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The vitamin A dimerization process refers to the non-enzymatic reaction by which two molecules of vitamin A join to form a dimer, leading to the production of toxic byproducts, such as A2E and other orange pigments, collectively termed vitamin A cycle byproducts (VAB). These dimers accumulate in the retinal pigment epithelium (RPE) and are strongly associated with the pathogenesis of Stargardt disease, age-related macular degeneration, and other retinal degenerative conditions. Inhibiting vitamin A dimerization, for example using deuterium-enriched vitamin A (C20D3-vitamin A, also called Gildeuretinol), can reduce the formation of these toxic byproducts and is being explored as a therapeutic approach for retinal diseases. Fundus autofluorescence is used as a clinical biomarker to track the accumulation of vitamin A dimers and related age-associated retinal changes.
Inhibition of hydrogen abstraction at carbon 20, thus slowing or inhibiting vitamin A dimer formation, reducing toxic byproducts (e.g., lipofuscin, A2E)
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