Abbott Biotechnology Ltd. v. Centocor Ortho Biotech, Inc.
| Decision Date | 16 April 2014 |
| Docket Number | Civil Action No. 09–40089–FDS. |
| Court | U.S. District Court — District of Massachusetts |
| Parties | ABBOTT BIOTECHNOLOGY LTD. and Abbvie Inc., Plaintiffs, v. CENTOCOR ORTHO BIOTECH, INC., Defendant. |
David P. Frazier, David Brian Kacedon, Michael A. Morin, Casey L. Dwyer, Cora Renae Holt, Finnegan, Henderson, Farabow, Garrett & Dunner, LLP, Washington, DC, Michael P. Angelini, Douglas T. Radigan, Bowditch & Dewey, LLP, Worcester, MA, Steven O'Connor, Finnegan, Henderson, Farabow, Garrett & Dunner, LLP, Reston, VA, Denise W. Defranco, Finnegan, Henderson, Farabow, Garrett & Dunner, L.L.P., Boston, MA, for Plaintiffs.
Dianne B. Elderkin, Matthew G. Hartman, Angela Verrecchio, Barbara L. Mullin, Matthew A. Pearson, Ruben H. Munoz, Steven D. Maslowski, Akin Gump Strauss Hauer & Feld LLP, Philadelphia, PA, Heather B. Repicky, Nutter, McClennen & Fish, LLP, Boston, MA, for Defendant.
MEMORANDUM AND ORDER ON MOTIONS FOR SUMMARY JUDGMENT
This is a patent dispute involving pharmaceutical products used to treat certain autoimmune diseases. Plaintiffs Abbott Biotechnology Ltd. and AbbVie Inc. (collectively “Abbott”) seek a judgment that the drug Simponi, manufactured by defendant Centocor Ortho Biotech, Inc. infringes its patents to the extent that it is used with the drug methotrexate to treat rheumatoid arthritis.1 Centocor seeks declarations of non-infringement and invalidity of Abbott's patents.
Both parties have moved for summary judgment. Centocor has moved on the grounds that (1) the claims are invalid for lack of a written description; (2) the claims are invalid for lack of enablement because the patents indicate only a small subset of the claimed invention, not the full scope; (3) the patents are invalid for failing to list a purported inventor; (4) some claims are invalid for lack of enablement because the patents enable the creation of antibodies by only one method; (5) Centocor did not willfully infringe the patent, if it did infringe at all; and (6) the patents are invalid because references prior to the filing date are prior art and Abbott did not diligently reduce its invention to practice. Abbott opposes Centocor's contentions, and has cross-moved for summary judgment on the grounds that (1) the 4SE3 antibody is not prior art; (2) references prior to the date it filed its patent applications are not prior art; and (3) the patents are not invalid for failure to list a purported inventor.
For the reasons set forth below, the motions will be granted in part and denied in part.
The following facts are undisputed, unless otherwise noted.
U.S. Patents No. 7,223,394 (the “'394 patent”) and No. 7,541,031 (the “'031 patent”) are part of a family of patents owned by Abbott. The parent patent, U.S. Patent No. 6,090,382 (the “'382 patent”), was filed in 1996 and issued in 2000. It is directed to certain human antibodies designed to attach to a naturally-occurring protein in the human body called tumor necrosis factor alpha (“hTNFa”).
Human TNFa is involved in regulation of the immune system, a role it performs by triggering inflammation in response to invasion by a foreign entity. Overproduction of hTNFa can lead to excessive inflammation that can result in tissue damage. This occurs in diseases such as rheumatoid arthritis, Crohn's disease, ankylosing spondylitis, and psoriasis. Such diseases are known as autoimmune diseases because of the way the body's own immune system—in this case, through hTNFa—targets healthy human tissue instead of foreign contaminants.
Antibodies are proteins that bind with harmful foreign substances, or “antigens,” such as viruses or bacteria. An antibody attaches itself to an antigen by binding with a portion of the antigen called an “epitope.” By occupying the antigen's epitope, the antibody diminishes the antigen's ability to bind with other receptors in the body, and therefore minimizes the harmful effect.
The human immune system rarely produces antibodies that target hTNFa, because hTNFa is a protein that the body itself produces, not a foreign contaminant. To prevent an overabundance of hTNFa from causing tissue damage, researchers have sought to develop an antibody that binds to hTNFa. The process of binding is known as “neutralization” of hTNFa. In order for an antibody to neutralize hTNFa effectively, it must attach to it with sufficient strength. The strength of an antibody's interaction with hTNFa is called its “affinity” for hTNFa. Affinity is expressed in term of Kd—the propensity that the objects will dissociate—and a lesser Kdindicates a higher affinity.2 Also, the longer that the antibody attaches to hTNFa, the more effective it is at neutralizing the antigen. The rate at which the antibody and antigen dissociate is expressed in terms of Koff, with a lower number indicating that the objects bind for a longer period of time.3
Researchers have long sought to develop antibodies that neutralize hTNFa and bind to it with high affinity. An antibody that inhibits hTNFa in this manner could become a treatment for, among other things, autoimmune diseases. In the 1980s, researchers invented a high-affinity, neutralizing anti-hTNFa antibody that derived from mouse DNA. It could not effectively treat human autoimmune diseases, however, because humans often exhibit adverse reactions to non-human antibodies.
The development of chimeric antibodies, or antibodies with components that derive from both mouse and human DNA, advanced treatment options for autoimmune diseases. Centocor, together with the Kennedy Institute, obtained a patent in 2001 that disclosed a method for treating arthritis by co-administering chimeric anti-hTNFa antibodies with a pre-existing drug called methotrexate. (See U.S. Patent No. 6,270,766 ).4 In 1999, the FDA approved Remicade, a drug manufactured by Centocor and based on chimeric antibodies, for treatment of rheumatoid arthritis.
During the same time period, Abbott was also seeking to develop effective antibodies. In 1993, BASF Bioresearch Corporation, later acquired by Abbott, and Cambridge Antibody Technology (“CAT”) were collaborating on the development of antibodies. Three CAT scientists, all of whom are inventors of the patents-in-suit, succeeded in isolating a human antibody called 4SE3 by July 1993. However, 4SE3 did not have the sought-after qualities, and does not fall within the scope of the claims of the patents-in-suit.
By April 14, 1995, BASF and CAT scientists had succeeded in isolating a high affinity, neutralizing anti-hTNFa antibody, which they labeled “D2E7.” BASF then undertook preclinical and clinical testing of the antibody.
At some point, BASF scientists conceived of the idea to co-administer such an antibody with methotrexate to treat rheumatoid arthritis. Abbott contends that one of the BASF scientists came up with the idea prior to the development of D2E7, because it was a well-known and obvious treatment. None of them has taken credit for the concept nor remembers who is responsible. Centocor contends that the idea was not obvious and that the BASF scientists co-opted the idea from Dr. Michael Weinblatt, who consulted with them about clinical development of an anti-hTNFa drug in January 1995. Dr. Weinblatt, however, denies that he introduced the concept to the BASF scientists.
In 1996, Abbott filed the '382 patent and for the first time disclosed a class of fully-human, high-affinity, neutralizing anti-hTNFa antibodies as well as certain uses of those antibodies. The '382 patent did not address co-administration of the antibodies with methotrexate.
From April 14, 1995, to February 10, 1997, other references to purportedly the same invention became public: two international patent applications, Kucherlapati WO 96/33735 and Kucherlapati WO 96/34096; the 1995 Kennedy Institute of Rheumatology Annual Report; two scientific papers, published in 1996 and 1997; a presentation by Dr. Salfeld, an Abbott scientist, in 1996; and two patent applications, U.S. Patent No. 6,075,081, filed April 27, 1995, and U.S. Patent No. 6,150,584, filed October 2, 1996.
Abbott filed two patent applications on February 10, 1997—the '394 and ' 031 patents, the patents-in-suit—that are continuations of a patent in the '382 family. The listed inventors were Jochen G. Salfeld and twelve others; Dr. Weinblatt was not included. The '394 patent, issued in 2007, is directed to a method for treating rheumatoid arthritis by administering the human anti-hTNFa antibody with methotrexate. The '031 patent, issued in 2009, shares the same specification and claims substantially the same invention. Both patents claim priority to the 1997 Patent Co-operation Treaty application; Abbott contends that the date of invention was, at the latest, April 14, 1995, when it first developed D2E7.
The patents describe a genus of human anti-hTNFa antibodies, of which D2E7 is a member. They define the genus by its functional characteristics: a high affinity for hTNFa, defined as a Kdof –10 –8 M or less; a slow rate of dissociation, defined as a Koffof –10 –8 sec –1 or less; and an ability to neutralize hTNFa in vitro and in vivo. The patents indicate possible methods of creating other antibodies within the genus, starting by making changes to D2E7, but do not indicate the total number of qualifying antibodies that exist.
Based on the technology disclosed in the '382 patent and its progeny—in particular, the '394 and '031 patents —Abbott developed a drug called Humira. The FDA approved Humira in December 2002 to treat rheumatoid arthritis, either alone or in combination with methotrexate or other DMARDs. Rheumatoid arthritis patients typically take a combination of Humira once every two weeks and methotrexate weekly, but may take Humira weekly when it is not prescribed in combination with methotrexate.
In the past decade, Centocor researchers also developed a fully-human, high-affinity, neutralizing...
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Abbott Biotechnology Ltd. v. Centocor Ortho Biotech, Inc.
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