Atopic Dermatitis (AD) is a chronic, relapsing, inflammatory skin disease characterized by erythema, dryness, edema, skin barrier dysfunction, immune dysregulation, and pruritus [1], [2], [3], [4]. In AD’s inflammatory skin lesions, there is thickening of the dermis, infiltration of leukocytes, T helper (Th) cells, and elevated levels of serum IgE, cytokines, and chemokines [5]. The Global Burden of Disease (GBD) study estimated the prevalence of AD to be 15-20% in children and up to 10% in adults [6], and its incidence has increased in both children and adults [7], [8]. The pathogenesis of AD is complex, involving abnormal immune, environmental, psychological, and other factors [1], [9]. Currently, its specific pathogenesis remains unclear. To further investigate the pathophysiology of AD, mouse models are indispensable and widely used as valuable tools. Nowadays, there are more than 20 mouse models of AD are available, which can be categorized as genetically engineered models, inbred models, exogenous drugs-induced models, and so on. In particular, exogenous drugs-induced models include hapten-induced mouse models, allergen-induced models, and MC903(calcipotriol)-induced model. They have the advantage of being practical, time-controllable, and widely applicable [3], [10]. However, there is currently a lack of comprehensive comparative studies on exogenous drug-induced AD mouse models, which hinders researchers' ability to choose among these models. In this paper, we will review the establishment methods, induction effects, and molecular mechanisms of various exogenous drug-induced models, and compare the advantages and weaknesses of each model, laying a solid foundation for further research on AD.