Atopic dermatitis stems from skin barrier abnormalities and immune dysregulation1-4

Overactive PDE4 results in excessive cytokines, which may lead to skin inflammation

Overactive PDE4 and atopic dermatitis

  • Atopic dermatitis is associated with excessive cytokines, which have been shown to contribute to the signs and symptoms of atopic dermatitis1-3
  • These cytokines are regulated at the intracellular level by overactive PDE4 enzymes in immune cells1,2
  • Overactive PDE4 degrades cAMP to AMP, resulting in overproduction of these inflammatory cytokines1,4
  • Overactive PDE4 may be one of the many potential factors involved in the pathophysiology of atopic dermatitis

EUCRISA works both above and below the skin to treat atopic dermatitis1-7

The first and only nonsteroidal topical monotherapy that inhibits PDE4 within the skin5

The specific mechanism(s) of action of crisaborole in atopic dermatitis is not well defined.

The active ingredient in EUCRISA, crisaborole 2%, is combined with a proprietary Emollient-rich Vehicle ointment.5,9 Ointments contain emollients, which can help lock in moisture and soften the skin.10

EUCRISA inhibits PDE4

  • Crisaborole penetrates into the skin1,5
  • Crisaborole inhibits PDE4 in inflammatory cells, resulting in increased intracellular cAMP levels1,5,6
  • Increased intracellular cAMP may result in reduced inflammatory cytokines, which is thought to reduce the signs and symptoms of atopic dermatitis3,5,7

Images for illustrative purposes only.
PDE4=phosphodiesterase 4; cAMP=cyclic adenosine monophosphate; AMP=adenosine monophosphate.

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  1. Jarnagin K, Chanda S, Coronado D, et al. Crisaborole topical ointment, 2%: a nonsteroidal, topical, anti-inflammatory phosphodiesterase 4 inhibitor in clinical development for the treatment of atopic dermatitis. J Drugs Dermatol. 2016;15(4):390-396.
  2. Chan SC, Reifsnyder D, Beavo JA, Hanifin JM. lmmunochemical characterization of the distinct monocyte cyclic AMP-phosphodiesterase from patients with atopic dermatitis. J Allergy Clin Immunol. 1993;91(6):1179-1188.
  3. Hanifin JM, Chan SC, Cheng JB, et al. Type 4 phosphodiesterase inhibitors have clinical and in vitro anti-inflammatory effects in atopic dermatitis. J Invest Dermatol. 1996;107(1):51-56.
  4. Sawai T, Ikai K, Uehara M. Cyclic adenosine monophosphate phosphodiesterase activity in peripheral blood mononuclear leucocytes from patients with atopic dermatitis: correlation with respiratory atopy. Br J Dermatol. 1998;138(5):846-848.
  5. EUCRISA® (crisaborole) Full Prescribing Information. December 2018.
  6. Freund YR, Akama T, Alley MRK, et al. Boron-based phosphodiesterase inhibitors show novel binding of boron to PDE4 bimetal center. FEBS Lett. 2012;586(19):3410-3414.
  7. Dong C, Virtucio C, Zemska O, et al. Treatment of skin inflammation with benzoxaborole phosphodiesterase inhibitors: selectivity, cellular activity, and effect on cytokines associated with skin inflammation and skin architecture changes. J Pharmacol Exp Ther. 2016;358(3):413-422.
  8. Paller AS, Tom WL, Lebwohl MG, et al. Efficacy and safety of crisaborole ointment, a novel, nonsteroidal phosphodiesterase 4 (PDE4) inhibitor for the topical treatment of atopic dermatitis (AD) in children and adults. J Am Acad Dermatol. 2016;75(3):494-503.e4.
  9. Data on file. Pfizer Inc., New York, NY.
  10. Eichenfield LF, Tom WL, Berger TG, et al. Guidelines of care for the management of atopic dermatitis: section 2. Management and treatment of atopic dermatitis with topical therapies. J Am Acad Dermatol. 2014;71(1):116-132.