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My CartCAS：210344-95-9
Storage：Powder:-20℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year
Purity：HPLC≥98%
Appearance：White to off-white Solid
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| CAS | 210344-95-9 |
| Name | Z-WEHD-FMK |
| Molecular Formula | C30H41FN4O12 |
| Molecular Weight | 668.66 |
| Solubility | Soluble in DMSO |
| Purity | HPLC≥98% |
| Appearance | White to off-white Solid |
| Storage | Powder:-20℃，2 years;Insolvent(Mother Liquid):-20℃，6 months;-80℃，1 year |
| MDL | MFCD00205201 |
| SMILES | O=C(N[C@@H](C(C)C)C(N[C@H](C(CF)=O)CC(OC)=O)=O)[C@H](CCC(OC)=O)NC([C@H](CC(OC)=O)NC(OCC1=CC=CC=C1)=O)=O |
| InChIKey | GBJVAVGBSGRRKN-JYEBCORGSA-N |
| InChI | InChI=1S/C30H41FN4O12/c1-17(2)26(29(42)33-20(22(36)15-31)13-24(38)45-4)35-27(40)19(11-12-23(37)44-3)32-28(41)21(14-25(39)46-5)34-30(43)47-16-18-9-7-6-8-10-18/h6-10,17,19-21,26H,11-16H2,1-5H3,(H,32,41)(H,33,42)(H,34,43)(H,35,40)/t19-,20-,21-,26-/m0/s1 |
| PubChem CID | 16760394 |
| Target Point | Caspase |
| Passage | Apoptosis |
| Background | Z-DEVD-FMK is a specific irreversible caspase-3 inhibitor. |
| Biological Activity | Z-DEVD-FMK 是一种特异性的不可逆的 caspase-3 抑制剂, IC50 为 18 μM[1-4]。 |
| IC50 | Caspase-3:18μM (IC50) [1-4] |
| In Vitro | 在不存在或存在50μMZ-DIPD-FMK或100μMZ-DEVD-FMK或50μMZ-LEHD-FMK的情况下，将N27细胞暴露于MPP +，然后通过酶促测定胱天蛋白酶-9和胱天蛋白酶-3的酶活性。分别在暴露后12和24小时进行测定。在N27细胞中暴露于300μMMPP+ 24小时导致胱天蛋白酶-3酶活性增加约2.5倍。 MPP +诱导的caspase-3酶活性增加被50μMZ-DIPD-FMK，100μMZ-DEVD-FMK和50μMZ-LEHD-FMK显着阻断[1]。 |
| In Vivo | 早期Z-DEVD-FMK(160 ng)治疗可改善小鼠严重受控皮层撞击(CCI)引起的创伤性CNS损伤后的运动和认知功能[2]。与用DMSO载体处理的创伤动物相比，用Z-DEVD-FMK(160ng)治疗显着改善神经学结果[p <0.01] [3]。 |
| Cell Experiment | 在存在或不存在0.1-50μMZ-DIPD-FMK或0.1-100μMZ-DEVD-FMK或50的情况下，将N27细胞和原代中脑神经元暴露于10-100μM6-OHDA或10-300μMMPP+在实验期间μMZ-IETD-FMK或Z-LEHD-FMK。在存在或不存在50μMZ-DEVD-FMK的情况下，将N27细胞与100μM6-OHDA孵育24小时或300μMMPP+孵育36小时，并通过MTT测定法测定细胞死亡，MTT测定法广泛用于评估细胞活力。 。处理后，将细胞在含有0.25mg / mL MTT的无血清培养基中于37℃温育3小时。使用SpectraMax酶标仪[1]，在570nm处测量来自四唑的甲an的形成，参比波长为630nm。 |
| Animal Experiment | 小鼠[2]使用雄性C57Bl / 6小鼠(20-25g)。对于在CCI后用Z-DEVD-fmk或媒介物治疗，在损伤后不同时间用异氟烷对小鼠进行再麻醉，置于立体定位装置中，并重新开放CCI伤口用于脑室内注射。在5分钟内注射Z-DEVD-FMK(160ng，在2μLDMSO中)或DMSO载体。使用大鼠[3]雄性Sprague Dawley大鼠(425±25g)。在TBI之前30分钟和之后6小时和24小时，通过输注泵以0.5μL/分钟的受控速率给予DMSO(5μL)载体或Z-DEVD-FMK(160ng在5μLDMSO中)。在损伤后的指定时间段，在戊巴比妥钠麻醉下(100mg / kg，ip)将动物断头，并迅速取出脑并解剖。假手术(对照)动物接受麻醉和手术，但未受到创伤。在TBI后1，4，12，24和72小时收集组织样品。将样品在干冰上冷冻并保持在-85℃。 |
| Data Literature Source | [1]. Kanthasamy AG， et al. A novel peptide inhibitor targeted to caspase-3 cleavage site of a proapoptotic kinase protein kinase C delta (PKCdelta) protects against dopaminergic neuronal degeneration in Parkinson's disease models. Free Radic Biol Med. 2006 Nov 15; 41 (10) :1578-89. [2]. Knoblach SM， et al. Caspase inhibitor z-DEVD-fmk attenuates calpain and necrotic cell death in vitro and after traumatic brain injury. J Cereb 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 traumatic brain injury. J Neurosci. 1997， 17 (19) ， 7415-7424. [4]. Huang MY， et al. Chemotherapeutic agent CPT-11 eliminates peritoneal resident macrophages by inducing apoptosis. Apoptosis. 2016 Feb; 21 (2) :130-42. |
| Unit | Bottle |
| Specification | 1mg 5mg |
Z-DEVD-FMK 是一种特异性的不可逆的 caspase-3 抑制剂。
Remark：These protocols are for reference only. Solarbio does not independently validate these methods.
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