Methods of treating skin disorders using anti-IL-31RA antibodies
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Publication Number
US-10611846-B2
Publication Date
2020-04-07
Expiration Date
Abstract
The present invention relates to methods of treating patients suffering from Contact dermatitis, Drug induced delayed type cutaneous allergic reactions, Toxic epidermal necrolysis, Cutaneous T cell Lymphoma, Bullous pemphigoid, Alopecia aereata, Vitiligo, Acne Rosacea, Prurigo nodularis, Scleroderma, Herpes simplex virus, or combination by administering an IL-31RA antagonist.
Core Innovation
The invention relates to IL-31RA antagonism for treatment of a skin disorder involving CLA+ T-cell involvement. The approach is described using IL-31/IL-31RA/OSMRbeta biology, where IL-31 expression is restricted to skin-homing CLA+ T cells and IL-31RA is expressed on epidermal keratinocytes and other skin infiltrating cells. Therapeutic compositions are defined around IL-31RA antagonism rather than IL-31 alone, targeting IL-31RA in skin-associated inflammatory pathways.
The document states that therapeutics include anti-IL-31RA antibodies and antibody fragments that bind specified IL-31RA amino-acid ranges. In particular, IL-31RA polypeptide forms are described, including a long form (SEQ ID NO:6; residues 20-519) and a short form (SEQ ID NO:8; residues 33-532), along with soluble receptor forms including soluble IL-31RA and IL-31RA/OSMRbeta soluble receptors. The invention therefore encompasses antibody antagonists directed to defined IL-31RA sequence regions and/or soluble receptor forms that function as IL-31RA antagonists.
The document provides experimental support showing IL-31-related activity in CLA+ cells and IL-31RA expression in diseased skin contexts. It describes human primary T-cell bioassays indicating IL-31 production primarily by activated CLA+ cells, and immunohistochemistry indicating IL-31RA upregulation in atopic dermatitis epidermis and expression on macrophages. It also describes a mouse model where anti-IL-31 antibody treatment reduces TARC and MDC, supporting a role of IL-31/IL-31RA signaling in skin disease-associated chemokine activity.
Claims Coverage
The partial content identifies one independent claim covering treatment of bullous pemphigoid using a therapeutically effective anti-IL-31RA antibody composition. The claim set includes dependent claims that specify neutralizing activity, permitted Fc-region immunoglobulin classes, and a humanized antibody attribute, yielding five inventive features centered on IL-31RA binding.
Treating bullous pemphigoid with anti-IL-31RA antibody binding IL-31RA residues 20-519
A method of treating a patient with a skin disorder by administering a therapeutically effective amount of a pharmaceutical composition comprising an anti-IL-31RA antibody and a pharmaceutically acceptable carrier, where the antibody binds amino acid residues 20-519 of SEQ ID NO:6, and wherein the skin disorder is bullous pemphigoid.
Neutralizing anti-IL-31RA antibody
The method includes using a neutralizing anti-IL-31RA antibody.
Fc region immunoglobulin class selection (IgG, IgA, IgD, IgM, or IgE)
The method is carried out using an anti-IL-31RA antibody whose Fc region is IgG, IgA, IgD, IgM, or IgE.
IgG Fc region
The method is performed using an anti-IL-31RA antibody whose Fc region is an IgG antibody.
Humanized anti-IL-31RA antibody
The method further provides that the anti-IL-31RA antibody is humanized.
Across the independent claim and its dependents, the claim coverage centers on administering a therapeutically effective anti-IL-31RA antibody composition for bullous pemphigoid, with the antibody binding IL-31RA residues 20-519 of SEQ ID NO:6. Dependent claims further require neutralizing activity, constrain Fc-region immunoglobulin classes including IgG specifically, and specify that the antibody is humanized.
Stated Advantages
Not explicitly described in patent.
Documented Applications
Not explicitly described in patent.
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