The present invention provides a method of treating ovarian cancer in a mammal in need of such treatment comprising administering an effective amount of a combination of gemcitabine, cisplatin or carboplatin, and 5-[2-tert-butyl-5-(4-fluoro-phenyl)-1H-imidazol-4-yl]-3-(2,2-dimethyl-propyl)-3H-imidazo[4,5-b]pyridin-2-ylamine.

The invention provides methods of treatment, pharmaceutical compositions, systems and kits appropriate for first line and/or adjunct therapy with antivenom using at least one active component, in some instances at least two active components and in other instances no more than two active components selected from the group consisting of a selective secretory PLA.sub.2 inhibitor (sPLA2 or PLA.sub.2 inhibitor), a metalloproteinase inhibitor, a serine protease inhibitor, antivenom, one or more acetylcholinesterase inhibitors or a nAChR agonist paired with a mAChR antagonist, a NMDA receptor antagonist and a spreading factor inhibitor to treat a subject who suffers from an envenomation, preferably at the time of envenomation and often within a period of less than about an hour after an envenomation or 6 hours after an envenomation and throughout the course of treatment at time with or without antivenom as an adjunct therapy after an envenomation by, for example, a snake or invertebrate.

The invention provides methods of treatment, pharmaceutical compositions, systems and kits appropriate for first line and/or adjunct therapy with antivenom using at least one active component, in some instances at least two active components and in other instances no more than two active components selected from the group consisting of a selective secretory PLA.sub.2 inhibitor (sPLA2 or PLA.sub.2 inhibitor), a metalloproteinase inhibitor, a serine protease inhibitor, antivenom, one or more acetylcholinesterase inhibitors or a nAChR agonist paired with a mAChR antagonist, a NMDA receptor antagonist and a spreading factor inhibitor to treat a subject who suffers from an envenomation, preferably at the time of envenomation and often within a period of less than about an hour after an envenomation or 6 hours after an envenomation and throughout the course of treatment at time with or without antivenom as an adjunct therapy after an envenomation by, for example, a snake or invertebrate.

Disclosed herein are pharmaceutical compositions and uses thereof in treating Parkinson’s disease. The pharmaceutical composition comprises an ethanol extract of an herbal mixture consisting of Artemisia argyi, Morus alba L., LeonurusjaponicusHoutt, Capsicum annuum L., Lophatherum gracile Brongn, Cur-cuma longa, and Glycyrrhiza uralensis; and a pharmaceutically acceptable excipient. The ethanol extract comprise 14 ingredients, including chlorogenic acid, leonurine, schaftoside, rutin, isochaftoside, isochlorogenic acid, 4, 5-dicaffeoylquinic acid, quercetin, apigenin, glycyrrhizic acid, bisdemethoxycurcumin, demethoxycurcumin, curcumin and artemisetin.

Disclosed herein are pharmaceutical compositions and uses thereof in treating Parkinson’s disease. The pharmaceutical composition comprises an ethanol extract of an herbal mixture consisting of Artemisia argyi, Morus alba L., LeonurusjaponicusHoutt, Capsicum annuum L., Lophatherum gracile Brongn, Cur-cuma longa, and Glycyrrhiza uralensis; and a pharmaceutically acceptable excipient. The ethanol extract comprise 14 ingredients, including chlorogenic acid, leonurine, schaftoside, rutin, isochaftoside, isochlorogenic acid, 4, 5-dicaffeoylquinic acid, quercetin, apigenin, glycyrrhizic acid, bisdemethoxycurcumin, demethoxycurcumin, curcumin and artemisetin.

The inventors have unexpectedly discovered that shock and/or potential multi-organ failure due to shock can be effectively treated by administration of liquid high-dose protease inhibitor formulations to a location upstream of where pancreatic proteases are introduced into the gastrointestinal tract. Most preferably, administration is directly to the stomach, for example, via nasogastric tube under a protocol effective to treat shock by such administration without the need of providing significant quantities of the protease inhibitor to the jejunum and/or ileum.

The inventors have unexpectedly discovered that shock and/or potential multi-organ failure due to shock can be effectively treated by administration of liquid high-dose protease inhibitor formulations to a location upstream of where pancreatic proteases are introduced into the gastrointestinal tract. Most preferably, administration is directly to the stomach, for example, via nasogastric tube under a protocol effective to treat shock by such administration without the need of providing significant quantities of the protease inhibitor to the jejunum and/or ileum.

The present invention discloses a selective butyrylcholinesterase inhibitor having a general formula (I) or a pharmaceutically acceptable salt thereof, a preparation method and use thereof. The treatment efficacy of Alzheimer’s disease, especially moderate to severe Alzheimer’s disease, is tested through butyrylcholinesterase inhibitory activity, selectivity screening and toxicity to nerve cells as a carrier, and it is found that it has good target activity in vitro, extremely high selectivity and drug safety, can be used as a lead substance for further development of the treatment of Alzheimer’s disease by selectively inhibiting butyrylcholinesterase.

The present invention discloses a selective butyrylcholinesterase inhibitor having a general formula (I) or a pharmaceutically acceptable salt thereof, a preparation method and use thereof. The treatment efficacy of Alzheimer’s disease, especially moderate to severe Alzheimer’s disease, is tested through butyrylcholinesterase inhibitory activity, selectivity screening and toxicity to nerve cells as a carrier, and it is found that it has good target activity in vitro, extremely high selectivity and drug safety, can be used as a lead substance for further development of the treatment of Alzheimer’s disease by selectively inhibiting butyrylcholinesterase.

The present invention relates to methods for enhancing Hypoxia inducible factor-1 (HIF) activity in a cell by contacting the cell with any one of the following compounds: 3,6-bis[2-(dimethylamino)ethoxy]-9h-xanthen-9-onedihydrochloride, 2,8-bis[dimethylaminoacetyl]dibenzofurin dihydrochloride hydrate, tilorone analog R-9536-DA, indoprofen, ciclopiroxolamine, tryptophan, ansindione, nabumetone, oxybendazole, albendazole, tropicamide, pramoxine hydrochloride, atenolol, mebendazole, carbetapentane citrate, monensin sodium, methoxyvone, hydroxyzine, phenazopyridine, clofoctol, ipraflavone, zomepirac, biochanin A, xylometazoline hydrochloride, fenbendazole, pirenzepine, triprolidine hydrochloride, daidzein, tripelennamine citrate, colchicines, aminopyridine, trimethoprim, helenine, hydroxyurea, amiodarone hydrochloride, clindamycin hydrochloride, sulfachlorpyridazine, mephenesin, semustine, clofivric acid, clofibrate, ibuprofen, hyoscyamime, nafcillin sodium, piperin, clidinium bromide, trioxsalen, hydralazine and HIF alpha protein fused to a carrier peptide.