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Mechanism of Action

Otezla® (apremilast) inhibits PDE4 intracellularly and has anti-inflammatory properties1-4
  • Mechanism of Action VideoButton to view the video that describes the mechanism of action of Otezla® (apremilast) in the treatment of psoriatic arthritis
  • Mechanism of Action Diagram – PDE4Button to view the diagram of the role of PDE4 and cAMP in controlling inflammation
  • Mechanism of Action Diagram – OtezlaButton to view the diagram of the mechanism of action of Otezla®

LEARN MORE ABOUT THE INTRACELLULAR MECHANISM OF ACTION OF OTEZLA IN THE VIDEO BELOW

The specific mechanism(s) by which Otezla exerts its therapeutic action in psoriatic arthritis is not well defined.4

PDE4, phosphodiesterase 4.

THE ROLE OF PDE4 AND cAMP IN CONTROLLING INFLAMMATION1-3

The interior of an inflammatory cell showing how phosphodiesterase 4 (PDE4) breaks down cyclic AMP into AMP

Inflammatory cella

  • Cyclic adenosine monophosphate (cAMP) is a second messenger for a variety of inflammatory mediators1
  • Phosphodiesterase 4 (PDE4) is a cAMP-specific PDE that has been shown to degrade cAMP to AMP in inflammatory cells1,4,5
  • The balance between cAMP and AMP within a cell may modulate the expression of pro-inflammatory and anti-inflammatory mediators3
a

Visual representation based on preclinical evidence.

Otezla is a non-biologic oral PDE4 inhibitor with a distinct mechanism of action4

The interior of an inflammatory cell showing how apremilast binds to phosphodiesterase 4 (PDE4) to inhibit the hydrolyzation of cyclic AMP in to AMP

Inflammatory cella

Otezla inhibits PDE4 intracellularly4

  • By elevating cAMP levels, Otezla is thought to indirectly modulate production of inflammatory mediators2,3
  • The specific mechanism(s) by which apremilast exerts its therapeutic action in patients with psoriatic arthritis is not well defined4
  • An exploratory PALACE 1 substudy evaluating 47 biomarkers, some of which are relevant in the pathophysiology of psoriatic disease, observed6-9,b,c:
    • An increase in anti-inflammatory mediators, such as IL-10
    • A decrease in pro-inflammatory mediators, such as TNF-α, IL-17A, and IL-23
a

Visual representation based on preclinical evidence.

b

Based on an exploratory PALACE 1 biomarker substudy of patients with active psoriatic arthritis (n = 150 peripheral blood plasma samples at baseline, weeks 4, 16, 24, and 40) for a total of 47 biomarkers using a validated, multiplexed immunoassay.

c

Prior exposure to a biologic was higher in the biomarker subset compared to the full patient population (48.8% vs 23.6%).

 

IL, interleukin; PALACE, Psoriatic Arthritis Long-Term Assessment of Clinical Efficacy; PDE4, phosphodiesterase 4; TNF, tumor necrosis factor.

References: 1. Moore AR, Willoughby DA. Clin Exp Immunol. 1995;101(3):387-389. 2. Schafer PH, Parton A, Gandhi AK, et al. Br J Pharm. 2010;159(4):842-855. 3. Schafer P. Biochem Pharmacol. 2012;83(12):1583-1590. 4. Otezla [package insert]. Summit, NJ: Celgene Corporation. 5. Soto FJ, Hanania NA. Curr Opin Pulm Med. 2005;11(2):129-134. 6. Schafer PH, Chen P, Fang L, Wang A, Chopra R. J Immun Res. 2015. doi:10.1155/2015/906349. 7. van Kujik AW, Reinders-Blankert P, Smeets TJ, Dijkmans BA, Tak PP. Ann Rheum Dis. 2006;65(12):1551-1557. 8. Ritchlin CT, Haas-Smith DH, Cappuccio J, Osterland CK, Looney RK. J Rheumatol. 1998;25(8):1544-1552. 9. Barnas JL, Ritlin CT. Rheum Dis Clin North Am. 2015;41(4):643-663.

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