+86-28-82633987
Product name: Cucurbitacin B
Synonym name: Amarin
Catalogue No.: BP0414
Cas No.: 6199-67-3
Formula: C32H46O8
Mol Weight: 558.712
Botanical Source: Bitter principle of fruits of Cucurbitaceae, also present in some other plants, e.g. Anagallis arvensis, Luffa acutangula, Luffa graveolens, Luffa echinata, Echinocystis fabacea, Iberis spp., Begonia tuberhybris-alba, Begonia heracleifolia, Bryonia alba,
Physical Description: White powder
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, up to kilograms
Inquire for bulk scale.
Descriptions:
Cucurbitacin B (cucB) is a triterpenoid constituent of Cucurbitaceae vegetables and a promising phytochemical for cancer prevention, cucB induces G(2) arrest and apoptosis through a STAT3-independent but ROS-dependent mechanism in SW480 cells.[1]
Cucurbitacin B has antiproliferative effect, can induce apoptosis by inhibition of the JAK/STAT pathway and potentiates antiproliferative effects of gemcitabine on pancreatic cancer cells, may be an effective, new approach for the treatment of ER-, Her2/neu amplified, and p53 mutant breast cancers.[2,3]
Combination of cucurbitacin B at a relatively low concentration with either of the chemotherapeutic agents, docetaxel (DOC) or gemcitabine (GEM) , shows prominent antiproliferative activity against breast cancer cells without increased toxicity, this promising combination should be examined in therapeutic trials of breast cancer.[4]
Cucurbitacin B has anti-cutaneous squamous cell carcinoma (CSCC) activity by inhibiting growth, arresting the cell cycle, and synergistically potentiate the anti-proliferative effect of cisplatin in CSCC.[5]
Cucurbitacin B a selective inhibitor of JAK2/STAT3 signaling, could promote dendritic cells (DCs) differentiation and improve antitumor immunity, also significantly reduce the frequency of imCs in patients with lung cancers and enhance the effect of p53-specific CTL on tumor 16HBE/BPDE cells.[6]
References:
[1] Yasuda S, Yogosawa S, Izutani Y, et al. Mol Nutr Food Res, 2010, 54(4):559–65.
[2] Thoennissen N H, Iwanski G B, Doan N B, et al. Cancer Res, 2009, 69(14):5876-84.
[3] Wakimoto N, Dong Y, O’Kelly J, et al. Cancer Sci, 2008, 99(9):1793–7.
[4] Aribi A, Sigal Gery ?, Lee D H, et al. Int J Cancer, 2013, 132(12):2730–7.
[5] Chen W, Leiter A, Yin D, et al. Int J Oncolo, 2010, 37(3):737-43.
[6] Lu P, Yu B, Xu J. Cancer Biother Radio, 2012, 27(27):495-503.
[7] Sun W, Chao Z M, Wang C, et al. Chinese Journal of Experimental Traditional Medical Formulae ,2014, 20(23):86-8.
HPLC of Cucurbitacin B
HNMR of Cucurbitacin B
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
146.4700
3.5000
3.2000
Low
null
No
No
No
Unknown
No
Positive
null
Cucurbitacin B (CAS No.: 6199-67-3) is a highly oxidized tetracyclic triterpene natural product widely found in plants of the Cucurbitaceae family. As an important member of the cucurbitacin family, cucurbitacin B has attracted widespread attention in recent years due to its remarkable biological activity, especially its potential in anti-tumor fields. Numerous in vivo and in vitro experiments have shown that cucurbitacin B can not only inhibit the proliferation, migration, and invasion of cancer cells, but also induce cell cycle arrest and promote apoptosis. In addition, its multiple pharmacological effects—anti-inflammation, antioxidant, antiviral, blood sugar-lowering, liver protection, and neuroprotection—make it a hot topic in natural product pharmacology research.
This review aims to systematically summarize the chemical structure and physicochemical properties of cucurbitacin B, plant origin, and extraction methods, thoroughly explore its pharmacological activity and mechanism of action, evaluate its druggability and pharmacokinetic characteristics, and finally look ahead to its clinical application prospects, aiming to provide a theoretical foundation and reference for related research.
Cucurbitacin B is a highly oxidized tetracyclic terpenoid compound, with a molecular formula of C_32H_46O_8 and a molecular weight of 542.7. Its core structure consists of four rings, containing multiple hydroxyl and ketone groups, exhibiting high polarity and complex stereochemical characteristics. The LogP value of cucurbitacin B is about 3.5, indicating moderate lipid solubility and facilitating oral absorption. Its topological pole surface area (TPSA) is 146.47 Ų, and it has 8 hydrogen bond acceptors, indicating that its molecules possess strong polarity and hydrogen bonding capabilities, which is significant for binding to biological targets.
The structural characteristics of cucurbitacin B give it unique bioactivity, but also bring certain pharmacokinetic challenges. Its lower blood-brain barrier penetration limits its potential for central nervous system diseases. Existing studies have not yet clarified its hepatotoxicity and cardiotoxicity; the hERG channel inhibition test results were negative, indicating a lower risk of cardiotoxicity. However, Ames' mutagenic test was positive, suggesting a possible genotoxicity risk, which should be closely monitored in subsequent drug development.
Cucurbitacin B is mainly distributed in the roots, stems, leaves, and fruits of plants in the Cucurbitaceae family, such as bitter melon (Momordica charantia), pumpkin (Cucurbita pepo), snake gourd (Trichosanthes kirilowii), and other related plants. Different plant species and their growth environments have significant effects on the content and composition of cucurbitacin B.
Traditional extraction methods mostly use organic solvent extraction methods, such as methanol, ethanol, or ethyl acetate, combined with ultrasound-assisted extraction or reflux extraction technologies to improve extraction efficiency. The extract undergoes steps such as concentration, separation, and column chromatography, and is finally purified and identified using techniques such as high-performance liquid chromatography (HPLC) or gas chromatography-mass spectrometry (GC-MS). In recent years, the application of supercritical CO_2 extraction and molecular blotting technology has provided new ideas for efficient and green extraction of cucurbitacin B.
Cucurbitacin B exhibits significant cytotoxicity in various tumor cell lines, inhibiting the proliferation, migration, and invasion of cancer cells. Its antitumor effects involve regulation of multiple signaling pathways, manifested as cell cycle blocking and promoting apoptosis. For example, in models of breast, lung, colorectal, liver, and pancreatic cancers, cucurbitacin B has shown good anti-tumor effects. In vivo experiments have also confirmed that it can significantly inhibit tumor growth and reduce the formation of metastases.
Cucurbitacin B demonstrates powerful anti-inflammatory activity by inhibiting the release of inflammatory mediators and regulating immune cell function. It can downregulate the expression of pro-inflammatory factors such as TNF-α, IL-6, and IL-1β, reducing inflammatory responses. At the same time, cucurbitacin B has the ability to eliminate free radicals and enhance antioxidant enzyme activity, effectively reducing oxidative stress damage.
Research shows that cucurbitacin B has inhibitory effects on various viruses, including hepatitis B virus (HBV), human immunodeficiency virus (HIV), and influenza virus. Its antiviral mechanism mainly works by interfering with viral replication, blocking the binding of viruses to host cells, and regulating immune responses.
Cucurbitacin B has shown glycemic lowering effects in diabetes models, possibly by improving insulin sensitivity and regulating the activity of enzymes related to glucose metabolism. Additionally, it has protective effects on the liver, reducing inflammation and fibrosis and promoting liver cell repair.
Cucurbitacin B exhibits neuroprotective effects in neurodegenerative disease models, mainly by slowing nerve damage and improving cognitive function through antioxidant, anti-inflammatory, and regulation of nerve cell apoptosis pathways.
The multi-target mechanism of cucurbitacin B forms the basis for its multiple pharmacological activities. The main targets include:
In addition, cucurbitacin B also regulates inflammatory responses and cell survival by regulating signaling pathways such as NF-κB, PI3K/Akt, and JAK/STAT.
Cucurbitacin B has a molecular weight of 542.7 and a LogP of 3.5, meeting certain lipophilicity requirements and facilitating cell membrane penetration and oral absorption. Its higher TPSA means stronger molecular polarity, which may limit its ability to pass through biofilms, especially its lower blood-brain barrier penetration.
Currently, data on hepatotoxicity and cardiotoxicity of cucurbitacin B are still unclear. The hERG channel inhibition test results are negative, suggesting good cardiac safety. However, positive Ames test results suggest potential genotoxicity risks and require special attention in subsequent safety evaluations.
Pharmacokinetic studies show that cucurbitacin B is absorbed orally relatively quickly, but its bioavailability is limited by its solubility and metabolic stability. Its main metabolic pathways may involve oxidative and binding reactions in the liver, and the activity and toxicity of these metabolites require further research. In vivo distribution studies show that cucurbitacin B accumulates in the liver, kidneys, and tumor tissues, but its concentration is lower in the central nervous system.
Cucurbitacin B, with its broad-spectrum pharmacological activity, especially its outstanding performance in the antitumor field, has good clinical development potential. Its multi-target and multi-pathway mechanism helps overcome tumor resistance and heterogeneity, making it suitable for combination drug strategies. In addition, the anti-inflammatory, antioxidant, and neuroprotective effects of cucurbitacin B also offer potential applications in chronic inflammation, autoimmune diseases, and neurodegenerative disorders.
However, the genotoxicity risks, pharmacokinetic limitations, and safety issues of cucurbitacin B remain major obstacles to clinical translation. Future research should focus on structural optimization, formulation improvement, and targeted delivery technologies to enhance bioavailability and safety. At the same time, systematic toxicological evaluation and preclinical studies are key to advancing the clinical application of cucurbitacin B.
In addition, combining modern drug design technologies, such as computer-aided drug design (CADD), multi-omics analysis, and precision medicine strategies, will help reveal the network of action of cucurbitacin B and optimize its clinical indications.
Cucurbitacin B, a widely sourced and biologically active natural compound, demonstrates outstanding antitumor and multiple pharmacological effects. Its complex molecular structure and multi-target mechanisms provide valuable models for natural drug research. Although there are currently certain safety and pharmacokinetic challenges, with advances in extraction and purification technologies, drug design, and delivery systems, cucurbitacin B is expected to become an important candidate for future natural product drug development.
Future research should strengthen systematic evaluation of the toxicology of cucurbitacin B, deepen molecular-level analysis of its mechanism of action, expand its clinical indications, and explore its synergistic effects with existing drugs to promote its transition from laboratory to clinical application, benefiting a broad patient base.
Shenshuai
Wenjing
Hedandan
