Repatha® is a first-in-class PCSK9 inhibitor10*

Repatha® inhibits PCSK9 to increase LDL receptors and decrease LDL-C.1

PCSK9 promotes LDL receptor degradation1

PCSK promotes LDL receptor degradation

Repatha® binds selectively and with high affinity to circulating PCSK9, preventing LDL receptor degradation1

Pharmacodynamics of Repatha®1

Repatha® reduced free PCSK9 in a concentration-related manner†

Following a single subcutaneous administration of Repatha® 140 mg or 420 mg:

  • maximum suppression of circulating free PCSK9 occurred within 4 hours
  • reduction of LDL-C from baseline reached nadir by 14 days (140 mg Q2W dose) and 21 days (420 mg QM dose)

See the Repatha® Product Monograph for more information.

Download Product Monograph

* Comparative clinical significance is unknown.↩
† Clinical significance is unknown.↩
LDL=low-density lipoprotein; ↩LDL-C=low-density lipoprotein cholesterol; ↩LDL-R=low-density lipoprotein receptor;↩ MOA=mechanism of action; ↩PCSK9=proprotein convertase subtilisin/kexin type 9; ↩Q2W=every 2 weeks;↩ QM=monthly↩

Enrol your patient today

You are now leaving the Repatha.ca website

The linked sites are not under the control of Amgen, and Amgen is not responsible for the content available on the linked sites. Such links do not imply Amgen's endorsement of material on any other site, and Amgen disclaims all liability with regard to your access to such linked websites. Amgen provides links to other Internet sites as a convenience to users, and access to such linked sites is at your own risk.

Proceed