UNIVERSITY OF SOUTH FLORIDA BOARD OF TRUSTEES v. USAMOTION for Partial Summary Judgment '094 Patent Claims are not Invalid for Prior InventorshipFed. Cl.November 5, 2018i THE UNITED STATES COURT OF FEDERAL CLAIMS UNIVERSITY OF SOUTH FLORIDA, BOARD OF TRUSTEES, Plaintiff, v. THE UNITED STATES OF AMERICA, Defendant. ) ) ) ) ) ) ) ) ) ) No. 15-1549 Judge Campbell-Smith MOTION BY USF FOR PARTIAL SUMMARY JUDGMENT – U.S. Patent 5,898,094 IS NOT INVALID BY REASON OF PRIOR INVENTORSHIP 35 USC §102(g) Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 1 of 22 ii TABLE OF CONTENTS TABLE OF CONTENTS ii TABLE OF AUTHORITIES iii I. STATEMENT OF MATERIAL FACTS NOTS IN DISPUTE 4 II. THE “INVENTION” OF THE ‘094 PATENT IS DEFINED BY ITS CLAIMS 8 III. BORCHELT DID NOT HAVE POSSESSION OF THE ACCELERATED ALZHEIMER’S PATHOLOGY REQUIREMENTS OF THE INVENTION BEFORE APRIL 25, 1997 11 V. CONCLUSION 15 Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 2 of 22 iii TABLE OF AUTHORITIES PAGE NO. CASES Altoona Publix Theatres v. Am. Tri-Ergon Corp., 294 US 477 9 Amkor Technology, Inc. v. International Trade Com’n, 692 F.2d 1250 (Fed. Cir. 2012) 2 Cooper v. Goldfarb, 154 F.3d 1321 (Fed. Cir. 1998) 2,12 Fleming v. Escort, Inc., 774 F.3d 1371 (Fed. Cir. 2014) 2 Heard v. Burton, 333 F.2d 239 (CCPA 1964) 12 Hitzeman v. Rutter, 243 F.3d 1345 (Fed. Cir. 2001) 11,14 Innova/Pure Water, Inc. v. Safari Water Filtration Systems, Inc., 38 F.3d 1111 (Fed. Cir. 2004) 9 Oka v. Youssefyeh, 849 F.2d 581 (Fed. Cir. 1988) 2 REG Synthetic Fuels v. Neste Oil Oyj, 841 F.3d 954 (Fed. Cir. 2016) 2 Smith v. Snow, 294 US 1 (1935) 9 Sumitomo Dainippon Pharma Co., Ltd., v. Emcure Pharmaceuticals, Limited, 2018 WL 4906268 at *1 (October 5, 2018 DNJ) 9 Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 3 of 22 iv STATUTES 35 U.S.C. §102(g) 2, 17 Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 4 of 22 1 Plaintiff University of South Florida, Board of Trustees, (hereinafter “USF”) hereby moves for entry of partial summary judgment that the patent-in-suit, U.S. Patent No. 5,898,094 (hereinafter “the ‘094 Patent”)(Ex. 10) is not invalid on the basis that the subject matter claimed was invented by another prior to the date of invention by the ‘094 Patent’s inventors, John Hardy and Karen Duff. The Final Invalidity Contentions of the United States (Docket 106) offers a narrative asserting that a research group led by David Borchelt and including Sangram Sisodia made the invention of the ‘094 Patent (Ex. 10) before Hardy and Duff, Docket 106, pp. 15–17. In fact the testimony proves quite the opposite. David Borchelt clearly and carefully explained on the record that he did not, and could not have, conceived of the subject matter claimed in the ‘094 Patent (Ex. 10) prior to Hardy and Duff’s invention thereof. To the contrary, Borchelt testified he made the conscious decision NOT to pursue research into that subject matter for a very clear and understandable reason. In Borchelt’s own words, David Borchelt, in 1995–1996, wanted something that would give him a result, “a development” he could publish earlier, and so focused on the chemistry of APP which could be detected early in the life of the experimental mice, as opposed to the invention of the ‘094 Patent (Ex. 10) which is focused on pathology which is not apparent until much later in the life of the mice. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 5 of 22 2 Where an issued patent is challenged as unpatentable under 35 U.S.C. §102(g)1 the burden on the challenger is to demonstrate, by clear and convincing evidence, that the invention was first reduced to practice by a party other than the patentees, or demonstrate prior conception of the invention coupled with reasonable diligence to a subsequent reduction to practice. Cooper v. Goldfarb, 154 F,3d 1321, 1327 (Fed. Cir. 1998). The prior inventor must have made the invention without abandonment, suppression or concealment of that invention. Fleming v. Escort, Inc., 774 F. 3d 1371, 1378 (Fed. Cir. 2014). In this case, the actual filing date of the ‘094 Patent (Ex. 10) is July 30, 1997. It is quite clear, however, that the invention of the ‘094 Patent (Ex. 10) was actually reduced to practice no later than April 25, 1997, the date Karen Duff wrote the detailed account of that reduction to practice and sent it to USF. The Government must prove Borchelt and Sisodia et al made the invention at issue and reduced it to practice before April 25, 1997; or conceived of it first followed by reasonable diligence to a reduction to practice after, in the absence of abandonment, suppression or concealment. REG Synthetic Fuels v. Neste Oil Oyj, 841 F.3d 954, 962 (Fed. Cir. 2016); Amkor Technology, Inc. v. International Trade Com'n, 692 F. 2d 1250, 1256 (Fed. Cir. 2012) citing Oka v. Youssefyeh, 849 F. 2d 581, 584 (Fed. Cir. 1988). 1 The ‘094 Patent (Ex. 10) was filed in July, 1997 and issued in 1999 and so is subject to the pre-AIA version of the statutes. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 6 of 22 3 This Motion is supported by a Statement of Material Facts, below, followed by an explanation as to why USF is entitled to judgment as a matter of law. Reference is made to deposition transcripts, as well as the ‘094 Patent (Ex. 10) and certain publications by Borchelt et al and others. By agreement, the parties have submitted the full transcripts of the depositions of witnesses taken during fact discovery – the deponents are referred to by their initials herein. These witnesses are Karen Duff (Ex. 1) (hereinafter “KD”); David Borchelt (Ex. 2) (hereinafter “DB”); Marcia Gordon (Ex. 4) (hereinafter “MG”); David Morgan (Ex. 5) (hereinafter “DM”); Stephen Snyder (Ex. 3) (hereinafter “SS”) and Sangram Sisodia (Ex. 6) (hereinafter “SNS”). The exhibits that are specific to this Motion are referenced as Ex. 10 (the ‘094 Patent), Ex. 15 (an article by Borchelt et al in Neuron dated 1996), Ex. 17 (an article by Borchelt et al in Genetic Analysis in December of 1996), Ex. 16, (an article by Borchelt et al in Neuron in October of 1997), Declaration of William Coppola (Ex. 7), and Declaration of Marcia Gordon (Ex. 8). All exhibits referred to in the Summary Judgment Motions filed by USF were submitted when the Motions themselves were filed, as attachments to USF’s Motion Submitting the Record for Summary Judgment Motions – thus, the Exhibits are attachments to that document filed immediately prior to the Motions for Summary Judgment on November 5, 2018. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 7 of 22 4 I. STATEMENT OF MATERIAL FACTS NOT IN DISPUTE 1. Hardy and Duff conceived of the invention of the Claims of the ‘094 Patent (Ex. 10) in 1995. KD (Ex. 1) 97: 9–13. 2. The Hardy/Duff conception of the invention is reflected in the NIH Grant Application (Ex. 18) submitted by USF naming Hardy as principal investigator dated September 29, 1995. (The grant application, Section IV, provided “We also aim to cross our PS-1 mice with normal and mutant APP mice to study the effect of PS gene manipulation on human APP.” Section IV). SS (Ex. 3) 30:13–34:20. 3. The Hardy/Duff invention claimed in the ‘094 Patent (Ex. 10) was subsequently published in a paper by Holcomb et al (Ex. 14) that referenced the NIH grant AG014633(Ex. 18) that was submitted by USF naming Hardy as principal investigator in 1995. SS (Ex. 3) 52:8–23. 4. Duff and Hardy disclosed the invention of the ‘094 Patent (Ex. 10) as an invention in September, 1996 on an invention disclosure form for the University of South Florida. KD (Ex. 1) 55:21–57:13. 5. The work at USF including breeding and cross-breeding the transgenic mice to reduce the invention of the ‘094 Patent (Ex. 10) to practice began no later than about the beginning of August of 1996. MG (Ex. 4), 71:14–25. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 8 of 22 5 6. Work on actually reducing the invention of the ‘094 Patent (Ex. 10) to practice by cross-breeding mice expressing the APPswe mutation with mice expressing a presenilin mutation and assessing and characterizing those mice began in August 1996 with “near daily diligence” at USF leading to an actual reduction to practice in April of 1997. Ex. 8, Declaration of Marcia Gordon, ¶¶ 6 - 7. 7. Duff characterized an actual reduction to practice of the invention claimed in the ‘094 Patent (Ex. 10) in a statement dated April 25, 1977 sent to USF’s Office of Patents and Licensing. KD (Ex. 1) 126: 3–135:5. 8. William Coppola, who was at USF’s Patent and Licensing office in 1997 confirmed receipt of the facsimile reflecting Karen Duff’s report on an actual reduction to practice as the type of thing he would have received from her in the course of his work. Ex. 7, Declaration of Coppola, ¶6. 9. Stephen Snyder, grant program administrator at NIH and the witness identified by the Government as its 30(b)(6) witness on matters pertaining to NIH funding specifically selected David Borchelt to be one of the members of the committee that would review the application for funding submitted by Hardy. SS (Ex. 3) 39:14–44:6 (“Dave Borchelt, with his background, was really an ideal candidate as a reviewer”). Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 9 of 22 6 10. All members of the review team that assessed the Hardy NIH grant application approved as grant AG014633(Ex. 18) were required to specifically note any conflicts of interest they might have in reviewing the application for grant, and if they had no conflicts, they were required to expressly so state. SS (Ex. 3)41: 20– 42:13. 11. David Borchelt at no time indicated he had a conflict of interest in reviewing the Hardy/Duff grant application that pertained to making transgenic mice expressing presenilin mutations and APP mutations and exhibiting accelerated Alzheimer’s Disease pathology. SS (Ex. 3). 44:5–21. 12. Borchelt testified that the doubly transgenic mice of Borchelt’s 1996 Neuron paper (Ex. 15) did not clearly show an increase in expression of Aß-42 over the singly transgenic mice, a feature of the invention of the ‘094 invention. DB (Ex. 2) 26: 6–10. 13. The study and results reflected in the Borchelt et al 1996 Neuron paper (Ex. 15) were based on mice sacrificed at a young age, before any amyloid deposits in the brain could form. DB (Ex. 2), 26:12–17. 14. Borchelt’s group made a decision in 1996 not to wait to conduct experiments on doubly transgenic mice to see if they would form amyloid plaques or deposits earlier than the parental lines because it would take too much time to Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 10 of 22 7 age the mice, and Borchelt wanted to publish something new before then. DB (Ex. 2), 30:17– 31:19. 15. The Borchelt 1996 Neuron publication (Ex. 15) does not reflect any information on amyloid deposits or accelerated Alzheimer’s Disease pathology in the brain of mice expressing both APPswe and presenilin mutations. DB (Ex. 2) 24: 22–31:19. 16. Another publication by Borchelt et al in 1996, Ex. 17, Genetic Analysis, was prepared and submitted before the Borchelt group had aged their mice and does not disclose if the doubly transgenic mice expressing the APPswee mutation and a presenilin mutation exhibited any accelerated Alzheimer’s Disease pathologies including amyloid deposits, reactive gliosis, loss of cognitive function, neurofibrillary tangles or significant neuronal loss. DB (Ex. 2) 35: 3–38:19. 17. Mice raised by Borchelt et al with presenilin mutations but not an APP mutation in 1996 exhibited no Alzheimer’s Disease pathology. (“I could find nothing wrong with them, no proteolysis, no nothing.”) DB (Ex. 2) 48: 9–49:16. 18. Borchelt et al continued their research on mice expressing a presenilin mutation and the APPswe mutation during 1997, which culminated in the publication of the third article on this study, Neuron October 1997, (Ex. 16) in which the doubly transgenic mice were aged sufficiently to observe amyloid deposits in the brain. DB (Ex. 2) 52:11–16. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 11 of 22 8 19. In the October, 1997 Neuron article (Ex. 16), the doubly transgenic mice were shown for the first time to have higher severity of amyloid deposits in the brain than singly transgenic presenilin mice. DB (Ex. 2) 55: 3–56:6. 20. Borchelt could not recall any presentation made by any member of his group on the results of the study on the amyloid deposits of the doubly transgenic mice before its publication in Neuron, October 1997 (Ex. 16). DB (Ex. 2) 56:12–59:2. 21. No patent application directed to the doubly transgenic mice reported on in the Neuron publications of 1996 and 1997 (Exs. 15 and 16 herein) was ever filed. DB (Ex. 2) 14: 7–16. 22. David Borchelt testified that he had a conflict of interest in cooperating with USF as a witness in this litigation, in that he stood to monetarily benefit if the ‘094 Patent (Ex. 10) was invalidated. DB (Ex. 2) 5:1–6:22. II. THE “INVENTION” OF THE ‘094 PATENT IS DEFINED BY ITS CLAIMS An issued United States Patent is presumed valid. To demonstrate invalidity due to prior invention, the United States needs to demonstrate that the invention as claimed, directed to mice exhibiting accelerated Alzheimer’s Disease pathology, was invented by Borchelt and his team before the conception and reduction to practice of it by Hardy and Duff. The invalidity contentions of the United States (Docket 106) nowhere indicate precisely what “invention” Borchelt and his team Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 12 of 22 9 of investigators is argued to have invented in advance of the conception and reduction to practice of the invention of the ‘094 Patent (Ex. 10). The Government’s argument, (Docket 106) 14–17, seems to suggest the invention is simply mice that express a presenilin mutation and the APPswe mutation. It is well established, however, that the invention is defined by the claims of the patent as it is claim language which points out the subject matter the patentee regards as his invention. Innova/Pure Water, Inc. v. Safari Water Filtration Systems, Inc., 381F. 3d 1111, 1115–16 (Fed. Cir. 2004) recently cited in Sumitomo Dainippon Pharma Co., Ltd. v. Emcure Pharmaceuticals, Limited, 2018 WL 4906268 at*1 (October 5, 2018 DNJ). This is not a new or newly recited principle. The Supreme Court of the United States has consistently identified the claims of a United Sates Patent as the sole measure of a patented invention. Smith v. Snow, 294 US 1, 11 (1935) (“The claims of the patent, not its specifications, measure the invention.”); Altoona Publix Theatres v. Am. Tri-Ergon Corp.294 US 477, 487 (“Under the statute it is the claims of the patent which define the invention.”) Applying this principle to the ‘094 Patent (Ex. 10), each of the claims requires, at a minimum, a mouse which expresses a transgene for the APPswe mutation, and a transgene for a presenilin mutation. The broadest of these Claims are 7 and 8 directed to transgenic mice, and Claims 10 and 11, directed to a method for screening expressed transgenes in Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 13 of 22 10 mice. These claims are the broadest product and method claims of the ‘094 Patent (Ex. 10) in that they are not restricted to any particular presenilin mutation. Nevertheless, each and every claim of the ‘094 Patent (Ex. 10) further requires that the mice in question exhibit accelerated Alzheimer’s Disease pathology. This Court construed this critical language in the Markman proceeding that culminated in this Court’s construction, Document 101. That construction means that each and every one of the claims requires that the doubly transgenic mouse recited have a characteristic of Alzheimer’s Disease pathology, such as the formation of deposits containing Aß in the brain, forming at least one month earlier than the singly transgenic or non-transgenic parents.2 Accordingly, USF respectfully submits that the burden rests on the United States to demonstrate by clear and convincing evidence that Borchelt’s team conceived of and reduced to practice the invention of a mouse that expresses the APPswe mutation, and a presenilin mutation, which mouse exhibits amyloid deposits in the brain at least a month before the singly transgenic (expressing either the presenilin mutation or the APPswe mutation) or wildtype (no mutations) corresponding mice did in their lifespan. 2 The Court noted that other Alzheimer’s Disease pathology features, including fibrillar Aß deposits, reactive gliosis, increased maze activity, neurofibrillary tangles, and massive neuronal loss fit within that definition. Document 101 at 14. While these are important hallmarks of Alzheimer’s Disease pathology, for the purposes of this Motion for Summary Judgment only, it is sufficient to focus on the formation of amyloid deposits in the brain. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 14 of 22 11 The undisputed facts show this is not something the United States can prove. David Borchelt testified that he made the conscious decision not to pursue that invention, or arrive at evidence of the invention, until after the conception and reduction to practice of that invention by USF. III. BORCHELT DID NOT HAVE POSSESSION OF THE ACCELERATED ALZHEIMER’S PATHOLOGY REQUIREMENTS OF THE INVENTION BEFORE APRIL 25, 1997 At a minimum, to prevail on the question of prior invention, the United States would have to demonstrate that Borchelt and his team had possession of the invention, and in particular, of the requirement that the mice of the ‘094 Patent (Ex. 10) claims exhibit accelerated Alzheimer’s Disease pathology prior to April 25, 1997, USF’s latest actual possible first reduction to practice. Indeed, the United States has not offered any criticism of the April 25, 1997 memo by Duff as a recitation demonstrating an actual reduction to practice by that date. It is, therefore, per statute, the date before which the United States must show possession of that invention by Borchelt et al. Demonstration of possession of this invention – a doubly transgenic mouse that exhibits accelerated Alzheimer’s Disease pathology as construed by this Court, must be shown by the government as of the date it alleges Borchelt et al made the invention of the ‘094 Patent (Ex. 10). Hitzeman v. Rutter, 243 F. 3d 1345, 1358 (Fed. Cir. 2001). This is reflected in the rule against “nunc pro tunc conceptions.” Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 15 of 22 12 Cooper v. Goldfarb, 240 F. 3d 1378, 2001 (Fed. Cir. 2001). As observed by the Court in Hitzeman: Nunc pro tunc conception involves the situation where an inventor actually possessed a claimed device at the time of his alleged conception, but failed to recognize the device’s inventive features at the time. As articulated in cases such as Heard [ Heard v. Burton, 333 F. 2d 239, 242–44 (CCPA 1964)] an inventor who failed to appreciate the claimed inventive features of a device at the time of his alleged conception cannot use his later recognition of those features to retroactively cure his imperfect conception. Heard, 333 F.2d at 243. To be sure, Borchelt has never argued or claimed such a conception. The United States government appears to be urging this result, pointing to Borchelt’s mice and the Neuron 1996 article (Ex. 15). It cannot successfully press this argument in the face of Borchelt’s testimony, however. David Borchelt himself testified that he did not make or have that conception in 1996. First, he testified that he did not believe that the mice he had made were reasonable models of Alzheimer’s Disease. DB (Ex. 2) p. 16, ll. 21 7:10 (“Others might have had the notion that you could make a mouse a mouse that would model Alzheimer’s disease, all right? Which is claimed by many that they have mice that model Alzheimer’s disease. I am not in agreement that those mice do that.”) Then Borchelt testified as to why he did not undertake the research and investigation required to determine whether the doubly transgenic mice he and his team made would exhibit accelerated Alzheimer’s Disease pathology. In a publish Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 16 of 22 13 or perish world, it would take too long, and others, like Hardy/Duff, might publish first. DB (Ex. 2) p. 31, ll. 9-17: We made the tactical decision that we could not wait – we could not wait to see whether our doubly transgenic mice would get amyloid plaques. It was going to be another six to nine months before those mice – I had the mice on the – by the time this paper was out, was submitted, I had the mice on the shelf aging to do the other part of the study. But we decided we could not wait, because we were well aware of others that were trying to do the same thing. As a consequence, although Borchelt and his team would publish three papers looking at the work they did on the doubly transgenic mice, neither of the first two, Ex. 15 in November of 1996, and Ex. 17 in December of 1996, make any reference to or description of accelerated Alzheimer’s Disease pathology. No reference is made in those articles to amyloid deposits in the brains of those mice or any other Alzheimer’s Disease pathology – the mice were simply too young to exhibit those features. As a result, it was not until October of 1997 that Borchelt’s team’s observations on the doubly transgenic mice expressing APPswe and a presenilin mutation was reported in Neuron 1997, Ex. 16. That was nearly four months after the ‘094 Patent filing (Ex. 10). Borchelt’s very first statement indicating the mice he and others studied exhibited accelerated Alzheimer’s disease pathology came twelve months after the provisional application filed October 21, 1996 (Ex. 11) which discloses the invention. Borchelt’s very first disclosure of mice with accelerated Alzheimer’s Disease pathology came a full Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 17 of 22 14 twenty-five months after the corroborated conception of the invention by Hardy and Duff in the grant application that matured into the grant designated AG014633 (Ex. 18). Thus, whether in fact the mice that Borchelt et al made in 1995-1997 would later exhibit accelerated Alzheimer’s Disease pathology inherently when they aged due to their transgenic pedigree or not, failure on the part of the Borchelt team to recognize or appreciate that phenomenon precludes any kind of conception prior to Hardy and Duff. As observed in Hitzeman at 1354– 56, whether or not the accelerated Alzheimer’s Disease pathology exhibited by the mice is inherent is beside the point – in the absence of Borchelt’s recognition of those properties, no conception of the invention of the ‘094 Patent (Ex. 10) was had by Borchelt and his team. Due to a conscious decision to not pursue pathology but rather only the chemistry of the APP protein (which took less time to appear), Borchelt and his team did not investigate the effects of co-expression of the APPswe mutation and a presenilin mutation on accelerated Alzheimer’s Disease pathology until after an actual reduction to practice of the invention by Duff. Borchelt, Sisodia and their co-researchers certainly made doubly transgenic mice, but they were not in possession of the invention of the ‘094 Patent (Ex. 10) until after Duff and Hardy had actually reduced it to practice. Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 18 of 22 15 The decision by Borchelt to deliberately NOT investigate the accumulation of amyloid deposits in the brains of the doubly transgenic mice until much later is consistent with another conscious decision made by Borchelt. Stephen Snyder, administrator at NIH and NIA for funding and grant applications, placed Borchelt on the review board considering the application for funding (Ex. 18) that was eventually granted to Mayo Clinic for the work embodying the invention of the ‘094 Patent (Ex. 10) conceived of by Hardy and Duff. If in fact Borchelt had intended to pursue that invention in 1995–1996 when the application was reviewed featuring the preparation of a “mouse model” of Alzheimer’s Disease exhibiting accelerated Alzheimer’s Disease pathology, he would have had to advise Snyder of his potential conflict of interest. In fact, Snyder testified that Borchelt never so advised him, and Borchelt was a strong supporter of the work proposed in the grant application. This is consistent only if in fact Borchelt – who testified he did not agree that the doubly transgenic mice were good models of Alzheimer’s Disease – did not intend to investigate the phenomenon of accelerated pathology in the time frame addressed by the grant, that is, until after 1996. IV. CONCLUSION John Hardy and Karen Duff conceived of the invention of the ‘094 Patent (Ex. 10), the doubly transgenic mice expressing the APPswe and presenilin mutation, exhibiting accelerated Alzheimer’s Disease pathology, no later than Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 19 of 22 16 September of 1995. They actually reduced it to practice no later than Duff’s memo of April 25, 1997. All of this occurred before David Borchelt and his research team published results for such doubly transgenic mice that reflect accelerated Alzheimer’s Disease pathology in October, 1997. To be sure, Borchelt et al were raising doubly transgenic mice in the same time frame that Hardy and Duff were at USF. Yet, while Hardy and Duff were looking at an Alzheimer’s Disease models that exhibited accelerated pathology, Borchelt and his team were focused on the chemistry of the APP protein, and sacrificed their mice long before those mice could ever exhibit accelerated Alzheimer’s Disease pathology. Those mice could not be models of Alzheimer’s Disease. Fundamentally, mammalian Alzheimer’s Disease models such as the doubly transgenic mice with accelerated pathology were not of interest to Borchelt until after Duff and Hardy made the invention of the ‘094 Patent (Ex. 10). Borchelt’s team simply did not have possession of the invention of the ‘094 Patent (Ex. 10), they did not invent that subject matter before Hardy and Duff. Any other conclusion must explain 1) Why Borchelt did not draw attention to his conflict of interest to Snyder and NIH earlier; 2) why the Borchelt team suppressed the news of that invention throughout 1995-1996; and 3) concealed it from the 1996 publications in Neuron and Genetic Analysis (Exs. 15 and 17). In the absence of compelling explanations for these actions, one can only conclude that Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 20 of 22 17 Hardy and Duff were the first to invent the subject matter of the ‘094 Patent (Ex. 10). The claims of that patent are not invalid over the work of Borchelt et al under 35 U.S.C. 102(g). Entry of judgment in accordance is respectfully requested. Respectfully submitted, Dated: November 5, 2018 OF COUNSEL: Jerry Stouck Email: stouckj@gtlaw.com GREENBERG & TRAURIG 2101 L Street, N.W., Suite 1000 Washington, DC 20037 (202) 331-3173 phone (202) 261-4751 facsimile s/Steven B. Kelber Steven B. Kelber Email: steve@kelberlawgroup.com THE KELBER LAW GROUP 1875 Eye Street, N.W., Fifth Floor Washington, D.C. 20006 240-506-6702-Telephone Counsel for Plaintiff University of South Florida, Board of Trustees Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 21 of 22 18 LIST OF EXHIBITS (cited in this Motion) Exhibit 1 Deposition Transcript of Karen Duff (referenced as “KD”) Exhibit 2 Deposition Transcript of David Borchelt (referenced as “DB”) Exhibit 3 Deposition Transcript of Stephen Snyder (referenced as “SS”) Exhibit 4 Deposition Transcript of Marcia Gordon (referenced as “MG”) Exhibit 5 Deposition Transcript of David Morgan (referenced as “DM”) Exhibit 6 Deposition Transcript of Sangram Sisodia (referenced as “SNS”) Exhibit 7 Declaration of William Coppola Exhibit 8 Declaration of Marcia Gordon Exhibit 10 U.S. Patent No. 5,898,094, issued April 27, 1999 (“094 Patent”) Exhibit 11 U.S. Provisional Patent Application 60/028,937, filed October 21, 1996 (“’937 Application”) Exhibit 14 Holcomb et al., 1998 Nature Medicine, 4:1, 97–100. Exhibit 15 Borchelt et al., 1996 Neuron, 17:1005–1013. Exhibit 16 Borchelt et al., 1997, Neuron, 19(4):939-4. Exhibit 17 Borchelt et al., 1996, Genetic Analysis, 13(6):159-63. Exhibit 18 NIH Funding Grant AG014663 (Awarded 1996). Case 1:15-cv-01549-PEC Document 117 Filed 11/05/18 Page 22 of 22
