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Review
. 2022 Mar 8:15:395-402.
doi: 10.2147/CCID.S266036. eCollection 2022.

Apremilast in the Treatment of Plaque Psoriasis: Differential Use in Psoriasis

Jia C Gao  1 , Albert G Wu  1 , Marissa N Contento  1 , Jacqueline M Maher  1 , Abigail Cline  2
Affiliations
Review

Apremilast in the Treatment of Plaque Psoriasis: Differential Use in Psoriasis

Jia C Gao et al. Clin Cosmet Investig Dermatol. .

Abstract

Small molecule medications like apremilast are emerging as promising options for patients with psoriasis and other inflammatory conditions. Apremilast was approved by the Food and Drug Administration in 2014 for the management of both psoriasis and psoriatic arthritis. Apremilast inhibits phosphodiesterase-4, which increases the intracellular levels of cyclic AMP, thereby reducing inflammatory cytokine production. This review aims to discuss the published evidence and evaluate the differential use of apremilast in plaque psoriasis of the body and scalp, nail psoriasis, and palmoplantar psoriasis. In clinical trials, apremilast effectively reduced the severity of different dermatological manifestations of psoriasis and improved patients' quality of life. It has an acceptable safety profile and is generally well-tolerated. Oral medications like apremilast offer an alternative route of administration which can be more convenient and appropriate for some patients. Additionally, pharmacoeconomic analyses of available anti-psoriatic systemic agents favor apremilast as a cost-effective therapeutic option.

Keywords: apremilast; biologic; cost-efficacy; efficacy; nail; palmoplantar; pharmacoeconomics; phosphodiesterase inhibitor; plaque psoriasis; safety; scalp; small molecule; systemic.

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Conflict of interest statement

The authors report no conflicts or competing interests in this work.

Figures

Figure 1
Figure 1
Mechanism of action of apremilast. In monocytes and dendritic cells, PDE4 degrades cAMP to AMP. When apremilast inhibits PDE4, intracellular cAMP levels increase and activate PKA. PKA activation results in phosphorylation of the transcription factors CREB and NF-κB. Phosphorylation leads to activation of CREB, which increases anti-inflammatory cytokines, such as IL-10. Phosphorylation of NF-κB results in inhibition of transcriptional activity, thereby decreasing expression of pro-inflammatory cytokines, including IL-23, TNF-α, and IFN-γ. The decreased production of inflammatory mediators reduces inflammation and proliferation of keratinocytes in psoriatic skin.
See this image and copyright information in PMC

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