Myocardial Infarction Therapeutics

Award Information
Agency:
Department of Health and Human Services
Branch
n/a
Amount:
$199,085.00
Award Year:
2009
Program:
SBIR
Phase:
Phase I
Contract:
1R43HL097464-01
Award Id:
93977
Agency Tracking Number:
HL097464
Solicitation Year:
n/a
Solicitation Topic Code:
n/a
Solicitation Number:
n/a
Small Business Information
CELDARA MEDICAL, LLC, 16 CAVENDISH CT, CENTERRA RESOURCE PARK, DRTC, LEBANON, NH, 03766
Hubzone Owned:
N
Minority Owned:
N
Woman Owned:
N
Duns:
828763263
Principal Investigator:
EBO DEMUINCK
(603) 650-3903
EBO.D.DEMUINCK@DARTMOUTH.EDU
Business Contact:
JAKE REDER
() -
jr@celdaramedical.com
Research Institution:
n/a
Abstract
DESCRIPTION (provided by applicant): Myocardial infarction (MI) is the leading cause of death in the developed world, including the United States. Each year over 8.1 million Americans have an MI; 30% die before reaching hospital and 10% die after hospitali zation. The goal of these studies is to advance a novel therapeutic approach to MI wound healing that is both strikingly effective and exactly contrary to conventional wisdom in order to help the 70% of MI victims that reach hospital. Temporary depletion o f dendritic cells (DC) during MI wound healing results in a 49% improvement in cardiac function and a 65% reduction in MI size in a murine model. Cardiac function is the greatest determinant of survival post-MI, and also has a significant effect on quality of life. The goal of this project is to begin to develop this seminal discovery into a therapy for humans. The drugs to be evaluated are antibody-toxin conjugates designed to deplete DC post-MI. Their observed effect on MI wound healing is noteworthy for at least two reasons. First, immunologists and cardiologists have conventionally thought that interfering with wound healing through the depletion of DC post-MI would result in catastrophe: i.e. weakened tissues (cardiac rupture) and no new vasculature. Th is has not been the case. Second, the beneficial effect of DC depletion is startling in its magnitude (49% improvement in heart function). In Phase I, we will study two transgenic mouse models which express human receptors (DEC 205 and mannose) on their DC to determine safety and efficacy of the two the human mAb conjugates which comprise our lead therapeutic candidates. Aim 1. is to determine efficacy of these drugs in the murine models. Aim 2. is to measure the toxicity, distribution and elimination of le ad drug candidate identified in Aim 1. A treatment that temporarily depletes DC is nothing short of a paradigm shift. Initial results suggest that this strategy may lead to a sharp reduction in mortality and profound improvements in the lives of victims of MI. PUBLIC HEALTH RELEVANCE: Heart attacks are the leading cause of death in the developed world. By temporarily depleting a cell type commonly associated with inflammatory and immune responses, we have been able to dramatically improve heart function aft er a heart attack in mice. The overall goal of this project is to advance these results toward a drug that will help humans.

* information listed above is at the time of submission.

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