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Molecular pathway and compounds for treating neuropathic chronic pain

Summary

Lead Inventors: Richard T. Ambron Ph.D., Donald W. Landry M.D., Ph.D.Problem or Unmet Need:Chronic pain occurs after an injury and persists, potentially indefinitely, even after healing of the wound site. When nociceptive (pain) sensory neurons are damaged, they are induced into a long-term hyperexcitablity (LTH) state that causes overstimulation of downstream neurons and results in long-term perceived pain. Current medications are not specific to this type of pain, and require heavy doses that often cause undesirable side effects. Identification of injury signals, pathways, and molecules involved in induction of LTH can lead to therapeutic compounds that relieve chronic pain in a directed manner. This technology describes a molecular signaling pathway, detailing how proteins activated at the injury site can mediate cellular changes that lead to LTH and cause persistent, chronic pain. One such molecule is protein kinase G (PKG). It is activated at the time of injury on site, subsequently transported via the axon to the cell body, where it induces a molecular signal cascade that leads to transcriptional changes that cause LTH. This technology details the PKG pathway and potential compounds that could inhibit activation of PKG, blocking the signaling cascade. This is based on the discovery of the tertiary structure of PKG and identification of molecules that bind to its active site and/or balanol analog. Also provided is the pharmaceutical composition for treating chronic pain by inhibiting LTH.

Technology Benefits

-- The delivery of the compounds can be done through transdermal patch, which could provide controlled release-- The compounds have high specificity to inhibit PKG -- Pain alleviating drugs that interfere with the LTH pathway have no effect on motor systems-- Since PKG is activated locally and thus treatment can also be local (injection or patch) -- one can reduce dosage, side effects, and treatment cost

Technology Application

-- Mechanism and potential compounds for treating neuropathic chronic pain-- PKG as a potential therapeutic target for treatment of neuropathic pain following injury, inflammation, or other types of nerve trauma-- Direct inhibition of the LTH pathway: allows for specific blockade of neuropathic pain with a low risk for side effects

Detailed Technology Description

This technology describes a molecular signaling pathway, detailing how proteins activated at the injury site can mediate cellular changes that lead to LTH and cause persistent, chronic pain. One such molecule is protein kinase G (PKG). It is ac...

*Abstract

None

*Inquiry

Jerry Kokoshka Columbia Technology Ventures Tel: (212) 854-8444 Email: TechTransfer@columbia.edu

*IR

1726

*Principal Investigator

*Publications

Sung YJ, Chiu DT, Ambron RT. Neuroscience. 2006 Aug 25;141(2):697-709.Sung YJ, Walters ET, Ambron RT. J Neurosci. 2004 Aug 25;24(34):7583-95.

*Web Links

Patent pending: US 2006/0216339 A1Patent pending: US20080176920

Country/Region

USA