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Sulfur mustard exposure degranulates mast cells in the dermis. Bifunctional indomethacin prodrug abrogates mast cell degranulation. Evidence suggests that inflammatory cells and mediators that they generate are important in the pathogenic responses to SM. In the present studies we investigated the role of mast cells in SM-induced skin injury using a murine vapor cup exposure model. 14 days after SM reduced skin inflammation and injury and enhanced tissue repair. These data suggest that reduced inflammation and injury in response to the bifunctional indomethacin prodrug may be due, at least in part, to abrogating mast cell degranulation.