De novo lipogenesis (DNL) plays a pivotal role in mammalian development, facilitating the production of fatty acids required for cellular functions like energy storage and membrane formation. The fatty acid synthase (FASN) enzyme is vital for this process, making it a target for therapeutic interventions in conditions like cancer and steatotic liver disease. The inhibitor denifanstat is undergoing clinical trials, showing promising results. However, complete inhibition of DNL can lead to adverse effects, underscoring the need for comprehensive research on FASN’s role to safely exploit its therapeutic potential.
FASN is the primary enzyme in de novo lipogenesis, condensing acetyl-CoA and malonyl-CoA to produce palmitate, a crucial fatty acid in mammals.
Denifanstat, a leading FASN inhibitor, is in various clinical trials and shows promise for treating metabolic diseases like MASLD and cancer.
Further studies indicate that while targeting FASN can treat metabolic diseases, complete loss of de novo lipogenesis may lead to negative effects such as decreased platelet production.
The structural complexity of the FASN enzyme highlights its role in synthesizing fatty acids, showing high homology to animal FASN-like polyketide synthases.
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