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Please Note: The technology listed below is not available to the public at this time. This technology is in the early stage of research and requires further development before it is ready for the marketplace. The VA is currently in the process of identifying potential companies who may be interested in licensing and/or further developing the technology through Cooperative Research and Development Agreements (CRADA). Through cooperative research initiatives such as these, it is our hope and goal that commercial products will be fully developed and made available to benefit veterans and others.
VA TECHNOLOGY OPPORTUNITY BRIEF
Ethanol Antagonist
(#00-029)
OPPORTUNITY:
The Department of Veterans Affairs (VA) is seeking a commercial partner to license and/or further develop this technology through a Cooperative R & D Agreement (CRADA) to expedite bringing it to market.
BACKGROUND:�
Maternal alcohol consumption during pregnancy can cause a variety of serious birth defects, with fetal alcohol syndrome (FAS) being the most serious.� Alcoholic individuals are at increased risk of brain damage through poor nutrition, liver disease and head trauma as well as through the direct and diverse actions of ethanol in its capacities as a neurotoxin.� Current therapies for alcoholism target alcohol dependency rather than the adverse effects that are associated with chronic ethanol ingestion. �Ethanol produces its toxicity in developing and adult nervous systems through a variety of mechanisms.� Recent evidence suggests that one important mechanism may be the inhibition by ethanol of cell adhesion mediated by the L1 cell adhesion molecule.� L1 plays a critical role in nervous system development, and brain lesions in children with fetal alcohol syndrome resemble those of children with mutations in the gene for L1.� L1 is expressed in the nervous system at early developmental stages and persists in the mature nervous system.� A number of studies suggest that L1 is involved in the synaptic plasticity associated with learning and memory.� Effects of ethanol on L1 might therefore contribute to the fetal alcohol syndrome, to memory disorders and even to addiction in adults.�
TECHNOLOGY OVERVIEW:
There is a need for drugs that can prevent fetal alcohol syndrome in women and prevent the adverse effects of ethanol on learning and memory in adults because the current therapies are limited to disease management, not to disease prevention.� The VA has discovered an antagonist to inhibit the effects of alcohol on cell-cell adhesion mediated by L1.� It also antagonizes the morphological effects of ethanol on proliferating neural cells and it prevents ethanol-induced cell-death and dysmorphology in mouse embryos.� The VA therefore hypothesizes that ethanol causes fetal alcohol syndrome and adult cognitive deficiencies in part through its action on L1, and that antagonists of this effect would help prevent these conditions.� Although the agonist is too toxic for human use, experiments in progress suggest that other related molecules are also ethanol antagonists.� The VA proposes to use molecules that block the effects of ethanol on L1 as potential therapeutic agents for ethanol-related disorders of the nervous system.�
TECHNICAL MERIT:�
The potential application of the ethanol antagonist would be in the prevention and treatment of fetal alcohol syndrome (FAS), but these compounds might also prove useful in preventing and treating cognitive disorders and alcohol dependence in adults.�� This technology has completed preliminary in vitro studies and has proved effective in mouse whole embryo culture.�
PATENT STATUS:
U.S. patent was issued on 3/19/02 (S/N 6,359,015).�
Federal Register: Aug. 31, 2001 (Vol. 66, No. 170) p. 46065
FOR MORE INFORMATION CONTACT:
Saleem Sheredos
Program Manager
Technology Transfer Program
Veterans Affairs
Office of Research & Development (12TT)
5th Floor
103 South Gay Street
Baltimore, MD 21202
202-380-5080
Fax 410.962.2141
e-mail: saleem.sheredos@va.gov