Jusneesiinol
Jusneesiinol is a lignan-class prostaglandin synthesis inhibitor and COX-1/COX-2 inhibitor that exerts central analgesic, peripheral analgesic, and antipyretic effects by inhibiting prostaglandin formation, antagonizing prostaglandin receptors, and inhibiting lipid peroxidation. Jusneesiinol can be used in research on pain and fever.
For research use only. We do not sell to patients.
- CAS No.: 216955-78-1
- Formula: C20H14O7
- Molecular Weight:366.33
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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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
[3]|
COX-1 |
COX-2 |
In Vitro
Jusneesiinol (compound 12) (25 μg/mL; 48 h) does not exhibit significant inhibitory activity against tumor cell proliferation in the tested cancer cell lines at a concentration of 25 μg/mL[3].
Jusneesiinol (10 mg; 20 min-overnight) undergoes dehydrogenation to yield retrohelioxanthin and justirumalin, hydrogenation to yield compound 4 and tetralin 11, and acetylation to form monoacetate 8[2].
Jusneesiinol (25 μg/mL) exhibits potent inhibitory activity against lipid peroxidation in the LUV assay[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:AGS, HCT-116, MCF-7, NCI H460, SF-268
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Concentration:25 μg/mL
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Incubation Time:48 h
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Result:Did not show significant inhibitory activity against gastric, colon, breast, lung or CNS cancer cell lines at 25 μg/mL.
Chemical Information
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CAS No. 216955-78-1
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Molecular Weight 366.33
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Formula C20H14O7
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SMILES
O=C1C=2[C@@H](C3=C([C@@H](O)C2CO1)C=CC4=C3OCO4)C=5C=C6C(=CC5)OCO6
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Structure Classification
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Initial Source
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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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Ferroptosis Solutions
Ferroptosis is an iron-dependent, non-apoptotic form of regulated cell death characterized by lethal lipid peroxidation and sensitivity to suppression by iron chelators or lipophilic radical-trapping antioxidants. The core pathway links cystine uptake through system Xc−, glutathione availability, GPX4-dependent detoxification of phospholipid hydroperoxides, iron-dependent oxidative reactions, and polyunsaturated-phospholipid metabolism into a cell-death program that is biochemically and morphologically distinct from apoptosis, necrosis, and autophagy. The ferroptosis pathway is experimentally linked to phenotype through chemical and genetic perturbation. Erastin induces ferroptosis by inhibiting cystine uptake through system Xc− and weakening antioxidant defenses, while GPX4 inhibition or depletion causes lipid peroxide accumulation and ferroptotic cancer-cell death. ACSL4 and oxidizable arachidonoyl- or adrenoyl-containing phosphatidylethanolamines shape ferroptosis sensitivity by con
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Jusneesiinol Related Classifications
HY-N21710 Related Classifications
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