ZD 2079 - CAS 178600-17-4
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Adrenergic Receptor
ZD 2079 is a β3-adrenoceptor agonist. ZD 2079 inhibits ob gene expression and circulating leptin levels in lean mice in vivo, and has the potential to treat obesity and type 2 diabetes.
Brife Description:
β3-adrenoceptor agonist
≥99% by HPLC
Related CAS:
146376-58-1 (free base)
4-[2-[[(2R)-2-Hydroxy-2-phenylethyl]amino]ethoxy]-benzeneacetic acid hydrochloride; Talibegron hydrochloride; Talibegron HCl, Talibegron hydrochloride, D-2079, ICI-D-2079, SCH-417849, ZD-2079, D2079, ICI-D2079, SCH417849, ZD2079
potential treatment of obesity and type II diabetes
Canonical SMILES:
1.Urinary tract toxicity in rats following administration of beta 3-adrenoceptor agonists.
Waghe M;Westwood R;Nunn G;Kalinowski A;Aldridge A Toxicol Pathol. 1999 Mar-Apr;27(2):165-70.
ZD7114, [(S)-4-[2-(2-hydroxy-3 phenoxypropylamine)ethoxy]-N-(2-methoxyethyl) phenoxyacetamide], and ZD2079, [(R)-N-(2-[4- (carboxymethyl)phenoxy]ethyl)-N-(beta-hydroxyphenethyl)ammonium chloride], are beta 3-adrenoceptor stimulants with selectivity for brown adipose tissue. ZD7144 is the hydrochloride salt of the S-enantiomer of the racemic amide ZD2079. They were developed as potential novel treatments for obesity and non-insulin-dependent diabetes mellitus. Male and female rats were dosed separately by gavage for a minimum of 28 days with 0, 10, 50, and 500 mg/kg/day of ZD7114 or with 0, 10, 30, and 150 mg/kg/day of ZD2079. Two further groups of male and female rats were dosed with 0 and 500 mg/kg/day of ZD7114 for 28 days and were then allowed a 6-wk, undosed withdrawal period. At high doses, both compounds caused urinary tract toxicity, which primarily affected the distal tubules and collecting ducts of the kidney via tubular necrosis. They also caused ureteric inflammation, cystitis, and accumulation of crystalline inclusions throughout the urinary tract. As a result of urinary tract toxicity, affected animals from one or both studies showed reduced red blood cell indices, lower platelet counts, and higher white cell counts.
2.Rapid inhibition of ob gene expression and circulating leptin levels in lean mice by the beta 3-adrenoceptor agonists BRL 35135A and ZD2079.
Trayhurn P;Duncan JS;Rayner DV;Hardie LJ Biochem Biophys Res Commun. 1996 Nov 12;228(2):605-10.
The acute effect of two selective beta 3-adrenoceptor agonists, BRL 35135A and ZD2079, on the expression of the ob gene and plasma leptin levels has been examined in mice. By 4-5 h after the administration of either beta 3-agonist to lean animals there was a major loss of ob mRNA from epididymal white adipose tissue. This was accompanied by a substantial fall in circulating leptin levels, as measured by an ELISA. Even 24 h after the first administration of beta 3-agonists, ob mRNA levels and circulating leptin levels remained low. In contrast to lean animals, treatment with BRL 35135A had only a minor effect on ob mRNA levels in obese (ob/ob) mice. Regulation of leptin production appears to involve a negative feedback loop to white adipose tissue through the sympathetic nervous system suppressing ob gene transcription via beta 3-adrenoceptors; an impairment in this loop is evident in the ob/ob mutant.
3.Effects of propranolol and L-NAME on beta-adrenoceptor-mediated relaxation in rat carotid artery.
MacDonald A;McLean M;MacAulay L;Shaw AM J Auton Pharmacol. 1999 Jun;19(3):145-9.
1. The properties of beta-adrenoceptors mediating vascular relaxation in rat isolated carotid artery were investigated. Ring segments of arteries were preconstricted with the thromboxane A2 receptor agonist U-46619 and relaxation to beta-adrenoceptor agonists determined. 2. Isoprenaline produced a concentration-dependent relaxation of U-44619-constricted arteries. The concentration-response curve (CRC) to isoprenaline was shifted to the right by propranolol (1 microM) although the shift was less (105 fold; pA2, 8.02) than would be expected for an effect of isoprenaline at classical beta-adrenoceptors (300-1000 fold; pA2, 8.5-9). L-NAME (100 microM) significantly reduced responses to isoprenaline, lowering the slope of the CRC and reducing the maximum response. 3. The selective beta3-adrenoceptor agonists, BRL 37344 and ZD2079, also produced concentration-dependent relaxation of the arteries. L-NAME (100 microM) shifted the BRL 37344 CRC to the right 15 fold with no reduction in the slope or maximum response. L-NAME (100 microM) had no significant effect on the ZD2079 CRC. 4. In conclusion, relaxation to isoprenaline in rat carotid artery is inhibited by propranolol in a manner suggesting a mixed population of classical (beta1-/beta2-) and atypical (beta3-) adrenoceptors.
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CAS 178600-17-4 ZD 2079

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