| 包装 | 价格(元) |
| 10mM (in 1mL Water) | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Cell lines | H9c2 cells |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
Reaction Conditions | 1 μg/ml, 2 hours |
Applications | H9c2 cells were treated with increased concentrations of Doxorubicin (0.1, 0.3, 0.5, and 1.0 μg/ml, equal to 0.17, 0.52, 0.85, and 1.71 μM separately) for 2 h, or treated with 0.3 μg/ml (equal to 0.52 μM) of Doxorubicin for the different time points. Doxorubicin induces strong AMPKα (Thr 172) and its downstream Acetyl-CoA carboxylase (ACC, Ser 79) phosphorylation in both time- and dose-dependent manner. AMPKα phosphorylation became obvious after 1 h of Doxorubicin treatment which was further sustained for at least 6 h. LKB1, the possible upstream kinase for AMPK, was also activated by Doxorubicin in H9c2 cells. |
Animal models | C57BL/10 mice |
Dosage form | Intraperitoneal injection, 20 mg/kg |
Applications | Five days after doxorubicin injection, mice displayed significantly impaired systolic (LVP, -29%; dP/dtmax, -45%), diastolic (dP/dtmin, -44%; stiffness, +275%), and global (SV, -61%; HR, -18%; CO,-68%) left ventricular (LV) function when compared with the placebo group. Both cardiac lipid peroxidation activity (+37%) and cardiac nitrotyrosine protein expression (+204%) were increased when compared with placebo mice. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Doxorubicin is a semi-synthesized anticancer agent derived from bacterial culture. [1] It is an anthracycline antibiotic. It is been widely used in blood cancers, solid tumors and sarcomas. Doxorubicin intercalates into DNA double strand and inhibits the progression of DNA topoisomerase II, stopping replication process. [2] Doxorubicin also induces histone eviction from open chromatin, causing DNA damage and epigenetic deregulation. [3] Doxorubicin is administrated intravenously. Approximately 75% of doxorubicin and its metabolites bind to plasma protein. Doxorubicin does not cross blood brain barrier. 50% of the drug is eliminated unchanged from the body mainly though bile excretion. The remaining undergoes one-electron reduction, two-electron reduction, and deglycosidation. The major metabolite is a potent membrane ion pump inhibitor, which is associated with cardiomyopathy. [4] References: |
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