[CAS NO. 169332-60-9] Ac-DEVD-CHO

Name: Ac-DEVD-CHO
Brand: Arctom Scientific
SKU: SLK-S7901

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PRODUCTS SPECIFICATIONS [169332-60-9]

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Catalog

SLK-S7901

Brand

Selleck

CAS

169332-60-9

DESCRIPTION [169332-60-9]

Overview

MDL	MFCD00671412
Molecular Weight	502.47
Molecular Formula	C20H30N4O11
SMILES	CC([C@@](NC([C@](NC([C@](NC(C)=O)([H])CC(O)=O)=O)([H])CCC(O)=O)=O)([H])C(N[C@@](C=O)([H])CC(O)=O)=O)C

For research use only.

Storage

3 years,-20°C,powder
1 years,-80°C,in solvent

Shipping

Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Concentration Volume Mass	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
50 mM	0.0398 mL	0.1990 mL	0.3980 mL

Description

Ac-DEVD-CHO (Caspase-3 Inhibitor I, N-Ac-Asp-Glu-Val-Asp-CHO) is a potent aldehyde inhibitor of Group II caspases with values of 0.2 nM and 0.3 nM for for and , respectively. Weak inhibition for caspase-2.

Targets

In vitro

Ac-DEVD-CHO is a potent inhibitor of caspase-3 (Ki = 230 pM). In contrast, caspase-2 cleaves the tetrapeptide substrate poorly and is only weakly inhibited by this aldehyde (Ki = 1.7 μM). Group III caspases are broadly inhibited by Ac-DEVD-CHO with Ki values ranging from 1 to 300 nM. Inhibition of caspase-3 by Ac-DEVD-CHO in isolated working-heart rat model significantly improves post-ischemic contractile recovery of stunned myocardium, even when given after the onset of ischemia. The mechanism(s) of protection by Ac-DEVD-CHO appear to be independent of apoptosis. Troponin I cleavage was not inhibited by Ac-DEVD-CHO.

In vivo

Ac-DEVD-CHO administered at the time of MI results in a 61% reduction in activated caspase-3 expression in cardiomyocytes (p<0.05), and an 84% reduction in cardiomyocyte apoptosis in the young animals. However, in the aging mice, caspase inhibition had no effect on activated caspase-3 expression or cardiomyocyte apoptosis. Ac-DEVD-CHO suppressed and/or delayed the progression of photoreceptor cell damage in rats and delays disease progression in rd gene-carring mice, which normally develop retinal degeneration early in life.

References

[1] Garcia-Calvo M, et al. J Biol Chem. 1998, 273(49):32608-13.
[2] Ruetten H, et al. J Am Coll Cardiol. 2001, 38(7):2063-70.
[3] Gyrd-Hansen M, et al. Mol Cell Biol. 2006, 26(21):7880-91.
[4] Boyle AJ, et al. Cardiovasc Ther. 2013, 31(6):e102-10.
[5] Airo Tsubura, et al. Acta Histochem. 2003, 36(4):263-270.