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

HPLC of Notoginsenoside Fe

Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃

Introduction/Overview

As a traditional Chinese medicinal herb, Panax notoginseng holds an important position in clinical TCM applications due to its remarkable effects of promoting blood circulation, removing blood stasis, stopping bleeding, and reducing swelling. Sanqi saponins, as the main active ingredient in Sanqi, have attracted widespread attention in recent years due to their diverse pharmacological activities. Notoginsenoside Fe is a natural triterpene saponin isolated from Sanqi, featuring a unique chemical structure and significant biological activity, especially showing potential therapeutic value in the field of neuroprotection. This paper aims to systematically review the chemical structure, physicochemical properties, plant origin, and extraction method of Sanqi saponin Fe, and, considering its pharmacological activity, mechanism of action, druggability evaluation, and clinical application prospects, comprehensively review the research progress of this compound and provide a theoretical basis for subsequent basic and clinical studies.

Chemical structure and physicochemical properties

The molecular formula of Sanqi saponin Fe is C_48H_78O_18, with a molecular weight of 917.14 Da, and it belongs to the pentacyclic triterpene saponin class. Its structural core is the typical framework of ginsenosides, connecting multiple glycoside residues to form a complex glycoside structure. The LogP value was 2.6873, indicating moderate lipid solubility, suitable for cell membrane penetration. Its extremely high polar surface area (TPSA 277.91 Ų) indicates strong molecular polarity and low water solubility (0.0674), which may limit its oral absorption and blood-brain barrier (BBB) penetration ability. Druggability analysis showed that Sanqi saponin Fe does not inhibit hERG channels, and the Ames test result was zero, indicating low genotoxicity risk and good safety.

Plant Origins and Extraction Methods

Sanqi saponin (Fe) mainly comes from the roots and rhizomes of Sanqi and is an important component in the Sanqi saponin population. Traditional extraction methods mostly use alcohol extraction combined with liquid chromatography separation technology. The specific process includes:

1. Raw material pretreatment: Dry Sanqi root is ground into fine powder to facilitate the extraction of active ingredients.
2. Solvent extraction: 70%-80% ethanol is commonly used for reflux extraction, with extraction time generally 2-3 hours, repeated 2-3 times to improve extraction efficiency.
3. Concentration and separation: After the extract is concentrated under reduced pressure to a certain concentration, it is separated and purified using silica gel column chromatography or reversed-phase high-performance liquid chromatography (RP-HPLC).
4. Purification identification: The structure and purity of Sanqi saponin Fe are confirmed using mass spectrometry (MS), nuclear magnetic resonance (NMR), and other techniques.

In recent years, the application of new technologies such as ultrasound-assisted extraction and microwave-assisted extraction has improved extraction efficiency and purity, reduced extraction time and solvent usage, and provided technical support for industrial production.

Pharmacological activity research

Sanqi saponin Fe has demonstrated significant pharmacological activity in various disease models, with abundant research achievements especially in the field of neuroprotection.

1. Neuroprotective effects

Panax notoginseng saponin Fe regulates multiple signaling pathways, reduces nerve cell damage, inhibits neuroinflammation, and promotes nerve repair. Its main manifestations are:

• Antioxidant activity: Activates the NFE2L2 (Nrf2) signaling pathway, enhances intracellular antioxidant enzyme expression, clears excess reactive oxygen species (ROS), and reduces oxidative stress damage.
• Anti-apoptotic effect: Upregulates the expression of BCL2 anti-apoptotic protein, inhibits CASP3 activation, and reduces neuronal apoptosis.
• Inhibits neurotoxic protein accumulation: regulates APP and BACE1 expression, reduces β-amyloid protein (Aβ) production, inhibits abnormal phosphorylation of MAP (tau protein), and alleviates neuronal fiber tangles.
• Regulates neurotransmitter metabolism: By inhibiting ACE activity, it prolongs the duration of acetylcholine action and improves cognitive function.
• Anti-inflammatory effect: Inhibits the MAPK1 signaling pathway, reduces the release of pro-inflammatory factors, and alleviates neuroinflammatory responses.

2. Other pharmacological activities

In addition to neuroprotection, Sanqi saponin Fe also exhibits antiplatelet aggregation, anti-inflammatory, anti-tumor, and cardiovascular protective effects, though the related mechanisms require further elucidation.

Mechanism of action and molecular targets

The neuroprotective effects of Sanqi saponin Fe involve multi-target and multi-pathway coordinated regulation, with main targets including:

• BCL2: As an anti-apoptotic protein, Sanqi saponin Fe upregulates its expression and blocks apoptosis signaling.
• APP and BACE1: regulate β-amyloid precursors and their lyases, reducing the formation of neurotoxic Aβ.
• MAPT: Regulates the phosphorylation state of tau protein to prevent nerve fiber tangles.
• NFE2L2: Activates antioxidant response elements and enhances cellular antioxidant capacity.
• SIRT1: Regulates cellular metabolism and stress responses through deacetylation, promoting neuron survival.
• MAPK1: Inhibits pro-inflammatory signal transduction, reducing neuroinflammation.
• ACHE: Inhibits acetylcholinesterase and enhances cholinergic neurotransmission.
• CASP3: Inhibits key apoptotic enzymes, reducing cell death.
• SNCA: Regulates α-synuclein to prevent protein aggregation associated with Parkinson's disease.

The coordinated regulation of these targets enables Panax notoginseng saponin Fe to demonstrate good therapeutic potential in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.

Druggability evaluation and pharmacokinetics

Analysis of the drug-like properties of Sanqi saponin Fe shows:

• The molecular weight is relatively large (917.14 Da), exceeding the ideal range for traditional oral drugs, which may affect oral bioavailability.
• The LogP was moderate (2.6873), which favored cell membrane penetration, but the high TPSA (277.91 Ų) limited its passive diffusion.
• Low water solubility (0.0674) may affect absorption and distribution.
• The blood-brain barrier penetration ability is low, indicating limited direct action on the central nervous system and relying on other mechanisms or drug administration methods.
• It has good safety, no hERG suppression, negative Ames test, and low genotoxicity risk.

Pharmacokinetics, there are few studies available. Preliminary data show that Sanqi saponin Fe is slowly absorbed orally and has a long plasma half-life. It is mainly metabolized by the liver, with excretion routes including bile and urine. Its low blood-brain barrier permeability suggests that in the future, drug carrier systems or structural modifications can enhance central nervous system targeting.

Prospects and outlooks for clinical applications

Based on the multi-target effects and good safety profile of Sanqi saponin Fe in neuroprotection, it has broad clinical application prospects, especially in the following areas:

1. Treatment of neurodegenerative diseases
   By regulating Aβ metabolism, tau protein phosphorylation, and oxidative stress, Sanqi saponin Fe is expected to become a potential therapeutic drug for cognitive impairment diseases such as Alzheimer's disease.

2. Cerebral ischemia-reperfusion injury
   Antioxidant and anti-inflammatory effects help alleviate nerve damage after stroke and promote nerve function recovery.

3. Parkinson's disease and other movement disorders
   By modulating SNCA and anti-apoptotic mechanisms, neuronal degeneration may be slowed.

4. Combination medication strategies
   Can be used in combination with existing drugs to exert synergistic effects and enhance efficacy.

Future research should focus on pharmacokinetic optimization of Sanqi saponin Fe, innovations in delivery pathways (such as nanocarriers, brain-targeted delivery systems), clinical safety, and efficacy evaluation. Additionally, in-depth analysis of its molecular mechanisms and multi-target synergistic effects helps promote its clinical translation.

Conclusion

Sanqi saponin Fe, as an important active ingredient in Sanqi, demonstrates broad medicinal value thanks to its unique chemical structure and multi-target neuroprotective effects. Despite limitations such as its large molecular weight and low blood-brain barrier permeability, improvements in modern drug design and delivery technology make Sanqi saponin Fe a promising new candidate for treating neurodegenerative diseases. In the future, it is necessary to strengthen pharmacokinetics, mechanistic research, and preclinical evaluation to lay a solid foundation for clinical application and promote innovative development of natural product pharmacology in the field of neurological disease treatment.