Antigen binding proteins

Abstract

Antigen binding proteins that bind β-amyloid peptide, in particular human β-amyloid peptide; methods of treating diseases or disorders characterised by elevated β-amyloid levels or β-amyloid deposits, particularly Alzheimer's disease and diseases or disorders affecting the eye or optic nerve characterised by elevated β-amyloid levels or β-amyloid deposits, including age related macular degeneration and glaucoma type diseases and β-amyloid dependent cataract formation, with said antigen binding proteins; pharmaceutical compositions comprising said antigen binding proteins; and methods of manufacture.

Description

FIELD OF THE INVENTION[0001]The present invention relates to antigen binding proteins, including antibodies, that bind β-amyloid peptide and in particular human β-amyloid peptide. The present invention also concerns methods of treating diseases or disorders characterised by elevated β-amyloid levels or β-amyloid deposits, particularly Alzheimer's disease and diseases or disorders affecting the eye or optic nerve characterised by elevated (β-amyloid levels or β-amyloid deposits, including age related macular degeneration, glaucoma type diseases and β-amyloid dependent cataract formation, with antigen binding proteins that bind β-amyloid peptide, particularly human β-amyloid peptide. Other aspects of the present invention will be apparent from the description below.BACKGROUND OF THE INVENTION[0002]Alzheimer's disease (AD) is the most common cause of age-related cognitive decline, affecting greater than 12 million individuals worldwide (Citron M (2002) Nat. Neurosci 5, Suppl 1055-1057)...

AI Technical Summary

Benefits of technology

[0082]The person skilled in the art appreciates that in order for an antigen binding protein (antigen binding protein A) to compete with an antibody comprising a heavy chain having the sequence set forth in SEQ ID No:27 and a light chain having the sequence set forth in SEQ ID No:28 (antibody B) for a specific binding site (β-amyloid), antigen binding protein A must be present in a sufficient amount to have an effect in said assay. In a particular embodiment, antigen binding protein A and antibody B are present in equimolar amounts. In another embodiment, the presence of antigen binding protein A reduces the binding of antibody B to β-amyloid in an ELISA assay by more than 10%, 20%, 30%, 40% or 50%. In another embodiment (β-amyloid is bound to an immunoassay plate in an ELISA assay. In another embodiment antigen binding protein A reduces the binding of antibody B to plate bound β-amyloid, whereas a non-β-amyloid-specific control does not.

Problems solved by technology

The potential for a disease-modifying therapy that slows and possibly halts the progression of the disease is enormous.

These considerable biological differences in the various transgenic mouse models used have made it difficult to compare the pharmacology and the efficiency of different approaches.

In this form of the disease, the degeneration of RPE results in the secondary death of macular rods and cones and in these cases this leads to the severe age-related vision loss.

In both forms of the disease, vision loss occurs due to the death of photoreceptor cells, although in wet AMD internal bleeding from the leaky vessels formed during CNV also causes vision loss.

However, currently there are no definitive means of treatment for the very prevalent atrophic form of AMD nor to prevent the progression of early dry AMD either to geographic atrophy or to wet AMD, (Petrukhin K (2007) Expert Opin Ther Targets 11: 625-639)

This may result in decreased levels of Aβcontaining drusen and / or local Aβ in the surrounding environment of the RPE and thereby interfere in both the early and later stages of AMD and treat the underlying cellular decline that causes the loss of vision.

It is a major cause of blindness in the world caused ultimately by increased intraocular pressure (IOP) and decreased visual acuity.

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