Alrestatin (sodium) - CAS 51876-97-2
Catalog number: 51876-97-2
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C14H8NNaO4
Molecular Weight:
277.21
COA:
Inquire
Targets:
Aldose Reductase
Description:
Alrestatin sodium is a specific inhibitor of aldose reductase (IC50 = 148 μM).
Purity:
≥98%
Appearance:
White crystalline solid
Synonyms:
Sodium;2-(1,3-dioxobenzo[de]isoquinolin-2-yl)acetate;
Solubility:
Soluble in DMSO
Storage:
Store at -20 °C
MSDS:
Inquire
Application:
A specific inhibitor of aldose reductase
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Grams-Kilos
Melting Point:
262 - 265 °C
InChIKey:
FKZUETPACPDEAD-UHFFFAOYSA-M
InChI:
1S/C14H9NO4.Na/c16-11(17)7-15-13(18)9-5-1-3-8-4-2-6-10(12(8)9)14(15)19;/h1-6H,7H2,(H,16,17);/q;+1/p-1
Canonical SMILES:
C1=CC2=C3C(=C1)C(=O)N(C(=O)C3=CC=C2)CC(=O)[O-].[Na+]
Current Developer:
Wyeth
1.Alrestatin: gastric acid antisecretory-antiulcer activity in the rat.
Lippmann W;Seethaler K;Borella LE;Pugsley TA Digestion. 1978;18(1-2):35-44.
Alrestatin sodium (AY-22,284-A) inhibited gastric acid secretion and decreased the volume of gastric juice produced in the pylorus-ligated rat when administered intraperitoneally or perorally. Pentagastrin-induced gastric acid output in the unanesthetized rat was antagonized. The pyloric ligation-induced ulcer formation in the rat was inhibited. Alrestatin sodium did not exhibit an anticholinergic profile. The drug did not block the norepinephrine neuronal uptake mechanism in rat brain or heart; it did not alter the endogenous norepinephrine concentration in the heart and decreased endogeneous brain norepinephrine concentration. Alrestatin sodium is an effective inhibitor of gastric acid secretion and ulcer formation in the rat.
2.Effect of alrestatin sodium on glucose-stimulated insulin secretion in the fasted anaesthetized rat.
Kobric M;Lippmann W Horm Metab Res. 1978 Nov;10(6):495-500.
In the anaesthetized fasted non-diabetic male intact rat, alrestatin sodium injected as a bolus (0.75 mmol/kg, i.v.) did not affect basal plasma insulin or glucose levels. However, in response to an intravenous glucose tolerance test, plasma insulin levels were significantly increased above the values observed in the animal during a control test. The decreases in plasma glucose levels after alrestatin were significantly greater than in the control study. In rat pancreatic preparations in vitro, alrestatin lowered the basal release of 3H-norepinephrine and also the release obtained with the catecholamine-releasing agent tyramine. A modulation of catecholamine release appears to be of importance in the mode of action of alrestatin with respect to the insulin secretion and plasma glucose levels. It is suggested that alrestatin may play a useful role in the therapy of diabetes mellitus since it can augment insulin secretion when glucose is administered to a fasted animal in which the acute insulin response has been shown to be like that of the human diabetic, and in addition, can lower arginine-stimulated glucagon secretion in the animal, the latter being a model of an action that is observed in the human diabetic.
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CAS 51876-97-2 Alrestatin (sodium)

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