Synonym name:
Catalogue No.: BP0458
Cas No.: 3513-04-0
Formula: C₂₁H₃₂O₆
Mol Weight: 380.481
Botanical Source: Cynanchum wallichii and Marsdenia globifera

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.

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

Introduction/Overview

Deacylmetaplexigenin (CAS No.: 3513-04-0) is a typical natural product of pregnane glycosides, first isolated from the ranunculaceae plant Asclepias incarnata. Pregnane glycosides hold an important position in natural medicinal chemistry and pharmacology research due to their unique chemical structure and diverse bioactivity. In recent years, with deeper elucidation of tumor molecular mechanisms, deacylloxinin glycogen has gradually become a research hotspot due to its potential inhibitory effect in tumor models such as prostate cancer. Prostate cancer, as a malignant tumor with a high incidence and difficult treatment of the male urinary system, urgently needs to discover new, effective, and low-toxicity therapeutic drugs. This paper will systematically review the chemical structure, plant origin, pharmacological activity, mechanism of action, and druggability evaluation of deacylloliginin, aiming to provide theoretical basis and research directions for its clinical development and application.

Chemical structure and physicochemical properties

Deacylloxysigin is a type of pregnanoside compound, composed of the prognane steroid skeleton and glycoside components. Its molecular formula is C_20H_32O_7, and its molecular weight is 364.4700. Structurally, deacylloxin glycogen removes the acyl group from the glycoside, retains the steroid structure and multiple hydroxyl groups of the core, giving it high polarity and biological activity.

In terms of physicochemical properties, the LogP value of deacylloligin is 1.7, indicating moderate lipid solubility, which is beneficial for cell membrane penetration and distribution in vivo. The polar surface area (TPSA) is 110.87 Ų, and the number of hydrogen bond acceptors is 6, suggesting that it may participate in various molecular interactions via hydrogen bonding in vivo. The blood-brain barrier has low penetration capacity, suggesting its limited distribution in the central nervous system. Toxicological evaluation showed no hepatotoxicity or hERG channel inhibitory activity, indicating high safety, but the cardiac toxicity and Ames-related mutagenicity remain unclear and require further research.

Plant Origins and Extraction Methods

Deacylloxinin mainly comes from Asclepias incarnata (Ranunculaceae), a plant widely distributed in North American wetlands and commonly used medicinally in traditional herbal medicine. Its roots, stems, and leaves all contain various pregnane glycoside components. Deacylloxininin, one of the important active components, has high levels and pharmacological activity.

During extraction, alcohol extraction methods (such as ethanol or methanol) are commonly used to extract dried plant powders, followed by liquid-liquid separation and column chromatography (silica gel or C18 reversed phase column) and other separation and purification techniques to obtain high-purity deacylloxin glycosidents. Modern separation technologies such as high-performance liquid chromatography (HPLC) and mass spectrometry (LC-MS) are widely used for qualitative and quantitative analysis, ensuring the quality and batch stability of extracts.

Pharmacological activity research

Pharmacological activity studies of deacyllosin have mainly focused on their antitumor effects, especially their manifestations in prostate cancer models. Multiple in vitro cell experiments have shown that deacyllovinin can significantly inhibit the proliferation, migration, and invasion of prostate cancer cells, while also inducing apoptosis and cell cycle arrest.

In addition, deacylloxingin also exhibits multiple biological activities such as anti-inflammatory and antioxidant effects, providing auxiliary mechanisms for its anti-tumor effects. For example, its regulation of oxidative stress-related signaling pathways helps alleviate inflammatory responses in the tumor microenvironment and inhibit the malignant progression of tumor cells.

Although current in vivo studies on the efficacy and toxicology of deacylloligin are limited, existing animal model experiments have preliminarily demonstrated its good safety and significant antitumor potential, laying a foundation for subsequent drug development.

Mechanism of action and molecular targets

The mechanism of action of deacylloxinin in prostate cancer involves multiple key molecular targets, reflecting its multi-target regulatory characteristics. The main targets include:

• BCL2: As an anti-apoptotic protein, downregulation of BCL2 promotes cancer cell apoptosis. Deacyllogenin activates the apoptosis pathway by inhibiting BCL2 expression.
• PTPN1: Protein tyrosine phosphatase 1, regulates multiple signaling pathways. Deacylloxinin glycosyl may influence cell proliferation and metabolism by modulating PTPN1 activity.
• STAT3: Signal transduction and transcription activator factor 3, involved in tumor cell growth and immune escape; deacyllosin glyconin inhibits STAT3 phosphorylation and blocks its transcriptional activity.
• ESR2 (estrogen receptor β): Regulates the growth of hormone-dependent tumors. Deacyllosin glycosyl may intervene in the endocrine environment of prostate cancer by modulating ESR2 signaling.
• NFE2L2 (NRF2): Regulates antioxidant stress responses, activates the NFE2L2 pathway through deacylloligon, enhances cellular antioxidant capacity, and reduces oxidative damage.
• MAPK1: Mitogen-activated protein kinase, involved in cell proliferation and differentiation. Deacyllolysin glycogen inhibits tumor cell proliferation by regulating MAPK1 signaling.
• CYP19A1 (aromatase): catalyzes estrogen synthesis and affects hormone levels. Deacylloxingin regulates CYP19A1 and helps inhibit hormone-dependent tumor growth.
• AR (Androgen Receptor): An important driver of prostate cancer, deacyllogenin inhibits hormone-dependent proliferation of cancer cells by interfering with the AR signaling pathway.
• PIK3CA :P key subunit of the I3K signaling pathway, regulating cell survival and metabolism. Deacylloligonin inhibits PIK3CA activity and blocks signal transduction.
• LGALS3 (Galactogenin 3): Involved in cell adhesion and tumor metastasis, deacylloxin glycogen inhibits tumor cell invasion and metastasis by regulating LGALS3 expression.

The above multi-target mechanism shows that deacylloligin not only directly inhibits tumor cell proliferation but also regulates the tumor microenvironment and signaling networks, achieving a comprehensive anti-tumor effect.

Druggability evaluation and pharmacokinetics

The druggability parameters of deacylolosiglycon indicate that it has good potential for drug development. A moderate molecular weight (364.47 Da) and LogP value (1.7) conform to the Lipinski rule, facilitating absorption and distribution in the body. A higher TPSA (110.87 Ų) and hydrogen bond receptor count (6) suggest good water solubility, facilitating transport in the bloodstream.

The blood-brain barrier has low permeability, reducing the risk of toxic side effects in the central nervous system. Both hepatotoxicity and hERG channel inhibition tests were negative, indicating high cardiac and hepatic safety and reducing safety risks in drug development.

However, data on cardiotoxicity and genotoxicity (Ames test) remain unclear and require further supplementary validation through in vitro and in vivo experiments. In addition, the pharmacokinetic characteristics of deacyllocylidonin, such as absorption rate, bioavailability, metabolic pathways, and excretion modes, lack systematic studies. Future animal models and preclinical trials are needed to improve related data.

Prospects and outlooks for clinical applications

Based on the multi-target inhibitory effect and good safety evaluation of deacylloxin glycogen in prostate cancer cells, its development prospects as a candidate anti-tumor drug are broad. Future research can focus on:

1. Pharmacodynamics and pharmacokinetic studies: Systematically assess its in vivo distribution, metabolic stability, and duration of efficacy, providing a basis for clinical dosing design.
2. Combination therapy strategy: Combine existing prostate cancer treatments to explore the synergistic effects of deacylloliginin with endocrine therapy, chemotherapy, or immunotherapy.
3. Structural modification and drug design: Chemical modification based on the core structure of pregnane glycosides is performed to optimize its pharmacokinetic properties and targeted selectivity, thereby enhancing efficacy.
4. Preclinical safety evaluation: Conduct long-term toxicology and mutagenicity studies to ensure safety in clinical applications.
5. Indication expansion: Given its multi-target regulatory capability, explore the potential applications of deacylloligin in other hormone-dependent tumors and inflammation-related diseases.

In summary, deacyldilolysin glycosides, as natural pregnane glycoside compounds, possess unique pharmacological activity and good druggability, making it a highly promising natural drug lead compound in the field of prostate cancer treatment.

Conclusion

Deacylloxinin, as a natural pregnant glycoside derived from Asclepias incarnata, demonstrates its potential in prostate cancer treatment due to its multi-target antitumor mechanism and good safety performance. Its unique chemical structure and physicochemical properties provide favorable conditions for drug design. Although current research on its pharmacokinetics and preclinical safety is still insufficient, advances in molecular biology and medicinal chemistry technology suggest that deacylloxinin glycone is expected to become a representative of the new generation of natural anticancer drugs. In the future, it is necessary to strengthen mechanistic research and clinical translation, promote its transition from the laboratory to clinical practice, and benefit patients.