Immunoglobulin constant region Fc receptor binding agents
AssigneesGliknik Inc., University of Maryland, Baltimore
InventorsScott E. Strome, Dan H. Schulze, David S. Block, Henrik Olsen
Life of this patent
Estimating the term…
Abstract
IVIG replacement compounds are derived from recombinant and/or biochemical creation of immunologically active biomimetic(s). These replacement compounds are then screened in vitro to assess each replacement compound's efficiency at modulating immune function. Particular replacement compounds are selected for further in vivo validation and dosage/administration optimization. Finally, the replacement compounds are used to treat a wide range of diseases, including inflammatory and autoimmune diseases.
Claims20
A method for binding human low affinity Fcγ receptors (FcγR) on effector cells comprising administering a recombinantly produced biomimetic composition to a population of effector cells, wherein the biomimetic composition comprises two or more human IgG4 Fc domains wherein each of the two or more human IgG4 Fc domains is capable of binding to a human low affinity FcγR, wherein the biomimetic composition binds to two or more human low affinity FcγRs, and wherein the biomimetic composition does not comprise either an antigen binding domain or a non-immunoglobulin protein, and wherein the human low affinity FcγR is an FcγRIIA, an FcγRIIB, or an FcγRIIIA receptor.
A method for binding human low affinity Fcγ receptors (FcγR) on effector cells comprising administering a recombinantly produced biomimetic composition to a population of effector cells, wherein the biomimetic composition comprises three or more human IgG4 Fc domains wherein each of the three or more human IgG4 Fc domains comprises an IgG4 CH2 and an IgG4 CH3 domain and is capable of binding to a human low affinity FcyγR, wherein the biomimetic composition binds to two or more human low affinity FcγRs, and wherein the biomimetic composition does not comprise either an antigen binding domain or a non-immunoglobulin protein, and wherein the human low affinity FcγR is an FcγRIIA, an FcγRIIIB, or an FcγRIIIA receptor.
Dependencies are inferred from the claim text.