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The nail plate is the hard, translucent, keratinized structure that forms the visible part of the human nail, serving primarily to protect the distal phalanges and enhance fine motor tasks and sensory perception [1]. It is composed of approximately 80-90 layers of dead, flattened keratinocytes (onychocytes) held together by intercellular glue and disulfide bonds, creating a dense, semi-permeable barrier [2]. While not a molecular target in the traditional pharmacological sense (such as a receptor or enzyme), the nail plate is a critical anatomical barrier and a site of drug delivery for treating conditions like onychomycosis and nail psoriasis [3]. Drugs such as efinaconazole and tavaborole are specifically engineered to penetrate this dense keratin matrix to reach the underlying nail bed where pathogens often reside [4]. A major challenge in targeting the nail plate is its low permeability to most topically applied substances, which often necessitates treatment regimens lasting several months to a year [5].
Passive diffusion and penetration of antifungal or anti-inflammatory agents through the dense keratinized matrix to reach the nail bed or act within the plate layers.
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