Z-DEVD-FMK - Caspase-3 抑制劑 - 生命科學(xué)試劑 - MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEZ-DEVD-FMKCat. No.: HY-12466CAS No.: 210344-95-9分式: CHFNO分量: 668.66作靶點: Caspase作通路: Apoptosis儲存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實驗 DMSO : 33.33 mg/mL (49.85 mM)* means soluble, but satur

2、ation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲備液1 mM 1.4955 mL 7.4776 mL 14.9553 mL5 mM 0.2991 mL 1.4955 mL 2.9911 mL10 mM 0.1496 mL 0.7478 mL 1.4955 mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲備液，并請注意儲備液的保存式和期限。體內(nèi)實驗請根據(jù)您的實驗動物和給藥式選擇適當(dāng)?shù)娜芙獍?，配制前請先配制澄清的儲備液，再依次添加助溶?為保證實驗結(jié)果的可靠性，體內(nèi)實驗的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使；澄清的儲備液可以根據(jù)儲存

3、條件，適當(dāng)保存；以下溶劑前的百分 指該溶劑在您配制終溶液中的體積占)：1. 請依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (3.74 mM); Clear solution2. 請依序添加每種溶劑： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (3.74 mM); Clear solution3. 請依序添加每種溶劑： 10% DMSO 90% corn oil1/3 Master of Small Molecules 您

4、邊的抑制劑師www.MedChemESolubility: 2.5 mg/mL (3.74 mM); Clear solutionBIOLOGICAL ACTIVITY物活性 Z-DEVD-FMK種特異性的不可逆的 caspase-3 抑制劑，IC50 為 18 M。IC50 & Target Caspase-318 M (IC50)體外研究 N27 cells are exposed to MPP+ in the absence or presence of 50 M Z-DIPD-FMK or 100 M Z-DEVD-FMKor 50 M Z-LEHD-FMK and then casp

5、ase-9 and caspase-3 enzymatic activities are determined by enzymaticassay at 12 and 24 h following exposure, respectively. Exposure to 300 M MPP+ for 24 h in N27 cellsresults in an approximately 2.5-fold increase in caspase-3 enzyme activity. MPP+-induced increases incaspase-3 enzyme activity are si

6、gnificantly blocked by 50 M Z-DIPD-FMK, 100 M Z-DEVD-FMK, and 50 M Z-LEHD-FMK 1.體內(nèi)研究 Early Z-DEVD-FMK (160 ng) treatment improves motor and cognitive function after traumatic CNS injuryinduced by severe controlled cortical impact (CCI) in the mouse 2. Treatment with Z-DEVD-FMK (160 ng)significantly

7、improves neurological outcome when compared with traumatized animals treated with DMSOvehicle (p 3.PROTOCOLCell Assay 1 N27 cells and primary mesencephalic neurons are exposed to either 10-100 M 6-OHDA or 10-300 MMPP+ in the presence or absence of 0.1-50 M Z-DIPD-FMK or 0.1-100 M Z-DEVD-FMK or 50 M

8、Z-IETD-FMK or Z-LEHD-FMK for the duration of the experiment. N27 cells are incubated with 100 M 6-OHDA for 24h or 300 M MPP+ for 36 h in the presence or absence of 50 M Z-DEVD-FMK and cell death is determinedby MTT assay, which is widely used to assess cell viability. After treatment, the cells are

9、incubated in serum-free medium containing 0.25 mg/mL MTT for 3 h at 37C. Formation of formazan from tetrazolium ismeasured at 570 nm with a reference wavelength at 630 nm using a SpectraMax microplate reader 1.MCE has not independently confirmed the accuracy of these methods. They are for reference

10、only.Animal Mice 2Administration 23 Male C57Bl/6 mice (20-25 g) are used. For treatment with Z-DEVD-fmk or vehicle after CCI, mice arereanesthetized with isoflurane at various times after injury, placed in a stereotaxic apparatus, and the CCIwound is reopened for intracerebroventricular injection. E

11、ither Z-DEVD-FMK (160 ng in 2 L DMSO), orDMSO vehicle is injected over a 5-minute period.Rats 3Male Sprague Dawley rats (42525 g) are used. DMSO (5 L) vehicle or Z-DEVD-FMK (160 ng in 5 L ofDMSO) is administered at a controlled rate of 0.5 L/min via an infusion pump at 30 min before and at 6 and24 h

12、r after TBI. At the designated time periods after injury, animals are decapitated under sodiumpentobarbital anesthesia (100 mg/kg, i.p.), and the brains are removed rapidly and dissected. Sham-operated2/3 Master of Small Molecules 您邊的抑制劑師www.MedChemE(control) animals received anesthesia and surgery

13、but are not subjected to trauma. Tissue samples arecollected 1, 4, 12, 24, and 72 hr after TBI. Samples are frozen on dry ice and kept at 85C.MCE has not independently confirmed the accuracy of these methods. They are for reference only.戶使本產(chǎn)品發(fā)表的科研獻 Cell Mol Life Sci. 2018 Mar;75(6):1117-1132. Anal C

14、hem. 2017 Sep 19;89(18):9788-9796. Cell Death Dis. 2019 Feb 11;10(2):118. J Cell Mol Med. 2019 Apr;23(4):2489-2504. Apoptosis. 2016 Feb;21(2):130-42.See more customer validations on HYPERLINK / www.MedChemEREFERENCES1. Kanthasamy AG, et al. A novel peptide inhibitor targeted to caspase-3 cleavage si

15、te of a proapoptotic kinase protein kinase C delta(PKCdelta) protects against dopaminergic neuronal degeneration in Parkinsons disease models. Free Radic Biol Med. 2006 Nov15;41(10):1578-89.2. Knoblach SM, et al. Caspase inhibitor z-DEVD-fmk attenuates calpain and necrotic cell death in vitro and af

16、ter traumatic brain injury. JCereb Blood Flow Metab. 2004 Oct;24(10):1119-32.3. Yakovlev AG, et al. Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumaticbrain injury. J Neurosci. 1997, 17(19), 7415-7424.4. Huang MY, et al. Chemotherapeutic agent CPT-11 eliminates peritoneal resident macrophages by inducing