This invention relates to inhibition of the complement signaling using an anti-C5 antibody. Specifically, the invention relates to methods of treating a complement-mediated disease or complement-mediated disorder in an individual by contacting the individual with an anti-C5 antibody.

The present invention provides for the treatment, prevention, and/or reduction of a risk of a disease, disorder, or condition in which aldehyde toxicity is implicated in the pathogenesis, including ocular disorders, skin disorders, conditions associated with injurious effects from blister agents, and autoimmune, inflammatory, neurological and cardiovascular diseases by the use of a primary amine to scavenge toxic aldehydes, such as MDA and HNE.

Compounds, tautomers and pharmaceutically acceptable salts of the compounds are disclosed, wherein the compounds have the structure of Formula Ia, ##STR00001##
as defined in the specification. Corresponding pharmaceutical compositions, methods of treatment, methods of synthesis, and intermediates are also disclosed.

The present invention relates to substituted pyrrolopyridinones and substituted pyrazolopyridinones which are inhibitors of BET proteins such as BRD2, BRD3, BRD4, and BRD-t and are useful in the treatment of diseases such as cancer.

Disclosed are compounds of Formulas (I), (II), (III), (IV), and (V): ##STR00001##
and/or a salt thereof, wherein R.sub.1 is —OH or —OP(O)(OH).sub.2, and X.sub.1, X.sub.2, X.sub.3, R.sub.2, R.sub.2a, R.sub.a, R.sub.b, and R.sub.c are defined herein. Also disclosed are methods of using such compounds as selective agonists for G protein-coupled receptor S1P.sub.1, and pharmaceutical compositions comprising such compounds. These compounds are useful in treating, preventing, or slowing the progression of diseases or disorders in a variety of therapeutic areas, such as autoimmune diseases and vascular disease.

The present invention relates to non-immunogenic RNA. This RNA forms the basis for the development of therapeutic agents for inducing tolerance towards an autoantigen and thus, for the treatment of autoimmune diseases.

Disclosed are a quinazolinone derivative, a preparation method therefor, a pharmaceutical composition, and applications. Provided are a compound represented by formula I, a pharmaceutically acceptable salt, a solvate, a crystal form, a eutectic crystal, a stereoisomer, an isotope compound, a metabolite, or a prodrug thereof. Generation or activity of a cell factor can be regulated, and accordingly, cancers and inflammatory diseases can be effectively treated. ##STR00001##

Provided herein are methods and compositions for treating inflammatory disease by the administration, to a patient in need thereof, of an inhibitor of IL-2R desensitization in combination with a low dose of IL-2. A low dose of interleukin-2 (IL-2) is sufficient to stimulate regulatory T lymphocytes (Tregs) without substantially inducing effector T lymphocytes (Teffs). In some embodiments, the inhibitor of IL-2R desensitization is a small molecule or drug. Is some embodiments the inhibitor is a NEDD8 activating enzyme (NAE) inhibitor. In some embodiments a combination therapy provides for a synergistic effect, where the combination of the inhibitor of IL-2R desensitization and low dose IL-2 provides an effect that is greater than the sum of either the inhibitor or low dose IL-2 administered as a single agent.

The invention provides compositions for establishing mixed chimerism in a subject. The compositions include CD34.sup.+ cells that have been column-purified from an apheresis product and CD3.sup.+ cells from an apheresis product that have not been purified through a column. The invention also provides methods of making and using such compositions.

The invention is fused heterocyclic compounds of formula (I), and salts thereof, compositions thereof, and methods of use therefor. In particular, disclosed herein are certain fused heterocyclic compounds that can be useful for inhibiting protein kinase, including Bruton's tyrosine kinase (Btk), and for treating disorders mediated thereby.

##STR00001##