Product name: Cucurbitacin E
Synonym name: alpha-Elaterin
Catalogue No.: BP0416
Cas No.: 18444-66-1
Formula: C₃₂H₄₄O₈
Mol Weight: 556.696
Botanical Source: Cucumis melo L.
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.




Chengdu Biopurify Phytochemicals Ltd. is a leading company in the research, development, manufacture and marketing of High Quality Phytochemicals and Extracts(especially Active Ingredients from Traditional Chinese Medicine，TCM), Natural Active Pharmaceutical Ingredients worldwide.
The main services:
A. Supply active ingredients and reference standards of TCM, from mgs to kgs scale
B. Custom extraction and purification, target Herb Active Ingredients
C. Custom synthesis and semi-synthesis for Natural Active Ingredients
D. CR(contract research), CM(contract manufacture) and PD(process development) services from lab scale, pilot scale to commercial scale(GMP is also available)
E. TCM compounds library for drug screen,more than 3000 compounds available, many of them are rare and unique.

HPLC of Cucurbitacin E

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

Introduction/Overview

Cucurbitacin E (CAS No.: 18444-66-1) is a class of triterpene natural products derived from plants in the Cucurbitaceae family. Due to its unique chemical structure and significant biological activity, it has attracted widespread attention in the field of natural product pharmacology in recent years. Cucurbitacin compounds are known for their strong cytotoxicity and antitumor activity, especially showing significant inhibitory effects in various cancer models. Cucurbitacin E, as an important member, can significantly inhibit the activity of the cyclin B1/CDC2 complex, a key cell cycle regulatory protein, demonstrating a potential anti-tumor mechanism and becoming a hot topic in anticancer drug development.

Colon cancer, as a malignant tumor of the digestive system with a high incidence and mortality rate worldwide, has a complex pathogenesis involving abnormal activation of multiple signaling pathways. Cucurbitacin E demonstrates multi-target, multi-pathway anti-tumor potential by regulating key molecular targets including AMPK, BCL2, STAT3, and MAPK1. This paper will systematically review the chemical structure and physicochemical properties of Cucurbitacin E, plant origin and extraction methods, pharmacological activity and mechanism of action, druggability evaluation, and pharmacokinetic characteristics, and explore its clinical application prospects in colon cancer treatment, aiming to provide theoretical basis and reference for subsequent research and drug development.

Chemical structure and physicochemical properties

Cucurbitacin E belongs to the triterpene class of compounds, with the chemical formula C32H44O8 and a molecular weight of 556.68. Its structure is based on the tetracyclic triterpene nucleus, featuring a typical cyclopentane and cyclohexane ring backbone. The molecule contains multiple hydroxyl and ketone groups, giving it rich functional group characteristics. The LogP value of Cucurbitacin E is about 3.0, indicating moderate lipid solubility, which facilitates penetration of cell membranes. Its topological pole surface area (TPSA) is 146.9 Ų, indicating high molecular polarity and a hydrogen bond acceptor count of 8. These physicochemical properties have significant implications for its bioavailability and targeting activity.

Structurally, cucurbitacin E contains multiple unsaturated bonds and oxidative functional groups; these structural features not only determine its biological activity but also affect its stability and metabolic pathways. Its large molecular weight and high polarity suggest that its pharmacokinetic performance should be optimized during drug design to improve absorption and distribution efficiency in vivo.

Plant Origins and Extraction Methods

Cucurbitin E is mainly found in plants of the Cucurbitaceae family, such as bitter melon (Momordica charantia), pumpkin (Cucurbita pepo), and other wild gourd species. Different plant species and their growth environments have significant effects on the content and composition of cucurbitacin E. Typically, cucurbitacin E is concentrated in the fruit and rhizome parts of plants.

There are various methods for extracting cucurbitacin E, mainly including solvent extraction, ultrasound-assisted extraction, and high-performance liquid chromatography (HPLC) separation and purification. Traditional solvent extraction often uses ethanol or methanol as solvents, combined with reflux extraction or ultrasound-assisted technologies to improve extraction efficiency. Subsequently, separation and purification are performed by silica gel column chromatography or reversed-phase HPLC to ensure the obtain high-purity cucurbitacin E.

In recent years, green extraction technologies such as supercritical CO2 extraction and microwave-assisted extraction have gradually been applied to cucurbitacin E extraction, aiming to improve extraction efficiency and reduce the use of organic solvents, aligning with the environmental trend of modern natural product extraction.

Pharmacological activity research

The pharmacological activity of cucurbitacin E focuses on its significant antitumor effects, especially its inhibitory effect in colon cancer cell lines. In vitro studies have shown that cucurbitacin E can effectively inhibit the proliferation of colon cancer cells, induce apoptosis, and block the cell cycle process. Its antitumor activity is closely related to its inhibition of the cyclin B1/CDC2 complex, blocking the G2/M phase transition and leading to cell cycle arrest.

In addition to anti-tumor properties, Cucurbitacin E also exhibits multiple biological activities such as anti-inflammatory and antioxidant properties. Its anti-inflammatory effect is mainly achieved by inhibiting the inflammatory mediator TNF-α and related signaling pathways, thereby reducing inflammatory responses and possessing potential immunomodulatory functions. Antioxidant activity helps reduce oxidative stress and protects cells from free radical damage.

Animal model studies further support the antitumor potential of cucurbitacin E, showing that it can effectively inhibit tumor growth, improve the tumor microenvironment, and have low toxicity, providing a solid safety foundation.

Mechanism of action and molecular targets

The pharmacological mechanisms of cucurbitacin E are complex and diverse, involving multiple signaling pathways and molecular targets. Its core mechanisms include:

1. Cell cycle regulation
   Cucurbitacin E blocks cells from transitioning from G2 phase to M phase by inhibiting cyclin B1/CDC2 complex activity, causing cell cycle arrest and inhibiting cancer cell proliferation.

2. AMPK signaling pathway activates
   As an energy-sensing molecule, AMPK (PRKAA1) is activated by cucurbitacin E, promoting cellular energy metabolism reprogramming, inducing autophagy and apoptosis, and inhibiting tumor cell growth.

3. Inhibition of the anti-apoptotic protein BCL2
   Cucurbitacin E downregulates BCL2 expression, disrupting intracellular anti-apoptotic balance and promoting mitochondrial pathway-mediated apoptosis.

4. STAT3 signaling pathway inhibition
   As a key transcription factor in various tumors, STAT3's activity is inhibited by cucurbitacin E, blocking the proliferation and metastasis ability of tumor cells.

5. Multidrug resistance-related protein ABCB1 regulates
   Cucurbitacin E can regulate the expression and function of ABCB1, reduce drug efflux from tumor cells, and enhance the sensitivity of chemotherapy drugs.

6. Targets related to inflammation and oxidative stress
   By inhibiting inflammatory mediators such as ALOX5 and TNF, Cucurbitacin E alleviates tumor-related chronic inflammatory responses and improves the tumor microenvironment.

7. Other signal path regulation
   Including multiple molecular targets such as TOP1, MAPK1, GSK3B, and PPARG, cucurbitacin E achieves comprehensive regulation of tumor cells through the synergistic action of multiple targets.

In summary, cucurbitacin E demonstrates strong antitumor activity through its multi-target and multi-pathway mechanisms, and its regulation of the cell cycle and signaling pathways provides a solid molecular basis for its pharmacological effects.

Druggability evaluation and pharmacokinetics

The druggability parameters of Cucurbitacin E indicate that it has certain potential for drug development. Although the molecular weight of 556.68 is relatively large, it is still within an acceptable range. The LogP was 3.0, indicating moderate lipid solubility and favorable cell membrane penetration. The TPSA value of 146.9 is relatively high, indicating strong polarity, which may affect oral absorption and bioavailability.

A hydrogen bond receptor count of 8 indicates that the molecule has strong hydrogen bond binding ability, which helps form stable complexes with target proteins, but may also limit its ability to cross lipid membranes. The low permeability of the blood-brain barrier suggests its limited distribution in the central nervous system, reducing the risk of CN toxicity.

Currently, safety data on the hepatotoxicity, cardiotoxicity, and hERG channel inhibition of cucurbitacin E are still insufficient and require further systematic toxicological studies to clarify these findings. The results of the Ames trial are unknown, and a genotoxicity assessment is needed to ensure its safety.

In terms of pharmacokinetics, current research is relatively limited. Preliminary in vivo experiments indicate that oral absorption of cucurbitacin E is limited, and its bioavailability may be reduced due to its higher polarity and metabolic enzyme activity. Its metabolic pathway may involve the hepatic cytochrome P450 enzyme system, and the activity and toxicity of these metabolites require further study. Its half-life and distribution characteristics in vivo remain to be clarified.

In summary, cucurbitacin E has a certain medicinal foundation, but its pharmacokinetic performance needs to be improved through structural modification and pharmacological optimization, enhancing in vivo stability and bioavailability.

Prospects and outlooks for clinical applications

With its multi-target anti-tumor mechanism and excellent cytotoxicity, Cucurbitacin E shows broad application prospects in the treatment of solid tumors such as colon cancer. By regulating the cell cycle, inducing apoptosis, and inhibiting multidrug resistance-related proteins, it may effectively overcome resistance to traditional chemotherapy drugs and enhance treatment outcomes.

In the future, cucurbitacin E is expected to become an important component of single drugs or combination chemotherapy regimens, exerting synergistic anti-cancer effects. Moreover, its anti-inflammatory and antioxidant properties provide new ideas for tumor microenvironment regulation, helping to comprehensively improve tumor treatment outcomes.

However, the clinical translation of cucurbitacin E still faces many challenges. First, it is necessary to thoroughly study its safety and toxicological characteristics to clarify potential side effects. Second, optimizing its pharmacokinetic performance and improving oral bioavailability and in vivo stability are key to achieving clinical application. Finally, systematic preclinical and clinical trials are conducted to verify efficacy and safety, pushing the process from the laboratory to clinical practice.

Future research can focus on structural modification of cucurbitacin E, development of nanocarrier delivery systems, and combined application with existing anticancer drugs to enhance therapeutic efficacy and clinical applicability. At the same time, modern molecular biology and pharmacological techniques are used to clarify the details of its mechanisms of action, providing theoretical support for precision treatment.

Conclusion

Cucurbitacin E, an important triterpene natural product in the Cucurbitaceae family, demonstrates tremendous potential in colon cancer treatment due to its unique chemical structure and multi-target antitumor activity. By inhibiting cyclin B1/CDC2 complex activity and regulating key molecular targets such as AMPK, BCL2, and STAT3, it achieves cell cycle blockade and apoptosis induction, demonstrating the advantages of multidimensional intervention in tumors by natural products.

Although current safety and pharmacokinetic data on cucurbitacin E are not yet complete, its favorable druggability parameters and preliminary pharmacological research provide a foundation for subsequent development. In the future, through structural optimization and innovations in drug delivery technology, Cucurbitacin E is expected to become a novel candidate for the treatment of colon cancer and other tumors.

In summary, Cucurbitin E not only enriches the natural anti-cancer drug stock, but also provides important scientific evidence for deeper understanding of tumor cell cycle regulation and multi-target therapeutic strategies. With ongoing research deepening, its clinical application prospects are promising.