| 產(chǎn)品編號(hào) | D50433 |
| 英文名稱 | Z-VAD(OMe)-FMK |
| 中文名稱 | |
| 別 名 | Z-VAD-FMK; Inhibitor Z-VAD-FMK; Caspase Inhibitor I; Z-Val-Ala-Asp(OMe)-FMK; N-Benzyloxycarbonyl-Val-Ala-Asp(O-Me) fluoromethyl ketone; Caspase Inhibitor; N-[芐氧羰基]-L-纈氨?；?N-[(1S)-3-氟-1-(2-甲氧基-2-氧代乙基)-2-氧代丙基]-L-丙氨酰胺; Caspase抑制劑; |
| 克 隆 號(hào) | |
| CAS | 187389-52-2 |
| 理論分子量 | kDa |
| 檢測(cè)分子量 | |
| 保存條件 | Store at -20℃. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| 產(chǎn)品介紹 |
基本信息： CAS：187389-52-2 分子式：C22H30FN3O7 分子量：467.49 序列：Z-Val-Ala-Asp-CH2F 純度：≥98% 產(chǎn)品簡(jiǎn)介： 作用靶點(diǎn)：Caspase; 作用通路：Apoptosis; 產(chǎn)品描述： Z-VAD-FMK是一種細(xì)胞滲透性的，不可逆泛caspase抑制劑 (Cell permeable pan caspase inhibitor)，可以抑制由Caspase激活導(dǎo)致的細(xì)胞凋亡。在THP.1 和 Jurkat T細(xì)胞中阻斷細(xì)胞凋亡的所有特性。 注意事項(xiàng)： 1. 如果每次使用量少，使用次數(shù)較多，請(qǐng)適當(dāng)分裝保存，避免反復(fù)凍融。 2. 如果希望適當(dāng)稀釋后再分裝保存，請(qǐng)使用DMSO進(jìn)行稀釋。 3. 本產(chǎn)品在較低溫度情況下會(huì)出現(xiàn)凝固，可在20-25℃水浴溫育片刻至全部融解后使用。 4. 為了您的安全和健康，請(qǐng)穿實(shí)驗(yàn)服并戴一次性手套操作。 體外研究： Z-VAD-FMK (10 mM) inhibits apoptosis in THP.1 cells. Z-VAD-FMK (10 μM) inhibits activation of PARP protease activity in control THP.1 cell lysates. Z-VAD-FMK (10 mM) inhibits the processing of CPP32 in intact THP.1 and Jurkat cells. Z-VAD-FMK (50 μM) cotreatment abolishes the apoptotic morphology of camptothecin-treated HL60 cells. Z-VAD-FMK (50 μM) blocks camptothecin-induced DNA fragmentation in HL60 cells. Z-VAD-FMK (50 μM) inhibits cell death following dSMN dsRNA-induced apoptosis in S2 cells. Z-VAD-FMK (50 μM) increases the percentage of transfected cells surviving from 26% to 63% in S2 cells. Z-VAD-FMK (> 100 μM) enhances TNFα-induced neutrophil apoptosis, lower concentrations (1-30 μM) completely blocks TNFα-stimulated apoptosis in human neutrophils. Z-VAD-FMK (10 mM) inhibits apoptosis in anterior stromal keratocytes. Z-VAD-FMK (10 mM) inhibits apoptosis in anterior stromal keratocytes detected with the TUNEL assay. 體內(nèi)研究： In vivo Z-VAD-FMK administration has been shown previously to be nontoxic and to prevent apoptosis in animal models. Intraperitoneal HK-GBS injection leads to preterm delivery, and pretreatment with Z-VAD-FMK delays preterm delivery in mice. In OVA-sensitized mice,treatment of z-VAD-fmk inhibits allergen-induced leukocyte infiltration. Systemic injection of the pan-caspase inhibitor z-VAD-fmk immediately before OVA challenge reduced inflammatory cell accumulation, mucus hypersecretion, and Th2 cytokine release in OVA-sensitized/challenged mice. Treatment with z-VAD-fmk blocked terminal differentiation of lens epithelial cells and keratinocytes, the differentiation of monocytes into macrophages, and the differentiation of erythroid progenitors. z-VAD-fmk attenuated allergen-induced airway inflammation and hyperreactivity. Treatment with z-VAD-fmk in vivo also prevented subsequent T cell activation ex vivo. |
