An 4-Second Procedure Towards cdk1 inhibitor Cell Cycle inhibitor

By comparison with the mass chromatography of FTZ and the rat serum samples from control group, the MS spectra for rat serum samples from FTZ treated group exhibited 27 peaks in common, which demonstrated that the 27 components from FTZ were absorbed into the rat blood after oral administration.

Ion chromatograms of dosed and controlled rat serum are shown in Figs. 2, 3 and 4. The MS spectra and retention behavior of 36 peaks for prototype components and metabolites are summarized in Table 6. The constituents in rat serum after oral administration of FTZ were identied using Cell Cycle inhibitor their retention time and mass spectra. As a result, peaks 1, 2, 22, 26 and 27 were original form compounds existing in Fructus Ligustri Lucidi, peaks 18 came from Rhizoma Coptidis, peaks 12, 16, 20, 21 and 23 resulted from Radix Notoginseng, peak 19 and 22 originated from Fructus Citri Sarcodactylis, peak 6 and 24 came from Cortex Eucommiae, peak 4 originated from Radix Salvia Miltiorrhiza.

By comparison with the literature data, this showed the same fragmentation pathway as the metabolite of ginsenoside Rh1/F1, so the two constituents were identied as the 25 hydroxyl Cell Cycle inhibitor ginsenoside Rh1/F1. Using the same method, M5 and M6 were identied as 20 / protopanaxatriol because they showed the m/z 477 ion in positive ion mode and m/z 493 and m/z 553 ions in negative ion mode. By comparison with the literature data, we suggested that M5 and M6 may be sapogenin which formed by loss of all glycosidic units from protopanaxatriol saponins. The MS and MS2 spectra and possible metabolic pathways of 25 hydroxy ginsenoside Rh1/F1 and protopanaxatriol in positive and negative ion mode are shown in Fig.

The results showed the same fragmentation pathway as the metabolite Cell Cycle inhibitor of ginsenoside Rb1 and ginsenoside Rd.