University of South Florida sues Jackson Laboratory of Bar Harbor, Maine over US patent 5,898,094
In suing Jackson Laboratory over claims of US Patent 5,898,094, the University of South Florida gives us an example of a university suing an entity that actually makes product.
Bizjournals notes of the dispute:
USF states that it owns the entire right, title and interest to the 094 Invention and was issued a patent on April 27, 1999 by the U.S. Patent and Trademark Office. In the patent, USF notes that so-called "transgenic animals" such as the mice at the center of this legal dispute are being used to "study neurodegenerative disorders, both to understand the underlying disease pathology as well as to test treatment protocols."
PsychoGenics, founded in 1999, has an exclusive license.to to USF's APP/PS1 double transgenic mice (US Patent No. 5,898,094), co-expressing the M146L presenilin 1(PS1) mutation and the double mutations at K670N/M671L (Swedish mutation) in the amyloid precursor protein (APP).
The first claim:
A transgenic mouse with enhanced Alzheimer's Disease related amyloid accumulation in its brain produced by:
producing an F1 generation mouse by crossing a first transgenic mouse whose genome comprises at least one transgene comprising a DNA sequence encoding mutant presenilin M146L operably linked to a promoter with a second transgenic mouse whose genome comprises at least one transgene comprising a DNA sequence encoding APP K670N,M671L operably linked to a promoter, wherein the first transgenic mouse expresses the DNA sequence encoding the mutant presenilin and wherein the second transgenic mouse expresses the DNA sequence encoding the APP; and
selecting from the offspring of the cross, those transgenic mice whose genome comprises at least one DNA sequence encoding mutant presenilin M146L operably linked to a promoter and at least one transgene comprising a DNA sequence encoding APP K670N,M671L operably linked to a promoter, and identifying an F1 mouse which express both transgenes such that the F1 mouse develops accelerated deposition of Aβ in its brain as compared to non-transgenic mice or either parental mouse.