Improving the Transfer of ERK siRNA Constructs Using Nanoporous Silica

Award Information
Agency:
Department of Health and Human Services
Branch
n/a
Amount:
$200,000.00
Award Year:
2007
Program:
STTR
Phase:
Phase I
Contract:
1R41CA126155-01A1
Award Id:
85422
Agency Tracking Number:
CA126155
Solicitation Year:
n/a
Solicitation Topic Code:
n/a
Solicitation Number:
n/a
Small Business Information
APOLLO SRI, LLC, 210 COLCHESTER AVE, BURLINGTON, VT, 05405
Hubzone Owned:
N
Minority Owned:
N
Woman Owned:
N
Duns:
143736614
Principal Investigator:
CHRISTOPHERLANDRY
(802) 656-3360
CHRISTOPHER.LANDRY@UVM.EDU
Business Contact:
TIMOTHYHICKEY
() -
jhickey@apollosri.com
Research Institute:
UNIVERSITY OF VERMONT

UNIVERSITY OF VERMONT AND ST AGRIC COLLEGE
85 SOUTH PROSPECT STREET
BURLINGTON, VT, 5405

Nonprofit college or university
Abstract
DESCRIPTION (provided by applicant): Our research is focused on the potential of acid-prepared mesoporous silica (APMS) as a delivery agent for siRNA constructs to inhibit the ERK1/2 and ERK5 pathways in the treatment of human malignant mesothelioma (MM). These pathways are critical to MM cell proliferation and chemoresistance. Our initial research suggests that APMS will be significantly more effective as a vehicle for uptake and delivery of siRNA constructs into the thoracic cavity than current alternativ es. Prior research shows that modified APMS effectively transfers DNA plasmids to epithelial and mesothelioma cells in vitro. APMS itself is not toxic to cells in vitro or after injection intranasally or intrathoracically into mice. The external surface of APMS can be modified for cell specific targeting and maximal uptake. The proposed research as three main goals: (1) engineer APMS for maximum and selective uptake by human MM cells in vitro; (2) study the kinetics of uptake of shRNA constructs into APMS; and (3) use shRNA-loaded APMS to block ERK1/2 and ERK5 pathways. Assuming the Phase I in vitro research validates our hypothesis that shRNA-loaded APMS both improves the uptake of the constructs to MM cells and significantly increases the interference of t he constructs with the ERK1/2 and ERK5 pathways, our Phase II research will involve the in vitro functional effects of shRNA-loaded constructs in human MM and in vivo work with a mouse xenograft model. In addition, we plan to expand our research to other s hRNA constructs that block other signaling pathways. Since a universal obstacle to all siRNA therapeutics is the delivery of the molecules into the cells, APMS offers the potential of revolutionizing the clinical opportunity for siRNA. Our primary focus is on the cancer drug market, a 36.9B in 2004.

* information listed above is at the time of submission.

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