The greatest risk factor for skin cancer is exposure to ultraviolet (UV) rays of the sun. Among the three types of solar radiation (UVA, UVB, UVC), UVB rays are most commonly associated with skin cancer. UVB exposure promotes the formation of cyclobutane pyrimidine dimers (CPDs) in the DNA of cells in the epidermal skin layers, which can lead to mutations as DNA repair machinery attempts to repair the damage. 

The glucagon-like peptide-1 receptor agonists (GLP1RAs) are a widely popularized drug class due to their notable success in promoting weight loss. The GLP1RAs, dulaglutide, exenatide, semaglutide, liraglutide, tirzepatide, and lixisenatide are FDAapproved for use in the treatment of obesity and type 2 diabetes mellitus (DM), particularly to reduce cardiovascular risk and improve glycemic control.^1,2,3 GLP1RAs work by mimicking glucagon-like peptide-1 (GLP-1), an incretin, that functions to subdue appetite, delay gastric emptying, and regulate homeostasis of glucose.

The role of the vehicle in topical prescription treatments is to deliver therapeutic concentrations of an active drug to a designated skin target site to support patient adherence and satisfaction, ideally without skin irritation. To achieve a pharmacological effect, the drug must be able to penetrate through the stratum corneum (SC) into the viable epidermis and dermis. The skin barrier is composed of terminally differentiated keratinocyte cells (corneocytes) and lipid lamellae, which prevent the movement of water out of the skin.