Product name: Tubeimoside II
Synonym name:
Catalogue No.: BP1416
Cas No.: 115810-12-3
Formula: C₆₃H₉₈O₃₀
Mol Weight: 1335.45
Botanical Source: Bolbostemma paniculatum（Maxim.）Franquet
Physical Description:
Type of Compound: Terpenoids

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:

Tubeimoside I, tubeimoside II, and tubeimoside III show anti-inflammatory, antitumor, and antitumor-promo ting effects.

References:

Acta Pharmacol Sin. 2001 May;22(5):463-8.    

Structure-activity relationship of tubeimosides in anti-inflammatory, antitumor, and antitumor-promoting effects.   

To study structure-activity relationship of tubeimosides isolated from Bolbostemma paniculatum for their anti-inflammatory, antitumor, and antitumor-promoting effects. 

METHODS AND RESULTS:

Tubeimoside I, Tubeimoside II, and Tubeimoside III were isolated from tubers of Bolbostemma paniculatum (Maxim) Franquet (Cucurbitaceae), a Chinese folk medicine,"Tubeimu", and their anti-inflammatory, anti-tumor, anti-tumorigenic activities, and acute toxicity were studied in vivo. Tubeimoside I, Tubeimoside II, and Tubeimoside III are all natural analogues of oleanane type of triterpenoid saponins from the same medicinal plant, and all show anti-inflammatory, antitumor, and antitumor-promo ting effects. However, the anti-inflammatory, anti-tumor, and anti-tumorigenic activities of Tubeimoside II are stronger than those of tubeimoside I, and the acute toxicity of Tubeimoside II is lower than that of tubeimoside I; the anti-inflammatory, anti-tumor, and anti-tumorigenic activities of Tubeimoside III are stronger than those of Tubeimoside II, and the acute toxicity of Tubeimoside III is also stronger than that of Tubeimoside II. 

CONCLUSIONS:

C-16 hydroxyl group of Tubeimoside II plays an important role in enhancing biological activity of Tubeimoside II and in decreasing its toxicity. The difference of chemical structure in B and/or C position between tubeimosides III and II plays an important role in enhancing biological activity and toxicity of Tubeimoside III. Therefore tubeimosidre II may be the most promising agent for cancer chemoprevention and chemotherapy among tubeimosides I, II, and III.    

HPLC of Tubeimoside II

HNMR of Tubeimoside II

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

Introduction/Overview

Tubeimoside II (TBMS-II) is a natural analogue of oleano-type triterpene saponin, mainly derived from the traditional Chinese medicinal herb Bolbostemma paniculatum) is separated and obtained. As one of the important active ingredients in traditional Chinese medicine fritillaria, TBMS-II has attracted widespread attention in the field of natural product pharmacology in recent years due to its remarkable anti-inflammatory and antitumor activities. Especially in the field of tumor treatment, TBMS-II demonstrates strong inhibitory effects on various cancer cells, particularly ovarian cancer, where the related mechanisms involve regulation of multiple signaling pathways and molecular targets. This paper aims to systematically review the chemical structure and physicochemical properties of TBMS-II, plant origin and extraction methods, pharmacological activity and mechanism of action, drug readiness evaluation, pharmacokinetic characteristics, and clinical application prospects, providing theoretical basis and research directions for subsequent drug development and clinical translation.

Chemical structure and physicochemical properties

TBMS-II belongs to the oleanotane-type triterpene saponin, with the molecular formula C₆₃H₉₉O₃₀ and a molecular weight of 1335.4470. Its structure is formed by the oleanokane-type triterpene nucleus connected by multiple glycosidic bonds, exhibiting typical saponin structural characteristics. The LogP value of TBMS-II is about 1.0177, indicating moderate lipophilicity, which facilitates membrane penetration without becoming overly hydrophobic. Its extremely high polar surface area (TPSA 465.4200) reflects the presence of polyhydroxyl and glycosyls, resulting in low water solubility (0.2570), which significantly affects its bioavailability and distribution in vivo.

From a physicochemical property perspective, TBMS-II has a large molecular weight and complex structure, with many hydrogen bond donors and acceptors, resulting in complex absorption and metabolic processes in vivo. Its blood-brain barrier penetration ability is relatively low, indicating its limited distribution in the central nervous system. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. Ames gene mutation test result was 0.0, indicating that TBMS-II does not show significant mutagenicity and is relatively safe.

Plant Origins and Extraction Methods

TBMS-II mainly originates from Bolbostemma paniculatum, a perennial herbaceous plant of the Cucurbitaceae family, widely distributed across many provinces in southern China. In traditional Chinese medicine, Fritillaria is used to treat abscesses, ulcers, scrofula, and other diseases. Its pharmacological active ingredients mainly include various triterpene saponins, among which TBMS-II is the most abundant and highly active component.

Common extraction methods for TBMS-II include solvent extraction, column chromatography separation, and high-performance liquid chromatography (HPLC) purification. Typically, methanol or ethanol is used as the extractor, and crude extracts are obtained by reflux extraction, followed by silica gel column chromatography or reversed-phase C18 columns for separation and purification. In recent years, the application of ultrasound-assisted extraction and microwave-assisted extraction technologies has improved extraction efficiency and purity. Purified TBMS-II can be structurally confirmed using modern analytical techniques such as mass spectrometry and nuclear magnetic resonance (NMR).

Pharmacological activity research

Anti-inflammatory activity

TBMS-II exhibited significant anti-inflammatory effects. In vitro experiments have shown that TBMS-II can inhibit the expression of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and nitric oxide synthase (NOS2), thereby reducing inflammatory responses. Its anti-inflammatory mechanism mainly works by inhibiting the activation of the nuclear factor κB (NF-κB) signaling pathway, reducing the release of inflammatory mediators, thereby protecting tissues.

Antitumor activity

TBMS-II exhibits good cytotoxicity across various tumor cell lines, especially showing significant inhibitory effects on ovarian cancer cells. Research has found that TBMS-II can induce tumor cell apoptosis, inhibit cell proliferation and migration, and block tumor angiogenesis. Its anti-tumor effects involve regulation of multiple signaling pathways and key molecules.

In ovarian cancer models, TBMS-II inhibits STAT3 activation by downregulating the anti-apoptotic protein BCL2, reduces the expression of multidrug resistance-related protein ABCB1, and enhances the sensitivity of chemotherapy drugs. Additionally, TBMS-II can regulate the oxidative stress-related transcription factor NFE2L2, inhibit matrix metalloproteinase MMP9, and reduce tumor cell invasion and metastasis. The effects on DNA topoisomerases TOP1 and TOP2A suggest that they may interfere with DNA replication and repair processes in tumor cells.

Mechanism of action and molecular targets

The mechanism of action of TBMS-II is complex, involving coordinated regulation of multiple targets and multiple pathways. The main targets and their mechanisms are as follows:

• BCL2: TBMS-II disrupts tumor cells' anti-apoptotic mechanisms by inhibiting BCL2 expression, promoting programmed cell death.
• STAT3: As a key transcription factor for tumor cell proliferation and immune escape, TBMS-II inhibits its phosphorylation and nuclear translocation, blocking the expression of downstream tumor-promoting genes.
• ABCB1: By reducing ABCB1 expression, TBMS-II alleviates drug efflux in tumor cells, reverses multidrug resistance, and enhances the efficacy of chemotherapy drugs.
• NFE2L2: Regulates cellular oxidative stress responses, enhances cellular antioxidant capacity, and slows the malignant progression of tumor cells.
• TOP1/TOP2A: Interferes with DNA topoisomerase activity, blocks DNA replication and repair, and leads to impeded tumor cell proliferation.
• ESR1: Affects estrogen receptor signaling and regulates hormone-dependent growth of tumor cells.
• NOS2: Inhibits induced nitric oxide synthase, reducing tumor promoters in the inflammatory microenvironment.
• PIK3CA: Blocks tumor cell survival and proliferation signals by inhibiting the PI3K/Akt signaling pathway.
• MMP9: Inhibits matrix metalloproteinases, reducing the ability of tumor cells to degrade and metastasize in the matrix.

The integrated regulation of these targets gives TBMS-II the advantage of multi-target synergistic effects in anti-tumor and anti-inflammatory effects.

Druggability evaluation and pharmacokinetics

The druggability evaluation of TBMS-II indicates that it has certain potential for drug development. Its large molecular weight and high polarity limit oral absorption, and its low water solubility also affects its bioavailability. Its LogP is moderate, which is favorable for cell membrane penetration, but the high TPSA value suggests limited transmembrane capability. The low permeability of the blood-brain barrier reduces the risk of central nervous system toxicity.

In terms of safety, TBMS-II does not inhibit hERG channels and carries a low risk of cardiotoxicity; Ames test is negative, indicating a low risk of genotoxicity. In vivo pharmacokinetic studies show that TBMS-II has a moderate half-life in the blood, mainly metabolized by the liver and excreted by the kidneys. Its metabolites still require further identification and toxicological evaluation.

To overcome its poor water solubility and low bioavailability, researchers have attempted to improve its pharmacokinetic properties by using nanocarriers, liposome encapsulation, and structural modification, thereby enhancing in vivo stability and targeting properties.

Prospects and outlooks for clinical applications

Given TBMS-II's significant anti-inflammatory and antitumor activity, especially its potential therapeutic value for refractory tumors such as ovarian cancer, its clinical application prospects are broad. Future research should focus on the following aspects:

1. Formulation optimization: Develop efficient delivery systems to improve the bioavailability and targeting of TBMS-II, reducing dose-related toxicity.
2. In-depth Mechanism Research: Using modern technologies such as genomics and proteomics to further elucidate the molecular mechanisms of TBMS-II action and its interactions with the tumor microenvironment.
3. Combination therapy strategies: Explore the synergistic effects of TBMS-II with existing chemotherapy or immunotherapy drugs to overcome tumor resistance and improve treatment outcomes.
4. Preclinical safety evaluation: Systematic toxicological and pharmacokinetic studies are conducted to ensure safety and efficacy, laying the foundation for clinical trials.
5. Clinical trial design: Conduct early clinical trials to evaluate TBMS-II's efficacy, safety, and dosage range, and promote its translation into clinical application.

Conclusion

As a natural triterpenoid saponin with multiple targets and mechanisms, Dermatitrosin B demonstrates excellent anti-inflammatory and anti-tumor activity, especially showing broad application potential in ovarian cancer treatment. Although there are certain challenges in druggability, modern drug formulation technologies and in-depth mechanistic research are expected to overcome these bottlenecks and achieve clinical translation. In the future, TBMS-II is expected to become an important candidate molecule for the development of natural anti-cancer drugs, offering new treatment options for cancer patients.