Abrocitinib is an oral Janus Kinase 1 selective inhibitor under investigation for the treatment of atopic dermatitis (AD). To support a phase 3 study design, dose-response modeling and simulation was used to predict the relationship between abrocitinib dose and clinical AD efficacy measures. Investigator’s Global Assessment (IGA) response (clear [0] or almost clear [1] with ≥2-grade improvement from baseline) at week 12 and Eczema Area and Severity Index (EASI) score over time were measured in a phase 2b, randomized, double-blind, proof-of-concept, dose-ranging trial in patients with moderate-to-severe AD (NCT02780167; N=245 IGA records [nonresponder imputation], N=2220 EASI records from 263 patients). IGA response at week 12 was adequately described by an Emax dose-response model (ie, landmark logistic regression). EASI score, from baseline through week 16, was adequately described across time by a linear dose-response model. The final models were used to simulate IGA response rates (as defined above) and EASI75 response rates (≥75% reduction in EASI score from baseline) in 1000 simulated trials with cohorts of 50 patients/dose. Simulations answered the question: what is the median (90% prediction interval) response rate at week 12 expected in a subsequent AD trial? The predicted rates for IGA response were 6% (0-14%), 26% (14-38%), and 38% (26-54%), and for EASI75 response were 21% (12-30%), 50% (38-62%), and 62% (52-74%) for placebo and abrocitinib doses of 100 mg and 200 mg, respectively. Based on these findings, once-daily abrocitinib doses of 100 mg and 200 mg were forecasted to provide clinically meaningful response relative to placebo in the current randomized, double-blind, placebo-controlled phase 3 trial in patients aged ≥12 years with moderate-to-severe AD.