CP 471474

Broad spectrum MMP inhibitor CAS# 210755-45-6

CP 471474

Catalog No. BCC2373----Order now to get a substantial discount!

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Quality Control of CP 471474

Number of papers citing our products

Chemical structure

CP 471474

3D structure

Chemical Properties of CP 471474

Cas No. 210755-45-6 SDF Download SDF
PubChem ID 9907286 Appearance Powder
Formula C16H16FN2O5S M.Wt 367.4
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO
Chemical Name 2-[[4-(4-fluorophenoxy)phenyl]sulfonylamino]-N-hydroxy-2-methylpropanamide
SMILES CC(C)(C(=O)NO)NS(=O)(=O)C1=CC=C(C=C1)OC2=CC=C(C=C2)F
Standard InChIKey QCOQJYRPDUMCNP-UHFFFAOYSA-N
Standard InChI InChI=1S/C16H17FN2O5S/c1-16(2,15(20)18-21)19-25(22,23)14-9-7-13(8-10-14)24-12-5-3-11(17)4-6-12/h3-10,19,21H,1-2H3,(H,18,20)
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 CP 471474

DescriptionBroad spectrum MMP inhibitor (IC50 values are 0.7, 0.9, 13, 16 and 1170 nM for MMP-2, MMP-13, MMP-9, MMP-3 and MMP-1 respectively). Attenuates early left ventricular dilation after experimental myocardial infarction in mice.

CP 471474 Dilution Calculator

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CP 471474 Molarity Calculator

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Preparing Stock Solutions of CP 471474

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.7218 mL 13.6091 mL 27.2183 mL 54.4366 mL 68.0457 mL
5 mM 0.5444 mL 2.7218 mL 5.4437 mL 10.8873 mL 13.6091 mL
10 mM 0.2722 mL 1.3609 mL 2.7218 mL 5.4437 mL 6.8046 mL
50 mM 0.0544 mL 0.2722 mL 0.5444 mL 1.0887 mL 1.3609 mL
100 mM 0.0272 mL 0.1361 mL 0.2722 mL 0.5444 mL 0.6805 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.

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Background on CP 471474

Broad spectrum MMP inhibitor (IC50 values are 0.7, 0.9, 13, 16 and 1170 nM for MMP-2, MMP-13, MMP-9, MMP-3 and MMP-1 respectively). Attenuates early left ventricular dilation after experimental myocardial infarction in mice.

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References on CP 471474

Recent perspectives of cerebral palsy (CP) in children: a review.[Pubmed:28353322]

Minerva Pediatr. 2017 Mar 27. pii: S0026-4946.17.04880-0.

The movement and posture disorder of cerebral palsy (CP) is presumed to mainly be a consequence of the motor disorder, but accompanying disturbances with sensations and perception have also been suggested to influence motor function. The heterogeneous condition of cerebral palsy (CP) is caused by an injury to the immature brain affecting movement and posture development. The attainment of standing and walking can be difficult and an assistive device to accomplish the tasks may be required for some children with CP. In this review, we enlightened the role of possible sensory and perceptual disturbances for standing difficulties in children with CP.

Mechanism study of humic acid functional groups for Cr(VI) retention: Two-dimensional FTIR and (13)C CP/MAS NMR correlation spectroscopic analysis.[Pubmed:28355575]

Environ Pollut. 2017 Jun;225:86-92.

Undissolved humic acid (HA) is known to substantially effect the migration and transformation of hexavalent chromium [Cr(VI)] in soils. The mechanisms of Cr(VI) retention in soils by undissolved HA have been reported; however, past studies are inconclusive about the types of HA functional groups that are involved in Cr(VI) retention and the retention mechanisms. Utilizing a two-dimensional correlation spectroscopy (2DCOS) analysis for FTIR and (13)C CP/MAS NMR, this study investigated the variations of HA function groups and molecular structures after reactions with aqueous Cr(VI) under different pH conditions. Based on the changing sequence of functional groups interpreted from the 2DCOS results, a four-step mechanism for Cr(VI) retention was determined as follows: (1) electrostatic adsorption of Cr(VI) to HA surface, (2) complexation of adsorbed Cr(VI) by carboxyl and ester, (3) reduction of complexed Cr(VI) to Cr(III) by phenol and polysaccharide, and (4) complexation of reduced Cr(III) by carboxylic groups. These functional groups that are involved in Cr(VI) retention were determined to occur in aromatic domains.

ACTIVLIM-CP a new Rasch-built measure of global activity performance for children with cerebral palsy.[Pubmed:28341237]

Res Dev Disabil. 2017 Jan;60:285-294.

OBJECTIVE: Children with cerebral palsy (CP) often have upper extremity (UE) and lower extremity (LE) impairments. While tools measuring separately UE and LE abilities are currently used, activities in which UE and LE are used in combination - numerous in everyday life - cannot be assessed because no instrument allows capturing global activity performance in children with CP. This study aimed to develop a clinical tool for measuring their global activity performance using the Rasch model. STUDY DESIGN: The caregivers of 226 children with CP (2-18 years old) answered a 154-item experimental questionnaire. Within 4-6 weeks, 129 of them filled in the questionnaire a second time. Responses were analyzed using the Rasch RUMM2020 software. RESULTS: The final 43 item scale presented a high reliability (R=0.98) and reproducibility (R=0.97). The item difficulty hierarchy was consistent over time and did not vary according to age, gender, or clinical form, allowing the follow-up of children from 2 to 18 years old. CONCLUSIONS: ACTIVLIM-CP is a unidimensional scale specifically developed to measure global activity performance in children with CP providing a reliable tool to follow children's evolution and document changes related to neurorehabilitation, especially where a combination of UE and LE is targeted. Its responsiveness is still to be tested.

Differences in inflammation, MMP activation and collagen damage account for gender difference in murine cardiac rupture following myocardial infarction.[Pubmed:17689559]

J Mol Cell Cardiol. 2007 Nov;43(5):535-44.

Cardiac rupture remains a fatal complication of acute myocardial infarction (MI) with its mechanism partially understood. We hypothesized that damage to the collagen matrix of infarcted myocardium is the central mechanism of rupture and therefore responsible for the difference in the incidence of rupture between genders. We examined left ventricular (LV) remodeling during the acute phase post-MI in 129sv mice. Following induction of MI, we monitored rupture events and assessed the extent of LV remodeling by echocardiography. Muscle tensile strength, content of insoluble and soluble collagen, expression and activity of matrix metalloproteinases (MMPs) and density of inflammatory cells were determined in the infarcted and non-infarcted myocardium. We then tested the effects of MMP inhibition on rupture. Compared to female mice, males with MI displayed greater extent of LV remodeling, reduced muscle tensile strength, loss of insoluble collagen, local inflammatory response and MMP-9 activation, changes associated with a 3 times higher incidence of rupture than in females. MMP-9 expression by circulating blood mononuclear cells was also increased in male mice with acute MI. Treatment of male mice with an MMP inhibitor reduced MMP activity and halved rupture incidence. Our findings demonstrate that the differences in the severity of inflammation, MMP activation and damage to collagen matrix account for gender difference in cardiac rupture. Our study illustrates the breakdown of fibril collagen as a central mechanism of cardiac rupture.

Selective matrix metalloproteinase inhibition reduces left ventricular remodeling but does not inhibit angiogenesis after myocardial infarction.[Pubmed:11839633]

Circulation. 2002 Feb 12;105(6):753-8.

BACKGROUND: Broad inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling after myocardial infarction (MI). However, it is not clear if selective MMP inhibition strategies will be effective or if MMP inhibition will impair angiogenesis after MI. METHODS AND RESULTS: We used a selective MMP inhibitor (MMPi) that does not inhibit MMP-1 in rabbits, which, like humans but unlike rodents, express MMP-1 as a major collagenase. On day 1 after MI, rabbits were randomized to receive either inhibitor (n=10) or vehicle (n=8). At 4 weeks after MI, there were no differences in infarct size or collagen fractional area. However, MMPi reduced ventricular dilation. The increase in end-diastolic dimension from day 1 to week 4 was 3.1+/-0.5 mm for vehicle versus 1.3+/-0.3 mm for MMPi (P<0.01). The increase in end-systolic dimension was 2.8+/-0.5 mm for vehicle and 1.3+/-0.4 mm for MMPi (P<0.05). Furthermore, MMPi reduced infarct wall thinning; the minimal infarct thickness was 0.8+/-0.1 mm for vehicle and 1.6+/-0.3 mm for MMPi (P<0.05). Interestingly, the MMPi group had increased numbers of vessels in the subendocardial layer of the infarct; the number of capillaries was increased in the subendocardial layer (46+/-4 vessels/field versus 17+/-3 vessels/field for vehicle; P<0.001), and the number of arterioles was also increased (4.0+/-0.8 vessels/field versus 2.0+/-0.4 vessels/field for vehicle; P<0.05). CONCLUSIONS: MMP inhibition attenuates left ventricular remodeling even when the dominant collagenase MMP-1 is not inhibited; furthermore, this selective MMP inhibition appears to increase rather than decrease neovascularization in the subendocardium.

Matrix metalloproteinase inhibition attenuates early left ventricular enlargement after experimental myocardial infarction in mice.[Pubmed:10368126]

Circulation. 1999 Jun 15;99(23):3063-70.

BACKGROUND: Extracellular matrix synthesis and degradation contribute to the morphological changes that occur after myocardial infarction (MI). METHODS AND RESULTS: We tested the hypothesis that inhibition of matrix metalloproteinases (MMPs) attenuates left ventricular remodeling in experimental MI. Seventy-one male FVB mice that survived ligation of the left anterior coronary artery were randomized to a broad-spectrum MMP inhibitor (CP-471,474) or placebo by gavage. Echocardiographic studies were performed before randomization (within 24 hours of surgery) and 4 days later and included short-axis imaging at the midpapillary and apical levels. Infarction as defined by wall motion abnormality was achieved in 79% of the procedures (n=56), and mortality rate during the 4-day protocol was 23% (9 of 36 on treatment vs 7 of 35 on placebo; P=NS). Baseline end-diastolic and end-systolic dimensions and areas were similar (P=NS) between treated and placebo groups. At follow-up, infarcted mice allocated to MMP inhibitor had significantly smaller increases in end-systolic and end-diastolic dimensions and areas at both midpapillary and apical levels compared with infarcted mice allocated to placebo (all P<0.05). In addition, infarcted animals that received MMP inhibitor had no change in fractional shortening (-3+/-13%), whereas animals that received placebo had a decrease in fractional shortening (-12+/-12%) (P<0.05). In an analysis stratified by baseline end-diastolic area, the effects of MMP inhibition on the changes in end-systolic area and end-diastolic area were most prominent in animals that had more initial left ventricular dilatation (both P<0.05). CONCLUSIONS: -Administration of an MMP inhibitor attenuates early left ventricular dilation after experimental MI in mice. Further studies in genetically altered mice and other models will improve understanding of the role of MMPs in left ventricular remodeling.

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