Patent classifications
A61K31/4412
Composition And Method for Modulating Hydrogen Ion Physiology Related to Weight Loss and Metabolism
A nutritional supplement composition that enhances the incorporation of calcium and other bone building elements in bone and that prevents bone breakdown, specifically due to the chronic metabolic acidosis that the typical Western diet generates each day. The transcription factor NFKB (Nuclear Factor Kappa B), which underlies some of this physiology, has also been shown to adversely affect fat metabolism. The enzymatic protein complex, AMP Kinase (Adenosine Monophosphate Kinase), a key regulator of energy metabolism, has been shown to reverse the effects of excessive NFKB activity on bone and fat metabolism. The novel nutrients modulate nutrient partitioning and fat metabolism in a human or animal so as to increase oxidation of fat, decrease storage of fat and promote increased storage of glycogen. They are composed of one or more of nutrients selected from the group consisting of Hesperidin, Berberine, Epigallocatechin 3-Gallate (EGCG), Resveratrol, Curcumin, Ginsenosides, Gingerols, Hispidulin, Honokiol, Magnolol and Quercetin. A method for modulating nutrient partitioning in a human involves orally or parenterally administering the aforementioned composition to the human or animal, preferably on a daily basis, for a therapeutically effective period of time. Preferably, the method further involves having the recipient follow a specific dietary regimen wherein the glycemic index is less than 60 and the daily calorie consumption from carbohydrates is less than about 50% and the daily calorie consumption from protein is at least about 20%. Optionally, the method further involves an exercise program, a stress reduction program and/or a blood donation program.
Composition And Method for Modulating Hydrogen Ion Physiology Related to Weight Loss and Metabolism
A nutritional supplement composition that enhances the incorporation of calcium and other bone building elements in bone and that prevents bone breakdown, specifically due to the chronic metabolic acidosis that the typical Western diet generates each day. The transcription factor NFKB (Nuclear Factor Kappa B), which underlies some of this physiology, has also been shown to adversely affect fat metabolism. The enzymatic protein complex, AMP Kinase (Adenosine Monophosphate Kinase), a key regulator of energy metabolism, has been shown to reverse the effects of excessive NFKB activity on bone and fat metabolism. The novel nutrients modulate nutrient partitioning and fat metabolism in a human or animal so as to increase oxidation of fat, decrease storage of fat and promote increased storage of glycogen. They are composed of one or more of nutrients selected from the group consisting of Hesperidin, Berberine, Epigallocatechin 3-Gallate (EGCG), Resveratrol, Curcumin, Ginsenosides, Gingerols, Hispidulin, Honokiol, Magnolol and Quercetin. A method for modulating nutrient partitioning in a human involves orally or parenterally administering the aforementioned composition to the human or animal, preferably on a daily basis, for a therapeutically effective period of time. Preferably, the method further involves having the recipient follow a specific dietary regimen wherein the glycemic index is less than 60 and the daily calorie consumption from carbohydrates is less than about 50% and the daily calorie consumption from protein is at least about 20%. Optionally, the method further involves an exercise program, a stress reduction program and/or a blood donation program.
SMALL-MOLECULE COVALENT INHIBITION OF RAL GTPASES
Disclosed herein are Ral-antagonist compounds that covalently bind to binding sites in RalA, and efficaciously inhibit Ral activity. The compounds include aryl sulfonyl fluoride compounds of the general structure of wherein X and Y are independently C or N, and R.sub.4 is C.sub.1-C.sub.4 alkyl, —OCH.sub.3, —OCH.sub.2CH.sub.3, —OCH(CH.sub.3).sub.2, —(SO.sub.2)CH.sub.3, —OH, or halo. These compounds expand Ral-inhibiting therapeutic options for treating Ral-driven cancers and one embodiment of the present disclosure is directed to the use of such compounds to treat cancer.
SMALL-MOLECULE COVALENT INHIBITION OF RAL GTPASES
Disclosed herein are Ral-antagonist compounds that covalently bind to binding sites in RalA, and efficaciously inhibit Ral activity. The compounds include aryl sulfonyl fluoride compounds of the general structure of wherein X and Y are independently C or N, and R.sub.4 is C.sub.1-C.sub.4 alkyl, —OCH.sub.3, —OCH.sub.2CH.sub.3, —OCH(CH.sub.3).sub.2, —(SO.sub.2)CH.sub.3, —OH, or halo. These compounds expand Ral-inhibiting therapeutic options for treating Ral-driven cancers and one embodiment of the present disclosure is directed to the use of such compounds to treat cancer.
Uttroside B and derivatives thereof as therapeutics for hepatocellular carcinoma
The present invention includes Uttroside B compositions and method for the treatment of hepatocellular carcinoma. Chemotherapeutic options for liver cancer are limited and the prognosis of HCC patients remains dismal. Sorafenib, is the only drug currently available for the treatment of hepatocellular carcinoma.
Uttroside B and derivatives thereof as therapeutics for hepatocellular carcinoma
The present invention includes Uttroside B compositions and method for the treatment of hepatocellular carcinoma. Chemotherapeutic options for liver cancer are limited and the prognosis of HCC patients remains dismal. Sorafenib, is the only drug currently available for the treatment of hepatocellular carcinoma.
Delayed release deferiprone tablets and methods of using the same
The invention is directed to pharmaceutical compositions such as tablets that exhibit delayed release properties when administered as either whole or half tablets. The invention is also directed to delayed release tablets comprising deferiprone for oral administration, for which twice daily administration is bioequivalent to the same daily dose of an immediate release tablet administered thrice daily. The invention is also directed to methods of making and using the same.
Delayed release deferiprone tablets and methods of using the same
The invention is directed to pharmaceutical compositions such as tablets that exhibit delayed release properties when administered as either whole or half tablets. The invention is also directed to delayed release tablets comprising deferiprone for oral administration, for which twice daily administration is bioequivalent to the same daily dose of an immediate release tablet administered thrice daily. The invention is also directed to methods of making and using the same.
Compositions and Methods for Treating Aging-Related Disorders
This invention provides a composition comprising at least three agents selected from the group consisting of alpha-ketoglutarate, malate, pterostilbene, micro-dosed lithium, glycine, ginger, Rhodiola rosea, acetyl glucosamine, vitamin C, glucosamine, fisetin, L-theanine, oxaloacetate, fumarate, succinate, hyaluronic acid, butyrate, anthocyanins, piperlongumine, quercetin, curcuminoids, caffeine, trehalose, and spermidine. This invention also provides related pharmaceutical compositions, methods for ameliorating hallmarks of aging, and articles of manufacture.
Compositions and Methods for Treating Aging-Related Disorders
This invention provides a composition comprising at least three agents selected from the group consisting of alpha-ketoglutarate, malate, pterostilbene, micro-dosed lithium, glycine, ginger, Rhodiola rosea, acetyl glucosamine, vitamin C, glucosamine, fisetin, L-theanine, oxaloacetate, fumarate, succinate, hyaluronic acid, butyrate, anthocyanins, piperlongumine, quercetin, curcuminoids, caffeine, trehalose, and spermidine. This invention also provides related pharmaceutical compositions, methods for ameliorating hallmarks of aging, and articles of manufacture.