The OTEZLA® international website

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OTEZLA HAS A UNIQUE MECHANISM OF ACTION IN PSORIASIS1

Targeting key intracellular signals to reduce inflammation2

  • Through intracellular PDE4 inhibition, OTEZLA reduces production of pro-inflammatory mediators and boosts production of anti-inflammatory mediators2
  • These mediators are implicated in the pathogenesis of psoriasis and psoriatic arthritis1,2
Inflammatory state, which involves pro-inflammatory mediators and anti-inflammatory mediators
Cross-section of human cell that illustrates OTEZLA® preventing the hydrolysis of cAMP to AMP
Representation of the increase in anti-inflammatory mediators, such as IL-10, and the decrease of pro-inflammatory mediators, such as IL-17

PDE4 is a key inflammatory mediator

  • PDE4 is active in immune cells, keratinocytes, and synovial cells
  • PDE4 converts cAMP to AMP, which increases inflammatory signaling

OTEZLA is an oral PDE4 inhibitor

  • Blocking PDE4 maintains intracellular cAMP levels higher than AMP
  • Higher levels of cAMP help lead to balanced immune signaling

Blocking PDE4 helps regulate immune signaling

  • Decreased production of pro-inflammatory mediators
  • Increased production of anti-inflammatory mediators
Phosphodiesterase 4 Phosphodiesterase 4
Adenosine monophosphate Adenosine monophosphate
Cyclic adenosine monophosphate Cyclic adenosine monophosphate

PDE4 inhibition helps regulate balance in the immune system2

IFN, interferon; IL, interleukin; TNF, tumor necrosis factor.

Watch the video

References:

  1. OTEZLA Summary of Product Characteristics. Amgen Europe B.V. Minervum 7061, 4817 ZK Breda, The Netherlands; 2020.
  2. Schafer PH, Parton A, Capone l, et al. Apremilast is a selective PDE4 inhibitor with regulatory effects on innate immunity. Cell Signal. 2014;26(9):2016-2029.
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OTEZLA is approved in 54 countries*
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