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Its copper coordination stabilizes the peptide structure, enhancing its bioavailability and interaction with target proteins and receptors

Homozygous null deletion of the Kat6a gene in mice causes foetal to perinatal death (depending on the genetic background), characterised by cleft palate, shortened jaws, cardiac septum defects, and interrupted aortic arch, as well as an anterior homeotic transformation of 19 body segments affecting the vertebral column and the nervous system (Voss et al, 2009, 2012

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[77] It is also known to be metabolized by the UDP-glucuronosyltransferase enzymes UGT1A3, UGT1A4, UGT1A6, UGT1A8, UGT1A9, UGT1A10, UGT2B7, and UGT2B15

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