Mevalonate Biosynthesis is a Metabolic Vulnerability of Gemcitabine-Resistant Pancreatic Cancer
Acquired gemcitabine resistance drives metabolic reprogramming that suppresses pyrimidine salvage while creating a therapeutically exploitable dependence on the mevalonate pathway. These findings identify pharmacologic inhibition of HMGCR as a metabolic vulnerability in gemcitabine resistance and support HMGCR expression as a candidate biomarker (measurable biological signal) for treatment stratification in PDAC patients.
Animal & Preclinical Data
Demonstrated in living animal models before large-scale human safety and dosing trials begin.