationship between LDL-C and CV event risk1,2

CV event rate by mean achieved LDL-C level with statin therapy, proven over 25 years of clinical trials1,2

Figure adapted from Raymond C, et al. Cleve Clin J Med. 2014;81:11-19.

Shows a scatterplot with best-fit line of major statin trials for secondary prevention of coronary heart disease events.


Statins alone may not be enough for recent myocardial infarction patients who remain at risk3

21% More than 1 in 5 post-MI patients had at least one additional MI, IS, UA, or PCI/CABG within 2 years.4

66% of patients in the United States with major ASCVD event(s) have elevated LDL-C ≥ 70 mg/dL.5

For very high-risk* patients who have suffered a recent myocardial infarction, updated ACC/AHA Guidelines recommend the addition of a PCSK9 inhibitor like Repatha® to further lower LDL-C and associated CV risk.3†

*Very high risk includes a history of multiple major ASCVD events or 1 major ASCVD event and multiple high-risk conditions.3

Class I: Add ezetimibe to maximal statin before adding PCSK9 inhibitor; Class IIa: If on clinically judged maximal LDL-C-lowering therapy and LDL-C ≥70 mg/dL, or non-HDL-C ≥100 mg/dL, adding a PCSK9 inhibitor is reasonable.3


Identifying recent MI patients who need more than a statin alone

In adults with established CVD


Tony, and patients like him, need more help protecting them from another CV event like a heart attack or stroke

*Hypothetical patient profile.

In adults with established CVD TONY*

Tony, and patients like him, need more help protecting them from another CV event like a heart attack or stroke

*Hypothetical patient profile.

Recent myocardial infarction

Presented to ER with NSTE-ACS, confirmed as NSTEMI as per elevated cardiac troponin

Underwent PCI within 24 hours of presentation and was admitted to the hospital


  • Sent home with dietary/lifestyle recommendations
  • Prescribed the following:
    • Rosuvastatin 40 mg QD (up-titrated from 20 mg post MI)
    • Aspirin 81 mg QD
    • Ticagrelor 90 mg BID
    • Ramipril 10 mg
    • Carvedilol 6.25 mg BID

Medical History

  1 month prior to MI Follow-up post discharge
LDL-C 112 mg/dL 105 mg/dL
HDL-C 45 mg/dL 47 mg/dL
TG 95 mg/dL 90 mg/dL
BMI 29.3 27.9
Rosuvastatin 20 mg 40 mg
  • History of hypertension
  • Current smoker (undergoing smoking cessation program)
  • TC=170 mg/dL

Statins + Repatha®

The Repatha® CV Outcomes Study (FOURIER) was designed to evaluate CV risk reduction by dramatically lowering LDL-C6

FOURIER was a double-blind, randomized, placebo-controlled, event-driven trial in 27,564 adult patients with established cardiovascular disease and with LDL-C ≥70 mg/dL and/or non-HDL-C ≥100 mg/dL despite high- or moderate-intensity statin therapy. Patients were randomly assigned to receive Repatha® (140 mg every 2 weeks or 420 mg once monthly) or placebo. The median follow-up duration was 26 months.6


of patients were receiving high- or moderateintensity statin therapy.7

≥40 to ≤85

year-old patients were enrolled.7


of patients had already experienced ≥1 MI.7

92 mg/dL

was the median baseline LDL-C for enrolled patients.7

Patients were treated with other CV medications6:

  • Anti-platelet agents (93%)
  • Beta-blockers (76%)
  • ACE inhibitor (56%)
  • ARB (23%)

For patients with established CVD,

Repatha® added to a statin reduced the risk of CV events more than statins alone6,7

Key secondary endpoint: composite of cardiovascular death, myocardial infarction, or stroke6,7

Repatha® added to a statin reduced the risk of composite CV events by 20% in a median of 2.2 years, and the benefit improved over time.6

  • Primary composite endpoint of time to CV death, MI, hospitalization for unstable angina, stroke, or coronary revascularization: HR 0.85 (95% CI, 0.79-0.92; P<0.0001)6


27% RRR6


22% RRR6

  • Stroke=21% RRR6
  • Key secondary composite endpoint of time to CV death, MI, or stroke: HR 0.80 (95% CI, 0.73-0.88; P<0.0001). ARR=2.0%6,7
  • Relative risk reductions for the primary and secondary composite endpoints were driven by a reduction in the risk of MI: HR 0.73 (95% CI, 0.65-0.82), stroke: HR 0.79 (95% CI, 0.66-0.95), and coronary revascularization: HR 0.78 (95% CI, 0.71-0.86)6

Observed HR for CV death: 1.05 (95% Cl, 0.88-1.25) and hospitalizations due to unstable angina: 0.99 (95% Cl, 0.82-1.18)6

Repatha® added to a statin provided an ARR of 2.9% in patients with a recent MI8

When compared to the overall study population, a greater ARR was observed in patients with a qualifying MI <2 years8

ARR of 2.0% in the overall Repatha® CV Outcomes Trial study population was evaluated at 36 months6,7

  • Repatha® reduced the risk of CV death, MI, or stroke by 24% in patients with a qualifying MI <2 years ago8
  • Analysis of 81% (n=22,351) of patients in Repatha® CV Outcomes Trial with MI as their qualifying event; median time from MI to enrollment in Repatha® CV Outcomes Trial was 3.3 years7
  • The observed HR for CV death was 1.05 (95% CI, 0.88-1.25) from the primary analysis6

For your high-risk CVD patients,

Repatha® added to a statin reduces risk of MI by dramatically reducing LDL-C6

Lipids are one of the most modifiable risk factors for the prevention of CV events.9

Repatha® added to a statin reduced composite CV event rates regardless of baseline LDL-C.10

View CV event rate

Repatha® has demonstrated a consistent safety profile across more than 26,000 patients.11

View safety profile

ACC/AHA=American College of Cardiology/American Heart Association; ARB=angiotensin II receptor blocker; ARR=absolute risk reduction; ASCVD=atherosclerotic cardiovascular disease; BID=twice daily; BMI=body mass index; CABG=coronary artery bypass graft; CI=confidence interval; CV=cardiovascular; CVD=cardiovascular disease; HDL-C=high-density lipoprotein cholesterol; HR=hazard ratio; IS=ischemic stroke; LDL-C=low-density lipoprotein cholesterol; MI=myocardial infarction; NSTE-ACS=non-ST-segment elevation acute coronary syndrome; NSTEMI=non-ST-elevation myocardial infarction; PCI=percutaneous coronary intervention; PCSK9=proprotein convertase subtilisin/kexin type 9; PRN=as needed; QD=once daily; RRR=relative risk reduction; TC=total cholesterol; TG=triglycerides; UA=unstable angina.

References: 1. Raymond C, Cho L, Rocco M, et al. New guidelines for reduction of blood cholesterol: Was it worth the wait? Cleve Clin J Med. 2014;81:11-19. 2. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;34:1383-1389. 3. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/ AACVPR/AAPA/ABC/ ACPM/ ADA/ AGS/ APhA/ASPC/NLA/PCNA Guideline on the management of blood cholesterol. J Am Coll Cardiol. 2019;73:e285-e350. 4. Li S, Peng Y, Wang X, et al. Cardiovascular events and death after myocardial infarction or ischemic stroke in an older Medicare population. Clin Cardiol. 2019;42:391-399. 5. Data on file, Amgen; 2020. 6. Repatha® (evolocumab) prescribing information, Amgen. 7. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and clinical outcomes in patients with cardiovascular disease. N Engl J Med. 2017;376:1713-1722. 8. Sabatine MS, De Ferrari GM, Giugliano RP, et al. Clinical benefit of evolocumab by severity and extent of coronary artery disease: an analysis from FOURIER. Circulation. 2018;138:756-766. 9. Yusuf S, Hawken S, Ôunpuu S, et al; on behalf of the INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-controlled study. Lancet. 2004;364:937-952. 10. Data on file, Amgen; 2017. 11. Data on file, Amgen; 2017.

In established CVD patients, regardless of baseline LDL-C,

Repatha® added to a statin reduced the risk of composite CV events1

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Reference: 1. Data on file, Amgen; 2017.

Important Safety Information

Contraindication: Repatha® is contraindicated in patients with a history of a serious hypersensitivity reaction to Repatha®. Serious hypersensitivity reactions including angioedema have occurred in patients treated with Repatha®.

Allergic Reactions: Hypersensitivity reactions (e.g. angioedema, 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 patients treated with Repatha® and occurring more frequently than placebo) were: nasopharyngitis, upper respiratory tract infection, influenza, back pain, and injection site reactions.

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.

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 most common adverse reactions (>5% of patients treated with Repatha® and occurring more frequently than placebo) were: 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 potential for immunogenicity with Repatha®.

Please see full Prescribing Information.