EnterostatinCAS# 117830-79-2 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 117830-79-2 | SDF | Download SDF |
PubChem ID | 3082883 | Appearance | Powder |
Formula | C21H36N8O6 | M.Wt | 496.57 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 0.70 mg/ml in sterile water | ||
Chemical Name | (2S)-2-[[(2S)-1-[2-[[(2S)-1-[(2S)-2-aminopropanoyl]pyrrolidine-2-carbonyl]amino]acetyl]pyrrolidine-2-carbonyl]amino]-5-(diaminomethylideneamino)pentanoic acid | ||
SMILES | CC(C(=O)N1CCCC1C(=O)NCC(=O)N2CCCC2C(=O)NC(CCCN=C(N)N)C(=O)O)N | ||
Standard InChIKey | ITZMJCSORYKOSI-AJNGGQMLSA-N | ||
Standard InChI | InChI=1S/C21H36N8O6/c1-12(22)19(33)29-10-4-6-14(29)17(31)26-11-16(30)28-9-3-7-15(28)18(32)27-13(20(34)35)5-2-8-25-21(23)24/h12-15H,2-11,22H2,1H3,(H,26,31)(H,27,32)(H,34,35)(H4,23,24,25)/t12-,13-,14-,15-/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. |
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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. |
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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. |
Description | N' terminal peptide fragment of procolipase that binds to the β-subunit of F1-ATPase. Activates the ERK and cAMP signaling pathways, and downregulates expression of Krüppel-like factor 4 (KLF4) and agouti-related peptide (AgRP) in vitro. Inhibits insulin secretion from pancreatic β-cells by downregulating expression of dynamin2 and altering protein trafficking. Reduces dietary fat intake via activation of CCK1, induces satiety, enhances memory-consolidation and exhibits hypocholesterolemic activity in vivo. Orally active. |
Enterostatin Dilution Calculator
Enterostatin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.0138 mL | 10.0691 mL | 20.1381 mL | 40.2763 mL | 50.3454 mL |
5 mM | 0.4028 mL | 2.0138 mL | 4.0276 mL | 8.0553 mL | 10.0691 mL |
10 mM | 0.2014 mL | 1.0069 mL | 2.0138 mL | 4.0276 mL | 5.0345 mL |
50 mM | 0.0403 mL | 0.2014 mL | 0.4028 mL | 0.8055 mL | 1.0069 mL |
100 mM | 0.0201 mL | 0.1007 mL | 0.2014 mL | 0.4028 mL | 0.5035 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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Enterostatin deficiency increases serum cholesterol but does not influence growth and food intake in mice.[Pubmed:19622781]
Am J Physiol Endocrinol Metab. 2009 Oct;297(4):E856-65.
A pentapeptide released from procolipase, Enterostatin, selectively attenuates dietary fat intake when administered peripherally or centrally. Enterostatin may act through the afferent vagus nerve and in the hypothalamus and amygdala, primarily in the central nucleus of the amygdala. To investigate the physiological role of endogenous Enterostatin, we created an Enterostatin-deficient, colipase-sufficient (Ent(-/-)) mouse. Ent(-/-) mice are viable, normally active, and fertile. They exhibit normal growth on low-fat and high-fat diets. Furthermore, Ent(-/-) mice develop diet-induced obesity, as do Ent(+/+) mice, and have normal responses to a two-macronutrient choice diet and to a switch from a high-fat to a low-fat diet. Levels of total serum (P = 0.004) and non-HDL (P
Effects of dietary fat and enterostatin on dopamine and 5-hydroxytrytamine release from rat striatal slices.[Pubmed:20599830]
Brain Res. 2010 Aug 19;1349:48-55.
Studies have demonstrated defects of DA and 5HT neurotransmission in dietary fat induced obese animals. In the present study, we used a perfusion system to assay the release of DA and 5HT from striatal slices preloaded with [(3)H]-DA or [(3)H]-5HT. The release of both DA and 5HT from striatal slices of rats fed a high fat diet for 10 days, but not 3 days, was reduced when compared to striatal slices taken from rats fed a low fat diet. Enterostatin, an endogenous pentapeptide inhibits dietary fat intake when administered peripherally and centrally in animals. The central mechanism for the action of Enterostatin is not yet determined even though several mechanisms have been suggested. We have shown that Enterostatin enhanced [(3)H]-DA release, but not [(3)H]-5HT release from striatal slices of rats that had been adapted to high fat diet for 10 days. The Enterostatin-induced increase in [(3)H]-DA release was blocked by nomifensine. Enterostatin did not alter [(3)H]-DA or [(3)H]-5HT release from striatal slices of rats adapted to high fat or low fat diet feeding for 3 days. These findings suggest that Enterostatin may inhibit dietary fat intake by blocking dopamine reuptake transport to increase central striatal DA release from rats that have acquired diminished dopamine signal after an adaptive period of fat consumption.
Effect of central enterostatin on fat intake in neonatal chicks.[Pubmed:23178475]
Neurosci Lett. 2013 Jan 15;533:60-4.
Enterostatin, a gut-brain pentapeptide cleaved from procolipase has been shown to inhibit fat intake in rodents after both peripheral and central administration. In this study, the effect of intracerebroventricular (ICV) injection of Enterostatin on fat intake was investigated in neonatal chicks. In Experiment 1, 3-h-fasted chicks fed a low-fat diet were injected with the various doses of Enterostatin. Experiment 2 was similar to experiment 1 except that the birds were fasted overnight. In Experiment 3, the 3-h-fasted and in Experiment 4, the overnight fasted chicks adapted to a high-fat diet received different doses of Enterostatin. ICV injection of Enterostatin caused a dose-dependent increase in high-fat diet intake in 3-h-fasted chicks whereas a decrease in high-fat intake was observed in chicks that were fasted overnight. However, low-fat diet intake was not affected by Enterostatin in either 3-h or overnight fasted chicks. These results suggest that Enterostatin acts within the brain of chicks to influence fat intake. It appears that in chicks, the eating effect of Enterostatin has a biphasic nature similar to those seen in rodents.