Skip to main content

MOA: MECHANISM OF ACTION

Discover the dupixent difference in copd

Not actual
DUPIXENT patients.

Not actual
DUPIXENT patients.

Up to 40% of COPD patients present with type 2 inflammation1-5,a

Multiple manifestations of
type 2 inflammation can
be seen in COPD

Mucus hypersecretion
and plugging6

Airway remodeling
and fibrosis7,8

Epithelial barrier
disruption8

Increased
FeNO8,b

Eosinophil
trafficking to the
lung tissues9,10

Parenchymal destruction11

How Dupixent Works

Increased risk of exacerbations8

The DUPIXENT Difference DUPIXENT is the only biologic that directly inhibits IL-4 and IL-13 signaling, two of the key drivers of type 2 inflammation12,*

  • *The mechanism of dupilumab action has not been definitively established.12

Watch the video below to learn more about the MOA of DUPIXENT

TYPE 2 INFLAMMATION DISRUPTS THE EPITHELIAL BARRIER, ALLOWING PENETRATION OF CIGARETTE SMOKE, PATHOGENS, POLLUTANTS, AND ALLERGENS8,11,13

Aeroallergens can activate dendritic cells directly, independent of the alarmin pathway

There are 3 alarmins released from the epithelium simultaneously that can each stimulate type 2 responses

IL-4 and IL-13 are two of the key cytokines that directly stimulate multiple inflammatory responses that lead to disease burden

  • a Based on findings from 5 studies in COPD patients without asthma. Eosinophil levels used to define type 2 inflammation ranged from ≥300 cells/μL to ≥340 cells/μL (blood), ≥2% in induced sputum, or 3% in peripheral blood. Percentages of patients with type 2 inflammation ranged from 12.3% to ~40%.1-5
  • b The role of FeNO in the characterization of COPD is uncertain.
  • COPD, chronic obstructive pulmonary disease; FeNO, fractional exhaled nitric oxide.

FREQUENTLY ASKED QUESTIONS