NOVEL NEUROPROTECTIVE AGENTS

Award Information
Agency: Department of Health and Human Services
Branch: N/A
Contract: N/A
Agency Tracking Number: 16782
Amount: $50,000.00
Phase: Phase I
Program: SBIR
Awards Year: 1991
Solitcitation Year: N/A
Solitcitation Topic Code: N/A
Solitcitation Number: N/A
Small Business Information
Neurotherapeutics Corp
11211 Sorrento Valley Rd #h, San Diego, CA, 92121
Duns: N/A
Hubzone Owned: N
Woman Owned: N
Socially and Economically Disadvantaged: N
Principal Investigator
 Paul Marangos
 (619) 455-6093
Business Contact
Phone: () -
Research Institution
N/A
Abstract
ACUTE NEUROLOGIC DISORDERS SUCH AS STROKE AND HEAD TRAUMA ARE PRESENTLY UNTREATABLE. RECENT BREAKTHROUGHS IN THE UNDERSTANDING OF HOW NEURAL TISSUE DEGENERATES, POST-ISCHEMIA, HAVE MADE POSSIBLE SEVERAL AVENUES OF THERAPEUTIC INTERVENTION FOR THESE DEVASTATING DISORDERS WHICH HOLD THE PROMISE OF SALVAGING MUCH OF THE BRAIN TISSUETHAT IS DESTROYED IN THE HOURS FOLLOWING STROKE OR HEAD TRAUMA. IT HAS BEEN SHOWN THAT EXCITATORY AMINO ACID (EAA) NEUROTRANSMITTERS, GLUTAMATE AND ASPARTATE ARE OVER RELEASED AFTER A STROKE AND THAT THIS ACTUALLY STIMULATES NERVE CELLS TO DEATH. THIS PROCESS IS CALLED EXCITOTOXICITYAND HAS LEAD TO THE DEVELOPMENT OF EAA RECEPTOR BLOCKERS AS A THERAPEUTIC STRATEGY. THESE AGENTS, ALTHOUGH EFFECTIVE, HAVE PROVEN TO HAVE UNACCEPTABLE SIDE EFFECTS. THE NEUROTHERAPEUTICS APPROACH IS TO INHIBIT THE RELEASE OF EAAS PRESYNAPTICALLY VIA BLOCKING THE N-TYPE CALCIUM CHANNELTHAT REGULATES EAA RELEASE. WE HAVE IDENTIFIED A GROUP OF AGENTS THAT ACTS AT N-TYPE CHANNELS. DURING PHASE I, WE WILL DEMONSTRATE EFFICACY OF THESE AGENTS IN AN IN VITRO AND IN VIVO MODEL SYSTEM OF NEUROPROTECTION. AN ATTEMPT TO OBTAIN SOME STRUCTURE ACTIVITY RELATIONSHIPS WILL ALSO BE MADE. IN PHASE II, WE WILL LAUNCH A MEDICINAL CHEMISTRY EFFORT TO DERIVATIZE THE AGENT CHARACTERIZED IN PHASE I. THE GOALS HERE ARE TO GENERATE AGENTS WITH GREATER POTENCY AT THE N-TYPE CALCIUM CHANNEL. ACUTE NEUROLOGIC DISORDERS SUCH AS STROKE AND HEAD TRAUMA ARE PRESENTLY UNTREATABLE. RECENT BREAKTHROUGHS IN THE UNDERSTANDING OF HOW NEURAL TISSUE DEGENERATES, POST-ISCHEMIA, HAVE MADE POSSIBLE SEVERAL AVENUES OF THERAPEUTIC INTERVENTION FOR THESE DEVASTATING DISORDERS WHICH HOLD THE PROMISE OF SALVAGING MUCH OF THE BRAIN TISSUETHAT IS DESTROYED IN THE HOURS FOLLOWING STROKE OR HEAD TRAUMA. IT HAS BEEN SHOWN THAT EXCITATORY AMINO ACID (EAA) NEUROTRANSMITTERS, GLUTAMATE AND ASPARTATE ARE OVER RELEASED AFTER A STROKE AND THAT THIS ACTUALLY STIMULATES NERVE CELLS TO DEATH. THIS PROCESS IS CALLED EXCITOTOXICITYAND HAS LEAD TO THE DEVELOPMENT OF EAA RECEPTOR BLOCKERS AS A THERAPEUTIC STRATEGY. THESE AGENTS, ALTHOUGH EFFECTIVE, HAVE PROVEN TO HAVE UNACCEPTABLE SIDE EFFECTS. THE NEUROTHERAPEUTICS APPROACH IS TO INHIBIT THE RELEASE OF EAAS PRESYNAPTICALLY VIA BLOCKING THE N-TYPE CALCIUM CHANNELTHAT REGULATES EAA RELEASE. WE HAVE IDENTIFIED A GROUP OF AGENTS THAT ACTS AT N-TYPE CHANNELS. DURING PHASE I, WE WILL DEMONSTRATE EFFICACY OF THESE AGENTS IN AN IN VITRO AND IN VIVO MODEL SYSTEM OF NEUROPROTECTION. AN ATTEMPT TO OBTAIN SOME STRUCTURE ACTIVITY RELATIONSHIPS WILL ALSO BE MADE. IN PHASE II, WE WILL LAUNCH A MEDICINAL CHEMISTRY EFFORT TO DERIVATIZE THE AGENT CHARACTERIZED IN PHASE I. THE GOALS HERE ARE TO GENERATE AGENTS WITH GREATER POTENCY AT THE N-TYPE CALCIUM CHANNEL.

* information listed above is at the time of submission.

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