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Z-DEVD-FMK

Catalog No.
A1920
Caspase-3 inhibitor
Grouped product items
SizePriceStock Qty
10mM (in 1mL DMSO)
$198.00
In stock
Evaluation Sample
$30.00
In stock
1mg
$61.00
In stock
5mg
$165.00
In stock
10mg
$275.00
In stock
25mg
$440.00
In stock
For scientific research use only and should not be used for diagnostic or medical purposes.

Tel: +1-832-696-8203

Email: [email protected]

Worldwide Distributors

Background

Z-DEVD-FMK (CAS 210344-95-9) is a tetrapeptide inhibitor primarily targeting caspase-3, a protease involved in apoptotic neuronal cell death. Beyond caspase-3 inhibition, Z-DEVD-FMK also directly suppresses calpain-mediated proteolysis, notably reducing calpain-induced spectrin degradation. In vitro studies confirm Z-DEVD-FMK attenuates necrotic neuronal death, independently of caspase-3 activity. In vivo, following traumatic brain injury (TBI) or cerebral ischemia, administration of Z-DEVD-FMK limits lesion size, reduces tissue damage, and improves functional neurological outcomes, likely due to combined inhibition of caspase-3 and calpain pathways.

References:

1. Garcia-Calvo M, Peterson EP, Leiting B, Ruel R, Nicholson DW, Thornberry NA (1998) Inhibition of human caspases by peptidebased and macromolecular inhibitors. J Biol Chem 273:32608–32613

2. Thornberry NA, Rano TA, Peterson EP, Rasper DM, Timkey T, Garcia-Calvo M, Houtzager VM, Nordstrom PA, Roy S, Vaillancourt JP, Chapman KT, Nicholson DW (1997) A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis. J Biol Chem 272:17907–17911

3. Yakovlev AG, Knoblach SM, Fan L, Fox GB, Goodnight R, Faden AI (1997) Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. J Neurosci 17:7415–7424

4. Clark RS, Kochanek PM, Watkins SC, Chen M, Dixon CE, Seidberg NA, Melick J, Loeffert JE, Nathaniel PD, Jin KL, Graham SH (2000) Caspase-3 mediated neuronal death after traumatic brain injury in rats. J Neurochem 74:740–753

5. S. M. Knoblach, D. A. Alroy et al, Caspase Inhibitor z-DEVD-fmk Attenuates Calpain and Necrotic Cell Death in Vitro and After Traumatic Brain Injury, Journal of Cerebral Blood Flow & Metabolism 24:1119–1132.

Product Citation

Chemical Properties

Physical AppearanceA solid
StorageStore at -20°C
M.Wt668.66
Cas No.210344-95-9
FormulaC30H41N4O12F
SynonymsCaspase-3 Inhibitor II,Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-FMK
Solubilityinsoluble in H2O; insoluble in EtOH; ≥60 mg/mL in DMSO
Chemical Namemethyl (4S)-5-[[(2S)-1-[[(3S)-5-fluoro-1-methoxy-1,4-dioxopentan-3-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-[[(2S)-4-methoxy-4-oxo-2-(phenylmethoxycarbonylamino)butanoyl]amino]-5-oxopentanoate
SDFDownload SDF
Canonical SMILESCC(C)C(C(=O)NC(CC(=O)OC)C(=O)CF)NC(=O)C(CCC(=O)OC)NC(=O)C(CC(=O)OC)NC(=O)OCC1=CC=CC=C1
Shipping ConditionSmall Molecules with Blue Ice, Modified Nucleotides with Dry Ice.
General tips We do not recommend long-term storage for the solution, please use it up soon.

Protocol

Cell experiment: [1]

Cell lines

WM9, WM35, WM98-1 and WM793 cells

Preparation method

The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37°C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.

Reaction Conditions

20 μM, 24 hours

Applications

To demonstrate the importance of caspase activation in TRAIL-induced apoptosis. Z-DEVD-FMK was added to melanoma cells along with TRAIL. Z-DEVD-FMK was only able to partially inhibit the cytotoxic effects of TRAIL. The decreased ability of Z-DEVD-FMK to inhibit death may result from the ability of the peptide to enter the cell.

Animal experiment: [2]

Animal models

Male C57Bl/6 mice with controlled cortical impact (CCI) injury

Dosage form

Intracerebroventricular injection, 160 ng.

Applications

To assess motor recovery, mice were tested for the ability to traverse a narrow, suspended beam during recovery over a 21-day period. Mice treated 1 hour after CCI performed significantly better than did vehicle controls on days 7, 14, and 21 after injury. Mice treated 4 hours after CCI performed significantly better than controls only on day 21 after injury, but this was an isolated observation, as they did not show a trend toward better performance compared with other treatment groups on any other testing day.

Other notes

Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal.

References:

[1] Griffith T S, Chin W A, Jackson G C, et al. Intracellular regulation of TRAIL-induced apoptosis in human melanoma cells. The Journal of Immunology, 1998, 161(6): 2833-2840.

[2] Knoblach S M, Alroy D A, Nikolaeva M, et al. Caspase inhibitor z-DEVD-fmk attenuates calpain and necrotic cell death in vitro and after traumatic brain injury. Journal of Cerebral Blood Flow & Metabolism, 2004, 24(10): 1119-1132.

Biological Activity

Z-DEVD-FMK is a cell-permeable, irreversible inhibitor of Caspase-3/CPP32. It is also an irreversible inhibitor of Caspase-6, Caspase-7, caspase-8, and Caspase-10.
Targets Caspase-3 Caspase-6 Caspase-7 Caspase-8 Caspase-10  
IC50            

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