49 results about "Tumour necrosis factor alpha" patented technology

The invention features a series of heterocyclic derivatives that inhibit tumor necrosis factor alpha (TNF-α) induced necroptosis. The heterocyclic compounds of the invention are described by Formulas (I)-(VIII) and by Compounds (I)-(I), (13)-(26), (27)-(33), (48)-(57), and (58)-(70). These necrostatins are shown to inhibit TNF-α induced necroptosis in FADD-deficient variant of human Jurkat T cells. The invention further features pharmaceutical compositions featuring necrostatins. The compounds and compositions of the invention may also be used to treat disorders where necroptosis is likely to play a substantial role.

The present disclosure describes the use of genetic variance information for genes involved in inflammatory or immunologic disease, disorder, or dysfunction. The variance information is indicative of the expected response of a patient to a method of treatment. Methods of determining relevant variance information and additional methods of using such variance information are also described.

The invention relates to a dermatological pharmaceutical composition for the treatment of skin inflammation diseases, such as dermatitis, atopic dermatitis, vitiligo, alopecia areata, acne, psoriasis and pruritus. The invention comprises a base anti-inflammatory agent, such as indometacin; one or more optional active ingredients selected alternatively from among at least a corticoid and an antibiotic; and a combination of topical antioxidants used to potentiate the anti-inflammatory effect, selected from among green tea, lipoic acid, curcumin, ascorbyl palmitate, Coenzyme Q10, resveratrol, Pycnogenol™, L-camosine, taurine, vitamin E, vitamin C, papaya extract, isoflavones, manganese, lycopene and quercetin. At least one of the topical antioxidants is a peroxisome proliferator-activated receptor-gamma (PPAR-γ) activator. The invention also includes at least one antioxidant substance with an antiproliferative effect on keratonocytes, e.g. manganese, and at least one substance that blocks tumour necrosis factor-alpha (TNF-α) or other cytokines that provoke the acute phase of the inflammatory reaction, also with an antiproliferative effect, e.g. pentoxifylline.

The invention relates to a method for preparing pig-bile-combination-type total bile acid. The method comprises the steps of extracting by utilizing ethanol, separating and purifying and drying. Proved by medicinal effectiveness tests for treating colonitis, the pig-bile-combination-type total bile acid prepared by utilizing the method provided by the invention has an inhibitory action on the increase of myeloperoxidase activity and tumor necrosis factor alpha content of model mice and has the advantages of inhibiting the secretion of proinflammatory cytokine, regulating the immune response, effectively blocking the damage of the immunoreactivity to an organism and achieving the purpose of treating colonic inflammation. The pig-bile-combination-type total bile acid prepared by utilizing the method provided by the invention can be adopted as a raw material to be made into various commonly-used preparation types such as tablets, capsules, powders, pills, granules, enemas and the like.

Compounds of formula 1:

are disclosed, wherein V is CH₂; W is S(O)_m; m is the integer 0, 1 or 2; U is O, C(O), CR₁₃R₁₄ or NR₁₅; where R₁₃ is H, alkyl; R₁₄ is H, OH, OR₁₃ or OCOR₁₃; R₁₅ is H, alkyl, cycloalkyl, alkenyl, C(O)R₁₃, C(O)OR₁₃ or alkylaminocarbonyl; R₁, R₂, R₃, R₄, R₅, R₆, R₇ and R₈ are as defined herein. These compounds are inhibitors of tumor necrosis factor-alpha (TNF-α) and are useful as medicaments for the treatment and prevention of disorders caused by increased TNF-α activity, in particular inflammations.

Aspects of the invention relate to topical and ocular formulations of spherical nucleic acids (SNA), as well as methods of use thereof and compositions thereof. The formulations may include an inhibitor such as an inhibitor of tumour necrosis factor alpha (TNFa), platelet-derived growth factor subunit A (PDGFA), platelet-derived growth factor subunit B (PDGFB), platelet-derived growth factor subunit C (PDGFC), platelet-derived growth factor subunit D (PDGFD), platelet-derived growth factor receptor alpha (PDGFRA), platelet-derived growth factor receptor beta (PDGFRB), platelet-derived growth factor receptor like (PDGFRL), vascular endothelial growth factor A (VEGFA), vascular endothelial growth factor B (VEGFB), vascular endothelial growth factor C (VEGFC) vascular endothelial growth factor D (VEGFD), vascular endothelial growth factor receptor-1 (VEGFR1), vascular endothelial growth factor receptor-2 (VEGFR2), vascular endothelial growth factor receptor-3 (VEGFR3), beta-2 adrenergic receptor (ADRB2), connective tissue growth factor (CTGF), interleukin 1 beta (IL1 β), interleukin 1 receptor-1 (IL1 R1), interleukin 1 receptor-2 (IL1R2), and interleukin 1 receptor-3 (IL1R3). Aspects of the invention further relate to nanostructures comprising self-assembling therapeutic oligonucleotides, such as antisense oligonucleotides, that are linked to a molecular species, wherein the molecular species is positioned in a core of the nanostructure and the oligonucleotides extend radially from the core.

The inhibitory oligonucleotides (ODNs) which strongly block NF-κB activation induced by TLR9 agonists and TLR7 agonists are provided. The production of proinflammatory cytokines, such as interleukin-6 and tumor necrosis factor alpha, is inhibited by the inhibitory-ODNs. Interferon production from human PBMC induced by TLR9 agonist is prevented by the inhibitory-ODNs. These ODNs can be used as a remedy for the treatment of immune-mediated disorders such as rheumatoid arthritis, systemic lupus erythematosus (SLE), sepsis, multiple organ dysfunction syndromes.

The present invention provides a RNA interferencefor inhibition of tumor necrosis factor a (TNFa) by silencing TNFa cell surface receptor TNF receptor-1 (TNFR1) mRNA expression, or by silencing TNFa converting enzyme (TACE/ADAM17) mRNA expression. Silencing such TNFa targets, in particular, is useful for treating patients having a TNFa-related condition or at risk of developing a TNFa-related condition such as the ocular conditions dry eye, allergic conjunctivitis, or ocular inflammation, or such as dermatitis, rhinitis, or asthma, for example.

The invention discloses an electrochemiluminescence detection method for a tumor necrosis factor alpha and a kit of the electrochemiluminescence detection method. According to the method, the tumor necrosis factor alpha is adopted as a detection target, a high quantum yield gold nano cluster electrochemiluminescence technique and an immunoassay technique are organically combined, a high quantum yield gold nano cluster electrochemiluminescence probe is prepared by using a reduction method, a manganese dioxide nano material is adopted as an electrochemiluminescence quenching agent, an electrochemiluminescence signal is recovered through a redox reaction between ascorbic acid generated from enzyme-linked immunosorbent assay and manganese dioxide, and the method is a high-performance electrochemiluminescence tumor necrosis factor alpha detection method based on the high quantum yield gold nano cluster probe. The method has a linear range of 0.06-31pg/mL for tumor necrosis factor alpha detection, and has a detection limit of 36fg/mL. The method has the characteristics of rapidness, accuracy, high sensitivity, good selectivity, good stability, small sample use amount and the like, and has relatively good clinical application prospects.

A new protein, named ACA1, has been isolated and purified from the medical fungi Antrodia camphorata using the technique of anion-exchange chromatography. ACA1, a glycoprotein with a molecular mass of 29 kDa, has a pI value of pH 5.3 and contains 118 amino acids in its peptide moiety. In addition, ACA1 contains methionine, half-cystine and histidine residues, which are not existent in FIP-fve and Ling Zhi-8. ACA1 is not able to agglutinate red blood cells from human and mouse. Moreover, ACA1 possesses immunomodulatory activities, which are demonstrated by their stimulatory activity toward RAW 264.7 macrophages and mouse splenocytes. ACA1 can directly enhance the production of tumor necrosis factor-alpha and nitric oxide by RAW 264.7 macrophages, and induce cell proliferation and interferon-gamma secretion by mouse splenocytes.

The invention discloses a protein segment of programmed death protein 2 analog, namely, the protein of region 2, and the application of the protein of the region 2 in preparing drugs for curing bacterial inflammation of the programmed death protein 2 analog. The protein of region 2 of the programmed death protein 2 analog realizes the function of restraining the tumor necrosis factor Alpha of a pro-inflammatory cytokine caused by bacterial LPS, thereby restraining the generating and developing of the inflammations caused by bacteria.

The present invention relates to vectors and compounds for the expression of recombinant soluble proteins. More particularly, the present invention relates to nucleic acid molecules, expression vectors, and host cells for the expression of recombinant soluble Tumour Necrosis Factor Alpha receptor (TNFR) - Human IgG Fc fusion protein. The invention further relates to methods for preparing recombinant soluble Tumour Necrosis Factor Alpha receptor (TNFR) - Human IgG Fc fusion protein using the host cells transfected with the expression vectors.

The present invention relates to Tumor Necrosis Factor-alpha (TNF-alpha or TNF-α) inhibiting peptides and process for the preparation thereof. The present invention further relates to a pharmaceutical composition comprising TNF-alpha inhibiting peptides of the present invention and uses thereof in treating TNF-alpha mediated inflammatory disorders.

The invention belongs to the field of biological medicines, and relates to a mutant protein vaccine aiming at tumor necrosis factor alpha (TNF-alpha) and applications of the mutant protein vaccine. The invention aims at providing the protein vaccine which is good in property and takes TNF-alpha as the target spot. According to the scheme, by immunizing the TNF-alpha mutant protein vaccine, the biological activity of the TNF-alpha mutant protein vaccine is inhibited, the cross immunologic reaction is generated in vivo, the biological functions of TNF-alpha are neutralized, and the autoimmune diseases and inflammatory diseases are inhibited. The protein vaccine aiming at TNF-alpha can be used for treating the autoimmune diseases and the inflammatory diseases and preventing the relapse of the autoimmune diseases and the inflammatory diseases.

The invention relates to a preparation method and an application of an effective component of artemisia sieversiana. The effective component is obtained as follows: a low-polarity component is obtained after artemisia sieversiana is subjected to conventional soaking extraction, heating reflux extraction, cold leaching extract, microwave assisted extraction or ultrasonic assisted extraction and removal of a solvent under reduced pressure, the low-polarity component is subjected to extraction with n-hexane after being dissolved and dispersed in water, an extraction part is dissolved in acetonitrile after being dried by distillation, filtrate is dried by distillation after filtration, and the effective component of the artemisia sieversiana is obtained. The effective component of the artemisia sieversiana, which is obtained with the method, proves in vitro that the effective component can be used for preventing and treating inflammation caused by excess of NO, TNF-alpha (tumor necrosis factor-alpha), IL-6 (interleukin-6) and MCP-1 (monocyte chemoattractant protein-1) and can be applied to anti-inflammatory drugs.

The invention provides novel peptide binders for streptavidin (SA), Taq polymerase and several human proteins: Prostate Specific Antigen (PSA), thrombin, Tumor Necrosis Factor Alpha (TNFα), and Urokinase-type Plasminogen Activator (uPA).

The present invention provides bispecific molecule comprising: (i) a first antigen binding portion which specifically targets the synovial microvasculature of arthritis patients and which binds to the same epitope as an antigen binding polypeptide comprising the amino acid sequence shown as SEQ ID No 11; and (ii) a second antigen binding portion which binds tumour necrosis factor alpha (TNF-α). The present invention also relates to the use of such bispecific molecules in the prevention and/or treatment of arthritis.