Echinoside A
Echinoside A is a saponin. Echinoside A can be isolated from sea cucumber. Echinoside A inhibits the catalytic activity of Top2α, reduces the noncovalent binding of Top2α to DNA. Echinoside A activates Caspase-3 and induces PARP cleavage. Echinoside A induces Apoptosis. Echinoside A has anticancer activity against prostate cancer, hepatocellular carcinoma, and S-180 sarcoma. Echinoside A exhibits antifungal activity against a variety of fungi, with a minimum growth inhibitory concentration range of 3.12 to 50.0 μg/mL, including potent activity against Aspergillus and Penicillium species.
For research use only. We do not sell to patients.
- CAS No.: 75410-53-6
- Formula: C54H87NaO26S
- Molecular Weight:1207.31
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
topoisomerase II alpha |
Caspase-3 |
In Vitro
Echinoside A (0.80-3.98 μM; 6-24 h) potently inhibits the proliferation of HepG2 cells in a dose-dependent manner, and reduces cell viability by 54.7% at 2.70 μM for 12 h[1].
Echinoside A (1.35-2.70 μM; 12 h) induces apoptosis in HepG2 cells in a dose-dependent manner in vitro[1].
Echinoside A (1.35-2.70 μM; 12 h) regulates the expression of cell cycle-related genes in HepG2 cells, upregulates the expression of p16 and p21, downregulates the expression of cyclin D1, but has no effect on p27[1].
Echinoside A (1.35-2.70 μM; 12 h) exerts no significant effect on the expression of NF-κB p65 protein in HepG2 cells[1].
Echinoside A (0.25-2 μM; 3 h for DNA fragmentation) induces concentration-dependent apoptosis and DNA fragmentation in human leukemia HL-60 cells[2].
Echinoside A exhibits antifungal activity against a variety of fungi, with a minimum growth inhibitory concentration range of 3.12 to 50.0 μg/mL, including potent activity against *Aspergillus* and *Penicillium* species[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human hepatocellular liver carcinoma HepG2 cells
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Concentration:1.35, 2.70 μM
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Incubation Time:12 h
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Result:Showed slightly increased percentages of early and late apoptotic cells compared to control cells.
Induced visible perinuclear chromatin condensation as bright green patches or fragments in cells treated with 2.70 μM.\nResulted in 18.1% total apoptotic cells (13.2% early apoptotic, 4.9% late apoptotic) at 1.35 μM for 12 h.
Resulted in 62.2% total apoptotic cells at 2.70 μM for 12 h.
Induced apoptosis in a dose-dependent manner.
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Cell Line:human hepatocellular liver carcinoma HepG2 cells
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Concentration:1.35, 2.70 μM
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Incubation Time:12 h
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Result:Increased the population of HepG2 cells in the G0/G1 phase from 67.9% to 75.2% at 2.70 μM for 12 h.
Increased the sub-G0/G1 cell population (indicative of apoptosis) from 1.83% to 21.21% at 2.70 μM for 12 h.
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Cell Line:human hepatocellular liver carcinoma HepG2 cells
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Concentration:1.35, 2.70 μM
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Incubation Time:12 h
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Result:Activated caspase-3 and induced PARP cleavage.\nHad no significant inhibitory effect on NF-κB p65 protein expression.
In Vivo
Echinoside A (1.5-3.0 mg/kg/day; i.v.; daily; 7 days) reduces S-180 sarcoma growth in KM mice[2].
Echinoside A (2.6-5.2 mg/kg; i.v.; weekly; 4 weeks) suppresses PC-3 prostate carcinoma xenograft growth in nude mice with T/C % values of 53.7% and 45.1%, respectively[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c (male, 17-22g, subcutaneous implantation of H22 hepatocarcinoma cells)[1]
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Dosage:0.5 mg/kg; 2.5 mg/kg
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Administration:i.p.; daily; 10 days
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Result:Reduced mean tumour weight to 1.53 ± 0.36 g, corresponding to a 33.8% tumour growth inhibition rate (P < 0.01).
Reduced mean tumour weight to 1.16 ± 0.22 g, corresponding to a 49.8% tumour growth inhibition rate (P < 0.01).
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Animal Model:KM mice (female, 7 weeks old, 18-22 g, specific pathogen-free, S-180 sarcoma model via s.c. inoculation)[2]
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Dosage:1.5 mg/kg/day; 3.0 mg/kg/day
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Administration:i.v.; daily; 7 days
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Result:Achieved a tumor growth inhibition rate of 52.0% at 1.5 mg/kg.
Achieved a tumor growth inhibition rate of 80.0% at 3 mg/kg.
Chemical Information
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CAS No. 75410-53-6
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Molecular Weight 1207.31
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Formula C54H87NaO26S
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SMILES
C[C@]12[C@]3([C@H](C=C4[C@@]2([H])CC[C@]5([H])[C@@]4(CC[C@@H](C5(C)C)O[C@H]6[C@@H]([C@H]([C@@H](CO6)OS(=O)(O[Na])=O)O)O[C@H]7[C@@H]([C@H]([C@@H]([C@H](O7)C)O[C@H]8[C@@H]([C@H]([C@@H]([C@H](O8)CO)O)O[C@H]9[C@@H]([C@H]([C@@H]([C@H](O9)CO)O)OC)O)O)O)O)C)O)[C@@]([C@@](C)(OC3=O)CCCC(C)C)(CC1)O
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Structure Classification
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Initial Source
Echinoside A was isolated from sea cucumber
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
Purity & Documentation
References
[1]. Zhao Q, et al. In vitro and in vivo anti-tumour activities of echinoside A and ds-echinoside A from Pearsonothuria graeffei. J Sci Food Agric. 2012;92(4):965-974. [Content Brief]
[2]. Li M, et al. Echinoside A, a new marine-derived anticancer saponin, targets topoisomerase2alpha by unique interference with its DNA binding and catalytic cycle. Ann Oncol. 2010 Mar;21(3):597-607. [Content Brief]
[3]. Kitagawa I, et al. Marine natural products. XIV. Structures of echinosides A and B, antifungal lanostane-oligosides from the sea cucumber Actinopyga echinites (Jaeger). Chem Pharm Bull (Tokyo). 1985 Dec;33(12):5214-24. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Echinoside A Related Classifications
HY-N17442 Related Classifications
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