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US 2002/0165197 A1Published application
Modulation of GSK-3beta activity and its different uses
OwnerPnina Fishman, Kamel Khaliliinventors
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OwnerPnina Fishman, Kamel Khaliliinventors
Estimating the term…
The present invention concerns the modulation of glycogene synthase kinase 3β (G3SK-3β) by an adenosine receptor ligand. Depending on the type of ligand, the modulation may be manifested by down-regulation or up-regulation of the kinase's activity. Thus, there is provided by the present invention a method and pharmacetical compositions for achieving a therapeutic effect involved in modulating GSK-3β activity in cells by the use of an adenosine receptor ligand or a combination of ARLs. When modulation involves activation of GSK-3β activity the ARL may be an adenosine A1 receptor agonist (A1RAg), an adenosine A3 receptor agonist (A3RAg), an adenosine A2 receptor antagonist (A2RAn) or any combination of the same, while when modulation involves inhabition of GSK-3β activity the ARL may be an adenosine A1 receptor antagonist (A1RAn), an adenosine A3 receptor antagonist (A3RAn), an adenosine A2 receptor agonist (A2RAg) or any combination of the same.
A method for a therapeutic treatment, comprising administering to a subject in need an effective amount of an active agent for achieving a therapeutic effect, the therapeutic effect comprises modulating GSK-3β activity in cells and said active agent is an adenosine receptor ligand (ARL).
A pharmaceutical composition for achieving a therapeutic effect in a subject in need, the therapeutic effect comprising modulating GSK-3β activity in target cells, the composition comprising a therapeutically effective amount of at least one active agent and one or more pharmaceutically acceptable additives, said active agent is an adenosine receptor ligand (ARL).
Use of an adenosine receptor ligand (ARL) for modulating GSK-3β activity in cells.
Use of an adenosine receptor ligand (ARL) for the preparation of a pharmaceutical composition for tie treatment of a disease or disorder which requires for its treatment suppression of GSK-3β activity.
Dependencies are inferred from the claim text.