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Z-IETD-FMK

Chemical structure for Z-IETD-FMK.
Chemical structure for Z-IETD-FMK.
Ordering information
Price ()
Catalog Number13305
Unit Size
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Additional ordering information
Telephone1-408-733-1055
Fax1-408-733-1304
Emailsales@aatbio.com
InternationalSee distributors
ShippingStandard overnight for United States, inquire for international
Physical properties
Molecular weight654.69
SolventDMSO
Storage, safety and handling
H-phraseH303, H313, H333
Hazard symbolXN
Intended useResearch Use Only (RUO)
R-phraseR20, R21, R22
StorageFreeze (< -15 °C); Minimize light exposure
UNSPSC12171501

OverviewpdfSDSpdfProtocol


Molecular weight
654.69
Z-IETD-FMK is a cell-permeable, irreversible caspase-8 inhibitor. It is widely used in cell apoptosis studies. Caspase-8 is a member of the cysteine proteases, which are implicated in apoptosis and cytokine processing. Like all caspases, caspase-8 is synthesized as an inactive single polypeptide chain zymogen procaspase and is activated by proteolytic cleavage, through either autoactivation after recruitment into a multimeric complex or trans-cleavage by other caspases. Thus, ligand binding-induced trimerization of death receptors results in recruitment of the receptor-specific adapter protein Fas-associated death domain (FADD), which then recruits caspase-8. Activated caspase-8 is known to propagate the apoptotic signal either by directly cleaving and activating downstream caspases or by cleaving the BH3 Bcl2-interacting protein, which leads to the release of cytochrome c from mitochondria, triggering activation of caspase-9 in a complex with dATP and Apaf-1. Activated caspase-9 then activates further "downstream caspases," including caspase-8. Knockout data indicate that caspase-8 is required for killing induced by the death receptors Fas, tumor necrosis factor receptor 1, and death receptor 3. Moreover, caspase-8-/- mice die in utero as a result of defective development of heart muscle and display fewer hematopoietic progenitor cells, suggesting that the FADD/caspase-8 pathway is absolutely required for growth and development of specific cell types.

Calculators


Common stock solution preparation

Table 1. Volume of DMSO needed to reconstitute specific mass of Z-IETD-FMK to given concentration. Note that volume is only for preparing stock solution. Refer to sample experimental protocol for appropriate experimental/physiological buffers.

0.1 mg0.5 mg1 mg5 mg10 mg
1 mM152.744 µL763.72 µL1.527 mL7.637 mL15.274 mL
5 mM30.549 µL152.744 µL305.488 µL1.527 mL3.055 mL
10 mM15.274 µL76.372 µL152.744 µL763.72 µL1.527 mL

Molarity calculator

Enter any two values (mass, volume, concentration) to calculate the third.

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References


View all 27 references: Citation Explorer
Role of caspases in CD95-induced biphasic activation of acid sphingomyelinase.
Authors: Stephan, Mario and Edelmann, Bärbel and Winoto-Morbach, Supandi and Janssen, Ottmar and Bertsch, Uwe and Perrotta, Cristiana and Schütze, Stefan and Fritsch, Jürgen
Journal: Oncotarget (2017): 20067-20085
Caspase-8 inhibition represses initial human monocyte activation in septic shock model.
Authors: Oliva-Martin, Maria Jose and Sanchez-Abarca, Luis Ignacio and Rodhe, Johanna and Carrillo-Jimenez, Alejandro and Vlachos, Pinelopi and Herrera, Antonio Jose and Garcia-Quintanilla, Albert and Caballero-Velazquez, Teresa and Perez-Simon, Jose Antonio and Joseph, Bertrand and Venero, Jose Luis
Journal: Oncotarget (2016): 37456-37470
Caspase blockade induces RIP3-mediated programmed necrosis in Toll-like receptor-activated microglia.
Authors: Kim, S J and Li, Jianrong
Journal: Cell death & disease (2013): e716
Cytokeratin 18 expression inhibits cytokine-induced death of cervical cancer cells.
Authors: Sullivan, Brian T and Cherry, Jessica A and Sakamoto, Hideo and Henkes, Luiz E and Townson, David H and Rueda, Bo R
Journal: International journal of gynecological cancer : official journal of the International Gynecological Cancer Society (2010): 1474-81
Non-canonical role for the TRAIL receptor DR5/FADD/caspase pathway in the regulation of MyoD expression and skeletal myoblast differentiation.
Authors: Freer-Prokop, Margot and O'Flaherty, John and Ross, Jason A and Weyman, Crystal M
Journal: Differentiation; research in biological diversity (2009): 205-12
ERK-1 MAP kinase prevents TNF-induced apoptosis through bad phosphorylation and inhibition of Bax translocation in HeLa Cells.
Authors: Pucci, Bruna and Indelicato, Manuela and Paradisi, Valentina and Reali, Valentina and Pellegrini, Laura and Aventaggiato, Michele and Karpinich, Natalie O and Fini, Massimo and Russo, Matteo A and Farber, John L and Tafani, Marco
Journal: Journal of cellular biochemistry (2009): 1166-74
T-2 toxin initially activates caspase-2 and induces apoptosis in U937 cells.
Authors: Huang, Peixin and Akagawa, Keisuke and Yokoyama, Yoshiko and Nohara, Kazunari and Kano, Kazutaka and Morimoto, Kanehisa
Journal: Toxicology letters (2007): 1-10
The death receptor pathway is not involved in alloreactive T-cell induced mitochondrial membrane permeability.
Authors: Grüllich, Carsten and McGoldrick, Suzanne and Zeiser, Robert and Finke, Jürgen
Journal: Leukemia & lymphoma (2005): 1207-16
Ceramide-induced apoptosis in rabbit corneal fibroblasts.
Authors: Kim, Tae-im and Pak, Jhang Ho and Tchah, Hungwon and Lee, Seung-ah and Kook, Michael S
Journal: Cornea (2005): 72-9
Pyranocoumarin(+/-)-4'-O-acetyl-3'-O-angeloyl-cis-khellactone induces mitochondrial-dependent apoptosis in HL-60 cells.
Authors: Fong, Wang-Fun and Zhang, Jin-Xia and Wu, Jimmy Yiu-Cheong and Tse, Kai-Wing and Wang, Cheng and Cheung, Hong-Yeung and Yang, Meng-Su
Journal: Planta medica (2004): 489-95