42 results about "Tumor necrosis factor α" patented technology

Methods and compositions for the prevention and treatment of all forms of atherosclerosis are described. Administration of compounds such as thalidomide, its analogs, hydrolysis products, metabolites, derivatives and precursors as well as additional compounds capable of inhibiting tumor necrosis factor α(TNF-α) are used in the invention. Also disclosed is the coating of prosthetic devices, such as stents, with the compounds of the invention for the prevention and / or treatment of restenosis.

The present invention relates to compositions and methods for treating related diseases or conditions by reducing tumor necrosis factor-alpha levels and / or by stimulating angiogenesis using alpha-7 nicotinic acetylcholine receptor (AChR) full agonists.

The present invention provides introduction of NF-κB decoy oligodeoxynucleotide into rat cranial nerve through a carotid artery during global brain ischemia. Polymerase chain reaction demonstrated that one hour after global brain ischemia, transfected NF-κB decoy oligodeoxynucleotide effectively suppressed expression of tumor necrosis factor α, interleukin 1β and intracellular adhesion molecule 1 messenger RNAs. Terminal deoxynucleotidyl transferase-mediated deoxyuridine nick-end labeling staining and immunohistochemistry using microtubule-associated protein 2 demonstrated that transfected NF-κB decoy oligodeoxynucleotide significantly attenuated neuronal damage seven days after global brain ischemia. Therapeutic transfection of NF-κB decoy oligodeoxynucleotide during brain ischemia may be effective for attenuation of neuronal damage, suggesting a strategy for protecting the cerebrum from global ischemia.

The enhydrazone esters for treating asthma, allergy, and inflammation relate to the use of two cyclohexenone derivatives and pharmaceutically acceptable salts thereof in the treatment of asthma, allergies, and inflammation. The esters have the formula:wherein R is ethyl or methyl. Administration of the esters inhibits the degranulation of eosinophils, the degranulation of mast cells, and the release or expression of tumor necrosis factor-α, thereby alleviating the debilitating symptoms of asthma, allergic reactions, and inflammatory responses.

The present invention relates to an orally administrable immunostimulatory product comprising microencapsulated cytokines, which are cells of fish, molluscs or crustaceans, and an enteroprotective polymer for protecting said cytokines Factors, preferably recombinant cytokines, such as tumor necrosis factor alpha (TNFα) overexpressed in the host microorganism.

The present invention belongs to the field of the application of genetic engineering and gene function, and it is directed to a new medical use of the gene encoding the recombinant soluble tumor necrosis factor α receptor (HusTNFR). The present invention made intervention to fulminant hepatic failure in mice by use of the long-acting recombinant human soluble tumor necrosis factor α receptor and the classic animal models of acute and sub-acute hepatic failure. The results showed that the long-acting soluble tumor necrosis factor α receptor of the present invention has a half-life extended more than 10 times, and it significantly decreased the mortality of model animals and has superior therapeutic effect for the treatment and / or prophylaxis of acute and sub-acute hepatic failure in model animals. These receptors have a noticeable therapeutic effect for the treatment and / or prophylaxis of acute and sub-acute hepatic failure in comparison with the non-long-acting HusTNFR.

The present invention relates to derivatives of 1,2-diaza-dibenzoazulene, to their pharmacologically acceptable salts and solvates, to processes and intermediates for the preparation thereof as well as to their antiinflammatory actions, especially to the inhibition of tumor necrosis factor-α (TNF-α) production and the inhibition of interleukin-1 (IL-1) production as well as to their analgetic action.

RNA interference is provided for inhibition of tumor necrosis factor α (TNFα) by silencing TNFα cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFα converting enzyme (TACE / ADAM17) mRNA expression. Silencing such TNFα targets, in particular, is useful for treating patients having a TNFα-related condition or at risk of developing a TNFα-related condition such as the ocular conditions associated with elevated intraocular pressure (IOP), including glaucoma and ocular hypertension.