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Ac-DEVD-CHO Sale

目录号 : GC32695

Ac-DEVD-CHO (Caspase-3 Inhibitor I, N-Ac-Asp-Glu-Val-Asp-CHO) is a potent 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 inhibition for caspase-2.

Ac-DEVD-CHO Chemical Structure

Cas No.:169332-60-9

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Sample solution is provided at 25 µL, 10mM.

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实验参考方法

Cell experiment:

OCLs are incubated with RANKL and treated with 0.5 mM SIN with or without the specific caspase-3 inhibitor Ac-DEVD-CHO (10 μM) for 24 h. At the end of the treatment, the cells are washed with PBS and are stained for 15 min with 10 μM Hoechst 33258 dye. Images of the staineing cells are captured with a fluorescent microscope. The differences are evaluated by counting the number of cells with apoptotic nuclear condensation in each well[4].

Animal experiment:

One hundred and two male mice are subjected to cecal ligation and puncture or sham operation. The animals are assigned into three equal groups (n=34) according to random number table: sham group, model group, and caspase-3 inhibitor (CI) group. Thirty minutes before CLP, Ac-DEVD-CHO (4 μg/g) is injected subcutaneously in CI group. The levels of blood urea nitrogen (BUN) and creatinine (Cr) are determined, and the concentrations of tumor necrosis factor-α (TNF-α), interleukins (IL-6 and IL-10) are measured by enzyme linked immunosorbent assay (ELISA), the renal cell apoptosis rate is determined by flow cytometry. The 4-day and 7-day survival rates of three groups of mice are observed[5].

References:

[1]. Garcia-Calvo M, et al.nhibition of human caspases by peptide-based and macromolecular inhibitors. J Biol Chem. 1998 Dec 4;273(49):32608-13.
[2]. Jinglin Wang, et al. A polysaccharide from Lentinus edodes inhibits human colon cancer cell proliferation and suppresses tumor growth in athymic nude mice. Oncotarget. 2017 Jan 3; 8(1): 610-623.
[3]. Junping Zhang, et al. Hypericin-mediated photodynamic therapy induces apoptosis of myoloma SP2/0 cells depended on caspase activity in vitro. Cancer Cell Int. 2015; 15: 58
[4]. Long-gang He, et al. Sinomenine induces apoptosis in RAW 264.7 cell-derived osteoclasts in vitro via caspase-3 activation. Acta Pharmacol Sin. 2014 Feb; 35(2): 203-210.
[5]. Liu LX, et al. The effect of caspase-3 inhibitor on the concentrations of serum inflammatory cytokines in sepsis related acute kidney injury induced by peritoneal cavity infection in mice. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Dec;22(12):736-9.

产品描述

Ac-DEVD-CHO (Caspase-3 Inhibitor I, N-Ac-Asp-Glu-Val-Asp-CHO) is a potent 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 inhibition for caspase-2.

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[1]. 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[2].

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[4]. 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[2].

[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.

Chemical Properties

Cas No. 169332-60-9 SDF
Canonical SMILES N-Acetyl-Asp-Glu-Val-Asp-al
分子式 C20H30N4O11 分子量 502.47
溶解度 Water : ≥ 50 mg/mL (99.51 mM) 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 1.9902 mL 9.9508 mL 19.9017 mL
5 mM 0.398 mL 1.9902 mL 3.9803 mL
10 mM 0.199 mL 0.9951 mL 1.9902 mL
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Research Update

Bcl-2△21 and Ac-DEVD-CHO Inhibit Death of Wheat Microspores

Front Plant Sci 2016 Dec 26;7:1931.PMID:28082995DOI:10.3389/fpls.2016.01931.

Microspore cell death and low green plant production efficiency are an integral obstacle in the development of doubled haploid production in wheat. The aim of the current study was to determine the effect of anti-apoptotic recombinant human B-cell lymphoma-2 (Bcl-2△21) and caspase-3-inhibitor (Ac-DEVD-CHO) in microspore cell death in bread wheat cultivars AC Fielder and AC Andrew. Induction medium containing Bcl-2△21 and Ac-DEVD-CHO yielded a significantly higher number of viable microspores, embryo-like structures and total green plants in wheat cultivars AC Fielder and AC Andrew. Total peroxidase activity was lower in Bcl-2△21 treated microspore cultures at 96 h of treatment compared to control and Ac-DEVD-CHO. Electron paramagnetic resonance study of total microspore protein showed a different scavenging activity for Bcl-2△21 and Ac-DEVD-CHO. Bcl-2△21 scavenged approximately 50% hydroxyl radical (HO•) formed, whereas Ac-DEVD-CHO scavenged approximately 20% of HO•. Conversely, reduced caspase-3-like activities were detected in the presence of Bcl-2△21 and Ac-DEVD-CHO, supporting the involvement of Bcl-2△21 and Ac-DEVD-CHO in increasing microspore viability by reducing oxidative stress and caspase-3-like activity. Our results indicate that Bcl-2△21 and Ac-DEVD-CHO protects cells from cell death following different pathways. Bcl-2△21 prevents cell damage by detoxifying HO• and suppressing caspase-3-like activity, while Ac-DEVD-CHO inhibits the cell death pathways by modulating caspase-like activity.

Dioscin Improves Pyroptosis in LPS-Induced Mice Mastitis by Activating AMPK/Nrf2 and Inhibiting the NF- κ B Signaling Pathway

Oxid Med Cell Longev 2020 Dec 30;2020:8845521.PMID:33488936DOI:10.1155/2020/8845521.

Dioscin, a natural steroid saponin, has been shown to have anti-inflammatory effects, but its protective mechanism against mastitis is still unknown. NLRP3 inflammasome and pyroptosis play important roles in the pathogenesis of many inflammatory diseases, including mastitis. The purpose of this study was to explore the effect of dioscin on lipopolysaccharide- (LPS-) induced mastitis in vivo and in vitro and its mechanism of action. In vivo experiments, dioscin can reduce the inflammatory lesions and neutrophil motility in mammary tissue. Moreover, dioscin also can reduce the production of proinflammatory factors such as interleukin-1 beta (IL-1β) and inhibit the activation of NLRP3 inflammasome in LPS-induced mice mastitis. In vitro experiments, the results showed that dioscin inhibited the inflammatory response and the activation of NLRP3 inflammasome, but the survival rate of mouse mammary epithelial cells (mMECs) induced by LPS+ATP is increased. Subsequently, the experiment convinces that dioscin can reduce LPS+ATP-induced mMEC pyroptosis by adding Ac-DEVD-CHO (a caspase-3 inhibitor). Further mechanistic studies demonstrate that dioscin can activate AMPK/Nrf2 to inhibit NLRP3/GSDMD-induced mMEC pyroptosis. In summary, this paper reveals a novel function of dioscin on mMEC pyroptosis and provides a new potential therapy of dioscin for the treatment and prevention of mastitis.

Effects of Z-VaD-Ala-Asp-Fluoromethyl Ketone (Z-VAD-FMK) and Acetyl-Asp-Glu-Val-Asp-Aldehyde(Ac-DEVD-CHO) on Inflammation and Mucus Secretion in Mice Exposed to Cigarette Smoke

Int J Chron Obstruct Pulmon Dis 2023 Feb 5;18:69-78.PMID:36777242DOI:10.2147/COPD.S385748.

Background and objectives: Smoking can lead to airway inflammation and mucus secretion through the nucleotide-binding domain-like receptor protein 3/caspase-1 pathway. In this study, z-VaD-Ala-Asp-fluoromethyl ketone(Z-VAD), a pan-caspase inhibitor, and acetyl-Asp-Glu-Val-Asp-aldehyde(Ac-DEVD), a caspase-3 inhibitor, were used to investigate the effect of caspase inhibitors on the expression of interleukin(IL)-1β and IL-8, airway inflammation, and mucus secretion in mice exposed to cigarette smoke(CS). Methods: Thirty-two C57BL/6J male mice were divided into a control group, Smoke group, Z-VAD group, and Ac-DEVD group. Except for the control group, the animals were all exposed to CS for three months. After the experiment, lung function was measured and hematoxylin and eosin staining and periodic acid-Schiff staining were performed. The levels of IL-1β, IL-8, and mucin 5ac(Muc5ac) in serum and bronchoalveolar lavage fluid(BALF) were determined by enzyme-linked immunosorbent assay. Results: Compared with the control group, the lung function of mice exposed to smoke was poorer, with a large number of inflammatory cells infiltrating around the airway, collapse of alveoli, expansion and fusion of distal alveoli, and formation of emphysema. The Z-VAD group was relieved compared with the smoke group. Airway inflammation was also reduced in the Ac-DEVD group compared with the Smoke group, but the degree of emphysema was not significantly improved. Although Z-VAD relieved airway inflammation and emphysema, Ac-DEVD only relieved inflammation. Z-VAD and Ac-DEVD decreased serum IL-1β and IL-8 levels. In BALF, IL-1β was decreased in Z-VAD group and IL-8 was highest in Smoke +Ac-DEVD group compared with control group and Ac-DEVD group. There was no significant difference in the expression of Muc5ac in serum. However, in BALF, levels of Muc5ac were higher in the smoking group and the lowest in the Ac-DEVD group. Conclusion: Mice exposed to smoke had decreased lung function and significant cilia lodging, epithelial cell shedding, and inflammatory cell infiltration, with significant emphysema formation. The pan-caspase inhibitor, Z-VAD, improved airway inflammation and emphysema lesions in the mice exposed to smoke and reduced IL-1β and IL-8 levels in serum. The caspase-3 inhibitor, Ac-DEVD, reduced airway inflammation, serum IL-1β and IL-8 levels, and Muc5ac levels in BALF, but it did not improve emphysema.

Amorphous alumina nanowire array efficiently delivers Ac-DEVD-CHO to inhibit apoptosis of dendritic cells

Chem Commun (Camb) 2014 Feb 7;50(10):1234-7.PMID:24336780DOI:10.1039/c3cc48088g.

To create an effective well-ordered delivery platform still remains a challenge. Herein we fabricate vertically aligned alumina nanowire arrays via atomic layer deposition templated by carbon nanotubes. Using these arrays, a caspase-3/7 inhibitor was delivered into DC 2.4 cells and blocked apoptosis, as confirmed by fluorescence microscopy.

Caspase-3 and its inhibitor Ac-DEVD-CHO in rat lens epithelial cell apoptosis induced by hydrogen in vitro

Chin Med J (Engl) 2003 Jul;116(7):1034-8.PMID:12890378doi

Objective: To investigate the role of caspase-3 and its inhibitor Ac-DEVD-CHO in rat lens epithelial cell apoptosis induced by hydrogen peroxide (H(2)O(2)) in vitro. Methods: Rat lenses were incubated in modified Eagle's medium containing 2 mmol/L H(2)O(2) to induce apoptosis in vitro. Apoptosis in lens epithelial cells was assessed by transmission electron microscopy and annexin V-propidium iodide (PI) double staining flow cytometry after 12, 24 and 48 h of incubation. The activity of caspase-3 was analyzed by western blotting. Results: Observations under transmission electron microscopy revealed that 2 mmol/L H(2)O(2) could effectively induce lens epithelial cell apoptosis in vitro. Caspase-3 activity increased during cell apoptosis and the peak measurement occurred at 24 h after treatment with H(2)O(2). Cell apoptosis was blocked by caspase-3 inhibitor Ac-DEVD-CHO. Conclusions: The activation of caspase-3 plays an important role in executing apoptosis in H(2)O(2)-treated lens epithelial cells and in the formation of cataract. The caspase-3 inhibitor Ac-DEVD-CHO may effectively prevent lens epithelial cell apoptosis caused by oxidative injury.