Pharmacokinetics of ginsenoside Rb1 and its metabolite compound K after oral administration of Korean Red Ginseng extract

Abstract

Compound K is a major metabolite of ginsenoside Rb1, which has various pharmacological activities in vivo and in vitro. However, previous studies have focused on the pharmacokinetics of a single metabolite or the parent compound and have not described the pharmacokinetics of both compounds in humans. To investigate the pharmacokinetics of ginsenoside Rb1 and compound K, we performed an open-label, single-oral dose pharmacokinetic study using Korean Red Ginseng extract. We enrolled 10 healthy Korean male volunteers in this study. Serial blood samples were collected during 36 h after Korean Red Ginseng extract administration to determine plasma concentrations of ginsenoside Rb1 and compound K. The mean maximum plasma concentration of compound K was 8.35±3.19 ng/mL, which was significantly higher than that of ginsenoside Rb1 (3.94±1.97 ng/mL). The half-life of compound K was 7 times shorter than that of ginsenoside Rb1. These results suggest that the pharmacokinetics, especially absorption, of compound K are not influenced by the pharmacokinetics of its parent compound, except the time to reach the maximum plasma concentration The delayed absorption of compound K support the evidence that the intestinal microflora play an important role in the transformation of ginsenoside Rb1 to compound K.

Ginsenoside compound K sensitizes human colon cancer cells to TRAIL-induced apoptosis via autophagy-dependent and -independent DR5 upregulation

“…The mean maximum plasma concentration of CK was 8.35±3.19 ng/ml (13.4±5 mM). 33 CK sensitized colon cancer cells to TRAIL at 50  μ M in this study, a concentration much less than the peak plasma concentrations achieved in volunteer during the test. Hence, the clinical application of CK was as guaranteed.…”

Metabolic profile and pharmacokinetics of polyphyllin I, an anticancer candidate, in rats by UPLC‐QTOF‐MS/MS and LC‐TQ‐MS/MS

“…Unlike the PPI concentration–time profile, PSA, TRL and DSN first occurred at 1, 2 and 3 h after administration of PPI in some rats and were slowly absorbed, distributed and eliminated. This phenomenon was also observed in other saponin studies (Kim, ; Zhu et al, ). The reason could be that PSA, TRL and DSN were first metabolized by intestinal microflora and then absorbed by the gastrointestinal tract.…”

“…The reason for this was not clear, but we inferred that the generation and absorption sites of the metabolites were different. In addition, the calculated pharmacokinetic parameters, especially that of the three metabolites, are highly variable, with coefficients of variation of 50-80%, which were observed during the other saponin studies (Kim, 2013;Shakya et al, 2012;Zhu et al, 2011). The diversity variation of intestinal microflora of individual rats might cause this phenomenon.…”

Ultra-fast liquid chromatography with tandem mass spectrometry determination of eight bioactive components of Kai-Xin-San in rat plasma and its application to a comparative pharmacokinetic study in normal and Alzheimer's disease rats

“…This phenomenon might be on account of pharmacological effects of GRb1, which may attenuate Aβ induced neurotoxicity and tau hyperphosphorylation , directly scavenge radical , and possess the anti‐neuroinflammation effect . The absorption and metabolism of GRb1 occur mainly in the intestine and partially in the stomach , which indicates that intestinal microflora and enzymes may play an important role in the absorption and elimination of GRb1 . In addition, some other ginsenosides (GRd as an example) could transform to GRb1 in the metabolic process.…”