Flufenamic Acid for the Treatment of Chronic Pain (27153)

Oral administration of flufenamic acid (FA) has a potent analgesic effect that can be exploited for the treatment of chronic pain. Chronic pain is an invalidating condition affecting a large number of people and no pharmacologic treatment has proven completely effective so far.

SIGNIFICANCE: Pain constitutes the primary reason driving people to seek health care. According to a 2006 from the National Center for Health Statistics, an estimated 76.5 million Americans report that they have had a problem with pain that persisted for more than 24 hours in duration. Of this group, 42% reported pain lasting more than one year. The annual cost of chronic pain in the United States, including healthcare expenses, lost income, and lost productivity, is estimated to be $100 billion.


Addresses urgent need of a large population. Targets neurons responsible for pain perception. Known pharmacokinetics.

BACKGROUND: Flufenamic acid, a molecule already used in human therapy as a non-steroidal anti-inflammatory drug, has potent analgesic effect in an animal model of neuropathic pain. The spared nerve injury model, a reliable animal model of chronic neuropathic pain, was used to test the effect of oral administration of FA. FA had a potent analgesic effect in all the animals tested.

The inventors show two synergistic mechanisms of action for flufenamic acid.

Flufenamic acid functions as an agonist of background potassium currents mediated by members of the KCNK channel family. The inventors have demonstrated that KCNK channels are expressed in dorsal root ganglia (DRG) neurons, which mediate peripheral pain perception. FA-dependent activation of KCNK channels in these neurons reduces their excitability and thus the perception of pain. Parallel experiments (on hippocampal neurons) also show that FA acts as a gating modifier of TTX-sensitive sodium channels, resulting in a current reduction. These channels contribute to the action potential generation in DRG cells (Blair and Bean 2003), which mediate pain perception. Thus this mechanism also inhibits DRG firing and can further enhance the analgesic effect.

Type of Offer: Licensing

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