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In the absence of any significant muscle or cardiac manifestations, the acute hepatic presentation of CPT1 deficiency cannot be distinguished on a clinical basis from other defects of long-chain fatty acid oxidation and conditions that present as a Reye-like illness
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It is a 46-residue peptide built entirely from D-amino acids in a reversed sequence, a design that confers high resistance to proteolytic degradation while preserving the spatial topology needed to engage its target
The risk of hepatotoxicity is also modulated by background liver disease, obesity or chemotherapy-related fatty liver (as in steatosis), alcohol consumption and genetic mutations in CYP2C9, CYP3A4 and UGT1A1 (213)
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