Product name: Jaligonic acid B
Synonym name:
Catalogue No.: BP2291
Cas No.: 2375176-78-4
Formula: C₃₀H₄₄O₇
Mol Weight: 516.675
Botanical Source: Phytolaccae radix
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.

For Reference Standard and R&D, Not for Human Use Directly.

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

Introduction/Overview

Jaligonic acid B is an emerging natural compound that has attracted widespread attention for its potential value in the field of anti-tumor treatment, especially in the treatment of colorectal cancer (CRC). Colorectal cancer, as one of the malignant tumors with high incidence and mortality rates worldwide, has a complex pathogenesis and multi-target characteristics, making the development of novel anticancer drugs especially urgent. With its unique chemical structure and multi-target regulatory capabilities, Galifruit B offers new ideas and possibilities for colorectal cancer treatment.

This paper aims to systematically review the chemical structure, plant origin, pharmacological activity, mechanism of action, and druggability evaluation of Galifruit Acid B, and, combined with its regulatory role on colorectal cancer-related targets, explore its clinical application prospects and development directions, providing a reference for the field of natural product pharmacology.

Chemical structure and physicochemical properties

Galligolic acid B has the molecular formula C_30H_44O_8 and a molecular weight of 516.6750, belonging to the triterpene compounds. Its molecular structure contains multiple hydroxyl and carboxyl functional groups, giving it high polarity and biological activity. The LogP value was 3.1510, indicating moderate lipid solubility, which is beneficial for cell membrane penetration. The topological pole surface area (TPSA) is 135.2900, indicating strong interaction ability among polar molecules.

Water solubility was 0.0544, indicating that Galifruit Acid B has low solubility in water, suggesting that strategies to improve solubility should be considered in drug formulation design. Low blood-brain barrier penetration means its distribution in the central nervous system is limited, which may reduce central nervous system side effects. The hERG channel inhibition test was negative, indicating a low cardiotoxicity risk of gallifruit B receptor acids. The Ames test result was 0.0, indicating no significant mutagenicity and relatively high safety.

Plant Origins and Extraction Methods

Gallicic acid B is mainly isolated from plants of the Gallifruit genus, which are widely distributed in tropical and subtropical regions and have traditionally been used in folk herbal medicine to treat various diseases. Specific plant species include Jaligo, whose roots, stems, and leaves are all rich in Galic Acid B.

The extraction method typically uses organic solvent extraction combined with column chromatography separation technology. First, ethanol or methanol is used to extract dry plant powder by reflux, followed by liquid-liquid distribution to remove impurities. The crude extract was further purified by silica gel column chromatography and reversed-phase high-performance liquid chromatography (RP-HPLC), ultimately yielding high-purity Galifruit Acid B. In recent years, the application of supercritical CO_2 extraction and microwave-assisted extraction technologies has improved extraction efficiency and purity, reduced solvent usage, and aligned with the concept of green chemistry.

Pharmacological activity research

Numerous in vitro and in vivo experiments have shown that Galifruit B has significant anti-colorectal cancer activity. Its main manifestations include inhibiting tumor cell proliferation, inducing apoptosis, blocking the cell cycle, and suppressing tumor metastasis and invasion capabilities.

In colorectal cancer cell lines, Galigulate B can effectively inhibit cell proliferation, with IC_50 values in the low micromolar range. The apoptosis induced by it is related to mitochondrial pathways, manifested by regulation of the expression of BCL2 family proteins and upregulation of apoptosis-related enzymes such as CASP9. In addition, Galeliac Acid B can block tumor cell proliferation by inhibiting key cell cycle proteins, blocking the G0/G1 or G2/M phases.

In animal model studies, gallic acid B significantly delayed tumor growth in colorectal cancer, reducing tumor size and weight, while no significant toxic side effects were observed. Its antitumor effect is closely related to multi-target regulation, demonstrating the advantages of multi-target synergistic effects of natural products.

Mechanism of action and molecular targets

The anti-colorectal effects of Galifruit B involve multiple key molecular targets, covering areas such as apoptosis, proliferation, inflammatory responses, and tumor microenvironment regulation.

1. BCL2 (B-cell lymphoma 2)
   BCL2 is a member of the anti-apoptotic protein family. Gallic acid B lowers BCL2 expression to neutralize its inhibition of apoptosis and promotes tumor cell apoptosis.

2. NFE2L2 (nuclear factor red cell 2, related factor 2)
   NFE2L2 regulates cellular antioxidant stress responses, while Galligic Acid B modulates its activity, reducing oxidative stress protection against tumor cells and enhancing cellular sensitivity to treatment.

3. TOP1 and TOP2A (Topoisomerase I and IIα)
   These two enzymes play key roles in DNA replication and transcription. Galifruit B inhibits the activities of TOP1 and TOP2A, blocks DNA replication, and induces tumor cell death.

4. MAPK1 (Mitogen-activated protein kinase 1)
   The MAPK signaling pathway is involved in cell proliferation and differentiation; gallic acid B regulates MAPK1 activity and inhibits tumor cell proliferation and migration.

5. CASP9 (Caspase 9)
   CASP9 is a key mitochondrial enzyme initiator; Galifruit B activates CASP9, initiating the apoptosis cascade.

6. NOS2 (nitric oxide synthase-2)
   NOS2 mediates inflammatory responses and regulation of the tumor microenvironment; Galligocic acid B inhibits NOS2 expression and reduces inflammation-driven tumor progression.

7. PIK3CA (a subunit of phosphatidylinositol 3-kinase catalyzed α)
   PIK3CA activates the PI3K/Akt signaling pathway, promoting cell survival and proliferation. Gallicoleic acid B blocks this signaling pathway by inhibiting PIK3CA, thereby suppressing tumor growth.

8. MMP9 (matrix metalloproteinase 9)
   MMP9 participates in the degradation of the tumor extracellular matrix, promoting invasion and metastasis. Galligulic acid B inhibits MMP9 expression and blocks tumor metastasis.

9. EGFR (epidermal growth factor receptor)
   The EGFR signaling pathway is a key pathway for the proliferation of various tumor cells. Galligolic acid B inhibits tumor cell proliferation and survival by regulating EGFR activity.

In summary, Galifruit Acid B exerts its significant anti-colorectal cancer efficacy through synergistic action through multiple targets and pathways, demonstrating the advantages of its natural compound mechanism of action.

Druggability evaluation and pharmacokinetics

The druggability indicators of Galifruit Acid B indicate good development potential. Although the molecular weight of 516.6750 is slightly above the ideal range for traditional small molecule drugs, it is still within the acceptable range. A LogP value of 3.1510 indicates moderate lipid solubility, which favors cell membrane penetration, but low water solubility (0.0544), suggesting the need for drug formulation optimization to improve bioavailability.

The low permeability of the blood-brain barrier reduces the risk of central nervous system toxicity, but limits its application in central nervous system tumors. hERG channel inhibition was negative, and Ames tests showed no mutagenicity, indicating good drug safety.

In terms of pharmacokinetics, current research is relatively limited. Preliminary in vivo pharmacokinetic data show that galliguic acid B is absorbed orally slowly, has a moderate plasma half-life, and is mainly metabolized by the liver. The activity of these metabolites still requires further research. In the future, systematic pharmacokinetic and toxicological studies are needed to clarify its in vivo kinetic characteristics and safe dose range.

Prospects and outlooks for clinical applications

Galifruit B, as a multi-target natural product against colorectal cancer, possesses significant antitumor activity and good safety, making it a potential new drug candidate in colorectal cancer treatment. Its multi-pathway coordinated regulatory mechanism is expected to overcome single-target drug resistance issues and improve treatment outcomes.

The future clinical application prospects are mainly reflected in the following aspects:

1. Monotherapy potential
   By further optimizing drug formulations and administration regimens, Galiguic Acid B is expected to enter clinical trials as a single anti-tumor drug.

2. Combined treatment strategies
   Galifruit B can be used in combination with existing chemotherapy drugs, targeted drugs, or immunotherapy drugs to exert synergistic effects, reduce toxic side effects, and improve efficacy.

3. Development of drug delivery systems
   To address its low water solubility, the development of novel delivery systems such as nanocarriers and liposomes will effectively improve its bioavailability and targeting.

4. Biomarker-guided treatment
   By targeting their respective targets, corresponding biomarkers are screened to achieve precision medicine and improve personalized treatment outcomes for patients.

However, the clinical translation of Galifruit Fruit B still faces many challenges, including insufficient systematic pharmacokinetics and toxicological evaluations, lack of preclinical safety data, and difficulties in standardizing production processes and quality control. In the future, it is necessary to strengthen multidisciplinary collaboration and promote the transformation from laboratory research to clinical applications.

Conclusion

As a natural triterpene compound with a unique structure and multi-target mechanism, Galifruit B shows broad application prospects in colorectal cancer treatment. Its remarkable antitumor activity, good safety, and multi-target regulatory capability provide a valuable example for the development of natural anti-cancer drugs.

In the future, through in-depth pharmacological research, pharmacokinetic optimization, and preclinical safety evaluations, Galifruit B is expected to become a novel candidate drug for colorectal cancer treatment. By combining modern drug development technologies with precision medicine concepts, it will further advance its clinical translational process, benefiting more patients.

In summary, research on Galifruit Acid B not only enriches the theoretical framework of natural product pharmacology but also provides new strategies and hope for colorectal cancer treatment, worthy of ongoing attention and investment from the research and pharmaceutical communities.