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Clusterin/ApoJ Facilitating the Delivery of GPI-Linked Membrane-Free Proteins to Mammalian Sperm Surface In Vitro Inventors:

Serial Number: Filing Date:

DeLeon, Patricia A.; Griffiths, Genevieve S. 60/855,500 October 31, 2006

Docket Number: UD07-13

The invention relates to a method for effectively delivering membrane-free bioactive proteins with a lipid anchor (GPI-linked proteins) to the surface of epididymal or ejaculated sperm. The process is facilitated or promoted in the presence of Clusterin/ ApoJ, a well-known lipid carrier, and the acquisition of these molecules, such as Sperm Adhesion Molecule 1 (SPAM1), can significantly impact sperm maturation and function. The invention is further directed to the previously unreported interaction between clusterin/ ApoJ and SPAM1 in both the epididymal luminal fluid (ELF) and the uterine luminal fluid (ULF). Tag and Target Drug Delivery System Inventors:

Serial Number: Filing Date:

Naik, Ulhas P.; Millili, Peter G. 60/921,119 March 29, 2007

Docket Number: UD07-17

The following invention is a novel drug delivery system containing an innovative approach to cancer cell targeting. Effective elimination of cancer cells can be achieved through a multi-staged process delivering cytotoxic agents with enhanced specificity. Combining the advantages of nanoparticle gene therapy with unique molecular biology approaches, this delivery system has the potential to significantly improve cancer treatment. Futhermore, the flexibility of this delivery system allows for individualized therapy, providing health-care professionals with multiple treatment options.


INVENTIONS - Technologies Available for Licensing

Oligonucleotide-Directed Base Modification in C. Elegans Inventors:

Serial Number: Filing Date:

Kmiec, Eric B.; Parekh-Olmedo, Hetal Provisional Filed January 29, 2007

Docket Number: UD07-22

Single-strand DNA oligonucleotides can be used to alter the genomic sequence of DNA in the nematode C. elegans. The oligonucleotides are introduced using a bacterial carrier system and have been found to direct the repair of a single base mutation — the mutation site analog of the human mutation responsible for muscular dystrophy. The evidence shows clear indications of phenotypic changes in the movement of the worm.

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