Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Carbohydrate doai
Reexamination Certificate
2000-07-10
2001-02-20
Henley, III, Raymond (Department: 1614)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Carbohydrate doai
C514S217000, C514S551000, C514S557000
Reexamination Certificate
active
06191117
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to pharmaceutical compositions, whose mechanisms of action(s) are at the kainate/AMPA receptor that can be used to treat the medical condition of obesity.
BACKGROUND OF THE INVENTION
Obesity is one of the most common medical disorders, which affects 30-40% of the population of which 10% may be severe and morbid. Complications of obesity include insulin resistance, diabetes mellitus, hypertension, cardiovascular disease, pseudotumor cerebri, hyperlipidemia, sleep apnea, cancer, pulmonary hypertension, cholecystitis, and osteoarthritis. The mortality from obesity is estimated at 300,000 to 400,000 per annum in the United States. Obesity in humans is commonly measured by the BMI (body mass index) which is the weight in kilograms divided by the height in meters squared. The degree of obesity is determined by comparisons against standard deviations above the means for males and females. The exact etiology of obesity is unknown but occurs when energy intake exceeds energy expenditure. The amount and distribution of body fat may have some genetic predisposition and be under some hormonal control. Hypothalamic structures, which have complex interconnections with the limbic system and other brain structures, control appetite. Some neurochemicals known to be involved in appetite control include: leptin, a substance released from adipose tissue, GLP-1 (glucagon-like peptidel) which promotes satiety, and neuropeptide-Y, a potent stimulator of appetite.
SUMMARY OF THE INVENTION
The present invention proposes a theory of obesity in which dysfunction of the AMPA/kainate and/or NMDA is a contributing etiology. Administration of drugs whose mechanism or action is antagonism of the AMPA/kainate receptor, with or without the combination of glycine-site antagonists, is proposed as a treatment for obesity.
REFERENCES:
Faught E, Wilder BJ, Ramsay RE, et al. “Topiramate placebo-controlled dose-ranging trial in refractory partial epilepsy using 600-, 800-, and 1000-mg daily dosages.” Neurology 46:1684-1690, 1996.
Privitera M, Fincham R, Penry J, et al. “Topiramate placebo-controlled dose-ranging trial in refractory partial epilepsy using 600-, 800-, and 1000-mg daily dosages.” Neurology 46:1678-1683, 1996.
Package insert. “Topamax (topiramate).” Raritan, NJ: Ortho McNeil Pharmaceutical, Dec. 1996.
Matsuo F, Bergen D, Faught, et al. “Placebo-controlled study of the efficacy and safety of lamotrigene in patients with partial seizures.” Neurology 43:2284-2291, 1993.
Brodie MJ, Richens A, Yuen AWC, et al. “Lamotrigene/Carbamazepine Monotherapy Trial Group. (No date aun.l) Double-blind comparison of lamotrigene and carbamezepine in newly diagnosed epilepsy.” Lancet 345:476-479.
Brodie MJ, Overstall PW, Giorgio L. “Multicentre, double-blind, randomized comparison between lamotrigene and carbamazepine in elderly patients with newly diagnosed epilepsy. The UK Lamotrigene Elderly Study Group.” Epilepsy Res. 37:81-87, 1999.
Steiner TJ, Dellaportas CI, Findley LJ, et al. “Lamotrigene monotherapy in newly diagnosed untreated epilepsy: a double-blind comparison with phenytoin.” Epilepsia 40:601-607, 1999.
Gilliam F, Vazquez B, Sackellares JC, et al. “An active-control trial of lamotrigene monotherapy for partial seizures.” Neurology 51:1018-1025, 1998.
Reunanen M, Dam M, Yuen AW. “A ramdomized open multicentre comparative trial of lamotrigene and carbamazepine as monotherapy in patients with newly diagnosed or recurrent epilepsy.” Epilepsy Res. 23:149-155, 1996.
Besag FM, Dulac O, Alving J, et al. “Long-term safety and efficacy of lamotrigene (Lamictal) in pediatric patients with epilepsy.” Seizure 6:51-56, 1997.
Sachdeo RC, Reife RA, Lim P, et al. “Topiramate monotherapy for partial seizures.” Epilepsia 38:294-300, 1997.
Rosenfeld WE, Sachdeo RC, Faught RE, et al. “Long-term experience with topiramate adjunctive therapy and as monotherapy in patients with partial onset seizures: retrospective survey of open-label treatment.” Epilepsia 38 (Suppl 1) 38:S34-S36, 1997.
Biton V. “Preliminary open-label experience with topiramate in primary generalized seizures.” Epilepsia 38(Suppl. 1): S42-S44, 1997.
Martin R. Kuzniecky R, Ho S, et al. “Cognitive effects of topiramate, gabapentin, and lamotrigine in healthy young adults.” Neurology 52:321-327, 1999.
Bassel Abou-Khalil. “Topiramate in the long-term management of refractory epilepsy.” Epilepsia 41 (Suppl 1): S72-S76, 2000.
Stanley BG, Butterfield BS, and RS Grewal. “NMDA receptor coagonist glycine site: evidence for a role in lateral hyptohalamic stimulation of feeding.” Am J Physiol. 73(42): R790-F796, 1997.
Bergen DC, Ristanovic K, Waicosky K, et al. “Weight loss in patients taking felbamate.” Clinical Neuropharm 18(1): 23-27, 1995.
Inui A. “Transgenic approach to the study of body weight regulation.” Pharmacological Reviews. 52(1): 35-61, 2000.
Wolf AM and GA Colditz. “Current estimates of the economic cost of obesity in the United States.” Obes. Res. 6:97-106, 1998.
Kaufman DW, JP Kelly, T Anderson et al. “Evaluation of case reports of aplastic anemia among patients treated with falbamate.” Epilepsia 38(12): 1265-1269, 1997.
Stanley BG, VL Willet, HW Donias, et al. “The lateral hypothalamus: a primary site mediating excitatory amino acid-elicited eating.” Brain Res. 630: 41-49, 1993.
Sorrels TL and E Bostock. “Induction of feeding by 7-chlorokynurenic acid, a strychnine-insensitve glycine binding site antagonist.” Brain Research 572: 265-268, 1992.
Stanley BG, VL Willet, HW Donias, et al. “Lateral hypothalamus NMDA receptors and glutamate as physiological mediators of eating and weight control.” Am. J. Physiol. 270 (39): R433-R449, 1996.
Meeker RB, RS Greenwood, and JN Hayward. “Glutamate receptors in the rat hypothalamus and pituitary.” Endocrinology 134: 621-629, 1994.
Stricker EM, AF Swerdloff, and MJ Zigmond. “Intrahypothalamic injections of kainic acid produce feeding and drinking deficits in rats.” Brain Research 158: 470-473, 1978.
Van den Pol A, JP Wuarin, and FE Dudeck. “Glutamate, the dominant excitatory transmitter in neuroendocrine regulation.” Science 250:1276-1278, 1990.
Stanley BG, LH Ha, LC Spears and MG Dee. “Lateral hypothalamic injections of glutamate, kainic acid, D,L-a-amino-hydroxy-5-methyl-isoxazole propionic acid or N-methyl-D-aspartic acid elicit intense transient eating in rats.” Brain Research 613: 88-95, 1993.
Wirtshafter D and R Trifunovic. “Stimulation of ingestive behaviors following injections of excitatory amino acid antagonists into the median raphe nucleus.” Pharmacol. Biochem. Behav. 30: 529-533, 1988.
Kuzniecky R, Hetherington H, Ho S, et al. “Topiramate increases cerebral GABA in healthy humans.” Neurology 51: 627-629, 1998.
Li LM, Nashef L., Moriarty J., et al. “Felbamate as add-on therapy.” Eur. Neurol. 36:146-148, 1996.
Privitera MD. “Topiramate: a new antipileptic drug.” Ann of Pharmacotherapy 31:1164-1173, 1997.
Pellock JM. “Felbamate.” Epilepsia 40 (Suppl 5):S57-S62, 1999.
Weiss S, Kemp DE, and L. Bauce. “Kainate evokes the release of endogenous glycine from striatal neurons in primary culture.” Neurosci Lett 107:205-210, 1989.
Henley III Raymond
Liniak, Berenato, Longacre & White LLC
LandOfFree
Methods of producing weight loss and treatment of obesity does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Methods of producing weight loss and treatment of obesity, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Methods of producing weight loss and treatment of obesity will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-2598394