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Abnormal keratin protein aggregates in the meibomian glands are a hallmark of obstructive Meibomian Gland Dysfunction (MGD), the leading cause of dry eye disease worldwide. In a healthy state, the meibomian gland ductal epithelium is non-keratinized or minimally keratinized to allow the free flow of meibum (lipids) to the ocular surface. However, pathological hyperkeratinization leads to the accumulation of keratinized material, forming plugs that obstruct the gland orifice and terminal duct (Jester et al., 2015; Knop et al., 2011). This obstruction results in lipid deficiency in the tear film, increased evaporation, and chronic inflammation of the ocular surface. Therapeutic interventions, such as the investigational drug AZR-MD-001 (Selenium sulfide), specifically target these aggregates by acting as a keratolytic agent. By breaking down the disulfide bonds within the keratin matrix and slowing the overproduction of keratinocytes, these treatments aim to restore gland patency and improve the quality of meibum secretion (Azura Ophthalmics, 2023).
Keratolytic activity via the reduction of disulfide bonds in keratin proteins; inhibition of keratinocyte proliferation and normalization of epithelial differentiation (Azura Ophthalmics, 2023; Knop et al., 2011).
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