You can now submit reviews for your favorite Tocris products. Your review will help other researchers decide on the best products for their research. Why not submit a review today?!Submit Review
Discontinued ProductZ-IETD-FMK (Cat. No. 2170) has been withdrawn from sale for commercial reasons.
Biological Activity for Z-IETD-FMK
Inhibitor of caspase-8. Blocks TNFα-induced cytochrome c release and apoptosis in human leukemic U937 cells. Also inhibits nuclear protein cleavage in Jurkat, MCF-7 and HeLa cells in vitro.
Technical Data for Z-IETD-FMK
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for Z-IETD-FMK
References for Z-IETD-FMK
References are publications that support the biological activity of the product.
Taimen and Kallajoki (2003) NuMA and nuclear lamins behave differently in Fas-mediated apoptosis. J.Cell Sci. 116 571 PMID: 12508117
Bang et al (2004) Differential response of MG132 cytotoxicity against small cell lung cancer cells to changes in cellular GSH contents. Biochem.Pharmacol. 68 659 PMID: 15276073
Partheniou et al (2001) c-IAP1 blocks TNFα-mediated cytotoxicity upstream of caspase-dependent and -independent mitochondrial events in human leukemic cells. Biochem.Biophys.Res.Comm. 287 181
View Related Products by Product Action
Keywords: Z-IETD-FMK, Z-IETD-FMK supplier, Caspases, 2170, Tocris Bioscience
Citations for Z-IETD-FMK
Citations are publications that use Tocris products.
Currently there are no citations for Z-IETD-FMK.
Reviews for Z-IETD-FMK
There are currently no reviews for this product. Be the first to review Z-IETD-FMK and earn rewards!
Have you used Z-IETD-FMK?
Submit a review and receive an Amazon gift card.
$50/€35/£30/$50CAN/¥300 Yuan/¥5000 Yen for first to review with an image
$25/€18/£15/$25CAN/¥75 Yuan/¥1250 Yen for a review with an image
$10/€7/£6/$10 CAD/¥70 Yuan/¥1110 Yen for a review without an image
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Cell Cycle and DNA Damage Research Product Guide
This product guide provides a review of the cell cycle and DNA damage research area and lists over 170 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Huntington's Disease Poster
Huntington's disease (HD) is a severe monogenic neurodegenerative disorder, which is characterized by the prevalent loss of GABAergic medium spiny neurons (MSN) in the striatum. This poster summarizes the effects of mutant huntingtin aggregation implicated in the pathology of HD, as well as highlighting the use of iPSCs for HD modeling.
Parkinson's Disease Poster
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.