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Caitlin M Brumfiel,1 Meera H Patel,2 Katheryn A Bell,1 Michael A Cardis3 1Georgetown University School of Medicine, Washington, DC, USA; 2Creighton University School of Medicine, Phoenix Regional Campus, Phoenix, AZ, USA; 3MedStar Washington Hospital Center/Georgetown University Hospital Department of Dermatology, Washington, DC, USACorrespondence: Caitlin M BrumfielGeorgetown University School of Medicine, 3900 Reservoir Road, Washington, DC, 20007, USATel +1 513-260-3948Email cmb373@georgetown.eduAbstract: Acne vulgaris is a common skin condition of the face and trunk that negatively impacts quality of life. Trifarotene is a new first-in-class fourth-generation topical retinoid that has been uniquely studied in the treatment of both facial and truncal acne. Through selective agonism of retinoic acid receptor (RAR)-gamma, the most predominant RAR isotype in the epidermis, trifarotene exerts more targeted, skin-specific effects than earlier generation retinoids. This narrative review summarizes all currently available literature regarding the use of trifarotene in acne vulgaris. We focus on efficacy, safety, and tolerability data and highlight quality of life outcomes and patient-reported satisfaction. Future clinical trials and the clinical applicability of this novel medication in the treatment of acne are also discussed.Keywords: acne vulgaris, trifarotene, retinoid, randomized controlled trials

Background: Cutaneous lichen planus (LP) is a recalcitrant, difficult-to-treat, inflammatory skin disease characterized by pruritic, flat-topped, violaceous papules on the skin. Baricitinib is an oral Janus kinase (JAK) 1/2 inhibitor that interrupts the signaling pathway of interferon (IFN)-γ, a cytokine implicated in the pathogenesis of LP., Methods: In this phase II trial, twelve patients with cutaneous LP received baricitinib 2 mg daily for 16 weeks, accompanied by in-depth spatial, single-cell, and bulk transcriptomic profiling of pre-and post-treatment samples., Results: An early and sustained clinical response was seen with 83.3% of patients responsive at week 16. Our molecular data identified a unique, oligoclonal IFN-γ, CD8+, CXCL13+ cytotoxic T-cell population in LP skin and demonstrate a rapid decrease in interferon signature within 2 weeks of treatment, most prominent in the basal layer of the epidermis., Conclusion: This study demonstrates the efficacy and molecular mechanisms of JAK inhibition in LP. Trial Registration Number : NCT05188521.