amibegron and Obesity

amibegron has been researched along with Obesity* in 3 studies

Reviews

1 review(s) available for amibegron and Obesity

ArticleYear
SR 58611A: SR 58611.
    Drugs in R&D, 2003, Volume: 4, Issue:6

    SR 58611A [SR 58611], a highly selective agonist for atypical beta3-adrenoceptors, inhibits intestinal motility. This (phenylethanol) aminotetraline sympathomimetic was originated by Sanofi as a potential treatment for irritable bowel syndrome but is now in development for depression. SR 58611A is currently in phase III trials for depression in France. A phase IIa trial of SR 58611A in patients with severe recurrent depression showed it to be superior to fluoxetine and well tolerated, while a phase IIb trial demonstrated comparable efficacy and tolerability to paroxetine. SR 58611A was in phase II clinical trials in France for irritable bowel syndrome but there is no record of active development of SR 58611A for this indication. SR 58611A had also been in phase IIa for the treatment of obesity but no recent development has been reported for this indication. SR 58878 is the acid metabolite of SR 58611A.

    Topics: Adrenergic beta-3 Receptor Antagonists; Animals; Antidepressive Agents; Clinical Trials as Topic; Depressive Disorder; Gastric Acid; Gastrointestinal Motility; Humans; Obesity; Tetrahydronaphthalenes

2003

Other Studies

2 other study(ies) available for amibegron and Obesity

ArticleYear
Effect of SR58611A, a potent beta-3 adrenoceptor agonist, on cutaneous wound healing in diabetic and obese mice.
    European journal of pharmacology, 2006, Jan-04, Volume: 529, Issue:1-3

    In diabetic patients, impairment of wound healing is a serious problem which represents a significant health burden. The effect of a highly selective beta-3 adrenoceptor agonist, SR58611A, on wound healing was assessed in animal models of type II diabetes. In db/db diabetic mice, a daily oral treatment with SR58611A (1, 3 and 10 mg/kg/day for two weeks) significantly reduced hyperglycaemia from 3 mg/kg/day onwards. The compound also normalized wound healing, starting from the lowest dose tested (1 mg/kg/day). SR58611A did not affect wound healing of control (lean) mice. An oral anti-diabetic agent, devoid of affinity for beta-3 adrenoceptors, troglitazone (130 mg/kg/day p.o.), normalized glycaemia but did not improve wound healing in db/db mice. Local application of SR58611A (200 microg/day in db/db mice) did not affect wound healing. SR58611A also normalized glucose levels in ob/ob mice, but only slightly improved wound healing in this strain. Moreover, in 17-week old db/db mice (i.e. severely insulin resistant) and in streptozotocin-induced diabetic mice, SR58611A slightly decreased hyperglycaemia and did not affect wound healing. In conclusion, SR58611A improves wound healing in animal models of non-insulin-dependent diabetes. This effect is not related to its effect on glucose levels, but probably implicates systemic effects of the compound.

    Topics: Administration, Oral; Adrenergic beta-3 Receptor Agonists; Adrenergic beta-Agonists; Animals; Blood Glucose; Diabetes Mellitus, Experimental; Male; Mice; Mice, Inbred C57BL; Obesity; Skin; Tetrahydronaphthalenes; Time Factors; Wound Healing

2006
SR 58611A: a novel thermogenic beta-adrenoceptor agonist.
    European journal of pharmacology, 1994, Jul-01, Volume: 259, Issue:2

    N(2S)-7-carbethoxymethoxy-1,2,3,4-tetrahydronaphth-2-yl]-(2R )-2-hydroxy-2-(3-chlorophenyl)ethanamine hydrochloride (SR 58611A) increased cyclic AMP levels in membrane homogenates from rat interscapular brown adipose tissue with an EC50 of 20 +/- 2 nM. Substitution of GTP with the GDP analog, guanosine-5'-O[thiodiphosphate], in the incubation medium suppressed the stimulation of adenylyl cyclase activity by SR 58611A. This compound also stimulated glycerol release from the brown fat cells, with an EC50 of 11 +/- 0.4 nM. Only at doses higher than 10 microM did the non-selective beta-adrenoceptor antagonists, propranolol and alprenolol, as well as the selective beta 1- and beta 2-adrenoceptor antagonists, (+-)-[2-(3-carbamoyl-4-hydroxy-phenoxy)- ethylamino]-3-[4(1-methyl-4-trifluoromethyl-2-imidazolyl)-phenoxy]-2 propanol (CGP 20712A) and erythro-(+-)-1-(7-methylindan-4-yloxy)-3-iso-propylamino butan-2-ol-hydrochloride (ICI 118,551), antagonize the SR 58611A-induced stimulation of both adenylyl cyclase activity and lipid metabolism. Since, at high doses, all these beta-adrenoceptor antagonists lack selectivity for beta 1- or beta 2-adrenoceptors, these results suggest that the beta-adrenoceptor agonist, SR 58611A, activates thermogenesis by acting on brown fat cell beta 3-adrenoceptors. This implies that this compound might be useful for treatment of obesity.

    Topics: Adenylyl Cyclases; Adipose Tissue, Brown; Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Animals; Cyclic AMP; Drug Interactions; Glycerol; Imidazoles; Lipid Metabolism; Male; Obesity; Propanolamines; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Tetrahydronaphthalenes

1994