Saccharomyces cerevisiae has been engineered to produce artemisinic acid (an immediate precursor to the anti-malarial drug artemisinin) through the introduction of a biosynthetic pathway from Artemsisia annua. Additionaly, the mevalonate pathway was altered to enhance flux from acetyl-CoA to the artemisinic acid. Further increase in product yields requires identification and genetic modification of the select metabolic pathways which currently hinder maximum product production. In this study, the central metabolic fluxes of S. cerevisiae are examined using ¹³C labeled galactose as the carbon source. The carbon labeling patterns of proteinogenic amino acids are probed using GC-MS, which provides constraints for calculation of metabolic flux distribution (assuming galactose uptake rate as initial flux is equal to 100). Preliminary results indicate that most of carbon substrate can not be fully oxidized by tricarboxylic acid (TCA) cycle (flux<50); instead, ex-cellular metabolites, including glycerol (flux=5~10), acetate (flux=10~15), and ethanol (flux=60~90) are the major carbon sinks. The pyruvate dehydrogenase bypass is not only the route for ethanol and acetate production, it also directly generates the main source of acetyl-CoA for the mevalonate pathway. However, less than 1% of total acetyl-CoA is converted to artemisinic acid. Most of the acetyl-CoA is either transported from cytosol into mitochondrion for oxidization by TCA cycle or utilized in fatty acid and ergosterol synthesis. Efforts to reduce ergosterol production have yielded elevated levels of artemisinic acid. It may be possible to channel more acetyl-CoA into mevalonate pathway by limiting acetyl-CoA transport to the mitochondrion or inhibiting ethanol and fatty acid synthesis.