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Abnormal keratin aggregates in the meibomian glands are a primary pathological driver of Meibomian Gland Dysfunction (MGD), which is the leading cause of evaporative dry eye disease (Source: StatPearls, Meibomian Gland Dysfunction). These aggregates arise from the hyperkeratinization of the ductal epithelium, where an overproduction of keratin proteins creates physical obstructions or plugs within the gland ducts (Source: Investigative Ophthalmology & Visual Science, Hyperkeratinization in MGD). This blockage prevents the normal secretion of meibum—the essential lipid layer of the tear film—leading to tear instability, ocular surface damage, and chronic inflammation. Therapeutic intervention focuses on the mechanical or chemical removal of these aggregates to restore ductal patency. For instance, selenium sulfide (AZR-MD-001) is utilized as a keratolytic agent to break down the disulfide bonds that stabilize the keratin structure (Source: Azura Ophthalmics, AZR-MD-001 Pipeline). By clearing these obstructive aggregates, the treatment aims to restore the flow of healthy lipids to the ocular surface and alleviate the symptoms of dry eye.
Keratolytic activity involving the reduction of disulfide bonds within keratin proteins to dissolve and remove obstructive aggregates from the gland ducts.
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