MOA: Mechanism of Action

DUPIXENT works beneath the surface, targeting IL-4 and IL-13 signaling, key sources of type 2 inflammation1-3

Choose DUPIXENT, a novel approach to treatment for appropriate uncontrolled moderate-to-severe atopic dermatitis patients

IL-4 and IL-13 have shared and distinct roles in Type 2 inflammation2

IL-4 perpetuates the type 2 inflammatory cascade and its effects through a positive feedback loop.4-7

IL-4 drives Th2 differentiation

Atopic dermatitis is a chronic, systemic, type 2 inflammatory disease—not a localized skin condition10-12

Both IL-4 and IL-13 are key mediators of type 2 inflammation and impact skin barrier dysfunction4-7:

  • Initial and continued Th2 differentiation and expansion4

IL-4 and IL-13
  • B cell class switching and IgE production4-6
  • Increase vascular adhesion and permeability5,8,9
  • Production of chemoattractants for inflammatory trafficking5,6
  • The itch-scratch cycle5,6
  • Induced barrier defects5-7

ILC2, type 2 innate lymphoid cells.

How DUPIXENT works

DUPIXENT helps repair the skin by targeting a key source of Type 2 inflammation.1,2,13,14

Watch the video to see how it works.

Not meant to depict the results of actual treatment with DUPIXENT.

DUPIXENT is the first and only dual inhibitor that works beneath the skin’s surface, specifically targeting IL‑4 and IL‑13 signaling to1,2,13:

  • Reduce epidermal hyperplasia
  • Modify lesional skin appearance
  • Modulate genes related to epidermal pathology in atopic dermatitis

Atopic dermatitis, or AD, is a chronic inflammatory skin disease that leads to dry, scaly, itchy skin and eczematous lesions. Moderate-to-severe AD is a potentially debilitating disease. The pathophysiology of AD is complex and multifactorial, involving immune and epidermal barrier components influenced by genetic and environmental factors. Patients with AD have a mix of lesional and nonlesional skin.

Though normal looking, nonlesional skin has persistent underlying inflammation due to activation of the immune system. In patients with AD, there are 2 main converging pathophysiological features: increased skin inflammation coupled with abnormalities of epidermal barrier structures and function.

Antigens are recognized by resident cells such as Langerhans cells and innate lymphoid type 2 cells and are presented to T cells in the skin and in lymph nodes driving immune inflammatory response in AD. This results in the initiation of a type 2, including Th2, immune response, such as IL-4, IL-13, and IL-31 release of chemokines. Cytokines that were historically known as Th2 cytokines, such as IL-4 and IL-13, are also produced by other cell types, including ILC2s, eosinophils, mast cells, basophils, and macrophages and are thus now known as type 2 cytokines.

In the acute phase of lesion development there is an increase in T cells and continued release of the type 2 cytokines IL-4 and IL-13, along with other cytokines and chemokines that promote inflammation. As the lesion progresses due to chronic disease, there is persistent type 2, including Th2, signaling. IL-4 and IL-13 are cytokines involved in the development of AD and play roles in the regulation of the immune response. IL-4 and IL-13 signal mainly through 2 receptor complexes.

The Type I receptor, consisting of IL-4Rα and γ-chain subunits, only binds IL-4. The Type II receptor, consisting of IL-4Rα and IL-13Rα1 subunits, is the primary receptor for IL-13 but also binds IL-4. In AD, increased levels of IL-4 and IL-13 lead to amplified signaling of type 2 cytokines and chemokines and activation of subsequent proinflammatory signaling pathways.

Dupilumab is a human monoclonal antibody that binds specifically to the IL-4Rα subunit of the receptor complexes for IL-4 and IL-13, two type 2 cytokines that play roles in the pathogenesis of AD. Dupilumab inhibits IL-4 signaling via the Type I receptor and both IL-4 and IL-13 signaling through the Type II receptor resulting in decreased IL-4 and IL-13 cytokine-induced responses, including the release of proinflammatory cytokines, chemokines, and IgE.

DUPIXENT is NOT an immunosuppressant or a steroid and requires NO initial lab testing or ongoing lab monitoring (according to the Prescribing Information)1

  • Immunosuppressive agents may inhibit multiple pathways2,13

DUPIXENT treats 3 indications driven in part by type 2 inflammation—demonstrating the important need for dual inhibition of IL-4 and IL-13 signaling1


  1. DUPIXENT Prescribing Information.
  2. Gandhi NA, Bennett BL, Graham NMH, Pirozzi G, Stahl N, Yancopoulos GD. Targeting key proximal drivers of type 2 inflammation in disease. Nat Rev Drug Discov. 2016;15(1):35-50.
  3. Guttman-Yassky E, Bissonnette R, Ungar B. Dupilumab progressively improves systemic and cutaneous abnormalities in patients with atopic dermatitis. J Allergy Clin Immunol. 2019;143(1):155-172.
  4. Palomares O, Akdis M, Martín-Fontecha M, Akdis CA. Mechanisms of immune regulation in allergic diseases: the role of regulatory T and B cells. Immunol Rev. 2017;278(1):219-236.
  5. Weidinger S, Beck LA, Bieber T, Kabashima K, Irving AD. Atopic dermatitis. Nat Rev Dis Primers. 2018;4(1):1. doi:10.1038/s41572-018-0001-z
  6. Rerknimitr P, Otsuka A, Nakashima C, Kabashima K. The etiopathogenesis of atopic dermatitis: barrier disruption, immunological derangement, and pruritus. Inflamm Regen. 2017;37:14. doi:10.1186/s41232-017-0044-7
  7. Brunner PM, Guttman-Yassky E, Leung DYM. The immunology of atopic dermatitis and its reversibility with broad-spectrum and targeted therapies. J Allergy Clin Immunol. 2017;139(4S):S65-S76.
  8. Patel KD. Eosinophil tethering to interleukin-4–activated endothelial cells requires both P-selectin and vascular cell adhesion molecule-1. Blood. 1998;92(10):3904-3911.
  9. Chen L, Lin SX, Amin S, Overbergh L, Maggiolino G, Chan LS. VCAM-1 blockade delays disease onset, reduces disease severity and inflammatory cells in an atopic dermatitis model. Immunol Cell Biol. 2010;88(3):334-342.
  10. De Benedetto A, Rafaels NM, McGirt LY, et al. Tight junction defects in patients with atopic dermatitis. J Allergy Clin Immunol. 2011;127(3):773-786.
  11. Sidbury R, Davis DM, Cohen DE, et al; American Academy of Dermatology. Guidelines of care for the management of atopic dermatitis: section 3. Management and treatment with phototherapy and systemic agents. J Am Acad Dermatol. 2014;71(2):327-349.
  12. Eyerich K, Eyerich S. Immune response patterns in non-communicable inflammatory skin diseases. J Eur Acad Dermatol Venereol. 2017;32(5):629-703.
  13. Guttman-Yassky E, Lio PA, Mallya UG, et al. Real-world effectiveness of dupilumab in atopic dermatitis: improvement in itch as assessed by the peak pruritus numerical rating scale (PNRS) in an electronic medical records dataset. Paper presented at: 24th World Congress of Dermatology (WCD); June 10-15, 2019; Milan, Italy.
  14. Callewaert C, Nakatsuji T, Knight R, et al. IL-4Rα blockade by dupilumab decreases Staphylococcus aureus colonization and increases microbial diversity in atopic dermatitis. J Invest Dermatol. 2020;140(1):191-202.e7.

Important Safety
Information and Indication

CONTRAINDICATION: DUPIXENT is contraindicated in patients with known hypersensitivity to dupilumab or any of its excipients.


Hypersensitivity: Hypersensitivity reactions, including generalized urticaria, rash, erythema nodosum, anaphylaxis and serum sickness or serum sickness-like reactions, were reported in <1% of subjects who received DUPIXENT in clinical trials. If a clinically significant hypersensitivity reaction occurs, institute appropriate therapy and discontinue DUPIXENT.

Conjunctivitis and Keratitis: Conjunctivitis and keratitis occurred more frequently in atopic dermatitis subjects who received DUPIXENT. Conjunctivitis was the most frequently reported eye disorder. Most subjects with conjunctivitis or keratitis recovered or were recovering during the treatment period. Advise patients to report new onset or worsening eye symptoms to their healthcare provider.

Reduction of Corticosteroid Dosage: Do not discontinue systemic, topical or inhaled corticosteroids abruptly upon initiation with DUPIXENT. Reductions in corticosteroid dose, if appropriate, should be gradual and performed under the direct supervision of a physician. Reduction in corticosteroid dose may be associated with systemic withdrawal symptoms and/or unmask conditions previously suppressed by systemic corticosteroid therapy.

Atopic Dermatitis Patients with Comorbid Asthma: Advise patients not to adjust or stop their asthma treatments without consultation with their physicians.

Parasitic (Helminth) Infections: It is unknown if DUPIXENT will influence the immune response against helminth infections. Treat patients with pre-existing helminth infections before initiating therapy with DUPIXENT. If patients become infected while receiving treatment with DUPIXENT and do not respond to anti-helminth treatment, discontinue treatment with DUPIXENT until the infection resolves.

ADVERSE REACTIONS: The most common adverse reactions (incidence ≥1% at Week 16) in adult patients with atopic dermatitis are injection site reactions, conjunctivitis, blepharitis, oral herpes, keratitis, eye pruritus, other herpes simplex virus infection, and dry eye. The safety profile in children and adolescents through Week 16 was similar to that of adults with atopic dermatitis. In an open-label extension study, the long-term safety profile of DUPIXENT in adolescents and children observed through Week 52 was consistent with that seen in adults with atopic dermatitis.

DRUG INTERACTIONS: Avoid use of live vaccines in patients treated with DUPIXENT.


  • Pregnancy: There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to DUPIXENT during pregnancy. Healthcare providers and patients may call 1-877-311-8972 or go to to enroll in or obtain information about the registry. Available data from case reports and case series with DUPIXENT use in pregnant women have not identified a drug-associated risk of major birth defects, miscarriage or adverse maternal or fetal outcomes. Human IgG antibodies are known to cross the placental barrier; therefore, DUPIXENT may be transmitted from the mother to the developing fetus.
  • Lactation: There are no data on the presence of DUPIXENT in human milk, the effects on the breastfed infant, or the effects on milk production. Maternal IgG is known to be present in human milk. The developmental and health benefits of breastfeeding should be considered along with the mother’s clinical need for DUPIXENT and any potential adverse effects on the breastfed child from DUPIXENT or from the underlying maternal condition.

Please see accompanying full Prescribing Information.


DUPIXENT is indicated for the treatment of patients aged 6 years and older with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable. DUPIXENT can be used with or without topical corticosteroids.