Atopic dermatitis (AD) was a chronic or recurrent heterogeneous inflammatory skin condition with significant economic and social consequences. atopic dermatitis was a complex illness influenced by a wide range of environmental and hereditary factors. Epidermal barrier failure, immunological dysregulation, and dysbiosis were the major contributors to the development of atopic dermatitis. Interleukin (IL)-13 was identified as a potentially important cytokine in the underlying inflammation of Alzheimer’s disease (AD). Advances in understanding the pathogenesis of Alzheimer’s disease had accelerated the development of tailored immunomodulatory medicines for the disease, such as tralokinumab, a selective IL-13 inhibitor.
A phase IIb clinical study found that a dosage schedule of 150 or 300 mg every two weeks efficiently treated moderate-to-severe atopic dermatitis in people with a tolerability profile that was acceptable. At 16 weeks of treatment, outcomes with tralokinumab monotherapy were superior to those with placebo in phase III clinical studies. In the great majority of patients, it was likewise well tolerated for up to 52 weeks. In addition, tralokinumab was well tolerated and efficacious when used in conjunction with topical corticosteroids, with a good risk-benefit profile.
These findings contributed to the growing body of evidence indicating IL-13 plays a role in AD pathogenesis, suggesting that tralokinumab might be a novel therapeutic option for moderate-to-severe AD.