Autoimmune diseaseImmunology & inflammationDermatology PopPKPKPDExposure-response

Dupilumab exposure and atopic-dermatitis response

Reference paper ↗

A coupled subcutaneous PK and indirect-response model linking dupilumab exposure to EASI and IGA response dynamics while accounting for patient and disease covariates.

Therapeutic
Dupilumab
Modality
Monoclonal antibody
Target
IL4R, CD124
Disease
Moderate-to-severe atopic dermatitis
Model type
PopPK, PKPD, Exposure-response

Complete model workspace

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Parameters
53
States
10
Equations
10
Derived outputs
12

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Adult severe AD 600 mg load, 300 mg every 2 weeks

How do dupilumab exposure and patient covariates shape the onset and depth of EASI and IGA response? Explore this intervention regimen through Central dupilumab concentration, EASI response, IGA response, Cumulative dupilumab exposure.

Starting result

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Starting configuration

Time: 0–112 day; step 7

InputDefaultAvailable range
Body weight76.1 kg38.05–114.1 kg
EASI IC5020.3 mg/L10.15–30.45 mg/L
EASI Imax0.266 dimensionless0.133–0.399 dimensionless
EASI effect half-life13.7 day6.85–20.55 day
IGA IC5027.1 mg/L13.55–40.65 mg/L

Expected readouts

Central dupilumab concentration · EASI response (dimensionless) · IGA response (dimensionless) · Exposure (AUC) (mg*day/L)

Adjustable model parameters

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More key parameters (1)

How the model represents the biology

A coupled subcutaneous PK and indirect-response model linking dupilumab exposure to EASI and IGA response dynamics while accounting for patient and disease covariates.

How does subcutaneous dupilumab exposure drive delayed EASI and IGA responses?A subcutaneous dupilumab dose passes through a depot and three transit stages, reaches central exposure, exchanges with a peripheral pool, undergoes linear and saturable elimination, and modulates empirical EASI and IGA response turnover.BIOLOGY OVERVIEWHow does subcutaneous dupilumab exposure drive delayed EASI and IGA responses?Subcutaneous doseDupilumab administrationDepot + transit chainThree staged absorption delaysCentral exposureDupilumab concentrationPeripheral poolReversible distributionPK eliminationLinear and saturable lossEASI + IGA turnoverEmpirical exposure-linkedresponsesCumulative exposureCentral concentration integralPRIMARY READOUTSCentral dupilumab concentrationCentral dupilumab concentr…EASI responseEASI responseIGA responseIGA responseCumulative exposureCumulative exposure

Solid arrows show modeled movement or change; two-headed arrows show reversible exchange; dashed arrows show modulation without material transfer.

Model scope: IL-4R binding, receptor occupancy, cytokine signaling, and lesion biology are not explicit; the pharmacodynamics are empirical exposure-linked response turnover.

Modeled relationships (6)
  • Subcutaneous dose → Depot + transit chain: SC input (flow)
  • Depot + transit chain → Central exposure: transit (flow)
  • Central exposure ↔ Peripheral pool: distribution (reversible exchange)
  • Central exposure → PK elimination: linear + saturable (loss)
  • Central exposure → EASI + IGA turnover: exposure effect (modulation)
  • Central exposure → Cumulative exposure: integrates C (production)

Modeled relationships: Subcutaneous dose to Depot + transit chain: SC input (flow); Depot + transit chain to Central exposure: transit (flow); Central exposure reversibly exchanges with Peripheral pool: distribution (reversible exchange); Central exposure to PK elimination: linear + saturable (loss); Central exposure to EASI + IGA turnover: exposure effect (modulation); Central exposure to Cumulative exposure: integrates C (production).

Primary readouts: Central dupilumab concentration; EASI response; IGA response; Cumulative exposure.

Found a scientific issue? Email helpdesk@unibiointelligence.com with model ID briggs_2023_dupilumab_ad_er_pkpd.

Research use only — not for patient-specific prediction or dosing advice.

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