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US 2017/0281756 A1Published application
Compositions and methods to selectively block pain induced by cold
AssigneeUniversity of Southern California
InventorDavid D. McKemy
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AssigneeUniversity of Southern California
InventorDavid D. McKemy
Estimating the term…
Tissue injury prompts the release of a number of proalgesic molecules that induce acute and chronic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli. In contrast, many proalgesics have no effect on cold sensitivity, or can inhibit cold-sensitive neurons and diminish cooling-mediated pain-relief (analgesia). Nonetheless, cold pain (allodynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mechanisms promoting pain versus those dampening analgesia. This disclosure establishes provides methods and compositions to treat cold allodynia induced by inflammation, nerve injury, and chemotherapeutics. One such therapy is the administration of antibodies against the GFRα3 ligand, artemin.
A method to treat and/or inhibit, and/or reduce pre-existing cold pain and/or pain that induced by NGF in a subject in need thereof, comprising administering to the subject of an effective amount of an agent that interferes with GFRα3 signaling in a cell expressing the GFRα3 receptor.
A method to treat and/or inhibit, and/or reduce pre-existing cold pain and/or pain that induced by NGF in a subject in need thereof, comprising administering to the subject of an effective amount of an agent that interferes with NGF receptor binding.
A method for the treatment of a disease or condition that relates to GFRα3 receptor signaling in a cell or tissue in a subject in need thereof, comprising administering to the subject an effective amount of an agent that interferes with GFRα3 signaling in the cell or the tissue expressing the GFRα3 receptor.
A method to identify a therapeutic agent to treat and/or inhibit, and/or reduce pre-existing cold pain and/or that induced by NGF in a subject in need thereof comprising contacting a cell that expresses an GFRα3 receptor with a test agent and assaying for interference with GFRα3 signaling in the cell, wherein an agent that interferes with GFRα3 receptor signaling is a potential therapeutic agent and an agent that does not interfere with GFRα3 receptor signaling is not a potential therapeutic agent.
Dependencies are inferred from the claim text.