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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 plaque psoriasis
  • Mechanism of Action Diagram – PDE4Button to view the diagram of the mechanism of action of PDE4
  • Mechanism of Action Diagram – OtezlaButton to view the diagram of the mechanism of action of Otezla®
  • Mechanism of Action QuizButton to access the mechanism of action quiz

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 psoriasis is not well defined.1

PDE4, phosphodiesterase 4.

PDE4 has been shown to be present within inflammatory cells2-7

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

Inflammatory cella

The role of phosphodiesterase 4 (PDE4) and cAMP in controlling inflammation

  • Cyclic adenosine monophosphate (cAMP) is a second messenger for a variety of inflammatory mediators2,5-7
  • PDE4 is a cAMP-specific PDE that has been shown to degrade cAMP to AMP in inflammatory cells2-6
a

Visual representation based on preclinical evidence.

OTEZLA INHIBITS PDE4 INTRACELLULARLY AND HAS ANTI-INFLAMMATORY PROPERTIES1-4

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,b

Otezla has a different MOA3

  • By elevating cAMP levels, Otezla is thought to indirectly modulate production of inflammatory mediators3
  • The specific mechanism(s) by which apremilast exerts its therapeutic action in patients with psoriasis is not well defined1
  • In a phase 2, open-label study, pharmacodynamic analyses of patients with plaque psoriasis treated with Otezla (n = 19) showed decreased6,c:
    • Lesional skin epidermal thickness
    • Expression of pro-inflammatory genes
    • Inflammatory cell infiltration
  • An exploratory ESTEEM 2 biomarker substudy evaluating 47 biomarkers, some of which are relevant in the pathophysiology of psoriasis, observed a decrease in pro-inflammatory mediators, such as IL-17F, IL-17A, IL-22, and TNF-α8-10,b
    • These biomarker analyses were exploratory and not designed to detect changes in biomarker levels or the relationship between biomarker change and clinical outcome8,9

aVisual representation based on preclinical evidence. bBased on an ESTEEM 2 substudy (Placebo n = 47; Otezla n = 83; peripheral blood plasma samples collected at baseline and weeks 4, 16, 32, 36, 40, and 44) using a validated multiplex immunoassay. High sensitivity assays were used to measure IL-17F, IL-17A, IL-22, and TNF-α.8,9 cPatients had recalcitrant plaque psoriasis, and skin biopsies were conducted at baseline, week 4, and week 12. Patients received oral Otezla 20 mg BID for 12 weeks.6

BID, twice daily; ESTEEM, Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis; IL, interleukin; PDE4, phosphodiesterase 4; TNF, tumor necrosis factor.

Learn more about the Otezla Mechanism of Action

The specific mechanism(s) by which Otezla exerts its therapeutic action in psoriasis is not well defined.1

Note: The Otezla Mechanism of Action quiz is optimized for desktop and tablet devices (768 pixel width and up) only.

References: 1. Otezla [package insert]. Summit, NJ: Celgene Corporation. 2. Schafer PH, Parton A, Gandhi AK, et al. Br J Pharm. 2010;159(4):842-855. 3. Schafer PH, Parton A, Capone L, et al. Cell Signal. 2014;26(9):2016-2029. 4. Schafer P. Biochem Pharmacol. 2012;83(12):1583-1590. 5. Schett G, Sloan VS, Stevens RM, Schafer P. Ther Adv Musculoskelet Dis. 2010;2(5):271-278. 6. Gottlieb AB, Matheson RT, Menter A, et al. J Drugs Dermatol. 2013;12(8):888-897. 7. Moore AR, Willoughby DA. Clin Exp Immunol. 1995;101(3):387-389. 8. Data on file, Celgene Corporation. 9. Krueger JK, et al. Presented at the European Academy of Dermatology and Venereology. Poster #P2081. September 28–October 2, 2016; Vienna, Austria. 10. Nestle FO, Kaplan DH, Barker J. N Eng J Med. 2009;361(5):496-509.

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Reference: 1. Data on file, Celgene Corporation.
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