Therapeutics targeting transforming growth factor beta family signaling
AssigneesThe Jackson Laboratory, University of Connecticut
InventorsSe-Jin Lee, Emily Germain-Lee
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Abstract
Provided herein are methods of inhibiting type 1 receptor and/or type 2 receptor signaling in subjects, optionally subjects with diseases associated with myostatin, type 1 receptor, and/or type 2 receptor signaling, or muscle loss and/or bone deterioration. Also provided are compositions for inhibition of type 1 receptor and/or type 2 receptor signaling.
Claims89
A method of increasing muscle weight, reducing body fat content, and/or improving glucose metabolism in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ALK4 and/or ALK5 signaling in the subject.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ALK4 and ALK5 signaling specifically in myofibers of the subject
A method of increasing muscle weight, reducing body fat content, and/or improving glucose metabolism in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ACVR2A and ALK5 signaling in the subject.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ACVR2A and ALK5 signaling specifically in myofibers of the subject
A method of increasing muscle weight, reducing body fat content, and/or improving glucose metabolism in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ACVR2B and ALK5 signaling in the subject.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ACVR2B and ALK5 signaling specifically in myofibers of the subject
A method of increasing muscle weight, reducing body fat content, and/or improving glucose metabolism in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) type I and/or type II receptor signaling in myofibers of the subject.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ALK4 and/or ALK5 signaling.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ACVR2A, ACVR2B, and/or TGFβRII signaling.
The method of any one of the preceding claims, wherein the agent or combination of agents inhibit(s) ACVR2A, ACVR2B, and TGFβRII signaling.
A method of increasing muscle weight, reducing body fat content, and/or improving glucose metabolism in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) (a) TGFβRII and/or (b) TGFβ1, TGFβ2, and/or TGFβ3 signaling in the subject.
A method of increasing bone mineral density, bone volume, and/or bone density in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ALK4 and/or ALK5 signaling in the subject.
A method of increasing bone mineral density, bone volume, and/or bone density in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ACVR2A and ALK5 signaling in the subject.
A method of increasing bone mineral density, bone volume, and/or bone density in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) ACVR2B and ALK5 signaling in the subject.
A method of increasing bone mineral density, bone volume, and/or bone density in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) type 1 and/or type 2 receptor signaling in osteoblasts of the subject.
A method of increasing bone mineral density, bone volume, and/or bone density in a subject, comprising administering to the subject an agent or a combination of agents that inhibit(s) (a) TGFβRII and/or (b) TGFβ1, TGFβ2, and/or TGFβ3 signaling in the subject.
Dependencies are inferred from the claim text.