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NOVO-118 as a therapeutic to promote remyelination in in vivo models of MS

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R41NS110159-01A1
Agency Tracking Number: R41NS110159
Amount: $353,084.00
Phase: Phase I
Program: STTR
Solicitation Topic Code: NINDS
Solicitation Number: PA18-574
Timeline
Solicitation Year: 2018
Award Year: 2019
Award Start Date (Proposal Award Date): 2019-09-15
Award End Date (Contract End Date): 2021-05-31
Small Business Information
7770 REGENTS RD 113 319, San Diego, CA, 92122-1937
DUNS: 078781043
HUBZone Owned: N
Woman Owned: N
Socially and Economically Disadvantaged: Y
Principal Investigator
 TRAVIS STILES
 (858) 324-6357
 travis.stiles@novoron.com
Business Contact
 ANDREW BRIGHT
Phone: (858) 324-5114
Email: a.taylor.bright@novoron.com
Research Institution
 UNIVERSITY OF VIRGINIA
 BOX 400195
CHARLOTTESVILLE, VA, 22904-4195
 Nonprofit college or university
Abstract
Project Summary Multiple sclerosisMSis a neurodegenerative disease in which myelin of the central nervous systemCNSis destroyed by a self reactive immune responseThis demyelination is accompanied by the death of the myelinating cells themselvesthe oligodendrocytesRepeated bouts of demyelination leave the denuded CNS neurons vulnerable to degradation and is the major cause of neuronal dysfunction and neurodegeneration in MSCurrent approved therapies for MS are aimed only at lessening the frequency of the auto immune attack and do not address the need for remyelinationWithout induction of remyelination to heal previous lesionsthe course of disease can only be slowed but not reversedThe CNS contains a large population of oligodendrocyte precursor cellsOPCthat have the potential to differentiate into mature oligodendrocytes and remyelinate denuded axonsAlthough OPCs are efficiently recruited into MS lesionsOPC differentiation into mature oligodendrocytesand subsequent remyelinationis inhibited in MSNovoron has discovered that the LRPreceptor is a key signaling molecule that prevents OPC differentiationBy abrogating LRPfunction using either genetic deletion or antagonismwe can increase OPC differentiation and restore the remyelinating capacity of the brainThe goal of this proposal is to transition from our preliminary data demonstrating our novel approach to remyelination to developing this technology into a viable human drugBy the end of this PhaseapplicationNovoron will possess the followinga lead drug candidate with an in vivo dose response profiledisease efficacy data in the cuprizone chemical demyelinating modelanddisease efficacy data in the autoimmunemediated EAE MS modelThese data will demonstrate the feasibility of our approach to healing MS leasions and preapre Novoron for an efficient comercialization focused PhaseapplicationProject Narrative Disability and death in multiple sclerosis result from neuronal damage that arises from demyelinationOligodendrocyte progenitor cellsOPCshave the ability to infiltrate areas of demylination and remyelinate denuded axonsthereby preventing neuronal damage and reversing disabilitybut their differentiation into mature myelinating oligodendrocytes is inhibited by debris within the lesion siteThe goal of this project is to further characterize and develop our lead molecule with the objective of creating the first therapeutic to overcome the suppression of OPC differentiation and restore myelination thereby overcoming the functional deficits that result from neuronal damage and loss

* Information listed above is at the time of submission. *

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