GPi 688

Allosteric glycogen phosphorylase inhibitor CAS# 918902-32-6

GPi 688

Catalog No. BCC6091----Order now to get a substantial discount!

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GPi 688: 5mg $138 In Stock
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Quality Control of GPi 688

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Chemical structure

GPi 688

3D structure

Chemical Properties of GPi 688

Cas No. 918902-32-6 SDF Download SDF
PubChem ID 10477191 Appearance Powder
Formula C19H18ClN3O4S M.Wt 419.88
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO and to 25 mM in ethanol
Chemical Name 2-chloro-N-[1-[(2R)-2,3-dihydroxypropyl]-2-oxo-3,4-dihydroquinolin-3-yl]-6H-thieno[2,3-b]pyrrole-5-carboxamide
SMILES C1C(C(=O)N(C2=CC=CC=C21)CC(CO)O)NC(=O)C3=CC4=C(N3)SC(=C4)Cl
Standard InChIKey UICNBXVDHCBKCE-PUODRLBUSA-N
Standard InChI InChI=1S/C19H18ClN3O4S/c20-16-7-11-6-13(22-18(11)28-16)17(26)21-14-5-10-3-1-2-4-15(10)23(19(14)27)8-12(25)9-24/h1-4,6-7,12,14,22,24-25H,5,8-9H2,(H,21,26)/t12-,14?/m1/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 GPi 688

DescriptionAllosteric glycogen phosphorylase inhibitor; acts at the indole site of glycogen phosphorylase. Inhibits glucagon-mediated hyperglycemia in vivo in the rat.

GPi 688 Dilution Calculator

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GPi 688 Molarity Calculator

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Preparing Stock Solutions of GPi 688

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.3816 mL 11.9082 mL 23.8163 mL 47.6327 mL 59.5408 mL
5 mM 0.4763 mL 2.3816 mL 4.7633 mL 9.5265 mL 11.9082 mL
10 mM 0.2382 mL 1.1908 mL 2.3816 mL 4.7633 mL 5.9541 mL
50 mM 0.0476 mL 0.2382 mL 0.4763 mL 0.9527 mL 1.1908 mL
100 mM 0.0238 mL 0.1191 mL 0.2382 mL 0.4763 mL 0.5954 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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References on GPi 688

An assessment of the in vivo efficacy of the glycogen phosphorylase inhibitor GPi688 in rat models of hyperglycaemia.[Pubmed:17934512]

Br J Pharmacol. 2007 Dec;152(8):1239-47.

BACKGROUND AND PURPOSE: Studies in cultured hepatocytes demonstrate glycogen synthase (GS) activation with glycogen phosphorylase (GP) inhibitors. The current study investigated whether these phenomena occurred in vivo using a novel GP inhibitor. EXPERIMENTAL APPROACH: An allosteric GP inhibitor, GPi688, was evaluated against both glucagon-mediated hyperglycaemia and oral glucose challenge-mediated hyperglycaemia to determine the relative effects against GP and GS in vivo. KEY RESULTS: In rat primary hepatocytes, GPi688 inhibited glucagons-mediated glucose output in a concentration dependent manner. Additionally GP activity was reduced and GS activity increased seven-fold. GPi688 inhibited glucagon-mediated hyperglycaemia in both Wistar (65%) & obese Zucker (100%) rats and demonstrated a long duration of action in the Zucker rat. The in vivo efficacy in the glucagon challenge model could be predicted by the equation; % glucagon inhibition=56.9+34.3[log ([free plasma]/rat IC50)], r=0.921). GPi688 also reduced the blood glucose of obese Zucker rats after a 7 h fast by 23%. In an oral glucose tolerance test in Zucker rats, however, GPi688 was less efficacious (7% reduction) than a glycogen synthase kinase-3 (GSK-3) inhibitor (22% reduction), despite also observing activation (by 45%) of GS in vivo. CONCLUSIONS AND IMPLICATIONS: Although GP inhibition can inhibit hyperglycaemia mediated by increased glucose production, the degree of GS activation induced by allosteric GP inhibitors in vivo, although discernible, is insufficient to increase glucose disposal. The data suggests that GP inhibitors might be more effective clinically against fasting rather than prandial hyperglycaemic control.

Sensitivity of glycogen phosphorylase isoforms to indole site inhibitors is markedly dependent on the activation state of the enzyme.[Pubmed:17016495]

Br J Pharmacol. 2006 Nov;149(6):775-85.

BACKGROUND AND PURPOSE: Inhibition of hepatic glycogen phosphorylase is a potential treatment for glycaemic control in type 2 diabetes. Selective inhibition of the liver phosphorylase isoform could minimize adverse effects in other tissues. We investigated the potential selectivity of two indole site phosphorylase inhibitors, GPi688 and GPi819. EXPERIMENTAL APPROACH: The activity of glycogen phosphorylase was modulated using the allosteric effectors glucose or caffeine to promote the less active T state, and AMP to promote the more active R state. In vitro potency of indole site inhibitors against liver and muscle glycogen phosphorylase a was examined at different effector concentrations using purified recombinant enzymes. The potency of GPi819 was compared with its in vivo efficacy at raising glycogen concentrations in liver and muscle of Zucker (fa/fa) rats. KEY RESULTS: In vitro potency of indole site inhibitors depended upon the activity state of phosphorylase a. Both inhibitors showed selectivity for liver phosphorylase a when the isoform specific activities were equal. After 5 days dosing of GPi819 (37.5 micromol kg(-1)), where free compound levels in plasma and tissue were at steady state, glycogen elevation was 1.5-fold greater in soleus muscle than in liver (P < 0.05). CONCLUSIONS AND IMPLICATIONS: The in vivo selectivity of GPi819 did not match that seen in vitro when the specific activities of phosphorylase a isoforms are equal. This suggests T state promoters may be important physiological regulators in skeletal muscle. The greater efficacy of indole site inhibitors in skeletal muscle has implications for the overall safety profile of such drugs.

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