摘要:
This invention relates to methods employing IL-1β-ligand/IL-1 receptor disrupting compounds such as IL-1β antibodies or IL-1 receptor antibodies, in the treatment and/or prevention of Familial Mediterranean Fever (FMF), in mammals, particularly humans.
摘要:
Human lubricating gels, methods and kits for delivering a therapeutic agent to a target tissue site beneath the skin of a patient utilizing human lubricating gel are provided, the human lubricating gel being capable of adhering to the target tissue site and comprising one or more biodegradable formulations containing an effective amount of the therapeutic agent. In various embodiments, the human lubricating gel is sprayable and hardens after contacting the target tissue site.
摘要:
Provided are protein, nucleic acid, and cellular libraries of single chain multivalent binding proteins (e.g., scDVD and scDVDFab molecules) and methods of using these of these libraries for the screening of single chain multivalent binding proteins using cell surface display technology (e.g., yeast display).
摘要:
The invention relates to a platform technology for production of antigen binding polypeptides having specificity for a desired target antigen which is based on the conventional antibody repertoire of species in the family Camelidae, and to antigen binding polypeptides obtained using this technology platform. In particular, the invention provides an antigen binding polypeptide comprising a VH domain and a VL domain, wherein at least one hypervariable loop or complementarity determining region (CDR) in the VH domain or the VL domain is obtained from a VH or VL domain of a species in the family Camelidae.
摘要:
The present invention relates to anti-IL-1 beta binding members and in particular to monovalent high potency IL-1 beta-binding antibody fragments being highly stable and soluble. Such binding members may be used in the treatment of inflammatory and other diseases as well as in diagnostics. Also provided are related nucleic acids, vectors, cells, and compositions.
摘要:
A method of treating a pathological syndrome includes administration of an activated form of ultra-low doses of antibodies to an antigen, wherein said activated form is obtained by repeated consecutive dilution combined with external impact, and the antigen is a substance or a pharmaceutical agent exerting influence upon the mechanisms of formation of this particular pathological syndrome.Pharmaceutical agent for treating a pathological syndrome contains activated form of ultra-low doses of monoclonal, polyclonal or natural antibodies to an antigen, wherein said activated form is prepared by means of repeated consecutive dilution and external treatment, predominantly based on homeopathic technology, and said antigen is a substance or a drug acting as a direct cause of the pathological syndrome or involved in regulation of mechanisms of its formation. At that, activated forms of ultra-low doses of antibodies are raised against antigens of exogenous or endogenous origin, against autologous antigens, fetal antigens; anti-idiotypic antibodies are used too.
摘要:
Techniques and devices for removing (filtering out) unwanted/inhibitory components (for example, products, byproducts and/or cell output such as inhibitory catabolic proteins) from a composition (for example, autologous fluid or serum) containing such unwanted/inhibitory components. The devices include at least one construct designed to contain a composition (for example, autologous fluid or serum) containing inhibitory/unwanted components (products, byproducts and/or output of cells such as inhibitory catabolic proteins). The construct is provided with interior walls including specific protein capturing means designed to remove the inhibitory/unwanted component(s) (for example, specific protein(s)) from the composition. Proteins targeted for capture include, but are not limited to, catabolic cytokines such as IL-1β, IL-α, IL-6, TNFα, IFNγ and MMPS as these proteins inhibit the healing process.
摘要:
The present invention includes compositions and methods for treating arthritic joints found in patients with autoinflammation, e.g., systemic onset juvenile idiopathic arthritis, by administering at the site of inflammation a therapeutically effective amount of at least one agent that reduces or blocks the bioavailability of interleukin-1β.