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ELAN PHARM. v. MAYO FOUNDATION FOR MEDICAL EDUC.

June 15, 2000

ELAN PHARMACEUTICALS, INC., AND ATHENA NEUROSCIENCES, INC., PLAINTIFFS,
V.
MAYO FOUNDATION FOR MEDICAL EDUCATION AND RESEARCH, DEFENDANT.



The opinion of the court was delivered by: Alsup, District Judge.

ORDER GRANTING DEFENDANT'S MOTION FOR SUMMARY JUDGMENT OF ANTICIPATION

INTRODUCTION

The issue on defendant's motion for summary judgment is whether a prior-art patent that discloses a "recipe" for producing transgenic mice, some of which will certainly end up with a particular characteristic and some of which won't, anticipates claims based on the same recipe but covering only those mice that end up with the particular characteristic.

STATEMENT

A suspected cause of Alzheimer's disease is the formation of plaque in the brain comprised residue from the break-down of an APP polypeptide. This residue is called AΣv, and the parties agree that it is always produced together with ATF-betaAPP, and vice versa. ATF-betaAPP is not suspected to form plaque. Searching for a cure to Alzheimer's disease, scientists screen various drugs on mice aimed at prohibiting or otherwise affecting the production of mice that produce AΣv (and therefore also ATF-betaAPP) are useful in this research. The mice that are used in these tests are the patented technology at issue in this case.

The patents-in-suit are United States Patent No. 5,612,486 and United States Patent No. 5,850,003, assigned to plaintiffs. Plaintiffs have asserted claims 1-3 of the `486 patent and claims 1-3 of the `003 patent. These claims cover rodents harboring a human gene with the Swedish mutation that produce ATF-betaAPP in a sufficient amount to be detectable in a brain homogenate. Independent claim 1 of the `486 patent provides as follows:

A transgenic rodent comprising a diploid genome comprising a transgene encoding a heterologous APP polypeptide having the Swedish mutation wherein the amino acid residues at positions corresponding to positions 595 and 596 in human APP695 are asparagine and leucine, respectively, wherein the transgene is expressed to produce a human APP polypeptide having the Swedish mutation, and wherein said polypeptide is processed to ATF-betaAPP in a sufficient amount to be detectable in a brain homogenate of said transgenic rodent.

Independent claim 1 of the `003 patent, parallel to Claim 1 of the `486 patent, provides as follows:

A transgenic rodent comprising a diploid genome comprising a transgene comprising in operable linkage a promoter, a DNA segment encoding a heterologous APP polypeptide and a polyandenylation site, wherein the APP polypeptide has the Swedish mutation whereby the amino acid residues at positions corresponding to positions 595 and 596 in human APP695 are asparagine and leucine, respectively, wherein the transgene is expressed to produce a human APP polypeptide having the Swedish mutation, and wherein said polypeptide is processed to ATF-betaAPP in a sufficient amount to be detectable in a brain homogenate of said transgenic rodent.

The remaining claims of each patent depend from these claims.

Not all transgenic rodents harboring a human gene with the Swedish mutation produce ATF-betaAPP in a sufficient amount to be detectable in a brain homogenate. The method disclosed in the patents-in-suit for making mice that produce a detectable amount of ATF-betaAPP is imperfect — that is, not all mice made according to the patents' disclosures will produce an amount of ATF-betaAPP detectable in a brain homogenate. Some of the mice made according to the patents' disclosures will not harbor the gene with the Swedish mutation. of those mice that do harbor the gene, some will not produce the APP polypeptide. of those that do produce the APP polypeptide, some will not process the APP polypeptide such that ATF-beta APP will be detectable in a brain homogenate.

The earliest date of conception for the claims in the patents-in-suit was June 30, 1993. Defendant has pointed to two references that pre-dated the conception of the claims at issue. The first was an article published in 1992 by Michael Mullan documenting his discovery of an APP mutation in a Swedish family — now called the Swedish mutation.

The second was a patent application filed by Mullan in 1992 that disclosed transgenic mice harboring a human APP gene with the Swedish mutation. The Mullan patent application disclosed the same recipe for making transgenic mice as was later disclosed in the patents-in-suit. Mullan disclosed making transgenic mice with the Swedish mutation; he described making constructs to use in making transgenic animals; he described the Swedish mutation at positions 670 and 671 in APP 770 (plaintiffs do not dispute that these are equivalent to positions 595 and 596 in APP695); he described making transgenic mice with the Swedish mutation that express the gene into a mutated protein; and he described the processing of APP into AΣv by enzymes. Mullan did not actually make the mice described and claimed in his patent. Mullan did not disclose looking for ATF-betaAPP as a proxy for Aσv.

In addition to the patents-in-suit, plaintiffs own a patent by the same inventors covering the brain-homogenate method for testing for ATF-betaAPP disclosed in the specifications of the patents-in-suit. That patent has not been asserted against Mayo because ...


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