A61K 31/216 - Esters, e.g. nitroglycerine, selenocyanates of carboxylic acids of acids having aromatic rings, e.g. benactizyne, clofibrate
A61P 1/16 - Drugs for disorders of the alimentary tract or the digestive system for liver or gallbladder disorders, e.g. hepatoprotective agents, cholagogues, litholytics
Disclosed is a therapeutic management method of hypertriglyceridemia in mammals. More specifically, the present invention relates to a method of reducing triglyceride in the blood stream of mammals, said method involving step of administering therapeutically effective amounts of Calebin A to said mammals to bring about the effects of reducing concentrations of serum triglycerides.
Disclosed is a therapeutic management method of hypercholesterolemia in mammals. More specifically, the present invention relates to a method of reducing high levels of circulating cholesterol (hypercholesterolemia) in the blood stream of mammals, said method involving step of administering therapeutically effective amounts of Calebin A to said mammals to bring about the effects of (i) reducing the amount of total blood cholesterol levels; (ii) reducing the concentrations of low density lipoproteins (LDL) and very low density lipoproteins (VLDL); (iii) increasing the concentrations of high density lipoproteins (HDL) and (iv) reducing concentrations of serum triglycerides.
A61P 9/10 - Drugs for disorders of the cardiovascular system for treating ischaemic or atherosclerotic diseases, e.g. antianginal drugs, coronary vasodilators, drugs for myocardial infarction, retinopathy, cerebrovascula insufficiency, renal arteriosclerosis
The present invention discloses the potential of Calebin A in inhibiting adipogenesis and applications thereof in obesity management. The present invention elucidates the potential of Calebin A to favorably modulate biochemical markers associated with obesity. Notable biomodulatory properties of Calebin A include inhibiting leptin production, increasing adiponectin expression and inhibiting local (adipocyte) and systemic inflammation caused by pro-inflammatory cytokines Tumor Necrosis Factor (TNF-.alpha.), Interleukin-6 (IL-6) and Interleukin-1 (IL-1.beta.).
patents