UNIQUE MOA THAT AFFECTS IL-4 AND IL-13 SIGNALING, IMPACTING TWO SOURCES THAT MEDIATE ALLERGIC AND EOSINOPHILIC INFLAMMATION

The mechanism of dupilumab action in asthma has not been established.1

DUPIXENT addresses Type 2 inflammation in appropriate patients with asthma1

Type 2 inflammation encompasses allergic and eosinophilic characteristics2,a-c:

DUPIXENT is indicated as an add-on maintenance treatment in patients with moderate-to-severe asthma aged 12 years and older with an eosinophilic phenotype or with oral corticosteroid dependent asthma. Limitation of Use: DUPIXENT is not indicated for the relief of acute bronchospasm or status asthmaticus.

MAKE DUPIXENT YOUR BIOLOGIC OF CHOICE FOR APPROPRIATE ASTHMA PATIENTS WITH TYPE 2 INFLAMMATION
  • aData from the 2005 and 2006 National Health and Nutrition Examination Survey (NHANES); N=310 adults. Total population reflected here is derived from individuals who had Type 2-mediated (eosinophilic and/or allergic) asthma, and excludes those individuals who had neither an eosinophilic nor allergic phenotype; N=257 adults.
  • bOverlap percentages may vary depending on the number of adults vs children, ongoing therapy, and IgE and eosinophil break points chosen.
  • cAlthough not defined by clinical guidelines, eosinophilic phenotype was defined in this study as blood eosinophil count ≥150 cells/μL; allergic phenotype was defined in this study as allergen-specific IgE ≥0.35 IU/mL.

Type 2 inflammation plays an important role in the pathogenesis of asthma1,3-5

DUPIXENT inhibits IL-4 and IL-13 signaling and decreases markers of airway inflammation, including1,3,6,7,d:

TOTAL AND ALLERGEN-SPECIFIC IgE Up to 70% reduction in total IgE from baseline

EOSINOPHILIC LUNG INFLAMMATION Despite the presence of normal or increased blood eosinophil levels

FeNO (a marker of lung inflammation)
Up to 35% reduction from baselinee

  • dEffects based on pharmacodynamic data from Trials 1 and 2.1
  • eFractional exhaled nitric oxide (FeNO) has not been established as useful for ruling in or ruling out a diagnosis of asthma; however, FeNO is higher in asthma that is characterized by Type 2 airway inflammation.8

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References:

  1. DUPIXENT Prescribing Information.
  2. Tran TN, Zeiger RS, Peters SP, et al. Overlap of atopic, eosinophilic, and TH2-high asthma phenotypes in a general population with current asthma. Ann Allergy Asthma Immunol. 2016;116(1):37-42.
  3. Robinson D, Humbert M, Buhl R, et al. Revisiting type 2-high and type 2-low airway inflammation in asthma: current knowledge and therapeutic implications. Clin Exp Allergy. 2017;47(2):161-175.
  4. Hammad H, Lambrecht BN. Dendritic cells and epithelial cells: linking innate and adaptive immunity in asthma. Nat Rev lmmunol. 2008;8(3):193-204.
  5. Corren J. Role of interleukin-13 in asthma. Curr Allergy Asthma Rep. 2013;13(5):415-420.
  6. Castro M, Corren J, Pavord ID, et al. Dupilumab efficacy and safety in moderate-to-severe uncontrolled asthma. N Engl J Med. 2018;378(26):2486-2496.
  7. Ravensberg AJ, Ricciardolo FLM, van Schadewijk A, et al. Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge. J Allergy Clin Immunol. 2005;115(4):779-785.
  8. Global Initiative for Asthma. Definition, description, and diagnosis of asthma. In: Global Strategy for Asthma Management and Prevention. https://ginasthma.org/. Updated 2019. Accessed March 26, 2020.