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

Cellular imagery of pcsk9 promoting LDL receptor degradation

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

Cellular imagery of Repatha® molecule binding selectively and with high affinity to circulating pcsk9, preventing ldl receptor degradation

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

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