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Case name
Therapeutic Compounds to Enhance Cognition, Counteract Depression and Treat Smoking Addiction
Owner
Website
University of Florida
http://technologylicensing.research.ufl.edu/technologie
s/13562_therapeutic-compounds-to-enhance-cognitioncounteract-depression-and-treat-smoking-addiction
description
Chemicals Selectively Modulate Cell Receptors Linked to Neurological Disorders in Humans and Other
Mammals
These compounds enable effective treatment of neurological disorders involving cognitive deficits (including
Alzheimer s and Parkinson s diseases), depression and drug dependences such as tobacco (nicotine) and betel nut
addictions. Neurological diseases including drug addictions are a major health cost to human societies. By 2030,
more than 8 million individuals will die annually from illnesses caused by tobacco use, while 600 million
individuals remain addicted to some form of betel nut or quid, a psychoactive substance that is carcinogenic.
Drugs available to help individuals quit an addictive habit often have undesirable side effects or are ineffective.
Researchers at the University of Florida have developed a variety of nicotinic receptor agonists (activators) based
on a marine natural product named anabaseine that selectively stimulate only one of a large number of nicotinic
receptors found in the mammalian brain; the alpha7 receptor is a major mediator of brain activity associated with
learning and memory. Stimulation of this receptor also has anti-inflammatory actions that are thought to be
involved in neuroprotective action in neurodegenerative disease animal models. On the other hand, antagonists
based on a plant compound, cytisine, are important in treating tobacco and other chemical addictions. Empirical
results suggest that when combined, the two types of compounds offer a more effective reduction in nicotine
addiction than currently available drugs.
Application
Safe and efficient treatment of neurological disorders and addictions
Advantages
Oral bioavailability and ready penetration of the blood-brain barrier for easy access to the brain,
minimizing invasive procedures and increasing simplicity of treatment
Improved pharmacokinetic properties such as potency and time period of effectiveness, increasing drug
efficiency
Selectively target particular nicotinic receptors, reducing dosage and side effects
Technology
These compounds target selective expression of alpha-7 and alpha-4-beta-2; nicotinic acetylcholine receptor
(nAChR) subtypes that impact cognition, mood, and neuroprotection. Research shows that alpha-4-beta-2 is
always associated with addiction. But fewer alpha-7 receptors are expressed if the host suffering from addiction
is stressed or suffering from depression. To treat depression, anabaseines can selectively promote alpha-7
receptors while acting as antagonists for alpha-4-beta-2 receptors, which would otherwise interfere with the
positive effects of the drug. When individuals suffering from nicotine addiction use nicotine, alpha-4-beta-2
rewards them, creating a dependence effect. To combat nicotine addiction, preliminary research suggests that
partial agonists modestly stimulate the same reward circuit of alpha-4-beta-2 receptors that nicotine does,
ultimately reducing cravings and blunting the peaks of receptor activation that cigarette smoking or betel quid
chewing would create. Unfortunately, available drugs that suppress the rewarding effects of nicotine by
inhibiting alpha-4-beta-2 receptors may cause worsened depression or even suicide. By using partial agonists for
alpha-7 receptors, drug developers can stimulate alpha-7 receptors unopposed by a concurrent alpha-4-beta-2
inhibitory effect and decrease the function of alpha-4-beta-2 nAChR to treat dependence while counteracting
depression.
Date
Case Ref.
2016-02-18 00:00:00
13562
Application number
US9440948
Applicants
University of Florida
Inventors
William R. Kem, Ferenc Soti, Jon Lindstrom Ph.D., Anne Rouchaud, Kristin Marie Andrud, Hong Xing,
Support:
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Classification
IPC classifications
CPC classifications
89646
89647
Bibliographic details:
Publication number
Publication date
2017-03-02
Priority number
Estimated expiry year
2017