I. Treatment of RA Includes early treatment, combined treatment: chemical drugs + chemical drugs, chemical drugs + biological drugs. Second, the treatment of RA drugs NASID: inhibit the inflammatory response, but itself can not change the progression of RA, aspirin, etc.; DMARDs: can delay the joint damage and insufficiency in the early stage of RA disease, alleviate the disease, but long-term use generally can not control the process of RA. Corticosteroids: reduce joint damage by inhibiting inflammation, but have many local side effects and are not suitable for long-term treatment; Biological agents: act by interfering with cytokine activity and inhibit the body’s autoimmune response to protect joints and relieve pain. Less. A new class of therapeutic drugs represented by TNFα antagonists is the most popular research at present. Third, new drug research Drug types: chemical drugs, therapeutic biologics, preventive biologics (vaccine class), natural drugs of traditional Chinese medicine; drug registration classification: new drugs (not listed at home and abroad), generic drugs (already listed in China, generic), imported drugs; new drugs of laboratory medicine: innovative drugs, effective monomers extracted from natural drugs or fermented extracts (can be declared as chemical drugs or traditional Chinese medicine), split optical isomers, the New compound preparations, change the route of administration of drugs, imitation of domestic and foreign listed drugs (will change), change the acid root base of the drug, change the dosage form of drugs. Biological drugs: not listed at home and abroad, monoclonal antibodies, gene therapy somatic cell therapy and its products, allergic reactive original products, microecological products containing unapproved strains of bacteria preparation, products with different preparation methods from those already on the market. Fourth, according to the different targets of RA drug research according to different targets of new drug research. At present, the main targets are TNFα, IL-6R, IL-17, CTLA4, CD20, JAK, etc. 1.TNFα: a cytokine that promotes inflammation, mainly produced by activated monocytes, macrophages and T cells. Excessive production of TNFα leads to histopathological changes, such as synovitis, cartilage matrix explanation and bone loss, which in turn leads to joint deformation and disability. 2. JAK kinase: a family of non-receptor-type complex kinases that are important signaling sensors for many cytokines, etc. JAK kinase inhibitors: Targeted blockade of JAK/STAT pathway to improve the pathophysiological process of RA. 3, SYK activity inhibitor: SYK is an immune signaling regulator, which has a key role in the signaling process of cells. In RA patients with increased levels of phosphorylated SYK in fibroblast-like synoviocytes, SYK signaling inhibitors can inhibit the active level of RA and may be a treatment for RA. 4. IL-17 targets: IL-17A is the central cytokine of the inflammatory T cell subpopulation. In RA, IL-17 affects fibroblasts and macrophages in synovial tissue, chondrocytes, and osteoblasts in bone. It can induce the production of proinflammatory cytokines. Neutralization of IL-17A is expected to alter the pathophysiology underlying immune-mediated disease and thus alleviate symptoms. 5, IL-6 RA pathology has elevated tissue or serum IL-6, and inhibition of the biological activity of IL-6 and/or its receptors is a novel approach to the treatment of RA. 6.CD6 monoclonal antibody: humanized anti-CD6 monoclonal antibody injection Indications: Combined with methotrexate for the treatment of active RA, psoriasis, etc.