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2mg |
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5mg |
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10mg |
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25mg |
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50mg |
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100mg |
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Purity: ≥98%
Ac-DEVD-CHO is a potent and specific aldehyde inhibitor of Group II caspases with Ki values of 0.2 nM and 0.3 nM for for caspase-3 and caspase-7, respectively. Weak caspase-2 inhibition. This aldehyde only moderately inhibits caspase-2 (Ki = 1.7 μM), which only cleaves the tetrapeptide substrate. Ac-DEVD-CHO has a broad inhibitory effect on group III caspases, with Ki values ranging from 1 to 300 nM. Even when given after the onset of ischemia, Ac-DEVD-CHO'scaspase-3inhibition significantly improves the stunned myocardium's post-ischemic contractile recovery in the isolated working-heart rat model. Ac-DEVD-CHO appears to have protection mechanisms that are separate from apoptosis. Ac-DEVD-CHO did not prevent troponin I cleavage.
Targets |
Caspase 3 (Ki = 0.23 nM); Caspase-8 (Ki = 0.92 nM); Caspase-7 (Ki = 1.6 nM); Caspase-10 (Ki = 12 nM); Caspase-1 (Ki = 18 nM); Caspase-6 (Ki = 31 nM); Caspase-9 (Ki = 60 nM); Caspase-4 (Ki = 132 nM); Caspase-5 (Ki = 205 nM); Caspase-2 (Ki = 1710 nM)
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ln Vitro |
Ac-DEVD-CHO is a potent inhibitor of caspase-3 (Ki = 230 pM). In contrast, this aldehyde only slightly inhibits caspase-2 (Ki = 1.7 μM) and exhibits poor cleavage of the tetrapeptide substrate. With Ki values ranging from 1 to 300 nM, Ac-DEVD-CHO significantly inhibits Group III caspases[1]. Even when administered after the onset of ischemia, Ac-DEVD-CHO'scaspase-3inhibition significantly improves post-ischemic contractile recovery of stunned myocardium in the isolated working-heart rat model. Ac-DEVD-CHO'sprotectivemechanism(s) seem to operate independently of apoptosis. Ac-DEVD-CHO[2] did not inhibit troponin I cleavage.
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ln Vivo |
Receiving Ac-DEVD-CHO at the time of MI causes a 61% decrease in the expression of activated caspase-3 in cardiomyocytes (p<0.05) and an 84% decrease in cardiomyocyte apoptosis in young animals. Caspase inhibition, however, had no impact on cardiomyocyte apoptosis or activated caspase-3 expression in the aging mice[4]. Ac-DEVD-CHO inhibited and/or postponed the development of photoreceptor cell damage in rats, as well as slows the disease's progression in rd gene-carrying mice, which typically experience retinal degeneration in their early years of life[2].
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Enzyme Assay |
Studies with peptide-based and macromolecular inhibitors of the caspase family of cysteine proteases have helped to define a central role for these enzymes in inflammation and mammalian apoptosis. A clear interpretation of these studies has been compromised by an incomplete understanding of the selectivity of these molecules. Here we describe the selectivity of several peptide-based inhibitors and the coxpox serpin CrmA against 10 human caspases. The peptide aldehydes that were examined (Ac-WEHD-CHO, Ac-DEVD-CHO, Ac-YVAD-CHO, t-butoxycarbonyl-IETD-CHO, and t-butoxycarbonyl-AEVD-CHO) included several that contain the optimal tetrapeptide recognition motif for various caspases. These aldehydes display a wide range of selectivities and potencies against these enzymes, with dissociation constants ranging from 75 pM to >10 microM. The halomethyl ketone benzyloxycarbonyl-VAD fluoromethyl ketone is a broad specificity irreversible caspase inhibitor, with second-order inactivation rates that range from 2.9 x 10(2) M-1 s-1 for caspase-2 to 2.8 x 10(5) M-1 s-1 for caspase-1. The results obtained with peptide-based inhibitors are in accord with those predicted from the substrate specificity studies described earlier. The cowpox serpin CrmA is a potent (Ki < 20 nM) and selective inhibitor of Group I caspases (caspase-1, -4, and -5) and most Group III caspases (caspase-8, -9, and -10), suggesting that this virus facilitates infection through inhibition of both apoptosis and the host inflammatory response[1].
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Cell Assay |
OCLs are incubated with RANKL and treated with 0.5 mM SIN for 24 hours, either with or without the particular caspase-3 inhibitor Ac-DEVD-CHO (10 μM). After the treatment, the cells are rinsed with PBS and stained for 15 min with 10 μM Hoechst 33258 dye. A fluorescent microscope is used to take pictures of the staining cells. By counting the number of cells with apoptotic nuclear condensation in each well, the differences are measured[4].
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Animal Protocol |
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References | |||
Additional Infomation |
Ac-Asp-Glu-Val-Asp-H is a tetrapeptide consisting of two L-aspartic acid residues, an L-glutamyl residue and an L-valine residue with an acetyl group at the N-terminal and with the C-terminal carboxy group reduced to an aldehyde. It is an inhibitor of caspase-3/7. It has a role as a protease inhibitor.
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Molecular Formula |
C20H30N4O11
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Molecular Weight |
502.47
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Exact Mass |
502.1911
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Elemental Analysis |
C, 47.81; H, 6.02; N, 11.15; O, 35.02
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CAS # |
169332-60-9
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Related CAS # |
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PubChem CID |
644345
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Sequence |
N-Acetyl-Asp-Glu-Val-Asp-al
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SequenceShortening |
Ac-DEVD-al
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Appearance |
White to off-white solid powder
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Density |
1.374g/cm3
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Boiling Point |
1021.1ºC at 760mmHg
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Flash Point |
571.3ºC
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Vapour Pressure |
0mmHg at 25°C
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Index of Refraction |
1.535
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LogP |
-2.6
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tPSA |
245.37
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SMILES |
CC(C)[C@@H](C(=O)N[C@@H](CC(=O)O)C=O)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CC(=O)O)NC(=O)C
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InChi Key |
UMBVAPCONCILTL-MRHIQRDNSA-N
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InChi Code |
InChI=1S/C20H30N4O11/c1-9(2)17(20(35)22-11(8-25)6-15(29)30)24-18(33)12(4-5-14(27)28)23-19(34)13(7-16(31)32)21-10(3)26/h8-9,11-13,17H,4-7H2,1-3H3,(H,21,26)(H,22,35)(H,23,34)(H,24,33)(H,27,28)(H,29,30)(H,31,32)/t11-,12-,13-,17-/m0/s1
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Chemical Name |
(4S)-4-[[(2S)-2-acetamido-3-carboxypropanoyl]amino]-5-[[(2S)-1-[[(2S)-1-carboxy-3-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-5-oxopentanoic acid
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Synonyms |
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
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Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
Solubility in Formulation 1: 100 mg/mL (199.02 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
 (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 1.9902 mL | 9.9508 mL | 19.9017 mL | |
5 mM | 0.3980 mL | 1.9902 mL | 3.9803 mL | |
10 mM | 0.1990 mL | 0.9951 mL | 1.9902 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.