| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
Cell lines | WM9, WM35, WM98-1 and WM793 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 | 20 μM, 24 hours |
Applications | To demonstrate the importance of caspase activation in TRAIL-induced apoptosis. Z-DEVD-FMK was added to melanoma cells along with TRAIL. Z-DEVD-FMK was only able to partially inhibit the cytotoxic effects of TRAIL. The decreased ability of Z-DEVD-FMK to inhibit death may result from the ability of the peptide to enter the cell. |
Animal models | Male C57Bl/6 mice with controlled cortical impact (CCI) injury |
Dosage form | Intracerebroventricular injection, 160 ng. |
Applications | To assess motor recovery, mice were tested for the ability to traverse a narrow, suspended beam during recovery over a 21-day period. Mice treated 1 hour after CCI performed significantly better than did vehicle controls on days 7, 14, and 21 after injury. Mice treated 4 hours after CCI performed significantly better than controls only on day 21 after injury, but this was an isolated observation, as they did not show a trend toward better performance compared with other treatment groups on any other testing day. |
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 | Z-DEVD-FMK is a tetrapeptide caspase inhibitor that is considered relatively selective for caspase-31, 2and has been widely used in in vitro and in vivo models of acute injury to delineate roles for caspase 3 in neuronal cell death. Intracerebroventricular injections of Z-DEVD-FMK improved function after LFP3. Intraparenchymal infusion of Z-DEVD-FMK over several days after combined CCI and hypoxia reduced lesion size, although functional outcome was not significantly improved in this model4(Clark et al., 2000). Z-DEVD-FMK was a potent inhibitor of calpain and that improvement observed after treatment with Z-DEVD-FMK may reflect, at least in part, this action. Early treatment with Z-DEVD-FMK improved neurologic function and reduced lesion volume. Z-DEVD-FMK reduces cell death and inhibits calpain in a model of in vitro necrosis and a cell free assay and Z-DEVD-FMK treatment inhibits calpain activity after TBIin vivo. Z-DEVD-FMK improved neurologic function and reduced tissue damage at an injury severity that showed predominantly necrotic neuronal cell death with minimal evidence of caspase 3 activation. Moreover, effective treatment with Z-DEVD-FMK was associated with reduced calpain-mediated -spectrin degradation. Z-DEVD-FMK was also neuroprotective, at concentrations lower than those routinely used to inhibit caspase 3, in anin vitromodel of necrotic neuronal cell death induced by maitotoxin. The present data show that treatment with Z-DEVD-FMK improves behavioral recovery, reduces tissue damage and prevents accumulation of calpain-mediated α-spectrin breakdown products when administered not later than 1 hour after injury in a TBI model that primarily shows necrosis. Z-DEVD-FMK also reduces necrotic neuronal cell death in vitro, and such neuroprotection is associated with inhibition of calpain, but not caspase 3 or cathepsin B. In addition, Z-DEVD-FMK reduces calpainmediated hydrolysis of casein, which indicates that Z-DEVD-FMK can directly inhibit calpain. This nonspecificproperty of Z-DEVD-FMK may account, at least in part, for its neuroprotective actions5. References: |
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