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TUMOR VACCINE:COVALENT LINK OF ANTIGEN TO DENDRITIC CELL

Award Information
Agency: Department of Health and Human Services
Branch: National Institutes of Health
Contract: 1R43CA097834-01
Agency Tracking Number: CA097834
Amount: $158,517.00
Phase: Phase I
Program: SBIR
Solicitation Topic Code: N/A
Solicitation Number: N/A
Timeline
Solicitation Year: N/A
Award Year: 2002
Award Start Date (Proposal Award Date): N/A
Award End Date (Contract End Date): N/A
Small Business Information
THERAPYX, INC. 4786 ENSER RD
EDEN, NY 14057
United States
DUNS: N/A
HUBZone Owned: No
Woman Owned: No
Socially and Economically Disadvantaged: No
Principal Investigator
 QIANG LOU
 () -
Business Contact
 RICHARD BANKERT
Phone: (716) 829-2701
Research Institution
N/A
Abstract

DESCRIPTION (provided by applicant): The ability of dendritic cells (DC) to activate naive T-cells has made them targets for the design of enhanced vaccination protocols. DC loaded with tumor antigens in vitro and injected into recipients, have induced protective immune responses in several different animal models, and some encouraging preliminary data have been reported with DC-based vaccination trials in humans. However, the intensity and durability of these vaccines are usually modest. Currently attempts to improve the efficacy of the DC vaccines have focused upon enhancing the efficiency of loading DC with a diverse array of antigens, and improving upon the entry of the exogenous antigens into the MHC Class I pathway. A simple chemical modification of the antigen has been used here to enhance the amount and duration of the antigen bound to DC and to direct the linkage of antigens to the extracellular domains of receptors on surface of DC. The covalent linkage of antigens to receptors (which include ones that target both MHC Class I and II processing pathways) proceeds without loss of viability or function of the DC and results in the internalization of the bound antigen-receptor complexes. The aim of this proposal is to establish whether the covalent linkage of antigens to DC significantly enhances the efficacy of a DC-based tumor vaccination strategy. In Aim 1 mice immunized with DC loaded with a chemically modified surrogate tumor antigen, beta-galactosidase, (beta-gal) will be compared to mice immunized with DC loaded with unmodified beta-gal for their ability to resist a challenge with a beta-gal transfected tumor (i.e. protective efficacy of the vaccine). In Aim 2 the ability of antigen covalently linked to DC to suppress and/or eradicate existing tumors will be assessed (i.e. therapeutic efficacy of the vaccine). In the final Aim, the protective and therapeutic efficacy of the enhanced and directed loading of DC will be tested using a bona fide tumor specific antigen, i.e. a B-cell tumor-associated immunoglobulin.

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

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