Introduction: Bullous pemphigoid (BP) is the most common autoimmune blistering disease. Drug-induced BP has been increasingly reported, with dipeptidyl peptidase-4 (DPP-4) inhibitors, particularly vildagliptin, emerging as a notable cause. The pathogenesis is thought to involve the disruption of immune tolerance and epitope spreading, leading to a broader autoimmune response against basement membrane antigens beyond the classic NC16A domain of BP180. This case series highlights the variable clinical spectrum and therapeutic challenges in vildagliptin-induced BP. Case: A 74-year-old male with type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia, and a history of stroke presented with a 2-month history of recurrent, pruritic, tense bullae. He had been on vildagliptin for 36 months. Histopathology confirmed subepidermal blistering, and direct immunofluorescence demonstrated linear IgG/C3 deposition at the dermo-epidermal junction, with positive anti-BP180 antibodies, diagnosing BP. Discontinuation of vildagliptin and initiation of systemic corticosteroids resulted in significant clinical improvement, allowing a rapid prednisolone taper to 5 mg daily without new bullae formation. A 62-year-old female with T2DM and dyslipidemia presented with bullous eruptions 3 months after initiating vildagliptin. Skin biopsy confirmed BP, revealing subepidermal blistering with eosinophils and linear C3/IgG deposition at the basement membrane zone. Vildagliptin was discontinued. Despite initial management with systemic corticosteroids, the disease course was refractory. The patient experienced a flare upon steroid taper and had persistent blistering on prednisolone 20 mg daily, necessitating the addition of azathioprine as a steroidsparing agent. Conclusion This case series illustrates the variable clinical course of vildagliptin-induced BP in which the therapeutic trajectories diverged significantly. Recognition of BP as a potential adverse effect of DPP-4 inhibitors is critical, and management should be individualized.