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Product name: Ecliptasaponin A
Synonym name: Ecliptasaponin A; Gleditsoside B; Gleditschoside B
Catalogue No.: BP0523
Cas No.: 78285-90-2
Formula: C36H58O9
Mol Weight: 634.851
Botanical Source: EcliptaprostrataL.
Physical Description:
Type of Compound: Terpenoids
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.
Description:
Ecliptasaponin A has protective effects against the pulmonary fibrosis induced by bleomycin via reducing the oxidative stress, lung tissue inflammation, and the subsequent epithelial-mesenchymal transition.
References:
J Ethnopharmacol. 2015 Dec 4;175:172-80.
Preventive effects of Ecliptae Herba extract and its component, ecliptasaponin A, on bleomycin-induced pulmonary fibrosis in mice.
Ecliptae Herba, a nourishing traditional Chinese medicine, is also a folk medicine for the treatment of lung diseases. To investigate the anti-fibrosis effects and the underlying mechanism of the extract of Ecliptae Herba and its potential active components.
METHODS AND RESULTS:
The resulting extract (EXT) was prepared from the 80% ethanol extract of Ecliptae Herba. After intratracheally administrated with bleomycin (BLM, 5mg/kg), mice were orally treated with EXT at 2.5, 1.25, 0.625 g/kg and eclipta saponin A (ESA) at 80 mg/kg once daily for 28 day. The bodyweight, survival rate, pathological changes of lung and levels of hydroxyproline (HYP) were used to evaluate the anti-fibrotic effects. The malonaldehyde (MDA), superoxidae dismutase (SOD) activity, and the protein expressions of matrix metalloproteinase (MMP)-2, 9, tissue inhibitor of metalloproteinase-1 (TIMP-1), cyclooxygenase-2 (COX-2), α-smooth muscle actin (α-SMA) and transforming growth factor-β1 (TGF-β1) in lung tissue were analyzed by kits or western blot. Compared with BLM group, EXT administration could significantly ameliorated the pathological changes of lung, decreased the HYP content, enhanced the SOD activity, and reduced the MDA content of lung tissues. In mechanism, EXT significantly alleviated the levels of COX-2, TGF-β1, MMP-2 and α-SMA, as well as elevated the ratio value of MMP-9/TIMP-1. Additionally, the anti-fibrosis effects of ESA, a large amount of saponins isolated from Eclipta prostrata , was also evaluated by the BLM-induced model. The results showed that ESA could block BLM-induced histological changes of lung tissue and decrease the high levels of TGF-β1 and α-SMA.
CONCLUSIONS:
Ecliptae Herba has protective effects against the pulmonary fibrosis induced by BLM via reducing the oxidative stress, lung tissue inflammation, and the subsequent epithelial-mesenchymal transition. The active chemical constituents may be involved with triterpenoid saponins, such as ESA.
HPLC of Ecliptasaponin A
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
156.9100
3.9377
2.0076
.0446
.7652
.4024
Low
85.8395
5.3237
No
No
Yes
No
No
No
0.0
Yes
No
No
No
Ecliptasaponin A is a pentacyclic triterpene saponin derived from Ecliptasaponin species, and has attracted widespread attention in recent years due to its multi-target and multi-pathway pharmacological activity. As an orally effective bioactive ingredient, Estasidin A demonstrates significant anti-tumor, anti-inflammatory, anti-fibrotic, antioxidant, and cartilage-protective effects, and also shows potential in regulating endocrine function. Its effects cover various malignant tumors such as lung cancer and breast cancer, and it also provides protection against cardiovascular diseases, immune inflammatory responses, and various pathological conditions including bone and joint diseases. This article will systematically review the chemical structure and physicochemical properties of Estadiasidin A, plant origin, and extraction methods, with a focus on its pharmacological activity and mechanism of action. Combining druggability evaluation and pharmacokinetic data, it will explore its clinical application prospects and development directions.
Estasidin A has the molecular formula C_36H_58O_11 and a molecular weight of 634.8510, belonging to the pentacyclic triterpenoid saponin class. Its structure includes a typical triterpene backbone, connecting multiple glycan residues and imparting high polarity and water solubility. The LogP value was 3.9377, indicating moderate lipophilus, which facilitates cell membrane penetration but does not easily accumulate excessively in lipophilic waters. The topological polar surface area (TPSA) was 156.91 Ų, indicating high polarity that may affect oral absorption and bioavailability. Water solubility is 0.0446 mg/mL, making it a low-solubility compound but still exhibiting some aqueous dispersibility. Low blood-brain barrier permeability suggests limited distribution in the central nervous system. The hERG suppression test results were negative, indicating a low risk of cardiotoxicity. Ames mutagenicity test was zero, indicating low genotoxicity risk and good safety.
Structurally, the triterpene core of Estasidin A provides a bioactive basis, while the glycosyl group may affect its solubility and receptor-binding properties. The surface activity of saponins may also promote their interaction with cell membranes, enhancing biological activity.
Eclipta glycoside A is mainly found in Eclipta spp., especially Eclipta prostrata L. Eclipta is a traditional Chinese medicinal herb, widely distributed in tropical and subtropical regions of Asia, Africa, and the Americas. The whole plant contains abundant triterpene saponins, flavonoids, and polyphenols. Estasidin A, as one of the important active components, has been reported multiple times.
Common methods for extracting Ebasidin A include:
Solvent extraction: Methanol, ethanol, or water-alcohol mixed solvents are used to extract dried Eclipta powder, utilizing its polar properties to dissolve saponin components.
Liquid-liquid partitioning and column chromatography purification: After the initial extraction solution is distributed to remove lipid-soluble impurities, it is separated and purified using silica gel columns, reversed-phase C18 columns, or resin columns, combined with gradient elution technology to improve purity.
High-Performance Liquid Chromatography (HPLC): Used for qualitative and quantitative analysis and further purification, ensuring the purity and structural identification of Ebasidin A.
In recent years, modern technologies such as ultrasound-assisted extraction and microwave-assisted extraction have also been applied to improve the extraction efficiency and purity of Estasidin A.
Research on the pharmacological activity of Estasidin A covers multiple aspects, including anti-tumor, anti-inflammatory, anti-fibrotic, antioxidant, cartilage protection, and endocrine regulation.
Estasidin A exhibits significant cytotoxicity in lung cancer cell lines, capable of inducing apoptosis and autophagy. Its mechanism mainly involves activating the ASK1/JNK signaling pathway, promoting intracellular stress responses and programmed cell death. In addition, Estasidin A also has inhibitory effects on breast cancer cells, with related targets including AMPK, BCL2, STAT3, ESR2, ABCB1, ABCG2, PRKCA, MAPT, MMP2, and LCK, demonstrating its multi-target regulatory characteristics. Estasidin A can regulate the energy metabolism, apoptosis signaling, and cell cycle of tumor cells, inhibiting tumor cell proliferation and migration.
Estasidin A exerts anti-inflammatory effects by inhibiting the HMGB1/TLR4/NF-κB signaling pathway, reducing the expression of pro-inflammatory cytokines and enzymes (such as COX-2 and MMP9). This mechanism effectively reduces tissue inflammatory responses, blocks the transformation of inflammation into fibrosis, and protects the cardiovascular system from chronic inflammatory damage. Its anti-fibrotic effect has been validated in multiple models, manifested as reduced collagen deposition and expression of fibrotic markers.
Estasidin A can enhance superoxide dismutase (SOD) activity, reduce levels of malondialdehyde (MDA), a lipid peroxidation product, and alleviate cellular damage caused by oxidative stress. Its antioxidant effects help protect the cardiovascular system and other vital organs from free radical damage, slowing disease progression.
By inhibiting the expression of matrix metalloproteinase 13 (MMP13) and modulating inflammatory factors, Estasidin A demonstrates cartilage-protective effects in bone and joint disease models. It can reduce cartilage degradation, suppress joint inflammation, and maintain structural and functional stability of joint tissues.
Estasidin A improves ovarian function and regulates sex hormone levels by upregulating estrogen receptor α (ESR1) expression, demonstrating its potential value in reproductive health. This action may provide new approaches for treating ovarian hypofunction and related endocrine disorders.
The multiple pharmacological effects of Estasidin A are attributed to its complex mechanism of action and regulation of multiple molecular targets.
ASK1/JNK pathway activation: Estasidin A induces apoptosis and autophagy in lung cancer cells by activating castanin kinase 1 (ASK1) and its downstream c-Jun aminoterminal kinase (JNK), promoting tumor cell death.
HMGB1/TLR4/NF-κB signaling inhibition: By inhibiting the high-mobility group protein B1 (HMGB1) and Toll-like receptor 4 (TLR4)-mediated nuclear factor κB (NF-κB) signaling pathway, Estathoside A reduces pro-inflammatory factor expression and exerts anti-inflammatory and anti-fibrotic effects.
Regulation of antioxidant enzyme activity: Estasidin A enhances SOD activity, scavenges superoxide radicals, reduces MDA formation, and lessens oxidative damage.
Matrix metalloproteinase inhibition: By downregulating MMP9 and MMP13 expression, Estasidin A inhibits extracellular matrix degradation, protecting cartilage and cardiovascular tissue structures.
Hormone receptor regulation: Estasidin A upregulates estrogen receptor α (ESR1) expression, regulates sex hormone balance, and improves reproductive system function.
Tumor-related multi-target regulation: including AMPK (PRKAA1), anti-apoptotic protein BCL2, signal transduction and transcription activator STAT3, estrogen receptor β (ESR2), multidrug resistance proteins ABCB1 and ABCG2, protein kinase Cα (PRKCA), microtubule-associated protein MAPT, and lymphocyte kinase LCK. Estasidin A affects tumor cell metabolism, proliferation, migration, and drug resistance by regulating these targets.
The druggability parameters of Estasidin A indicate that it has certain potential for drug development. A larger molecular weight (634.85 Da) and higher TPSA (156.91 Ų) may limit its oral absorption efficiency, but its moderate LogP (3.94) helps with cell membrane penetration. Low water solubility (0.0446 mg/mL) suggests the need for formulation optimization to improve bioavailability.
The blood-brain barrier has low permeability, reducing the risk of central nervous system side effects. hERG channel inhibition was negative, indicating a lower risk of cardiotoxicity and better safety. The Ames test was negative, with low genotoxicity risk and meeting drug safety requirements.
Currently, pharmacokinetic research on Estadiasidin A is limited. Preliminary data indicate that it is well absorbed orally, widely distributed in the body, and metabolized mainly through hepatic enzyme systems, with bile excretion as the main pathway. In the future, further systematic pharmacokinetic and toxicological evaluations are needed to provide a basis for clinical development.
With its multi-target and multi-mechanism pharmacological activity, Estasidin A demonstrates broad clinical application potential. In the field of anti-tumor treatment, especially lung and breast cancer, it may be used as an adjunct or combination therapy to enhance therapeutic outcomes and overcome drug resistance. Its anti-inflammatory and anti-fibrotic properties give it potential application value in cardiovascular diseases, liver fibrosis, and other chronic inflammatory diseases.
In addition, the antioxidant and cartilage-protective effects of Evactoside A offer new ideas for the prevention and treatment of bone and joint diseases. Its ability to regulate endocrine function also opens new possibilities for treating female reproductive health-related diseases.
Future research should focus on preclinical safety evaluation, pharmacokinetic optimization, and formulation development of Estasidin A. At the same time, based on its multi-target mechanism of action, systematic network pharmacology and translational medicine research are being carried out to promote its clinical application.
As a pentacyclic triterpene saponin with multiple biological activities, Estasidin A demonstrates broad pharmacological effects and good safety profile. By regulating multiple signaling pathways and key molecular targets, it exerts multiple effects including anti-tumor, anti-inflammatory, anti-fibrotic, antioxidant, and cartilage protection. Although its pharmacokinetics and clinical research are still in the early stages, Estasidin A holds great potential as a candidate molecule for natural product drug development. In the future, it is necessary to strengthen mechanistic research, drug optimization, and clinical translational work to promote the application of Estasidin A in the treatment of various diseases and benefit patients.
Shenshuai
Wenjing
Hedandan
