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Ozoralizumab (trade name Nanozora) is a trivalent anti-tumour necrosis factor alpha (TNFα) nanobody designed for the treatment of inflammatory diseases. [1] Ozoralizumab was developed by Pfizer Inc, and now belongs to Ablynx NV. Ablynx has licensed the rights to the antibody in China to Eddingpharm.
A single-domain antibody is a peptide chain of about 110 amino acids long, comprising one variable domain (V H) of a heavy-chain antibody, or of a common IgG.These peptides have similar affinity to antigens as whole antibodies, but are more heat-resistant and stable towards detergents and high concentrations of urea.
This list of over 500 monoclonal antibodies includes approved and investigational drugs as well as drugs that have been withdrawn from market; consequently, the column Use does not necessarily indicate clinical usage. See the list of FDA-approved therapeutic monoclonal antibodies in the monoclonal antibody therapy page.
Several bsAb drugs have been approved by the US FDA / EMA and over 180 are currently in clinical trials. The first bispecific antibody to gain regulatory approval, blinatumomab , targets CD19 on B cells and CD3 on T cells, leading to the activation of T cells and the destruction of B cells. [ 31 ]
Talquetamab was approved for medical use in both the United States [9] [13] [14] and the European Union [15] in August 2023. The US Food and Drug Administration (FDA) considers it to be a first-in-class medication .
The FDA has signed off MoonLake Immunotherapeutics AG's (NASDAQ: MLTX) Phase 2 study of the nanobody sonelokimab in patients with active psoriatic arthritis (PsA). This is a global clinical study ...
The European Commission approved Inotuzumab ozogamicin [15] as a monotherapy for the treatment of adults with relapsed or refractory CD22-positive B-cell precursor acute lymphoblastic leukemia (ALL) on June 30, 2017 under the trade name Besponsa® (Pfizer/Wyeth), [16] followed on August 17, 2017 by the FDA.
Efgartigimod alfa as a drug is an antibody fragment that binds to the neonatal Fc receptor. When this binding happens, the IgG recycling process is blocked. The amount of circulating IgG decreases and therefore prevents the acetylcholine receptors from being degraded by the autoantibodies that are responsible for the myasthenia gravis. [14]