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Synonym name: Embelic acid; Embeliaquinone
Catalogue No.: BP0530
Cas No.: 550-24-3
Formula: C17H26O4
Mol Weight: 294.391
Botanical Source: Embelia ribes, Embelia tsjersium-cottam, Embelia barbeyana, Embelia robusta, Embelia kilimandscharica, Ardisia humilis, Rapanea umbellata, Connarus ritchiei, , Myrsine africana, Myrsine semiserrata, Myrsine capitellata
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Can be supplied from milligrams to grams.
For Reference Standard and R&D, Not for Human Use Directly.
Inquire for bulk scale.
HPLC of Embelin
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
74.6000
4.1259
1.5438
.0357
1.7828
7.0888
Low
93.0238
2.5163
Yes
Yes
No
No
No
No
0.0
No
No
No
No
Embelin, chemically known as 5-hydroxy-2-octyl-1,4-anthraquinone, CAS number 550-24-3, is a natural small molecule compound derived from plants, widely recognized in the field of natural product pharmacology due to its diverse pharmacological activities. As a non-peptide cell-permeable XIAP (X-linked inhibitor of apoptotic protein) inhibitor, anthbesin demonstrates significant antiproliferative and pro-apoptotic effects in various tumor cells, especially showing good anticancer potential in models of malignant tumors such as prostate cancer, oral squamous cell carcinoma, and breast cancer. In recent years, with in-depth research into its molecular mechanisms, anthbesin has been found to regulate multiple signaling pathways, including NF-κB, the caspase family, and autophagy-related pathways, enabling multi-target intervention in tumor cells. In addition, anthrobinin also demonstrates certain biological activities in anti-inflammation, antioxidant, and antibacterial aspects, indicating broad application prospects as a drug lead compound.
This paper aims to systematically review the chemical structure and physicochemical properties of anthrobin, its plant origin and extraction methods, conduct an in-depth analysis of its pharmacological activity and mechanism of action, evaluate its druggability and pharmacokinetic characteristics, explore its clinical application potential and development prospects, and provide theoretical basis and research directions for subsequent drug development and clinical translation.
The chemical core of anthraquinone is the anthraquinone framework, with a molecular formula of C17H26O4 and a molecular weight of 294.3910. Its structure includes a 1,4-anthraquinone core, a 5-position hydroxyl modification, and a 2-position connected octyl side chain, giving it strong hydrophobicity and membrane permeability. The LogP value of anthrobinin was 4.1259, indicating high lipid solubility, which facilitates penetration of cell membranes but may limit its water solubility. Its polar surface area (TPSA) is 74.6 Ų, and moderate polarity helps maintain a certain level of bioavailability. Low water solubility (0.0357 mg/mL) suggests that solubility improvement strategies should be considered in formulation development. Anthbesin does not inhibit hERG channels, and Ames-induced mutagenic test results are negative, indicating high safety and low toxicological risk.
The chemical structure is relatively stable, and the anthraquinone framework endows it with certain antioxidant capacity. The hydroxyl and long-chain alkyl side chains in the structure provide diverse interaction sites for binding to target proteins, promoting their specificity and selectivity.
Anthrobin is mainly found in the plant Embelia ribes Burm. f. (Ganbeigu) and its related species are among the main active components of this genus. Embelia ribes are widely distributed in India and Southeast Asia, and have traditionally been used to treat various diseases such as parasitic infections, inflammation, and tumors.
Common methods for extracting anthracetin include solvent extraction with intrinsic extraction, ultrasound-assisted extraction, and hot reflux extraction. Ethanol or methanol is generally used as extraction solvents to improve extraction efficiency. After liquid-liquid separation and column chromatography purification, high-purity anthracetin can be obtained. In recent years, supercritical CO2 extraction technology has also been applied to extract anthrobin, offering advantages of high efficiency and environmental friendliness.
During purification, methods such as silica gel column chromatography and reversed-phase high-performance liquid chromatography (RP-HPLC) are commonly used for separation and identification. Structural confirmation largely relies on nuclear magnetic resonance (NMR), mass spectrometry (MS), and infrared spectroscopy (IR) analysis.
As a XAP inhibitor, anthrobinin exhibits significant anti-proliferative effects across various tumor cell lines. As a member of the apoptotic inhibition protein family, XAP can inhibit the activity of caspase-3, caspase-7, and caspase-9, blocking the apoptosis signaling pathway. Anthrobin, by binding to XAP, releases its inhibition of caspase and induces tumor cell apoptosis.
In prostate cancer cells, anthbesin has an IC50 of about 4.1 μM, effectively inhibiting cell growth and activating caspase-9, initiating endogenous apoptosis. Research on oral squamous cell cells shows that anthrobinin not only induces apoptosis but also activates autophagy, suggesting a diverse anti-tumor mechanism.
In the field of breast cancer, anthbesin inhibits tumor cell proliferation, migration, and drug resistance by regulating multiple key molecular targets such as AMPK, BCL2, STAT3, and ESR2. Its regulation of ABC transporters ABCB1 and ABCG2 is expected to overcome multidrug resistance (MDR) and enhance chemotherapy efficacy.
Anthrobin can inhibit the NF-κB signaling pathway, reduce the expression of inflammatory mediators such as TNF-α, IL-6, and IL-1β, and exhibit good anti-inflammatory activity. It blocks NF-κB-regulated anti-apoptotic and metastatic gene products, further enhancing its antitumor effects.
In addition, anthrobinin also regulates immune cell function, promoting macrophage activation and cytokine secretion, thereby enhancing the body's immune surveillance capabilities.
Anthrobinin also exhibits certain antioxidant, antibacterial, and antiparasitic activities, broadening its pharmacological application range. Its antioxidant effect is mainly attributed to the electron donor properties of the anthraquinone structure, which can scavenge free radicals and reduce oxidative stress damage.
The core mechanism of anthbesin focuses on inhibiting the XAP protein, releasing inhibition of the caspase family, and activating intracellular apoptosis signaling. The specific mechanisms include:
XIAP inhibition: Anthbesin directly binds to the BIR3 domain of XIAP, blocking its binding to caspase-9, promoting caspase-9 activation, and initiating mitochondria-dependent endogenous apoptosis pathways.
Inhibition of NF-κB signaling pathway: Anthrobin inhibits IκB kinase (IKK) activity, blocks IκB degradation, suppresses NF-κB transfer from the cytoplasm to the nucleus, and reduces the expression of anti-apoptotic proteins and transfer-related genes.
Autophagy induction: In oral squamous cell cell cells, anthbesin activates the AMPK signaling pathway, promotes the expression of the autophagy-related protein LC3-II, induces cellular autophagy, and synergistically promotes cell death.
Multi-target regulation: In breast cancer cells, anthbesin modulates various signaling molecules such as STAT3, BCL2, PRKCA, and MMP2, inhibiting tumor cell proliferation, migration, and drug resistance.
ABC transporter regulation: Anthrobinin affects the expression or function of ABCB1 and ABCG2, reduces drug efflux, and enhances intracellular accumulation of chemotherapy drugs.
In summary, anthbesin achieves effective inhibition of tumor cells through the synergistic regulation of multiple signaling pathways, offering advantages of multiple targets and mechanisms.
Anthbesin has a molecular weight of 294.39, meeting the drug affinity criteria of the Lipinski rule. A LogP value of 4.13 suggests high lipid solubility, which facilitates cell membrane penetration, but low water solubility (0.0357 mg/mL), which may limit its oral bioavailability and formulation development. Its TPSA is 74.6 Ų, making it suitable for cell absorption.
The low penetration ability of the blood-brain barrier suggests that anthbesin is limited in drug development for the central nervous system, but this also reduces the risk of CN toxicity. The hERG channel inhibition test was negative, indicating a low risk of cardiotoxicity. Ames-induced mutagenic test results were zero, indicating low genotoxicity risk and good safety.
In terms of pharmacokinetics, the absorption, distribution, metabolism, and excretion (ADME) characteristics of anthrobinin still require systematic study. Current studies show that anthbesin is absorbed slowly orally and has limited bioavailability, so its pharmacokinetic performance may need to be improved through nanocarriers, liposomes, or other delivery systems. Metabolic pathways are inferred mainly through oxidation and binding reactions via hepatic enzyme systems, and the activity and safety of metabolites require further evaluation.
As a natural XAP inhibitor, anthrobasin has significant clinical translation potential due to its significant antitumor activity and good safety. Its application prospects are particularly prominent in various malignant tumors such as prostate cancer, oral squamous cell carcinoma, and breast cancer. By targeting and inhibiting apoptotic inhibition proteins and regulating multiple signaling pathways, anthbesin is expected to become a leading compound for the next generation of anticancer drugs.
In future clinical development, the following aspects need to be closely monitored:
Dosage Formulation Optimization: To address its poor water solubility and low bioavailability, new delivery systems such as nanoparticles, liposomes, or solid dispersions are developed to increase in vivo exposure levels and therapeutic efficacy.
Combination Strategies: Combining anthbesin with traditional chemotherapy drugs or targeted drugs may overcome multidrug resistance and enhance antitumor efficacy, warranting in-depth study.
Safety evaluation: Systematic toxicological and pharmacokinetic studies are essential for preclinical practice to ensure the long-term safety and tolerability of anthbesin.
Indication expansion: Due to its anti-inflammatory and immunomodulatory activities, anthbesin has potential in inflammatory diseases, autoimmune diseases, and infectious diseases that are worth exploring.
Clinical trial design: Conduct early clinical trials to clarify the maximum tolerated dose, pharmacokinetic parameters, and preliminary efficacy of anthrobin, laying the foundation for subsequent clinical development.
As a natural compound with multiple targets and mechanisms, anthrobin demonstrates excellent antitumor activity and good safety, showing potential as a novel anticancer drug. By inhibiting the XAP protein and blocking the NF-κB signaling pathway, it effectively induces tumor cell apoptosis and autophagy, thereby inhibiting tumor growth and metastasis. Meanwhile, druggability evaluations of anthbesin indicate it has a solid foundation for drug development, but issues of water solubility and bioavailability still need to be addressed.
In the future, combining modern drug formulation technology with precision medicine strategies, Xunbesu is expected to play an important role in the field of cancer treatment. Systematic pharmacokinetics, toxicology, and clinical research will drive it from the laboratory to clinical settings, bringing new treatment options for cancer patients. The in-depth development and multidisciplinary integration of natural product pharmacology will provide solid support for the drug development of anthbesin and similar compounds.
Shenshuai
Wenjing
Hedandan
