Ac-IETD-CHO (trifluoroacetate salt) is a caspase 8 inhibitor that can prevent the focal adhesion kinase (Fak) from being cleaved by caspase, with an IC50 value of 200nM [1]. Ac-IETD-CHO can prevent caspase-8 from cleaving Bid protein, prevent the loss of mitochondrial membrane potential, and inhibit cell apoptosis[2]. Ac-IETD-CHO has been widely used to inhibit DNA fragmentation and prevent various types of cell apoptosis caused by non-steroidal anti-inflammatory drugs[3].
In vitro, Ac-IETD-CHO treatment (300µM) for 24 hours significantly inhibited the death of MOLT-4N1 cells after 1.8Gy X-ray radiation, and promoted cell survival[4]. Treatment with 100µM Ac-IETD-CHO for 9 hours significantly prevented the reduction in the expression of CD31 and CD47 on the surface of Jurkat cells induced by etoposide[5].
References:
[1] Gervais F G, Thornberry N A, Ruffolo S C, et al. Caspases cleave focal adhesion kinase during apoptosis to generate a FRNK-like polypeptide[J]. Journal of Biological Chemistry, 1998, 273(27): 17102-17108.
[2] Yamada H, Tada-Oikawa S, Uchida A, et al. TRAIL causes cleavage of bid by caspase-8 and loss of mitochondrial membrane potential resulting in apoptosis in BJAB cells[J]. Biochemical and biophysical research communications, 1999, 265(1): 130-133.
[3] Inoue A, Muranaka S, Fujita H, et al. Molecular mechanism of diclofenac-induced apoptosis of promyelocytic leukemia: dependency on reactive oxygen species, Akt, Bid, cytochrome and caspase pathway[J]. Free Radical Biology and Medicine, 2004, 37(8): 1290-1299.
[4] Nakano H, Shinohara K. Time sequence analysis of caspase-3-independent programmed cell death and apoptosis in X-irradiated human leukemic MOLT-4 cells[J]. Cell and tissue research, 2002, 310(3): 305-311.
[5] Azuma Y, Nakagawa H, Dote K, et al. Decreases in CD31 and CD47 levels on the cell surface during etoposide-induced Jurkat cell apoptosis[J]. Biological and Pharmaceutical Bulletin, 2011, 34(12): 1828-1834.
Ac-IETD-CHO (trifluoroacetate salt)是一种caspase 8抑制剂，可阻止focal adhesion kinase (Fak)被caspase裂解，IC50值为200nM[1]。Ac-IETD-CHO能阻止caspase-8裂解Bid蛋白，防止线粒体膜电位丧失，并抑制细胞凋亡[2]。Ac-IETD-CHO已被广泛用于抑制DNA片段化，并预防非甾体抗炎药引起的多种类型细胞凋亡[3]。
在体外，300µM的Ac-IETD-CHO处理经1.8Gy X射线照射的MOLT-4N1细胞24小时，显著抑制了细胞死亡，并促进了细胞存活[4]。100µM的Ac-IETD-CHO处理9小时，显著阻止了依托泊苷诱导的Jurkat 细胞表面CD31和CD47表达的下调[5]。