Product name: Notoginsenoside Fe
Synonym name:
Catalogue No.: BP1009
Cas No.: 88105-29-7
Formula: C₄₇H₈₀O₁₇
Mol Weight: 917.14
Botanical Source: Panax notoginseng（Burk.）F.H.Chen
Physical Description:
Type of Compound: Triterpenoids

Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle

Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.

The product could be supplied from milligrams to grams
Inquire for bulk scale.

Description:

Notoginsenoside Fe can induce gap junction-mediated intercellular communication (GJIC) reductions; and gap junctions have been shown or are believed to be involved in the pathogenesis of many inherited and acquired human diseases, agents that regulate the GJIC function may facilitate prevention and treatment of GJIC-involved diseases.

References:

Planta Med., 2001, 67(5):417-22.    

Effects of ginsenosides from Panax ginseng on cell-to-cell communication function mediated by gap junctions.   

Gap junctions have been shown or are believed to be involved in the pathogenesis of many inherited and acquired human diseases. Agents that regulate the gap junction-mediated intercellular communication (GJIC) function may facilitate prevention and treatment of GJIC-involved diseases.

METHODS AND RESULTS:

In the present study we examined the effects of 27 ginsenosides isolated from Panax ginseng on GJIC. The results show that compounds 1 (oleanolic acid), 2 (ginsenoside-R0), 3 (ginsenoside-Rb1), 5 (ginsenoside-Rb2), 7 (ginsenoside-Rd), 8 (ginsenoside-Rg3), 12 (panaxadial), 13 (notoginsenoside-R4), 17 [ginsenoside-Rg2 (20S)], 18 (ginsenoside-Rf), and 26 (ginsenoside-F3) did not obviously affect GJIC, whereas compounds 4 (ginsenoside-Rc), 6 (ginsenoside-Rb3), 9 (ginsenoside-Rd2), 10 (Notoginsenoside Fe), 11 (ginsenoside-Rh2),14 (ginsenoside-Ra1), 15 (ginsenoside-Re), 16 [ginsenoside-Rg2 (20R)], 19 (ginsenoside-Ia), 20 [ginsenoside-Rh1 (20S)], 21 [ginsenoside-Rh1 (20R)], 22 (ginsenoside-F1), 23 (protopanaxatriol), 24 (panaxatriol), 25 (ginsenoside-Rg1), and 27 (chikusetsaponin-L8) induced GJIC reductions at various degrees. Compounds 2, 7, and 8 protected against the tyrosine phosphatase inhibitor vanadate-induced GJIC reduction, while compounds 1, 5, 7, and 17 inhibited the cytokine interleukin 1 alpha (IL-1alpha)-induced reduction in GJIC. Nevertheless, no compounds protected against the protein kinase C (PKC) activator 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced GJIC inhibition. On the other hand, GJIC reductions induced by compounds 6, 9,10, 20, 21, 22, 24, and 25 were inhibited by the tyrosine kinase (TK) inhibitor genistein, while GJIC reductions induced by compounds 6, 9, 14, 16, 19, 21, and 24 were attenuated in the presence of the PKC inhibitor calphostin C. However, GJIC reductions induced by compounds 4, 23, and 27 were not inhibited either by genistein or by calphostin C. 

CONCLUSIONS:

These data indicate that various mechanisms are responsible for effects of ginsenosides on GJIC.    

HNMR of Notoginsenoside Fe