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Caspase-3/7 Inhibitor I

Caspase-3/7 inhibitor CAS# 220509-74-0

Caspase-3/7 Inhibitor I

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Product Name & Size Price Stock
Caspase-3/7 Inhibitor I:10mg $257.00 In stock
Caspase-3/7 Inhibitor I:20mg $437.00 In stock
Caspase-3/7 Inhibitor I:50mg $1028.00 In stock
Caspase-3/7 Inhibitor I:100mg $1799.00 In stock
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Chemical structure

Caspase-3/7 Inhibitor I

3D structure

Chemical Properties of Caspase-3/7 Inhibitor I

Cas No. 220509-74-0 SDF Download SDF
PubChem ID 9840223 Appearance Powder
Formula C14H16N2O5S M.Wt 324.4
Type of Compound N/A Storage Desiccate at -20°C
Solubility >16.2mg/mL in DMSO
Chemical Name 5-[(2S)-2-(methoxymethyl)pyrrolidin-1-yl]sulfonyl-1H-indole-2,3-dione
SMILES COCC1CCCN1S(=O)(=O)C2=CC3=C(C=C2)NC(=O)C3=O
Standard InChIKey SLQMNVJNDYLJSF-VIFPVBQESA-N
Standard InChI InChI=1S/C14H16N2O5S/c1-21-8-9-3-2-6-16(9)22(19,20)10-4-5-12-11(7-10)13(17)14(18)15-12/h4-5,7,9H,2-3,6,8H2,1H3,(H,15,17,18)/t9-/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 Caspase-3/7 Inhibitor I

DescriptionA potent, cell-permeable, and specific, reversible inhibitor of caspase-3 (Ki = 60 nM) and caspase-7 (Ki = 170 nM).
TargetsCaspase-3Caspase-7    
IC5060nM170nM    

Protocol

Cell experiment: [1]

Cell lines

Human Jurkat T 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

50 μM

Applications

Cells were treated with camptothecin to induce cell death, and the ability of the compound to inhibit cell death was assessed by FACS analysis. A good correlation exists between relative cell-based activities of the compound with its in vitro isolated caspase 3 or 7 inhibition activites. The compound exhibited 54% inhibition of apoptosis at 50 μM and 22% at 10 μM.

Animal experiment:

Animal models

Dosage form

Application

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] Lee D, Long S A, Murray J H, et al. Potent and selective nonpeptide inhibitors of caspases 3 and 7. Journal of medicinal chemistry, 2001, 44(12): 2015-2026.

Caspase-3/7 Inhibitor I Dilution Calculator

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Preparing Stock Solutions of Caspase-3/7 Inhibitor I

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.0826 mL 15.4131 mL 30.8261 mL 61.6523 mL 77.0654 mL
5 mM 0.6165 mL 3.0826 mL 6.1652 mL 12.3305 mL 15.4131 mL
10 mM 0.3083 mL 1.5413 mL 3.0826 mL 6.1652 mL 7.7065 mL
50 mM 0.0617 mL 0.3083 mL 0.6165 mL 1.233 mL 1.5413 mL
100 mM 0.0308 mL 0.1541 mL 0.3083 mL 0.6165 mL 0.7707 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 Caspase-3/7 Inhibitor I

1. Tissue inhibitor of metalloproteinases-3 moderates the proinflammatory status of macrophages. Am J Respir Cell Mol Biol. 2013 Nov;49(5):768-77. doi: 10.1165/rcmb.2012-0377OC.
Abstract
TIMP-3 is involved in the regulation of inflammation where, in the absence of TIMP3, macrophages are more likely to be differentiated into proinflammatory (M1) cells.
2. [X-linked inhibitor of apoptosis protein (XIAP) and Survivin suppression on human pancreatic cancer cells Panc-1 proliferation and chemosensitivety]. Beijing Da Xue Xue Bao. 2013 Apr 18;45(2):242-9.
Abstract
The effects of inhibition of XIAP, Survivin or both on cell proliferation and chemosensitivity of Panc-1 cells have been investigated and compared.
3. [Effect of aurora kinase B inhibitor AZD1152 in the treatment of cisplatin-resistant ovarian carcinoma]. Zhonghua Fu Chan Ke Za Zhi. 2013 Jan;48(1):46-50.
Abstract
The effect of AZD1152 alone or in combination with cisplatin has been investigated in the treatment of cisplatin-resistant ovarian carcinoma.
4. Targeting X-linked inhibitor of apoptosis protein inhibits pancreatic cancer cell growth through p-Akt depletion. World J Gastroenterol. 2012 Jun 21;18(23):2956-65. doi: 10.3748/wjg.v18.i23.2956.
Abstract
The regulation of XIAP gene by lentivirus-mediated shRNA has been investigated for its effect in the treatment of pancreatic cancer.

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Background on Caspase-3/7 Inhibitor I

Caspase-3/7 inbibitor I is a potent, reversible, isatin sulfonamide-based inhibitor of caspase-3 (KI(app) = 60 nM) and caspase-7 (KI(app) = 170 nM). Is a weaker inhibitor of caspase-9 (Ki(app) = 3.1 mM). It Has only a trivial effect (Ki(app) >25 mM) on the activities of caspase-1, caspase-2, caspase-4, caspase-6, and caspase-8. It has been shown to inhibit apoptosis in camptothecin treated Jurkat cells (IC50 ~50 µM). Also it has been reported to inhibit apoptosis in chondrocytes (44% inhibition at 10 µM and 98% inhibition at 50 µM). Selectivity for caspases-3 and 7 involves unique hydrophobic residues in the S2 pocket surrounding the catalytic cysteine residue. [1] [2] In some systems inhibition of caspases-3 and -7 can prevent apoptosis and may therefore have important therapeutic implications. [3]

A potent, cell-permeable, and specific, reversible inhibitor of caspase-3 (Ki = 60 nM) and caspase-7 (Ki = 170 nM).

References:
1. Lee, D., et al. 2001. J. Med. Chem. 44, 2015.
2. Lee, D., et al. 2000. J. Biol. Chem. 275, 16007.
3. Clements, K. M., Burton‐Wurster, N., Nuttall, M. E., & Lust, G. (2005). Caspase‐3/7 inhibition alters cell morphology in mitomycin‐c treated chondrocytes. Journal of cellular physiology, 205(1), 133-140.

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References on Caspase-3/7 Inhibitor I

Synthesis of 7-halogenated isatin sulfonamides: nonradioactive counterparts of caspase-3/-7 inhibitor-based potential radiopharmaceuticals for molecular imaging of apoptosis.[Pubmed:25358116]

J Med Chem. 2014 Nov 26;57(22):9383-95.

N-Alkylated (S)-7-halogen-5-[1-(2-methoxymethylpyrrolidinyl)sulfonyl]isatins were developed as a new group of nonradioactive reference compounds for future radiotracers. Inhibitor potency studies of these compounds suggest that the binding pockets readily accommodate both the 7-halogen substituents and aliphatic side chains (methyl to n-butyl) as well as some omega-fluorinated analogues (3-fluoropropyl and 4-fluorobutyl) at the isatin nitrogen. Indeed, compared to the halogen free parent compounds, some 7-halogenated derivatives exhibited slightly improved inhibitory potencies with IC50 values up to 2.6 nM (caspase-3) and 3.3 nM (caspase-7), respectively. Moreover, the 7-position of isatin, a potential cytochrome P450 hydroxylation site, was substituted by I, Br, Cl, and F to potentially enhance the metabolic stability of isatin sulfonamides. As an example, the radiotracer [(18)F]39 that was produced by (19)F/(18)F isotope exchange was shown to be stable in human blood serum after incubation at 37 degrees C for at least 90 min.

A novel nonpeptidic caspase-3/7 inhibitor, (S)-(+)-5-[1-(2-methoxymethylpyrrolidinyl)sulfonyl]isatin reduces myocardial ischemic injury.[Pubmed:12450570]

Eur J Pharmacol. 2002 Dec 5;456(1-3):59-68.

The efficacy of a novel, nonpeptidic, caspase 3/7-selective inhibitor, (S)-(+)-5-[1-(2-methoxymethylpyrrolidinyl)sulfonyl]isatin (MMPSI) for reducing ischemic injury in isolated rabbit hearts or cardiomyocytes was evaluated. MMPSI (0.1-10 microM) evoked a concentration-dependent reduction in infarct size (up to 56% vs. control; IC(50)=0.2 microM). Furthermore, apoptosis (DNA laddering, soluble nucleosomes) was reduced in the ischemic area-at-risk. MMPSI inhibited recombinant human caspase-3 with an IC(50)=1.7 microM. Apoptosis in H9c2 cells after 16-h simulated ischemia and 2-h simulated reperfusion was significantly reduced by MMPSI in a concentration-dependent manner (IC(50)=0.5 microM); similar effects were observed in isolated adult rabbit cardiomyocytes (IC(50)=1.5 microM). These data support an important role for caspase-3/7 in mediating myocardial ischemic injury. Furthermore, these data indicate that cardioprotection via caspase-3/7 inhibition is attainable via a small molecule (nonpeptidic) inhibitor, a necessary step in making this approach therapeutically viable.

Combination of the histone deacetylase inhibitor depsipeptide and 5-fluorouracil upregulates major histocompatibility complex class II and p21 genes and activates caspase-3/7 in human colon cancer HCT-116 cells.[Pubmed:27509880]

Oncol Rep. 2016 Oct;36(4):1875-85.

Epigenetic anticancer drugs such as histone deacetylase (HDAC) inhibitors have been combined with existing anticancer drugs for synergistic or additive effects. In the present study, we found that a very low concentration of depsipeptide, an HDAC inhibitor, potentiated the antitumor activity of 5-fluorouracil (5-FU) in a human colon cancer cell model using HCT-116, HT29, and SW48 cells via the inhibition of colony formation ability or cellular viability. Exposure to a combination of 5-FU (1.75 microM) and 1 nM depsipeptide for 24 and 48 h resulted in a 3- to 4-fold increase in activated caspase-3/7, while 5-FU alone failed to activate caspase-3/7. Microarray and subsequent gene ontology analyses revealed that compared to 5-FU or depsipeptide alone, the combination treatment of 5-FU and depsipeptide upregulated genes related to cell death and the apoptotic process consistent with the inhibition of colony formation and caspase-3/7 activation. These analyses indicated marked upregulation of antigen processing and presentation of peptide or polysaccharide antigen via major histocompatibility complex (MHC) class (GO:0002504) and MHC protein complex (GO:0042611). Compared with vehicle controls, the cells treated with the combination of 5-FU and depsipeptide showed marked induction (3- to 8.5-fold) of expression of MHC class II genes, but not of MHC class I genes. Furthermore, our global analysis of gene expression, which was focused on genes involved in the molecular regulation of MHC class II genes, showed enhancement of pro-apoptotic PCAF and CIITA after the combination of 5-FU and depsipeptide. These results may indicate a closer relationship between elevation of MHC class II expression and cellular apoptosis induced by the combination of depsipeptide and 5-FU. To the best of our knowledge, this is the first study to report that the combination of 5-FU and depsipeptide induces human colon cancer cell apoptosis in a concerted manner with the induction of MHC class II gene expression.

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