[Federal Register Volume 68, Number 246 (Tuesday, December 23, 2003)]
[Notices]
[Pages 74243-74244]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-31653]


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DEPARTMENT OF HEALTH AND HUMAN SERVICES

National Institutes of Health


Government-Owned Inventions; Availability for Licensing

AGENCY: National Institutes of Health, Public Health Service, DHHS.

ACTION: Notice.

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SUMMARY: The inventions listed below are owned by an agency of the U.S. 
Government and are available for licensing in the U.S. in accordance 
with 35 U.S.C. 207 to achieve expeditious commercialization of results 
of federally-funded research and development. Foreign patent 
applications are filed on selected inventions to extend market coverage 
for companies and may also be available for licensing.

ADDRESSES: Licensing information and copies of the U.S. patent 
applications listed below may be obtained by writing to the indicated 
licensing contact at the Office of Technology Transfer, National 
Institutes of Health, 6011 Executive Boulevard, Suite 325, Rockville, 
Maryland 20852-3804; telephone: (301) 496-7057; fax: (301) 402-0220. A 
signed Confidential Disclosure Agreement will be required to receive 
copies of the patent applications.

Improved Endogenous Opioid Anti-Nociception With Reduced 
Neurodegeneration, Hyperalgesia, Allodynia and Tolerance

    Amina Woods, Toni Shippenberg, and Lawrence Sharp (NIDA).
    U.S. Provisional Application No. 60/459,830 filed 01 Apr 2003 (DHHS 
Reference No. E-276-2001/0-US-01).
    Licensing Contact: Norbert Pontzer; (301) 435-5502; 
[email protected].
    Endogenous opioid peptides and receptors evolved to modulate 
nociceptive input in response to injury. One of those peptides, 
dynorphin, acts on the kappa opioid receptor subtype to produce 
analgesia without sedation, respiratory depression or constipation. 
Prior to this invention, dynorphin was not an acceptable analgesic 
because of certain severe toxic side effects, when given in doses 
higher than physiological concentrations, mainly NMDA mediated 
neurotoxicity. Dynorphin produces its deleterious side effects by 
producing an NMDA mediated motor paralysis. In disease states such as 
stroke, spinal cord injury or neuropathic pain, activation of NMDA 
receptors by endogenous dynorphin may lead to neurodegeneration, 
hyperalgesia and allodynia. Tolerance to opiate drugs may also be 
mediated by the NMDA actions of dynorphin. This invention provides 
materials and methods to block NMDA receptor activation by dynorphin 
thus allowing the use of exogenous dynorphin as a beneficial 
nociceptive agent without side effects and preventing pathological 
actions of endogenous dynorphin in response to injury. Experimental 
data demonstrate: (1) attenuation of motor activity deficits, flaccid 
paralysis and mechanical allodynia produced by dynorphin 
administration; (2) reduction of infarct size and locomotor deficits 
after cerebral ischemia; (3) the reduction of morphine tolerization; 
and (4) so far no visible side effects.

Pain Control by the Selective Local Ablation of Nociceptive Neurons

    Michael Iadarola and Zoltan Olah (NIDCR).
    PCT/US01/09425 filed 22 Mar 2001, published as WO 02/076444 (DHHS 
Reference No. E-109-2000/0-PCT-02).
    Licensing Contact: Norbert Pontzer; (301) 435-5502; [email protected].
    The vanilloid receptor (VR) is a cation channel predominantly 
expressed on the peripheral processes and perikarya of nociceptive 
primary afferent neurons. Previous studies have shown that activation 
of the peripheral receptors by agonists such as capsaicin from hot 
peppers, or the much more potent resiniferatoxin, produces acute pain 
sensation which may be followed by desensitization. These inventors 
discovered that administration of VR agonists in the vicinity of 
neuronal cell bodies expressing the VR receptor can actually destroy 
those cells. To control pain and inflammatory disorders, the present 
invention provides methods and kits for the selective ablation of pain 
sensing neurons. For example, the intraganglionic administration of a 
VR agonist selectively ablates primary afferent nociceptive neurons 
without impairing other sensory modalities. This invention will greatly 
enhance the ability to control pain, inflammation and other conditions 
mediated by nociceptive neurons while sparing mental function and other 
sensations.
    This research has been described, in part, in Olah et al., J. Biol. 
Chem., 276, pp. 11021-11030, 2001.


[[Page 74244]]


    Dated: December 17, 2003.
Steven M. Ferguson,
Director, Division of Technology Development and Transfer, Office of 
Technology Transfer, National Institutes of Health.
[FR Doc. 03-31653 Filed 12-22-03; 8:45 am]
BILLING CODE 4140-01-P