Product name: Siamenoside I
Synonym name:
Catalogue No.: BP1304
Cas No.: 126105-12-2
Formula: C₅₄H₉₂O₂₄
Mol Weight: 1125.31
Botanical Source: Siraitiae fructus
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:

Siamenoside I is one of the mogrosides that has several kinds of bioactivities, it exhibits maltase inhibitory effect with the IC50 value of 12 mM.

References:

J Atheroscler Thromb. 2002;9(2):114-20.    

Sweet elements of Siraitia grosvenori inhibit oxidative modification of low-density lipoprotein.    

This study examined the ability of sweet elements extracted from Siraitia grosvenori (SG) to inhibit the oxidation of LDL. 

METHODS AND RESULTS:

We monitored the formation of conjugated diene during copper-mediated LDL oxidation in the presence or absence of sweet elements of whole extract of SG (SG extract) or cucurbitane glycosides (CGs) purified from SG extract as sweet elements. CGs consist of Mogroside IV (Mog.IV), Mogroside V (Mog.V), 11-Oxo-mogroside V (11-Oxo-mog.V), and Siamenoside I (Sia.I). In addition, the effect of these elements on human umbilical vein endothelial cell (HUVEC)- mediated LDL oxidation was tested by measuring production of lipid peroxides. SG extract inhibited copper-mediated LDL oxidation in a dose-dependent fashion, but neither glucose nor erythritol suppressed the oxidation. Among CGs, 11-Oxo-mog.V significantly inhibited LDL oxidation, and prolongation of the lag time during LDL oxidation by 11-Oxo-mog.V was dose-dependent. The lag time (119.7 +/- 8.9 min) in the presence of 200 microM 11-Oxo-mog.V was significantly longer than that (76.8 +/- 5.5 min) of control (p < 0.01). In addition, SG extract and 11-Oxo-mog.V inhibited HUVEC-mediated LDL oxidation in a dose-dependent manner. 

CONCLUSIONS:

These results demonstrate that SG extract can inhibit LDL oxidation and that 11-Oxo-mog.V, a sweet element of SG extract, provides the anti-oxidative property of SG which might reduce the atherogenic potential of LDL.    

J Agric Food Chem. 2005 Apr 20;53(8):2941-6.    

Triterpene glycosides of Siraitia grosvenori inhibit rat intestinal maltase and suppress the rise in blood glucose level after a single oral administration of maltose in rats.   

The effect of the crude extract from Siraitia grosvenori Swingle (SG-ex) on the postprandial rise in blood glucose level was investigated. 

METHODS AND RESULTS:

The increase in plasma glucose level in response to the oral administration of maltose was significantly suppressed in rats when SG-ex was given orally 3 min before the maltose administration. There was, however, no effect when glucose was administered instead, suggesting that the antihyperglycemic effect of SG-ex is elicited by inhibition of maltase in the small intestinal epithelium. In vitro, SG-ex inhibited rat small intestinal maltase. Similar effects were also observed both in vivo and in vitro when the concentrate of the sweet elements (triterpene glycosides) prepared from SG-ex was used. Furthermore, the main sweet element of SG-ex, mogroside V, and some minor elements such as mogroside IV, Siamenoside I, and mogroside III also exhibited maltase inhibitory effect with IC50 values of 14, 12, 10, and 1.6 mM, respectively. 

CONCLUSIONS:

These results suggest that SG-ex exerts anti-hyperglycemic effects in rats by inhibiting maltase activity and that these effects are at least partially exerted by its sweet elements, triterpene glycosides.    

HPLC of Siamenoside I

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

Introduction/Overview

Siamenoside I is a natural sweet-glycoside compound isolated from Siraitia grosvenorii, belonging to the triterpene glycoside family. As a traditional Chinese medicine and natural sweetener, Luo Han Guo has attracted attention for its low calorie, high sweetness, and various bioactive properties. In recent years, Cymenin I has become a research hotspot in the field of natural product pharmacology due to its unique chemical structure and broad biological activity, especially its potential therapeutic effects in malignant tumors such as liver cancer. This paper provides a systematic review of the chemical structure and physicochemical properties of Symmenin I, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and clinical application prospects, aiming to provide scientific evidence for further development and application of this compound.

Chemical structure and physicochemical properties

The molecular formula of Symmenin I is C54H88O28, with a molecular weight of 1125.3060. Its chemical structure belongs to the triterpene saponin class, with a core of a pentacyclic triterpene backbone connecting multiple glycan residues to form a typical sweet glycoside structure. This structure imparts high polarity to Symmenin I, resulting in a large topological pole surface area (TPSA) of 397.52 Ų and a LogP value of 1.4533, indicating moderate lipid solubility and strong hydrophilicity. The water solubility index was 0.3664, indicating a certain solubility in water, but solubility is still affected by the number and structure of sugar groups. Symmenin I has a complex molecular structure, contains multiple hydroxyl and glycosidic bonds, is relatively stable, and does not inhibit the hERG channel. Ames-induced mutagenic test results were zero, indicating high safety.

Plant Origins and Extraction Methods

Cymenin I is mainly isolated from the fruit of monk fruit (Siraitia grosvenorii). Monk fruit belongs to the gourd family, native to southern China, and its fruit is rich in glycoside compounds. Traditional extraction methods typically use water or alcohol extraction, combined with multi-step separation and purification techniques to obtain high-purity Cymenin I.

The specific extraction process includes: first, crush the dried monk fruit pulp, then reflux extraction with hot water or 70% ethanol. After the extract is concentrated, column chromatography (such as silica gel column, reversed-phase C18 column) is used to separate the sweet glycoside components. Further purification was performed by high-performance liquid chromatography (HPLC), combined with mass spectrometry (MS) and nuclear magnetic resonance (NMR) technologies for structural identification. In recent years, the application of ultrasound-assisted extraction (UAE) and microwave-assisted extraction (MAE) technologies has improved extraction efficiency and purity, supporting industrial-scale production.

Pharmacological activity research

Cymenin I exhibits a variety of biological activities, especially in anti-tumor, anti-inflammatory, antioxidant, and immunomodulatory effects.

Anti-liver cancer activity

Liver cancer is a malignant tumor with a high incidence and mortality rate worldwide. Cymenin I has demonstrated effects in inhibiting tumor cell proliferation, inducing apoptosis, and inhibiting metastasis in various in vitro and in vivo liver cancer models. Its anti-liver cancer activity mainly regulates tumor-related signaling pathways, manifested by cell cycle arrest, regulation of apoptosis-related protein expression, and reduced invasion and migration capacity.

Anti-inflammatory and antioxidant effects

Cymenin I can significantly inhibit the production of inflammatory mediators, reduce the expression of pro-inflammatory cytokines such as TNF-α and IL-6, and alleviate inflammatory responses. At the same time, it has the ability to scavenge free radicals, enhance cellular antioxidant enzyme activity, and protect cells from oxidative stress damage.

Immunomodulatory effects

Research shows that Cymenin I can regulate immune cell function, enhance macrophage phagocytic ability, promote lymphocyte proliferation, regulate cytokine secretion, and improve the body's immune defense capabilities.

Mechanism of action and molecular targets

The anti-liver cancer effects of Cymenin I involve multiple key molecular targets and signaling pathways, mainly including:

• BCL2: As an anti-apoptotic protein, its downregulation promotes apoptosis in liver cancer cells.
• STAT3: Cymenin I inhibits STAT3 activation, blocking its function of promoting tumor cell proliferation and immune evasion.
• TOP1: By regulating topoisomerase I activity, it interferes with DNA replication and transcription processes, inhibiting tumor cell proliferation.
• TERT: Inhibits telomerase reverse transcriptase activity, limiting the unlimited proliferation capacity of tumor cells.
• PIK3CA/AKT1: Intervenes in the PI3K/AKT signaling pathway, inhibiting cell survival and metabolic activity.
• MMP9: Downregulates stromal metalloproteinase 9, inhibiting stromal degradation and metastasis in tumor cells.
• EGFR: Blocks epidermal growth factor receptor signaling, inhibiting cell proliferation and migration.
• TP53: Activates tumor suppressor protein p53, promoting cell cycle arrest and apoptosis.
• NFKB1: Inhibits the NF-κB signaling pathway, weakens inflammatory responses and tumor promotion.

The synergistic regulation of these targets enables Cymenin I to inhibit liver cancer development from multiple angles and pathways, demonstrating its potential as a multi-target anti-tumor drug.

Druggability evaluation and pharmacokinetics

The druggability parameters of Cymenin I indicate that it has certain potential for drug development. A larger molecular weight (1125.3060) and a higher TPSA (397.52) suggest that its oral bioavailability may be limited, but a moderate LogP value (1.4533) favors cell membrane permeability. A water solubility index of 0.3664 indicates that its solubility in the aqueous phase is reasonable, which is beneficial for formulation development.

Low blood-brain barrier permeability, reducing the risk of central nervous system toxicity. No hERG channel inhibition, reducing the risk of cardiotoxicity. A negative Ames test indicates a low genotoxicity risk.

Although systematic pharmacokinetic (PK) data are currently lacking, based on its structural characteristics, Symmenin I may undergo glycoside hydrolysis and liver metabolism in the body. Future studies on in vivo absorption, distribution, metabolism, and excretion (ADME) are needed to optimize administration routes and formulations to improve bioavailability.

Prospects and outlooks for clinical applications

Cymenin I, as a naturally derived polysaccharide compound, has good safety and multi-target antitumor activity, showing broad application prospects especially in liver cancer treatment. Its multi-target mechanism helps overcome resistance issues with single-target drugs, and combined with modern drug design technologies, it is expected to develop into a novel anti-liver cancer drug.

In addition, the anti-inflammatory, antioxidant, and immunomodulatory effects of Symmenin I also offer potential applications in chronic inflammatory diseases, metabolic syndromes, and immune-related disorders. Future research should focus on:

1. In-depth mechanism research: Using techniques such as genomics and proteomics to comprehensively analyze the molecular action network.
2. Pharmacokinetic and toxicological assessment: Systematic evaluation of in vivo behavior and safety, laying the foundation for clinical translation.
3. Dosage form optimization and delivery route exploration: improving oral bioavailability or developing local delivery systems.
4. Preclinical and clinical trials: Verify efficacy and safety to promote clinical application.

Through multidisciplinary collaboration, Cymenin I is expected to become a key breakthrough in the development of natural anti-tumor drugs.

Conclusion

Cymenin I, as an important sweet glycoside component in monk fruit, has become a hot topic in natural product pharmacology research due to its unique chemical structure and significant biological activity, especially its potential in liver cancer treatment. Its multi-target and multi-mechanism characteristics offer new ideas for antitumor drug development. Although challenges remain in pharmacokinetics and clinical applications, with deeper research and technological advancements, Cymenin I is expected to become a star molecule in the field of natural anti-tumor drugs, driving the clinical translation of natural drugs. In the future, systematic basic and applied research will provide solid scientific support for its development and utilization, promoting its widespread application in the treatment of liver cancer and related diseases.