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Orally ingested ginsenoside passes through the stomach and small intestine without decomposition by either gastric juice or liver enzymes into the large intestine, where ginsenoside is deglycosylated by colonic bacteria followed by transit to the circulation. Colonic bacteria cleave the oligosaccharide connected to the aglycone stepwise from the terminal sugar to afford the major metabolites, 20S-protopanaxadiol 20-O-beta-D-glucopyranoside (M1) and 20S-protopanaxatriol (M4). These metabolites are further esterified with fatty acids. The resultant fatty-acid conjugates are still active molecules that are sustained longer in the body than parental metabolites. Accumulating evidence strongly suggests that ginsenoside is a prodrug that is activated in the body by intestinal bacterial deglycosylation and fatty acid esterification.
Hideo Hasegawa (2004) studied this question.