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Coronary Post-Dilatation Catheter

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R43AG044958-01A1
Agency Tracking Number: R43AG044958
Amount: $395,476.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: NIA
Solicitation Number: PA12-088
Solicitation Year: 2013
Award Year: 2013
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
10101 Alliance Rd
United States
DUNS: 182472162
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 (513) 475-6618
Business Contact
Phone: (513) 475-6618
Research Institution

DESCRIPTION (provided by applicant): The goal of this proposal is to develop tumor necrosis factor (TNF )-inhibiting compounds as neuroprotectant drugs for treating Alzheimer's disease (AD). Current FDA-approved AD interventions are symptomatic treatments with limited efficacy which do not affect AD etiology or modify the course of disease progression. Thus, a critical need exists for a novel AD treatment directed towards AD pathophysiology. Recent studies implicate the neuroinflammatory cytokine TNF- as a key mediator in AD- associated neurodegenerative pathology. Multiple preclinical and clinical studies indicate that TNF is a druggable molecular target to modify the course of AD progression. P2D, inc. is developing a novel TNF inhibitor, PD2015 (3,6' dithiothalidomide), a dithionylated analog of thalidomide as an anti-AD drug candidate for in vivo efficacy testing in a mouse model of AD. PD2015 exhibits 1800% greater TNF inhibition in vitro than its parent, thalidomide. The applicant organizationrecently published work demonstrating the efficacy of PD2015 in 3xTg AD mice [52]. A 50 mg/kg PD2015 i.p. dose administered daily for two months significantly improved working memory (*Plt0.05) in 3xTg AD mice. PD2015 also significantly modulated brain TNF levels after daily treatment for two months in 3 x Tg AD mice. Recent preliminary studies with chronic oral PD2015 dosing (50 mg/kg) demonstrate improved cognition. In contrast, thalidomide did not improve working memory or block brain TNF levels in 3xTg AD mice. Taken together, these data strongly suggest that PD2015 is a good anti-AD drug candidate. The proposed preclinical study is designed to evaluate the oral efficacy of chronic low doses of PD2015 administration across a 12-fold dose range in symptomatic 6 mo. old 3xTg AD mice. Specific Aim 1A): Determine the effect of chronic oral administration of PD2015 on cognitive function in 3xTg AD mice. Specific Aim 1B): Determine the effect of PD2015 on indicators of neuroinflammation and AD- associatedpathology including TNF- levels, Ass1-40/Ass1-42 levels, microglial activation, tau, phospho-tau, synaptophysin, SNAP-25 in 3xTg AD mice. PUBLIC HEALTH RELEVANCE PUBLIC HEALTH RELEVANCE: Alzheimer's Disease (AD) is a significant neurological problem affecting 4.5 million of our senior U.S. citizens. The present research aims to develop an effective drug that can be taken orally to target the underlying neuroinflammation in AD to modify disease progression and improve cognitive function and blockthe underlying AD-associated pathology.

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

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