Ginsenoside F2

Catalog No. BCN1245
CAS RN 62025-49-4
Molecular Weight 785.01
Molecular Formula C42H72O13
Database [PubChem]:382163248
[ChEBI]:77145
[PCIDB]:30389

Definition

A ginsenoside found in Panax species that is dammarane which is substituted by hydroxy groups at the 3β, 12β and 20 pro-S positions, in which the hydroxy groups at positions 3 and 20 have been converted to the corresponding β-D-glucopyranosides, and in which a double bond has been introduced at the 24-25 position.

Standard InChI

InChI=1S/C42H72O13/c1-21(2)10-9-14-42(8,55-37-35(51)33(49)31(47)25(20-44)53-37)22-11-16-41(7)29(22)23(45)18-27-39(5)15-13-28(38(3,4)26(39)12-17-40(27,41)6)54-36-34(50)32(48)30(46)24(19-43)52-36/h10,22-37,43-51H,9,11-20H2,1-8H3/t22-,23+,24+,25+,26-,27+,28-,29-,30+,31+,32-,33-,34+,35+,36-,37-,39-,40+,41+,42-/m0/s1

Biological Activity

Ginsenoside F2 has the anti-cancer activity, it induces apoptosis in breast cancer stem cells (CSCs) by activating the intrinsic apoptotic pathway and mitochondrial dysfunction, also induces the formation of acidic vesicular organelles, recruitment of GFP-LC3-II to autophagosomes, and elevation of Atg-7 levels, suggests that F2 initiates an autophagic progression in breast CSCs. [1]
Ginsenoside F2 suppresses hair cell apoptosis and premature entry to catagen more effectively than finasteride, it decreases the expression of TGF-β2 and SCAP proteins,   this study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.[2]
Ginsenoside F2 could be a new potential chemotherapeutic drug for glioblastoma multiforme (GBM) treatment by inhibiting the growth and invasion of cancer, the anticancer activity might be mediated through inhibition of proliferation judged by Ki67 and apoptosis induced by activation of caspase-3 and -8.[3]
Ginsenoside F2 may reduce obesity via the inhibition of adipogenesis in the 3T3-L1 cell line.[4]

Product information

English website: Ginsenoside F2
Japanese website: Ginsenoside F2
Chinese website: Ginsenoside F2

References

[1] Mai T T, Moon J Y, Song Y W, et al. Cancer Lett, 2012, 321(2):144–53.
[2] Shin H S, Park S Y, Hwang E S, et al. Biol Pharm Bull, 2014, 37(5):755-63.
[3] Shin J Y, Lee J M, Shin H S, et al. J Ginseng Res, 2012, 36(1):86-92.
[4] Siraj F M, Sathishkumar N, Kim Y J, et al. J Enzym Inhib Med Ch, 2014, 30(1):9-14.
[5] Zhou W, Li J, Li X, et al. J Sep Sci, 2008, 31(6-7):921-5.