Ascochlorin
Ascochlorin (Ilicicolin D), an isoprenoid antibiotic, mediates its anti-tumor effects predominantly through the suppression of STAT3 signaling cascade. Ascochlorin induces apoptosis. Anti-inflammatory activity.
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- CAS No.: 26166-39-2
- Formule: C23H29ClO4
- Masse moléculaire:404.93
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Chemical Information
- Protocole
- Pureté et documentation
- Références
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Help & FAQs
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Activité biologique
Description
IC50 & Target
[3]|
STAT3 |
Apoptosis |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| A549 | IC50 |
0.9 μM
Compound: 7
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Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by CCK8 assay
Cytotoxicity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by CCK8 assay
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[PMID: 34781681] |
| C3H 10T1/2 | IC50 |
1 μM
Compound: 1
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Concentration required for inhibition of C3H10T1/2 progenitor cell growth
Concentration required for inhibition of C3H10T1/2 progenitor cell growth
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[PMID: 12954063] |
| HepG2 | IC50 |
0.9 μM
Compound: 7
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Cytotoxicity against human HepG2 cells assessed as reduction in cell viability incubated for 48 hrs by CCK8 assay
Cytotoxicity against human HepG2 cells assessed as reduction in cell viability incubated for 48 hrs by CCK8 assay
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[PMID: 34781681] |
| MDA-MB-231 | IC50 |
2.2 μM
Compound: 12
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Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability incubated for 24 hrs by CellTiter-Glo luminescent assay
Cytotoxicity against human MDA-MB-231 cells assessed as reduction in cell viability incubated for 24 hrs by CellTiter-Glo luminescent assay
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[PMID: 34516133] |
| MDA-MB-468 | IC50 |
1.1 μM
Compound: 12
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Cytotoxicity against human MDA-MB-468 cells assessed as reduction in cell viability incubated for 24 hrs by CellTiter-Glo luminescent assay
Cytotoxicity against human MDA-MB-468 cells assessed as reduction in cell viability incubated for 24 hrs by CellTiter-Glo luminescent assay
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[PMID: 34516133] |
In Vitro
Ascochlorin (Ilicicolin D) (10-50 μM; 24-72 hours) inhibits the viability of HepG2, HCCLM3 and Huh7 cells in a time and dose dependent manner[3].
Ascochlorin (50 μM; 48 hours) induces apoptosis in HCC cells[3].
Ascochlorin (1-50 μM) significantly suppresses the production of nitric oxide (NO) and prostaglandin E2 (PGE2) and decreases the gene expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) in a dose-dependent manner. Ascochlorin inhibits the mRNA expression and the protein secretion of interleukin (IL)-1β and IL-6 but not tumor necrosis factor (TNF)-α in LPS-stimulated RAW 264.7 macrophage cells. Ascochlorin suppresses nuclear translocation and DNA binding affinity of nuclear factor-κB (NF-κB). Ascochlorin down-regulates phospho-extracellular signal-regulated kinase 1/2 (p-ERK1/2) and p-p38[2].
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:HepG2, HCCLM3, Huh7 cells
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Concentration:10, 25, 50 μM
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Incubation Time:24, 48, 72 hours
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Result:Inhibit the viability of three different HCC cell lines tested (HepG2, HCCLM3 and Huh7) in a time and dose dependent manner.
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Cell Line:HepG2 cells
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Concentration:50 μM
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Incubation Time:48 hours
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Result:Inhibited expression of the cell cycle regulator protein cyclin D1, the anti-apoptotic proteins Bcl-2, Mcl-1, survivin and XIAP, and the invasive gene product MMP-9.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Eight week-old athymic balb/c nude female mice (HCCLM3-Luc2 tumors)[3]
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Dosage:2.5 mg/kg, 5 mg/kg
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Administration:I.p.; day 0, 1, 2, 3, 13, 15, 17, 20, 22, 24, 27, 29 and 31
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Result:Induced significant inhibition of tumor growth.
Chemical Information
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CAS No. 26166-39-2
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Masse moléculaire 404.93
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Formule C23H29ClO4
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SMILES
O=CC1=C(O)C(C/C=C(C)/C=C/[C@]2(C)[C@@H](C)C(CC[C@H]2C)=O)=C(O)C(Cl)=C1C
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Synonyms
Ilicicolin D
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Initial Source
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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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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Cotton Pellet Granuloma
Cotton pellet granuloma is a classical in vivo chronic inflammation model used to evaluate the anti-inflammatory potential of test substances by measuring their ability to inhibit granuloma tissue formation around an implanted foreign body (cotton pellet) in rodents. The method is based on the biological response to a sterile implanted material, which induces proliferative phase inflammation characterized by fibroblast proliferation and collagen-rich granuloma formation, and the final readout reflects the extent of chronic inflammatory tissue growth surrounding the pellet. In multiple preclinical pharmacological evaluations, inhibition of cotton pellet-induced granuloma formation has been used as an indicator of anti-inflammatory activity in both synthetic and natural product screening contexts.
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Carrageenan-Induced Paw Edema
Carrageenan-induced paw edema is an acute inflammation model in which intraplantar injection of carrageenan induces localized inflammatory swelling characterized by vascular permeability, leukocyte infiltration, and production of inflammatory mediators such as prostaglandins and cytokines, making it widely used to evaluate anti-inflammatory agents in vivo. The resulting paw volume or thickness increase is quantified over time as a direct readout of inflammatory intensity and drug efficacy, typically reflecting cyclooxygenase-mediated prostaglandin-driven edema formation and immune cell recruitment in peripheral tissue[20].
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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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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Pureté et documentation
Références
[1]. Min-Wen JC, et al. Molecular Targets of Ascochlorin and Its Derivatives for Cancer Therapy. Adv Protein Chem Struct Biol. 2017;108:199-225. [Content Brief]
[2]. Lee SH, et al. Anti-Inflammatory Effect of Ascochlorin in LPS-Stimulated RAW 264.7 Macrophage Cells Is Accompanied With the Down-Regulation of iNOS, COX-2 and Proinflammatory Cytokines Through NF-κB, ERK1/2, and p38 Signaling Pathway. J Cell Biochem. 2016 Apr;117(4):978-87. [Content Brief]
[3]. Dai X, et al. Ascochlorin, an isoprenoid antibiotic inhibits growth and invasion of hepatocellular carcinoma by targeting STAT3 signaling cascade through the induction of PIAS3. Mol Oncol. 2015 Apr;9(4):818-33. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Ascochlorin Related Classifications
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