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Mechanism of Action

Otezla® (apremilast) inhibits PDE4 intracellularly and has anti-inflammatory properties1-4
  • Mechanism of Action Video
  • Mechanism of Action Diagram
  • 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

Otezla is an oral, non-biologic inhibitor of PDE41

Phosphodiesterase 4 (PDE4) has been shown to be present within inflammatory cells2-7

The role of PDE4 and cAMP in controlling inflammation

learn about the role of PDE4 and cAMP in controlling inflammation

Inflammatory cell

Visual representation based on preclinical evidence

  • 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 cells2-5,6

Otezla inhibits PDE4 intracellularly and has anti-inflammatory properties1-4

Otezla has a different MOA3

Inflammatory cell

Visual representation based on preclinical evidence

  • By elevating cAMP levels, Otezla is thought to indirectly modulate production of inflammatory mediators3
  • In a phase 2 open-label study, patients with plaque psoriasis treated with Otezla (n = 19) showed decreased6,8:
    • Lesional skin epidermal thickness
    • Expression of pro-inflammatory genes
    • Inflammatory cell infiltration
  • The specific mechanism(s) by which apremilast exerts its therapeutic action in patients with psoriasis is not well defined1

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.

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