bombesin receptor subtype 3

04/01/2013 - "Our study provides important information for evaluating BRS-3 as a potential therapeutic target for the treatment of obesity."
10/15/2018 - "These results confirm that BRS-3 and/or its agonist are a potential therapeutic tool for obesity/diabetes."
10/15/2018 - "Its expression was reduced in skeletal muscle from obese and/or diabetic patients, and BRS-3 KO-mice developed obesity. "
01/01/2017 - "Based on the obese phenotype of male BRS-3-deficient mice, BRS-3 has been considered an attractive target for obesity treatment. "
01/01/2015 - "The development of potent, selective BRS-3 agonists demonstrates promise as a novel approach to treat obesity/diabetic states. "

01/01/2018 - "Bombesin receptor subtype 3 (BRS-3) is a GPCR that is expressed in the CNS, peripheral tissues, and tumors. "
10/01/2006 - "Immunoreactive GRP-R and BRS-3 receptors were in many cases predominantly confined to the plasma membrane and uniformly present on nearly all tumor cells. "
06/30/2000 - "A higher incidence of BRS-3 expression was observed in samples with tumor Stage IV (4/4, 100%) compared with Stage III (1/17, approximately 6%). "
05/08/2003 - "New tool substances may help to unravel the physiological role of the human orphan receptor BRS-3 and its possible use as a drug target for the treatment of obesity and cancer. "
06/30/2000 - "Our study indicates that GRPR and NMBR are widely distributed in human ovarian carcinomas with BRS-3 being found in Stage IV tumors. "

12/08/2011 - "Starting from a high-throughput screening lead, we prepared a series of BRS-3 agonists with improved potency and pharmacokinetic properties, of which compound 8a caused mechanism-based, dose-dependent food intake reduction and body weight loss after oral dosing in diet-induced obese mice. "
04/01/2010 - "After oral administration, compound 9 had sufficient exposure in diet induced obese mice to demonstrate efficacy in lowering food intake and body weight via BRS-3 activation."
03/01/2008 - "To determine whether their obesity is a result of increased food intake or a defect in energy regulation, we matched the caloric intake of BRS-3 KO mice to wild-type (WT) ad libitum (ad lib)-fed controls over 21 wk. Although BRS-3 KO ad lib-fed mice were 29% heavier, the body weights of BRS-3 KO pair-fed mice did not differ from WT ad lib-fed mice. "
02/01/2012 - "Studies indicate that the orphan BRS-3 is an important regulator of body weight, energy expenditure, and glucose homeostasis. "
01/01/2012 - "Compelling experimental evidence has accumulated indicating that the orphan BRS-3 is an important regulator of body weight, energy expenditure, and glucose homeostasis. "

01/01/2018 - "To address its potential importance, in this study, we examined the frequency/relative quantitative expression of human BRS-3 compared to GRPR/NMBR and the effects of its activation on cell-signaling/growth in 13 different human lung-cancer cell-lines. "
01/01/2018 - "These results suggest that similar to GRPR/NMBR, BRS-3 should receive increased attention as possible approach for the development of novel treatments and/or diagnosis in lung-cancer."
01/01/2018 - "These results suggest that human BRS-3, similar to GRPR/NMBR, is frequently ectopically-expressed by lung-cancer cells in which, it is functional, affecting cell signaling/growth. "
01/01/2017 - "The ability of BA1 to elevate cytosolic Ca2+ in human lung cancer cells transfected with BB1R, BB2R, and BRS-3 was antagonized by AM-37 and ST-36. "
02/01/2015 - "ML-18 and EMY-98 inhibited specific (125)I-BA1 (DTyr-Gln-Trp-Ala-Val-βAla-His-Phe-Nle-NH2)BB(6-14) binding to NCI-H1299 lung cancer cells stably transfected with BRS-3 with IC50 values of 4.8 and >100μM, respectively. "

01/01/2012 - "Studies in mice showed robust BRS-3 expression in the hypothalamic satiety centers, and genetic receptor inactivation resulted in obesity, diabetes, and hypertension. "
11/13/1997 - "Mice lacking functional BRS-3 developed a mild obesity, associated with hypertension and impairment of glucose metabolism. "
01/01/2015 - "Since the initial observation that BRS-3 knockout mice develop obesity, hypertension, impaired glucose metabolism and hyperphagia, there have been numerous studies of the mechanisms involved and the development of selective BRS-3 agonists/antagonists, which have marked effects on body weight, feeding and glucose/insulin homeostasis. "