| Catalogue number |
C104608 |
| Chemical name | Kobophenol A |
| CAS Number | 124027-58-3 |
| Synonyms | 5-[(2S,3R,4S,5S)-4-[(2S,3S)-3-[(2R,3R)-3-(3,5-dihydroxyphenyl)-6-hydroxy-2-(4-hydroxyphenyl)-2,3-dihydrobenzofuran-4-yl]-6-hydroxy-2-(4-hydroxyphenyl)-2,3-dihydrobenzofuran-4-yl]-2,5-bis(4-hydroxyphenyl)-3-oxolanyl]benzene-1,3-diol |
| Molecular Weight | C56H44O13 |
| Formula | 925.0 |
| Purity | 98% |
| Physical Description | Powder |
| Solvent | Chloroform, Dichloromethane,DMSO |
| Storage | Stored at 2-8°C, Protected from air and light, refrigerate or freeze |
| Applications | Antimicrobial.
Kobophenol A inhibited AChE activity in a dose-dependent manner, and the IC50 values of Kobophenol A was 115.8mM.
Neuronal death induced by the withdrawal of tropic support was ameliorated by Kobophenol A. The protective effect of Kobophenol A against nitrosative/oxidative or mitochondrial damages resulted in the inhibition of the ROS, intracellular calcium ion level, and mitochondrial transmembrane potential changes on SH-SY5Y cells.
Direct NO donor sodium nitroprusside (SNP) that has been recognized as an inducer of apoptosis in various cell lines significantly induced cell death and NO production in MG-63 cells. Coincubation of Kobophenol A in SNP-treated MG-63 cells resulted in a significant protection against NO-induced cell death. This is associated with increase in intracellular reactive oxygen species (ROS) scavenging activity and the inhibition of decrease in mitochondrial membrane potential (MMP) by Kobophenol A. We also found that Kobophenol A inhibited the down-regulation of Bcl-2 and Bcl-XL, whereas the level of Bax expression was decreased by Kobophenol A treatment in SNP-treated MG-63 cells. Furthermore, Kobophenol A inhibited SNP-induced phosphorylation of JNK and c-Jun, and SNP-induced reduction in NF-κΒ and AP-1 activities, implicating that protective effect of Kobophenol A may occur through the regulation of JNK, NF-κΒ and AP-1 signaling pathways. Together, these findings suggest that Kobophenol A has a protective effect against NO-mediated osteoblast apoptosis and might be a plausible candidate for treatment of inflammatory bone diseases relevant to osteoblast cell death.
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| References | 1. Tetrahedron Letters, 1989, 30(29), 3785-3788.
2. Phytochemistry, 1991, 30, 649.
3. Biol. Pharm. Bull., 2002, 25(1) 125-127.
4. Bioorganic & Medicinal Chemistry Letters, 2007, 17(7), 1879-1882.
5. International Immunopharmacology, 2011, 11(9), 1251-1259.
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| Size | Price(USD) | Discount |
| 5mg | Inquiry | N/A |
| 10mg | Inquiry | N/A |
| 25mg | Inquiry | N/A |
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