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Z-DEVD-FMK

Caspase-3 inhibitor CAS# 210344-95-9

Z-DEVD-FMK

Catalog No. BCC1137----Order now to get a substantial discount!

Product Name & Size Price Stock
Z-DEVD-FMK:10mg $208.00 In stock
Z-DEVD-FMK:20mg $354.00 In stock
Z-DEVD-FMK:50mg $832.00 In stock
Z-DEVD-FMK:100mg $1456.00 In stock
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Chemical structure

Z-DEVD-FMK

3D structure

Chemical Properties of Z-DEVD-FMK

Cas No. 210344-95-9 SDF Download SDF
PubChem ID 16760394 Appearance Powder
Formula C30H41N4O12F M.Wt 668.66
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Caspase-3 Inhibitor II,Z-Asp(OMe)-Glu(OMe)-Val-Asp(OMe)-FMK
Solubility DMSO : ≥ 33.33 mg/mL (49.85 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name methyl (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
SMILES CC(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
Standard InChIKey GBJVAVGBSGRRKN-JYEBCORGSA-N
Standard InChI InChI=1S/C30H41FN4O12/c1-17(2)26(29(42)33-20(22(36)15-31)13-24(38)45-4)35-27(40)19(11-12-23(37)44-3)32-28(41)21(14-25(39)46-5)34-30(43)47-16-18-9-7-6-8-10-18/h6-10,17,19-21,26H,11-16H2,1-5H3,(H,32,41)(H,33,42)(H,34,43)(H,35,40)/t19-,20-,21-,26-/m0/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Z-DEVD-FMK

Description 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.
TargetsCaspase-3Caspase-6Caspase-7Caspase-8Caspase-10  

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.

Reacting condition

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,

Application

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.

Z-DEVD-FMK Dilution Calculator

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Z-DEVD-FMK Molarity Calculator

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Preparing Stock Solutions of Z-DEVD-FMK

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.4955 mL 7.4776 mL 14.9553 mL 29.9106 mL 37.3882 mL
5 mM 0.2991 mL 1.4955 mL 2.9911 mL 5.9821 mL 7.4776 mL
10 mM 0.1496 mL 0.7478 mL 1.4955 mL 2.9911 mL 3.7388 mL
50 mM 0.0299 mL 0.1496 mL 0.2991 mL 0.5982 mL 0.7478 mL
100 mM 0.015 mL 0.0748 mL 0.1496 mL 0.2991 mL 0.3739 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Research Update of Z-DEVD-FMK

2. [Effects of intracerebroventricular administration of a caspase-3 inhibitor Z-DEVD-FMK on behavior of rats]. Zh Vyssh Nerv Deiat Im I P Pavlova. 2006 Mar-Apr;56(2):247-56.
Abstract
Intracerebroventricular administration of Z-DEVD-FMK, a caspase-3 inhibitor, had effects on the active avoidance learning of rats, where it decreased the number of avoidance reactions and impaired the development of several components of the active avoidance performance.

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Background on Z-DEVD-FMK

Z-DEVD-FMK is a tetrapeptide caspase inhibitor that is considered relatively selective for caspase-31, 2 and has been widely used in in vitro and in vivo models of acute injury to delineate roles for caspase 3 in neuronal cell death. Intracerebroventricular injections of Z-DEVD-FMK improved function after LFP3. Intraparenchymal infusion of Z-DEVD-FMK over several days after combined CCI and hypoxia reduced lesion size, although functional outcome was not significantly improved in this model4 (Clark et al., 2000).

Z-DEVD-FMK was a potent inhibitor of calpain and that improvement observed after treatment with Z-DEVD-FMK may reflect, at least in part, this action.

Early treatment with Z-DEVD-FMK improved neurologic function and reduced lesion volume. Z-DEVD-FMK reduces cell death and inhibits calpain in a model of in vitro necrosis and a cell free assay and Z-DEVD-FMK treatment inhibits calpain activity after TBI in vivo.

Z-DEVD-FMK improved neurologic function and reduced tissue damage at an injury severity that showed predominantly necrotic neuronal cell death with minimal evidence of caspase 3 activation. Moreover, effective treatment with Z-DEVD-FMK was associated with reduced calpain-mediated -spectrin degradation. Z-DEVD-FMK was also neuroprotective, at concentrations lower than those routinely used to inhibit caspase 3, in an in vitro model of necrotic neuronal cell death induced by maitotoxin.

The present data show that treatment with Z-DEVD-FMK improves behavioral recovery, reduces tissue damage and prevents accumulation of calpain-mediated α-spectrin breakdown products when administered not later than 1 hour after injury in a TBI model that primarily shows necrosis. Z-DEVD-FMK also reduces necrotic neuronal cell death in vitro, and such neuroprotection is associated with inhibition of calpain, but not caspase 3 or cathepsin B. In addition, Z-DEVD-FMK reduces calpainmediated hydrolysis of casein, which indicates that Z-DEVD-FMK can directly inhibit calpain. This nonspecificproperty of Z-DEVD-FMK may account, at least in part, for its neuroprotective actions5.

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.

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References on Z-DEVD-FMK

The caspase-3 inhibitor (peptide Z-DEVD-FMK) affects the survival and function of platelets in platelet concentrate during storage.[Pubmed:24724067]

Blood Res. 2014 Mar;49(1):49-53.

BACKGROUND: Although apoptosis occurs in nucleated cells, studies show that this event also occurs in some anucleated cells such as platelets. During storage of platelets, the viability of platelets decreased, storage lesions were observed, and cells underwent apoptosis. We investigated the effects of caspase-3 inhibitor on the survival and function of platelets after different periods of storage. METHODS: Platelet concentrates were obtained from the Iranian Blood Transfusion Organization in plastic blood bags. Caspase-3 inhibitor (Z-DEVD-FMK) was added to the bags. These bags along with control bags to which no inhibitor was added were stored in a shaking incubator at 22 for 7 days. The effects of Z-DEVD-FMK on the functionality of platelets were analyzed by assessing their ability to bind to von Willebrand factor (vWF) and to aggregate in the presence of arachidonic acid and ristocetin. Cell survival was surveyed by MTT assay. RESULTS: At day 4 of storage, ristocetin-induced platelet aggregation was significantly higher in the inhibitor-treated (test) than in control samples; the difference was not significant at day 7. There was no significant difference in arachidonic acid-induced platelet aggregation between test and control samples. However, at day 7 of storage, the binding of platelets to vWF was significantly higher in test than in control samples. The MTT assay revealed significantly higher viability in test than in control samples at both days of study. CONCLUSION: Treatment of platelets with caspase-3 inhibitor could increase their functionality and survival.

[Experimental study on treatment of rabbits optic nerve injury with Caspase-3 inhibitor z-DEVD-fmk].[Pubmed:21211221]

Zhonghua Yan Ke Za Zhi. 2010 Dec;46(12):1084-9.

OBJECTIVE: To observe the effects of caspase-3 inhibitor Z-DEVD-FMK on optic nerve injury of rabbits. METHODS: It was an experimental study. Two to three month-old rabbits were used in this study. The rabbit model of optic nerve injury was created by fluid percussion brain injury device (FPI). DMSO (5 microl 2% solution) was injected intravitreally to the left eyes (control group). Caspase-3 inhibitor Z-DEVD-FMK (5 microl) was injected intravitreally to the right eyes (experimental group). Flash-visual evoked potential (F-VEP) and histopathological examination of the retina were used to check the variations in optic nerve injury at 1, 4, 7, 10, 14, and 21 days after the treatment. Immunohistochemistry was used to detect the expression of caspase-3 in the retina. T-test, variance analysis, q-test and linear correlation analysis were used to analyze these data. RESULTS: At the 7th day after treatment, the latency of F-VEP P1 in experimental group was shorter than that in the control group [(90.50+/-7.61) ms vs (113.59+/-12.92) ms, t=4.060, P<0.05] and the number of retinal ganglion cells (RGC) in the experimental group was greater than that in the control group (237.62+/-8.50 vs 207.03+/-11.04, t=-5.843, P<0.05). Both of these trends continued to the 21st day after treatment [(67.97+/-7.93) ms vs. (134.22+/-8.50) ms, t=13.950, P<0.05; 156.32+/-8.45 vs. 207.13+/-12.21, t=-10.307, P<0.05]. The absorbency (A) of caspase-3 in the experimental group (0.396+/-0.023) was lower than that in the control group (0.458+/-0.024) and this difference was statistically significant (t=6.200, P<0.05) at the 7th day after treatment. The latency of F-VEP P1 and the absorbency of caspase-3 in the retina were positively correlated with each other (r=0.95, P<0.05). CONCLUSION: Z-DEVD-FMK is effective in treating rabbit optic nerve injury by inhibiting the expression of caspase-3 in the retina. It can promote the recovery of optic nerve function.

[Effects of intracerebroventricular administration of a caspase-3 inhibitor Z-DEVD-FMK on behavior of rats].[Pubmed:16756133]

Zh Vyssh Nerv Deiat Im I P Pavlova. 2006 Mar-Apr;56(2):247-56.

Rats received intracerebroventricular injections of Z-DEVD-FMK (caspase-3 inhibitor) or z-FA-FMK (control peptide) in a dose of 3 nmol. Administration of Z-DEVD-FMK significantly decreased the number of avoidance reactions in some blocks of trials in active avoidance (shuttle box) learning. However, only slight effect of the caspase inhibitor across the session was found. Z-DEVD-FMK impaired development of some essential components of the two-way active avoidance performance, such as escape reaction, conditioned fear reaction, and inter-trial crossings. Z-DEVD-FMK did not impair working memory in the spontaneous alternation behavior paradigm. Z-DEVD-FMK affected neither emotionality nor locomotor activity in the open-field test. It also did not influence behavior in the light-dark chamber. Measurement of caspase-3 activity in rat brain regions involved in active avoidance learning revealed Z-DEVD-FMK-related inhibition of the enzyme activity most pronounced (about 30%) in the fronto-parietal cortex; a similar effect was close to significant in the hippocampus. The results suggest the involvement of brain caspase-3 in selected forms of learning.

Caspase-3 inhibitor Z-DEVD-FMK enhances retinal ganglion cell survival and vision restoration after rabbit traumatic optic nerve injury.[Pubmed:25588462]

Restor Neurol Neurosci. 2015;33(2):205-20.

PURPOSE: Vision loss after traumatic optic nerve injury is considered irreversible because of the retrograde loss of retinal ganglion cells (RGCs) which undergo apoptosis. Because the second messenger caspase-3 plays a major role in apoptosis, we now evaluated the efficacy of the specific caspase-3 inhibitor, Z-DEVD-FMK, in a rabbit model of fluid percussion injury (FPI) which mimics traumatic optic nerve injury in humans to enhance cell survival and improve vision. METHODS: Survival of RGCs and recovery of vision were studied using retinal morphological markers and visual evoked potentials (VEP), respectively. The FPI traumatized animals were treated in their right eye with a single intravitreal or peribulbar injection of Z-DEVD-FMK 30 min post-injury compared to 2% DMSO control injections in their left eye. RESULTS: Intravitreal Z-DEVD-FMK, but not control injections, led to down-regulation of capase-3 and reduced, in a dose-dependent manner, RGCs apoptosis from 7 to 21 days post-injury. These morphological improvements were accompanied by vision restoration as documented by VEP. The neuroprotection after intravitreal injection of Z-DEVD-FMK was more effective than the peribulbar application. CONCLUSIONS: The caspase-3 inhibitor Z-DEVD-FMK is neuroprotective by inhibiting RGCs apoptosis when injected 30 min after optic nerve damage and significantly promotes restoration of vision. A controlled clinical trial is now needed to evaluate the efficacy and safety of Z-DEVD-FMK in humans.

Description

Z-DEVD-FMK is a specific and irreversible caspase-3 inhibitor with IC50 of 18 μM.

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