Discontinued Product

Z-WEHD-FMK (Cat. No. 2167) has been withdrawn from sale for commercial reasons.
Description: Caspase-5 inhibitor
Chemical Name: Benzyloxycarbonyl-Trp-Glu(OMe)-His-Asp(OMe)-fluoromethylketone
Literature (5)

Biological Activity for Z-WEHD-FMK

Caspase-5 inhibitor. Inhibits ECyd-induced rRNA fragmentation in mouse mammary tumor and human fibrosarcoma cells.

Technical Data for Z-WEHD-FMK

M. Wt 763.78
Formula C37H42FN7O11
Sequence WEHD

(Modifications: Trp-1 = Z-Trp, Glu-2 = Glu(OMe), Asp-4 = (OMe)-fluoromethylketone)

Storage Store at -20°C
Smiles [H]N([C@@H](CC1=CNC2=C1C=CC=C2)C(=O)N[C@@H](CCC(=O)OC)C(=O)N[C@@H](CC1=CNC=N1)C(=O)N[C@@H](CC(=O)OC)C(=O)CF)C(=O)OCC1=CC=CC=C1

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.

References for Z-WEHD-FMK

References are publications that support the biological activity of the product.

Naito et al (2002) Anticancer mechanisms of 1-(3-C-ethynyl-beta-D-ribo-pentofuranosyl)cytosine (ECyd, TAS-106). Nucl.Acids Res.Suppl. 2 241

View Related Products by Target

View Related Products by Product Action

View all Caspase Inhibitors

Keywords: Z-WEHD-FMK, Z-WEHD-FMK supplier, Caspase-5, inhibitors, inhibits, Caspases, Proteinases, Proteases, 2167, Tocris Bioscience

Citations for Z-WEHD-FMK

Citations are publications that use Tocris products.

Currently there are no citations for Z-WEHD-FMK.

Reviews for Z-WEHD-FMK

There are currently no reviews for this product. Be the first to review Z-WEHD-FMK and earn rewards!

Have you used Z-WEHD-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

Submit a Review

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

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 150 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

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. 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 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 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

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.