Reference

Use of substituted pyrazole compounds for the treatment of cardiovascular risk factors caused by metabolic syndrome

All Rights Reserved. Use of substituted pyrazole compounds for the treatment of cardiovascular risk factors caused by metabolic syndrome. Buschmann, Helmut H. (Laboratorios del Dr. Esteve, S.Chemicals with cas numbers 168273-06-1 and 168272-90-0 also play role. A., Spain). PCT Int. Appl. WO 2007009701 A2 25 Jan 2007, 46pp. DESIGNATED STATES: W: AE, AG, AL, AM, AT, AU, AZ, BA, BB, BG, BR, BW, BY, BZ, CA, CH, CN, CO, CR, CU, CZ, DE, DK, DM, DZ, EC, EE, EG, ES, FI, GB, GD, GE, GH, GM, HN, HR, HU, ID, IL, IN, IS, JP, KE, KG, KM, KN, KP, KR, KZ, LA, LC, LK, LR, LS, LT, LU, LV, LY, MA, MD, MG, MK, MN, MW, MX, MZ, NA, NG, NI, NO, NZ, OM, PG, PH, PL, PT, RO, RS, RU, SC, SD, SE, SG, SK, SL, SM, SY, TJ, TM, TN, TR, TT, TZ, UA, UG, US, UZ, VC; RW: AT, BE, BF, BJ, CF, CG, CH, CI, CM, CY, DE, DK, ES, FI, FR, GA, GB, GR, IE, IS, IT, LU, MC, ML, MR, NE, NL, PT, SE, SN, TD, TG, TR. (English). (World Intellectual Property Organization). CODEN: PIXXD2. CLASS: ICM: A61K. APPLICATION: WO 2006-EP6975 15 Jul 2006. PRIORITY: EP 2005-384014 15 Jul 2005; US 2005-705451P 5 Aug 2005. DOCUMENT TYPE: Patent CA Section: 1 (Pharmacology) The present invention relates to the use of substituted pyrazole compds. for the treatment of metabolic syndrome in humans and animals and to corresponding medicaments. Specifically claimed are medicaments contg. substituted pyrazoline compds. of general formula I (wherein R1 = H or a linear, branched, (un)substituted, or (un)satd. C1-4-alkyl; R2, R3, R4, R5 and R6, R7, R41= H, linear or branched C1-6-alkyl, halo, CH2F, etc.) for the treatment of cardiovascular risk factors caused by metabolic syndrome. For example, in obese mice fed with high fat diet, example compd. II was an inhibitor of high blood levels of triglycerides. .

Modulation of morphine-induced Fos-immunoreactivity by the cannabinoid receptor antagonist SR 141716

Some chemicals with cas registry numbers like 52-26-6 and 168273-06-1 are also used. Modulation of morphine-induced Fos-immunoreactivity by the cannabinoid receptor antagonist SR 141716. Singh, M. E.; Verty, A. N. A.; Price, I.; McGregor, I. S.; Mallet, P. E. ( School of Psychology, University of New England, Armidale 2351, Australia). Neuropharmacology, 47(8), 1157-1169 (English) 2004 Elsevier B.V. CODEN: NEPHBW. ISSN: 0028-3908. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) A growing body of evidence suggests the existence of a functional interaction between opioid and cannabinoid systems. The present study further investigated this functional interaction by examg. the combined effects of morphine and the cannabinoid receptor antagonist SR 141716 on Fos-immunoreactivity (Fos-IR), a marker for neural activation. Male albino Wistar rats were treated with SR 141716 (3 mg/kg, i.p.), morphine HCl (10 mg/kg, s.c.), vehicle, or SR 141716 and morphine combined (n = 6 per group). Rats were injected with morphine or its vehicle 30-min after administration of SR 141716 or its vehicle and perfused 3 h later. Locomotor activity and body temp. were both increased in the morphine-treated group and SR 141716 significantly inhibited these effects. Morphine increased Fos-IR in several brain regions including the caudate-putamen (CPu), cortex (cingulate, insular and piriform), nucleus accumbens (NAS) shell, lateral septum (LS), bed nucleus of the stria terminalis (BNST), median preoptic nucleus (MnPO), medial preoptic nucleus (MPO), hypothalamus (paraventricular, dorsomedial and ventromedial), paraventricular thalamic nucleus (PV), amygdala (central and basolateral nuclei), dorsolateral periaqueductal gray, ventral tegmental area (VTA), and Edinger-Westphal nucleus. SR 141716 alone increased Fos-IR in the cortex (cingulate, insular and piriform), NAS (shell), LS, BNST, hypothalamus (paraventricular, dorsomedial and ventromedial), PV, amygdala (central, basolateral and medial nuclei), VTA, and Edinger-Westphal nucleus. SR 141716 attenuated morphine-induced Fos-IR in several regions including the CPu, cortex, NAS (shell), LS, MnPO, MPO, paraventricular and dorsomedial hypothalamus, PV, basolateral amygdala, VTA, and Edinger-Westphal nucleus (EW). These results provide further support for functional interplay between the cannabinoid and opioid systems. Possible behavioral and physiol. implications of the interactive effects of SR 141716 on morphine-induced Fos-IR are discussed. .