Full opinion text
MEMORANDUM DECISION AND ORDER DENYING PLAINTIFFS’ MOTION FOR PRELIMINARY INJUNCTION ROBERT J. SHELBY, District Judge. On June 13, 2013, the Supreme Court issued a unanimous decision holding that “genes and the information they encode are not patent eligible simply because they have been isolated from the surrounding genetic material.” Association for Molecular Pathology v. Myriad, Genetics, Inc. (AMP), — U.S. -, 133 S.Ct. 2107, 2120, 186 L.Ed.2d 124 (2013). This case arises in the aftermath of that decision. Plaintiff Myriad Genetics, Inc. (Myriad) is recognized as the winner in the “race” to locate and sequence the BRCA1 and BRCA2 genes. Myriad invested millions of dollars, including money obtained via public grants, in an effort to locate and sequence those genes in the early-to-mid-1 990s. Once it did, Myriad sought and obtained related patents, some of which will begin to expire in August 2014. Myriad also developed and commercialized tests to screen people for the presence of harmful variations in these genes. Myriad launched its flagship ‘BRACAnalysis’ test in 1996 and debuted its ‘myRisk’ test in 2013. Ford Deck at ¶¶ 1-3, 8 (Dkt. 6). Between 1997 and 2013, Myriad’s revenue from its BRACAnalysis test steadily increased, and now totals more than $2 billion. Kearl Decl. at 6 (Dkt. 107). Myriad earned that revenue by carefully guarding its patent rights and preventing others from providing screening tests for the BRCA1 and BRCA2 genes. From the mid-1990s, until the Supreme Court’s AMP decision, Myriad was the lone provider of full-sequence BRCA1 and BRCA2 tests in the United States. Ford Deck at ¶ 8. Within days of the Supreme Court’s AMP decision, Defendant Ambry Genetics Corporation (Defendant) announced plans to sell tests less expensive than Myriad’s to screen BRCA1 and BRCA2 genes. Since then, other companies have followed suit — publicly offering such tests or announcing plans to do so. Soon after Defendant announced it would begin to offer BRCA1 and BRCA2 testing, Plaintiffs filed this action, complaining that Defendant’s genetic testing infringes several of Plaintiffs’ patents. Plaintiffs now move the court for a preliminary injunction enjoining Defendant’s sales or offers to sell “genetic tests including a BRCA1 or BRCA2 panel” pending trial on the merits. Plaintiffs’ Motion focuses on ten claims in the patents-in-suit: 1) four claims to pairs of synthetic DNA strands, called “primers”; and 2) six methods claims for analyzing BRCA1 and BRCA2 sequences. Plaintiffs argue these claims remain patent eligible after the AMP litigation, and that Defendant’s testing infringes the patents containing these claims. Plaintiffs contend an injunction is necessary to prevent irreparable harm to their pricing structure, share of the BRCA1 and BRCA2 testing market, corporate reputation, and other exclusive benefits they might enjoy during the remainder of their patents’ terms. Defendant opposes Plaintiffs’ Motion, arguing that Plaintiffs cannot show that they are likely to succeed on the merits of their infringement claims because Defendant has raised a “substantial question” concerning the subject matter eligibility of Myriad’s BRCA1 and BRCA2-related patents, particularly in light of the recent AMP litigation. Defendant further contends there are substantial questions concerning whether: 1) its testing infringes Plaintiffs’ patent claims; 2) the patents at issue are invalid because the inventions they claim were anticipated and obvious; and 3) the patents are invalid due to indefiniteness or lack of written description. Defendant also argues that Plaintiffs will suffer no immediate, irreparable harm to their pricing, market share, or reputation. Finally, Defendant asserts that its business will be devastated and the public interest harmed if an injunction issues because the public would lose access to less expensive, more complete, and more innovative cancer testing. On September 11 and 12, and October 7, 2013, the court received testimony and argument on Plaintiffs’ Motion. Additionally, the parties have submitted numerous declarations from experts. Having carefully considered the relevant authorities, briefing from the parties and amici, oral argument, testimony, and the evidence, the court concludes Plaintiffs are not entitled to a preliminary injunction. The court finds that although Plaintiffs have shown they are likely to be irreparably harmed if an injunction does not issue, Defendant has raised substantial questions concerning whether any of the patent claims at issue in Plaintiffs’ Motion are directed toward patent eligible subject matter under 35 U.S.C. § 101. In light of Defendant’s showing, Plaintiffs are unable to establish that they are likely to succeed on the merits of their claims. Neither have Plaintiffs established that the equitable factors support issuance of the requested injunction. Having failed to satisfy their burden, Plaintiffs’ Motion for Preliminary Injunction must be denied. I. FACTUAL BACKGROUND A. The Parties 1. Plaintiffs Myriad is a Delaware molecular diagnostic corporation with its principal office in Salt Lake City, Utah. The University of Utah is a Utah nonprofit educational and research institution in Salt Lake City. The University of Pennsylvania is a Pennsylvania nonprofit educational and research institution in Philadelphia. The Hospital for Sick Children is a pediatric health care and research facility located in Toronto, Ontario. Endorecherche is a Canadian medical research corporation in Ste-Foy, Quebec. Myriad owns the following patents-in-suit: the '155, '400, '379, '721, '497, '510, '258, '237, '776, and '571 Patents. See supra note 4 (listing complete numbers for patents-in-suit). Myriad is the exclusive licensee of the '999, '282, '441, '492, and '857 Patents. The University of Utah is the owner or co-owner of three patents at issue in this case, the '999, '282, and '441 Patents. The University of Utah, University of Pennsylvania, the Hospital for Sick Children, and Endorecherche are the co-owners of the '857 and '492 Patents. The University of Utah Research Foundation, also a Plaintiff, has received from Myriad over $40 million in royalties under some of the patents at issue in this case over the past two decades. Pershing Deck at ¶ 4 (Dkt. 112). 2. Defendant Defendant is a clinical diagnostic and genomic services company in Aliso Viejo, California. In the hours after the Supreme Court issued its AMP decision, Defendant announced that it would begin offering a number of its own tests that include BRCA1 and BRCA2 screening. Defendant now offers a menu of at least six tests that include screening for BRCA1 and BRCA2: a combined BRCA1/BRCA2 test, BRCA Plus, Breast-Next, PancNext, Ova Next, and Cancer-Next. Chao Decl. at ¶ 16, Exhs. B-G (Dkt. 56). Defendant’s BRCA1/BRCA2 test is available for $2,200 — substantially less than the price for comparable testing offered by Myriad. Id. 3. Amici The court permitted the filing of a joint Amicus Curiae brief in support of Defendant’s Opposition to Plaintiffs’ Motion for Preliminary Injunction. (Dkt. 79.) Amici are the American Civil Liberties Union (ACLU) and ACLU of Utah Foundation, Inc. (ACLU Utah), Public Patent Foundation (PUBPAT), Association for Molecular Pathology (AMP), Breast Cancer Action (BCAction), and the AARP. The ACLU and PUBPAT represented the individual and organizational plaintiffs in the AMP litigation, including two of the amici here, AMP and BCAction. AARP also filed amicus briefs in the AMP litigation. The ACLU describes itself as a “nationwide, nonprofit, nonpartisan organization with over 500,000 members” with the stated goal of protecting rights protected under the Constitution. Id. at 4. ACLU Utah is a regional affiliate of the ACLU. Id. PUBPAT is a not-for-profit legal services organization affiliated with the Benjamin N. Cardozo School of Law and is concerned with patent policy issues. Id. at 4-5. AMP is “an international not-for-profit professional association representing over 2,000 physicians, doctoral scientists and medical technologists who perform laboratory testing based on knowledge derived from molecular biology, genetics and genomics.” Id. at 5. AMP claims an interest in this matter because, in its view, the issues in this case will impact “the provision of and innovation in genetic testing.” Id. BCAction is “a national, grassroots advocacy and education organization” working to end breast cancer. It holds itself out as “the watchdog of the breast cancer movement.” Id. AARP is a “nonpartisan, nonprofit organization with a membership dedicated to addressing the needs and interests of people age fifty and older,” seeking to “enhance the quality of life for all by promoting independence, dignity, and purpose.” Id. at 6. AARP’s mission is focused, in part, on healthcare-related issues. Id. B. Background on Genetics Plaintiffs and Defendant generally do not dispute the core scientific principles underlying the genetics issues in this case. Here, the court relies upon expert declarations and testimony submitted by Plaintiffs and Defendant. 1. DNA Genes are the units responsible for inheritance of discrete traits, such as the color of peas in a peapod. Kay Decl. at ¶ 15 (Dkt. 103); Tait Decl. at ¶ 32 (Dkt. 54). Genes are made from segments of deoxyribonucleic acid, or DNA. DNA is an integral component of chromosomes, the complex structures that carry genes and which are located within most cells of the human body. Pribnow Decl. at ¶ 18 (Dkt. 65); Kay Decl. from AMP Litigation at ¶ 131 (Dkt. 34-4). The human genome, the “whole of the genetic information of an organism,” is comprised of about 22,000 genes residing in 23 pairs of chromosomes. Tait Decl. at ¶ 32. Every cell in the human body contains a complete copy of the human’s genome. DNA is a chemical compound containing within its molecular structure the genetic information necessary to code for most, if not all, aspects of embryogenesis, development, growth, metabolism, and reproduction. Pribnow Decl. at ¶ 22. At its most basic level, a DNA molecule is composed of five chemical elements: carbon, hydrogen, oxygen, nitrogen, and phosphorus. Kay Decl. at ¶ 12. But DNA is unique from other molecules in that it encodes — provides the blueprint for — our highly organized, intricate, complex internal structures, and serves as the template for the complex molecules that allow us to extract, transform, and utilize the energy that is present in our environment. It can be said that DNA contains information necessary for all life functions. Aug. 23, 2013 Tutorial (Jackson) at 8:3-10, 8:22-9:18 (Dkt. 117); Nuss-baum Decl. at ¶¶ 41-65 (Dkt. 61); Pribnow Decl. at ¶ 33; Pribnow 2nd Decl. at ¶¶ 21-24 (Dkt. 132). It is DNA’s unique, informational aspect that sets it apart from other biological molecules. Tait Decl. at ¶ 32. The information in DNA is stored in the sequence of adjacent bases within the DNA strand through what is termed a “nucleotide sequence.” Scientists often refer to DNA as a “polynucleotide,” reflecting that DNA consists of a contiguous chain of chemical units called “deoxyribo-nucleotides.” Pribnow Decl. at ¶¶ 22-23. The standard nucleotides in vertebrate DNA contain four different bases: adenine, thymine, cytosine, and guanine. As shorthand, scientists often denote nucleotides by the first letter of the names of their bases: “A” for adenine; “G” for guanine; “T” for thymine; and “C” for cytosine. These bases are linked together by chemical bonds via a sugar-phosphate backbone. Kay Decl. at ¶ 12. A DNA molecule is typically represented by the linear order of the nucleotide sequence. Scientists can extract DNA from cells in the body. Such DNA is known as extracted “genomic” DNA or gDNA. Scientists can also chemically synthesize DNA. Whether genomic or synthetic, all DNA uses the same four nucleotides, -and the information encoded in a specific nucleotide sequence is the same. Pribnow Decl. at ¶¶ 19-21, 27, 52-54; Pribnow 2nd Decl. at ¶¶ 5-11. DNA often exists as a double helix, with two intertwined strands. This structure is made possible because each base in one strand is paired via hydrogen bonds with another base in the other, complementary strand. Kay Decl. at ¶ 14. To better understand DNA’s role as an informational molecule, one must understand the rules of base pair complementarity, or “Watson-Crick” base pairing, named after two of the scientists credited with deducing the structure of DNA upon recognizing the critical importance of base pair complementarity. Pribnow Decl. at ¶28. In Watson-Crick pairing, A pairs exclusively with T, while C pairs only with G. Id. at ¶¶ 28-29. The informational aspects of DNA are based on associations between the nucleotides that are governed by the natural law of Watson-Crick base pairing. Nussbaum Decl. at ¶¶ 41-65; Pis.’ Reply Br. at 5 (Dkt. 98); Pribnow Decl. at ¶¶ 28-50. A single-stranded DNA molecule has “directionality,” meaning that the two ends of the molecule are chemically different. The “beginning” of a DNA molecule is called the 5' (5 prime)-end and the “end” of the molecule is called the 3' (3 prime)end. Kay Decl. at ¶ 17. DNA also contains regions that can code for protein molecules. Protein-coding segments of native DNA are contained in “exons.” Id. at ¶ 18. In humans, protein-coding exonic DNA sequences are typically interrupted by intervening DNA sequences known as “introns” that do not code for proteins, but may contain regulatory elements — which control when a cell activates a gene. Id. DNA replicates through a complex process. Pribnow Decl. at ¶ 36. During replication, the DNA double helix is “unwound” and separated into single strands. Id. Single-stranded DNA binding proteins maintain DNA in its single-stranded conformation, preventing the strands from reassociating through Watson-Crick base pairing. Pribnow 2nd Decl. at ¶¶ 30-32. The two single strands of DNA then become templates for the synthesis of the strand that will form the opposite strand in a new double helix. Pribnow Decl. at ¶¶ 36-38; Pribnow 2nd Decl. at ¶¶ 13-17. DNA replication is “primed” by the presence of a short RNA primer that the enzyme responsible for synthesizing new DNA — “DNA polymerase” — -uses as a starting point to synthesize the new DNA strand. Pribnow 2nd Decl. at ¶¶ 13-17. The opposite strands are synthesized according to Watson-Crick base pairing rules, resulting in two identical copies of the original DNA sequence. Id. The entire genomic DNA of all human cells — all forty-six chromosomes’ worth (in twenty-three chromosome pairs) — is completely copied from end to end during each replication cycle. Pribnow Decl. at ¶ 37. Thus, all base pairs comprising the genome are exposed in an extended single-stranded form during each replication event. Id. In humans, this occurs trillions of times during the life of every person. Id. Both the integrity of the structure and the nucleotide sequence of each single strand of the entire double helix are critical for maintaining the fidelity of replication during the vast number of cell division events that occur. Id. A change in the gene sequence is called a genetic “variant” or “polymorphism.” Any change, even to a single nucleotide, can constitute a variant. Some variants are harmless. Others, termed “mutations,” can cause disease or increase the risk of disease. Disease conditions in humans frequently are due to mutations in an individual’s copy of a single gene that gives rise to a protein different from the normal, or “wild-type,” protein expressed in persons without the disease. The genetic mutation that is responsible for such protein alteration may be determined and may be observed relatively easily through analysis of a person’s DNA sequence from a human sample. Tait Decl. at ¶ 34. These mutations can be found in exons or introns, although it is often easier for geneticists to identify disease-causing mutations in exons. Hence, mutation screens often concentrate on examining DNA sequences containing exons. Kay Decl. at ¶ 19. In some instances, there is not enough information about a variant to classify it— the variant’s effect on the body is currently unknown. Such a variant is termed a “variant of unknown significance,” or “YUS.” The significance of the variant may be determined over time though the collection and analysis of more data for that variant. Swisher Decl. at ¶ 40 (Dkt. 59); Nussbaum Decl. at ¶¶ 66-68. Through further investigation, most VUS results are ultimately reclassified as either deleterious or benign. The vast majority are reclassified as benign. Of course, the number of VUS reported is inversely proportional to the completeness of a genetic database. The more mutations discovered and characterized, the fewer VUS results will be returned. Nussbaum Decl. at ¶¶ 66-67. 2. RNA RNA, or ribonucleic acid, is a chemical compound with four bases: guanine, cytosine, uracil, and adenine. Kay Decl. at ¶ 20. Thus, instead of DNA’s thymine base, RNA contains uracil. Id. Common abbreviations of the RNA bases are: “G” for guanine, “C” for cytosine, “U” for uracil, and “A” for adenine. Id. Each base, together with one sugar and one phosphate molecule, makes up one repeating unit known as an RNA nucleotide. Id. Also like DNA, RNA is formed by a strand of bases that are linked together via a sugar-phosphate backbone. Id. The structures of the sugar-phosphate backbone of RNA and DNA, however, are different; while RNA contains a ribose sugar, the sugar component of DNA is a deoxyribose. Id. Because of these differences in structure, RNA usually exists as a single strand instead of the double helix associated with DNA. Id. DNA is generally more stable than RNA. Id. RNA is generated in the body from DNA in a process called “transcription.” Id. at ¶ 21. During transcription of RNA from DNA, a discrete segment of the DNA unwinds, and the bases of the DNA molecule act as “clamps” that hold the bases of the newly forming RNA in place while the chemical bonds of the sugar-phosphate backbone are formed. Id. This process is mediated by a structure in the cell known as RNA polymerase. Id. A newly transcribed RNA molecule (transcript), or precursor messenger RNA (pre-mRNA), is processed to result in a mature messenger RNA (mRNA). Id. at ¶ 22. Pre-mRNA contains nucleotides that are eliminated during a process called “splicing.” Id. This involves splicing the introns out of the pre-mRNA, while the exons are ligated, or joined together, to form the intact mRNA molecule. Id. 3. Proteins Proteins are generally large, complex molecules that play many Critical roles in the body. Id. at ¶ 23. They are required for the structure, function, and regulation of the body’s tissues and organs. Id. Proteins are made up of hundreds or thousands of smaller units called amino acids, which are attached to one another in long chains. Id. There are 20 different amino acids that can be combined to make a protein. Id. The sequence of amino acids determines each protein’s unique 8-dimen-sional structure and its specific function. Id. Proteins are translated from mRNA through a process called “translation.” Id. at ¶ 24. During translation, mRNA serves as a template to assemble a protein. Id. Three consecutive bases in an mRNA molecule constitute a “codon,” which codes for one of the twenty amino acids. Id. Pairing interactions take place between an mRNA molecule and another RNA molecule known as tRNA, which serves as an adaptor during protein translation. Id. Specifically, sets of three nucleotides in the coding region of an mRNA react with three nucleotides in a tRNA in such a way as to cause the amino acid linked to the tRNA molecule to be chemically transferred to the growing polypeptide (a chain of amino acids linked together by peptide bonds) destined to become a protein. Id. The bases of the mRNA serve as “clamps” to hold the amino acids in place while the chemical bonds between the individual amino acids are formed. During translation, the mRNA template, the tRNA, the newly-forming polypeptide chain, and the next amino acid reside in a multi-protein complex called a ribosome. Id. Once a protein is translated it typically undergoes post-translational or chemical modifications that are important for the protein’s function. Id. The genetic code describes which codons code for which amino acids. Id. at ¶ 25. For example, the codon adenine-thymine-guanine encodes the amino acid methionine. Id. Thus, the chemical composition of an mRNA molecule determines the amino acid composition of a protein. Id. 4. cDNA Complementary DNA, or “cDNA,” is commonly synthesized from a mature mRNA in a reaction catalyzed by a protein known as reverse transcriptase. Id. at ¶ 26. cDNA is so named because each base in the cDNA can bind to a base in the mRNA from which the cDNA is synthesized. Id. In other words, it is “complementary” to the mRNA from which it is synthesized. Id. cDNA can be structurally different from native DNA. Most notably, cDNA made from an mRNA does not contain introns. Id. at ¶ 27. DNA generally contains intronic sequences — although DNA fragments may contain only exons. cDNA is also functionally different from DNA. Id. at ¶28. Most critically, DNA contains regulatory sequences. Id. These regulatory sequences are not present in cDNA because they are not present in the mRNA from which the cDNA is synthesized. Id. 5. Primers and Probes A primer is a short, synthetic, single-stranded DNA molecule that binds specifically to an intended target nucleotide sequence. Id. at ¶ 29. The sequence of the primer is necessarily complementary to the target sequence, so that the bases of the primer and the bases of the target sequence bind to each other. Id. In human genetic testing, primers bind to human gene sequences that are an exact match according to the law of Watson-Crick base pairing. Pribnow Decl. at ¶ 91. Binding a primer to its target sequence is the first step in amplifying a segment of DNA — the production of multiple copies of a specific DNA segment for DNA sequencing reactions or other molecular characterization. Id.; Kay Decl. at ¶¶ 29-30. Scientists create primers. In so doing, they consider primer size and other aspects, such as the exact portion of the DNA segment targeted. Pribnow 2nd Decl. at ¶ 8. These considerations are dictated by the nucleotide sequence of the DNA segment to which the primer is intended to bind. Id. For example, if the targeted sequence is a naturally occurring BRCA1 or BRCA2 sequence, the starting points for primer creation necessarily must be the complement of the naturally occurring BRCA1 or BRCA2 sequences flanking the specific DNA region the scientist wishes to amplify. Id. Because the primers in a pair are designed to “hybridize” to their BRCA primer binding sites per Watson-Crick base pairing rules, the BRCA primers must contain sequences identical to the BRCA sequence directly opposite its binding sites. Id. Typical primer pairs used in the most common method of DNA amplification, polymerase chain reaction (see discussion of polymerase chain reaction infra Part I.B.6.), are between 15 to 18 nucleotides or 25 to 30 nucleotides in length. Roa Deck at ¶ 16 (Dkt. 63); Pribnow Deck at ¶ 91. To hybridize well to a person’s DNA, the length of the nucleotide sequence of the primer that binds to the sample DNA should be at least 15 nucleotides long. Roa Deck at ¶¶ 16, 21-22. In addition to sequences that are identical to naturally occurring DNA sequences, primers may have additional appended sequences on their ends, such as “Next Generation Sequencing (NGS) adaptor sequences.” These adaptor sequences do not hybridize to the targeted genetic sequence. Elliott Deck ¶¶ 15-17 (Dkt. 47); Elliott 2nd Deck at ¶¶ 4-5 (Dkt. 136). Neither do they affect a primer pair’s function in hybridizing to portions of a targeted DNA sequence. The primer pairs bind to and prime the same portion of the DNA sequence regardless of the presence or makeup of any such appended molecule. Elliott Deck at ¶¶ 15-17; Elliott 2nd Deck at ¶¶ 4-5. Genetic testing methods can also utilize “probes.” Pribnow Deck at ¶ 85. Probes are similar to primers in that they are short segments of DNA that are capable of hybridizing to a DNA segment according to the rules of Watson-Criek base pairing. Id. A probe is used to detect the presence or absence of a particular DNA sequence in a DNA sample. Tait Deck at ¶26. Thus, as with primers, the composition of a probe is dictated by the DNA sequence a scientist wants to identify. Id. at ¶ 24. The probe’s DNA sequence is a complement to the sequence of DNA the probe will be used to detect, so that the probe will hybridize to the DNA target through Watson-Crick base pairing. Pribnow Deck at ¶¶ 85-87; Tait Deck at ¶¶ 22-26. Primers and probes may utilize sequences that can hybridize to the sequence that would be present in a cDNA of the gene. In other words, primers and probes can hybridize to exonic-only sequences. But, primers and probes are not cDNA. Pribnow Deck at ¶ 86. cDNA is typically not used as a primer or probe. Id. at ¶ 84. In the genetic testing that Plaintiffs contend their patent claims cover, cDNA may not be used much at all. Id. Rather, one simply amplifies a segment of DNA and uses it to interrogate a gene for medically important mutations. Id. cDNA is not typically used as a probe or primer in genetic testing in part because it is too large. Id. In addition, primers often are designed to hybridize to noncoding regions of the gene (introns) in order to copy the sequence of the intron immediately adjacent to the exon, in addition to the exon itself, thus mirroring the native nucleotide sequence. Id. Since cDNA does not contain introns, it cannot be used as a primer in this application. Id. Genomic DNA extracted from the body is not typically used as primers or probes, although it would be possible to do so. Id. at ¶ 88. Using probes and primers in genetic testing, including BRCA testing, does not fundamentally change the DNA that is analyzed. Pribnow Deck at ¶ 87. More specifically, primers and probes do not alter the underlying, naturally occurring DNA sequence that is being read. Id. Therefore, they do not alter the underlying DNA’s functional properties or identity for the purposes of genetic testing. Id. At the time of Myriad’s patents, the techniques for creating primers were well known in the art. Primers were generally created using commercially available “oli-gonucleotide synthesizing machines.” See '282 Patent col. 16 11.43-48 (BRCA1); '492 Patent col. 15 11.30-37 (BRCA2). As with primers, the creation and use of DNA probes in genetic testing experiments was well known and widely used prior to August 1994, when Myriad submitted its application for the first of the patents at issue in Plaintiffs’ Motion. Tait Decl. at ¶ 26; '282 Patent col. 15 11.9-20, col. 17 11.15-32, col. 21 11.34-col. 22 1.25. Probe hybridization results from Watson-Crick base pairing between two complementary strands of nucleic acids. Hybridization, a form of binding between molecules, occurs as a result of the inherent chemical properties of nucleic acid molecules and gives double-stranded DNA its characteristic helical structure. Tait Decl. at ¶ 22. 6. Polymerase Chain Reaction Many copies of an input DNA are required to sequence genes. Those who want to sequence and test human genes utilize methods for amplifying — creating copies — of a segment of genomic DNA products. Kay Decl. at ¶ 31; Pribnow Decl. at ¶ 17. Whether produced in a laboratory or by nature, amplified DNA is indistinguishable from the original DNA that was copied, both in its chemical structure and, importantly, the sequence information contained in the DNA. Pribnow Decl. at ¶ 19. The most widely used DNA amplification method is the polymerase chain reaction (PCR). Kay Decl. at ¶32. PCR mimics the processes of DNA replication in the cell. Pribnow Decl. at ¶¶ 55-59; Pribnow 2nd Decl. at ¶¶ 13-17. When PCR is used in conjunction with a targeted segment of genomic DNA, numerous exact duplicates are synthesized, and these are indistinguishable in sequence and chemical composition from the targeted genomic DNA. Id. PCR was developed in the 1980s by Dr. Kary Mullís at Cetus Corporation to develop exact duplicates — “amplicons”—of DNA segments. Pribnow Decl. at ¶ 16; Tait Decl. at ¶¶ 29-31. In 1989, the publication Science identified PCR and its use of a DNA polymerase from a thermophilic bacterium, Thermus aquaticus (Taq DNA polymerase), as the “Molecule of the Year,” and Dr. Mullís won the Nobel Prize in Chemistry for his invention in 1993. Tait Decl. at ¶ 29. Thus, as the asserted patents acknowledge, PCR was a well-understood and routine activity in the scientific community prior to the time Myriad filed its August 1994 application corresponding to those asserted patents, and prior to the identification of the BRCA1 or BRCA2 gene sequences. Id. at ¶ 31; '441 Patent col.1711.21-37. In any presently known process for analyzing a human’s genes, the first step is to obtain a person’s blood, saliva, or a cultured cell sample. DNA is then extracted from this sample. This extracted, genomic DNA represents a person’s “diploid” genome, as it contains two copies of each autosomal (non sex chromosome) gene. Roa Decl. at ¶ 3; Pribnow Decl. at ¶ 55. The genomic DNA is then “fragmented,” or cut into small pieces, often through sonication or biochemical shearing. The fragmentation randomly cuts -all parts of the DNA into many randomly sized pieces. These fragments are typically about 1000 nucleotides long, but smaller fragments can be created. Roa Decl. at ¶ 4; Pribnow Decl. at ¶ 55. The PCR process begins by mixing the fragmented genomic DNA with: 1) a ther-mostable DNA polymerase enzyme; 2) a pool of all four DNA nucleotides (A, C, T and G); and 3) a great excess of single-stranded primer pairs. Kay Decl. at ¶ 32; Pribnow Decl. at ¶¶ 55-59; Pribnow 2nd Decl. at ¶¶ 13-1'; Tait Decl. at ¶¶ 23-29. One primer in the pair is complementary to one end of the region to be amplified on one strand of the template DNA molecule and the other primer in the pair is complementary to the other end of the region to be amplified on the other strand of the template DNA. Kay Decl. at ¶ 32. Next, several steps occur in a cyclical reaction, as depicted in the illustration below. First, the template-primers mixture is heated so that the bonds linking the two strands of the template DNA molecule are overcome, causing the strands to separate. Id. at ¶ 33. This is called denaturation. Id. Second, the mixture is cooled enough to allow one copy of each primer to bind to its complementary template DNA sequence, in a process called annealing. Id. Third, the DNA polymerase adds nucleotides to the 3'-end of each of the primers in an order complementary to the template DNA. Id. This extension reaction results in the generation of a copy of each strand of the template DNA — amplification. Id. The number of copied DNA molecules doubles with each PCR cycle. Id. A typical PCR runs for 20-30 cycles and results in the accumulation of millions of copies— amplicons — of the template DNA. Id. It is essential that the amplieons contain exactly the same information contained in the DNA segment to be amplified, particularly where the amplicons will be used in testing. A patient and her doctor may make treatment decisions based on the information contained in the patient’s sequence of nucleotides, as reflected in the amplicons generated from her DNA. Aug. 23, 2013 Tutorial Tr. (Jackson) at 13:4-11, 23:16-24:3, 30:6-31:13; Sept. 11, 2013 Hearing Tr. (Roa) at 112:4-17; Pribnow 2nd Decl. at ¶¶ 33-35. For example, whether the information in a woman’s BRCA1 or BRCA2 genes predisposes her to an increased risk of hereditary breast or ovarian cancer can be determined by analyzing the sequence of at least portions of her BRCA1 and BRCA2 genes. The am-plicons generated during PCR enable this evaluation. Sept. 11, 2013 Hearing Tr. (Roa) at 105:1-15, 111:20-25, 112:1-15; Pribnow Decl. at ¶¶ 64-70; Pribnow 2nd Decl. at ¶¶ 33-35. 7. Sequencing After PCR, the resulting amplified DNA can be sequenced. This means that the specific nucleotide (adenine (“A”), thymine (“T”), cytosine (“C”), or guanine (“G”)) in each position of the DNA is identified or “read.” The identified sequence of an individual person’s gene or genes is commonly called a “germline” sequence, meaning the gene sequence that a person inherited at birth. Roa Decl. at ¶ 24. Two types of sequencing are at issue in this case: dideoxy sequencing (also known as Sanger sequencing) and Next-Generation Sequencing (NGS). Both types mimic DNA cell replication by using primers, DNA polymerase, and nucleotides — some of which have been chemically modified, but in ways that do not alter their Watson-Crick pairing functions. Aug. 23, 2013 Tutorial Tr. (Jackson) at 24:4-25; Elliott Decl. at ¶¶ 23-31; Tait Decl. at ¶¶ 35-36. Sanger sequencing was developed in 1977 and is named for its inventor, Frederick Sanger. NGS was not developed until the 2000s. Aug. 23, 2013 Tutorial Tr. (Roa) at 26:20-27:1; Sept. 11, 2013 Hearing Tr. (Roa) at 116:4-8; Tait Decl. at ¶¶ 35-37. Defendant’s testing employs both Sanger sequencing and NGS. Elliott Decl. at ¶¶ 23-31; Elliott 2nd Decl. at ¶¶ 14-16; Tait Decl. at ¶¶ 35-36. By the time Myriad submitted its first application corresponding to the asserted patents in August 1994, the laboratory techniques used to accomplish hybridization, amplification, and sequencing for the purpose of observing a genomic, or “native” gene sequence in a human sample were well understood, widely used, and fairly uniform insofar as any scientist engaged in obtaining the sequence of a gene in a human sample would likely have relied on the same techniques and general approach. Tait Decl. at ¶ 37. Likewise, the laboratory materials, reagents, and protocols to accomplish these tasks were well known and widely available in the art by that time, as the asserted patents acknowledge. Tait Decl. at ¶ 31;'441 Patent col. 17 11.20-27 (“These methods are well known and widely practiced in the art.”). Plaintiffs’ patents state that “the practice of the present invention employs, unless otherwise indicated, conventional techniques of chemistry, molecular biology, microbiology, recombinant DNA, genetics, and immunology.” See, e.g., '282 Patent eol.25 11.50-55. a. Sanger Sequencing Sanger sequencing includes, among other things, the application of artificial DNA nucleotide analogues known as dideoxynu-cleotide chain terminators to the amplified DNA. Either the primers or the terminators have labels or tags, such as fluorescent dyes or radioactive phosphorus, that can be read during sequencing of the DNA to identify what type of nucleotide is present at each position in the gene. Roa Decl. at ¶ 25; Elliott Decl. at ¶¶ 35-39. Improvements in the Sanger method by 1987 led to automation of the sequencing process. These Sanger sequencing methods were widely used well before the first of Myriad’s August 1994 applications corresponding to the asserted patents had been filed, and prior to the identification of the BRCA1 or BRCA2 gene sequences. Tait Decl. at ¶ 36. b. Next Generation Sequencing (NGS) NGS does not rely on the termination of DNA synthesis for resolution of a DNA’s sequence. Unlike Sanger sequencing, NGS does not use dideoxy sequencing. Elliott Decl. at ¶¶ 24-25. Instead, DNA molecules are “sequenced by synthesis” through a process where tagged (e.g., fluorescent) nucleotides are added to a growing synthetic DNA molecule in a controlled, stepwise fashion. As nucleotides are incorporated into the new synthetic molecules, the corresponding tag is released. This release is detected by a machine utilizing a technology similar to a camera that detects the flash of the fluorescent tag. Each nucleotide (A, T, C, and G) has a unique color fluorescent tag attached so that the machine can detect which nucleotides were added, and in which order. Roa Decl. at ¶ 26; Elliott Decl. at ¶¶ 20, 24-25, 29-31. 8. Large Rearrangement Analysis In addition to gene sequencing techniques like Sanger sequencing and NGS, scientists may also employ “large rearrangement analysis.” This analysis enables scientists to determine if a person’s gene contains large nucleotide deletions or sequence duplications which may not be observed during the sequencing processes described above. Two common examples of large rearrangement analysis are multiplex ligation-dependent probe amplification (MLPA) and microarray. Roa Decl. at ¶ 30; Elliott Decl. at ¶¶ 40-42. Both MLPA and micro-array processes use probes with a series of nucleotides precisely complementary to a piece of a single strand of the gene to be analyzed, such as BRCA1 or BRCA2 genes. MLPA uses pairs of probes that hybridize to adjacent segments of the target gene sequence and, after being hybridized, are chemically fused or “ligated” to form a single molecule. MLPA probes are chosen to be complementary to an “allele” in a gene, which refers to a form of the gene having a certain specific nucleotide sequence, such as a wild-type sequence, variant sequence, or mutation sequence of interest, and thus may be called a “wild-type” or a “mutated” allele. For large rearrangement testing, probes are targeted to parts of the gene that may contain deletions or duplications and are typically designed to detect deletion or duplication of one or more exons. Roa Decl. at ¶ 31; Elliott Decl. at ¶¶ 42-44, 47-52. In the MLPA process, multiple synthetic probes are used containing various specific nucleotide sequences that target sequences of the parts of the gene to be analyzed (e.g., typically one pair of probes for each exon). The probes also include generic “primer tail” nucleotide sequences that allow for PCR probe amplification. MLPA probes are designed to assess large deletion or duplication mutations in or near coding exons in the gene. MLPA uses pairs of probes containing target gene sequences that are adjacent to each other. The probes hybridize to any of the DNA fragments that are complementary to those probes. Matching probes that hybridize next to each other are then ligated to form a longer oligonucleotide. Because the probes also have primer tail sequences, the resulting ligated DNA is then amplified through PCR and labeled with flúores-cent tags. Roa Decl. at ¶ 32; see Elliott Decl. at ¶¶ 43-46. The resulting amplified MLPA products are analyzed and compared using computer software. By comparing the relative copy number of MLPA products in a patient against a wild-type control, the presence of a large deletion or duplication can be detected. For example, if certain probes hybridize at approximately 50 percent the amount the hybridization obtained in a wild-type control, it means that there was no section of the gene to which those probes were complementary in one of the patient’s expected two copies of the gene, indicating a deletion in the relevant region in one of the patient’s copies of the gene. Conversely, a 50 percent increase in MLPA probes in a certain region indicates duplication of that region in the gene. Roa Decl. at ¶ 33; see Elliott Decl. at ¶¶ 46-48. The hybridization of the probes is detected and quantified by amplification of the ligated longer probe. Conversely, if the region where the probe would normally hybridize has been deleted on one or more of the patient’s chromosomes, then less-than-expected hybridization and ligation will take place and less than the expected amount of amplification will result. In this way, detecting hybridization, or the lack of hybridization, allows scientists to compare a patient’s DNA sequence to a wild-type sequence and determine whether mutations are present. For this reason, using MLPA to detect an alteration in DNA necessarily requires detection of the wild-type allele through hybridization of the probes. Roa Decl. at ¶ 34; see Elliott Decl. at ¶¶ 46-48. “Microarray,” another form of large rearrangement analysis, uses a solid surface, such as a glass slide, with a collection of microscopic spots to which different DNA probes are attached. A microarray process employing comparative genomic hybridization (microarray-CGH) uses patient genomic DNA that is fragmented into small pieces. Synthetic products can be generated from the fragmented patient DNA by primer extension and labeling with a specific fluorescent dye. Similar products can be generated from fragmented wild-type DNA that is labeled with a different fluorescent dye. Alternatively, genomic fragments can be directly labeled with fluorescent dyes. A mixture containing equal amounts of differentially labeled products representing patient genomic and wild-type DNA are hybridized to the mi-croarray slide with immobilized probes tiled across the entire coding region of BRCA1 and BRCA2. Roa Decl. at ¶ 35; see Elliott Decl. at ¶¶ 51-53. Following hybridization, the microarray slides are scanned and the relative dye intensities are analyzed and quantified. Equal amounts of the two dye signals indicate a normal result or, in other words, show that no large rearrangement has been detected. In contrast, if there is a relative decrease in the amount of patient’s dye signal relative to wild-type dye signal, then deletion in one copy of the BRCA1 or BRCA2 gene regions covered by the affected probes is indicated. Conversely, if there is a relative increase in a patient’s dye signal, then that result indicates a duplication of the gene region corresponding to those probes. The resulting data obtained in the microarray-CGH analysis allows for identification of large genomic deletions or duplications in the BRCA1 or BRCA2 genes. These large rearrangements can occur anywhere in the gene, and may involve a single exon, multiple exons, or even the entire gene coding region. Roa Decl. at ¶ 36; see Elliott Decl. at ¶ 53. Microarray-CGH necessarily requires hybridization of sample DNA to a probe specific for the gene of interest, such as BRCA1 of BRCA2, and detection of that hybridization product. The resulting data allows identification of both the existence of the allele of interest and the existence of large mutations in a patient’s germline sequence, i.e., comparing the sequence of the patient’s BRCA1 or BRCA2 gene to wild-type, by comparing probe hybridization relative to the wild-type BRCA1 or BRCA2. Because the microarray process is performed by comparing the hybridization of the patient’s allele to the hybridization of the wild-type allele, this process necessarily requires detection of the wild-type allele through hybridization. Roa Decl. at ¶ 37. C. The Race to Locate and Sequence BRCA1 and BRCA2 Breast cancer is by far the most often diagnosed type of cancer among women, affecting about one in eight women. Swisher Decl. at ¶ 19. Among the entire population of men and women combined, breast cancer is the second most diagnosed cancer. The National Cancer Institute (NCI) estimates approximately 232,340 new cases of female breast cancer and 2,240 new cases of male breast cancer will have been diagnosed in the United States in 2013. Id. The NCI estimates that breast cancer will have caused approximately 39,620 female deaths and 410 male deaths in the United States in 2013. Id. Ovarian cancer is the eighth most common cancer in women. Although less common than breast cancer, it causes more deaths in the Western world than any other gynecologic cancer. Id. at ¶ 21. In the 1980s, breast cancer patients mobilized to increase public awareness of the breast cancer epidemic. Due to these efforts and those of breast cancer organizations, the Department of Defense created a research program devoted to breast cancer research. Between 1990 and 2008, the annual funding for this research increased from $90 million to $2.1 billion. Partha-sarathy Decl. from AMP Litigation at ¶ 10 (Dkt. 34-7). Also during the 1980s, scientists from the United States, England, France, Germany, Japan, and other countries were competing to first identify the nucleotide sequences linked to breast cancer. In 1989, various European and American research laboratories participated in an International Breast Cancer Linkage Consortium. Id. at ¶ 11. In 1990, a research group led by Mary-Claire King at the University of California, Berkeley announced that it had discovered that the Breast Cancer Susceptibility Gene 1 (BRCA1) was located on chromosome 17. With this discovery, research teams around the world intensified efforts to be the first to sequence the BRCA1 gene. Id. at ¶ 11. Among them were different teams led by Dr. King; Dr. Mark Skol-nick, co-founder of Myriad; and Dr. Michael Stratton of the Institute for Cancer Research, London (ICR). Id. In September 1994, Dr. Skolnick’s group at Myriad — including researchers from the National Institute for Environmental Health (NIEH), an agency of the National Institutes of Health (NIH) — announced that they had sequenced the BRCA1 gene. Id. at ¶ 11. They won a hard-fought “race,” as journalists reported at the time: The race to find the breast-cancer gene has been one of the most closely-watched and publicized of a host of gene hunts in recent years. The pursuit of the gene was triggered in late 1990 when Mary-Clare King, a geneticist at the University of California at Berkeley, stunned the cancer-research community by pinpointing the the [sic] gene’s approximate location. About a dozen laboratories around the world, including Dr. King’s, have been intensely probing a tiny region of genetic material since then. In the past few months, scientists said they had identified about 30 genes in the approximate region but had pared the search down to about four to six likely culprits. Dr. Skolnick said the first hint they had latched onto the gene came about two months ago. Since then they have worked to identify its structure. Scientists Say They’ve Found Gene That Causes Breast Cancer, The Wall Street Journal, September 14, 1994 (Dkt. 114-2). By the time this discovery was publicly announced in September 1994, Myriad had applied for patents related to BRCA1, including the '282 and '441 Patents. After the sequencing of BRCA1, many scientists thought there was at least one more gene linked with breast cancer, and the search for that gene continued. Id. at ¶ 12. By 1994, the existence of a ‘BRCA2 gene’ and its location on chromosome 13q was known, as described by Plaintiffs in the background of the invention section of the '441 Patent: Intense efforts to isolate the BRCA1 gene have proceeded since it was first mapped in 1990. [citations omitted]. A second locus, BRCA2, has recently been mapped to chromosome 13q (Wooster et. al., 1994) and appears to account for a proportion of early-onset breast cancer roughly equal to BRCA1, but confers a lower risk of ovarian cancer. '441 Patent col. 2 1.46 — col. 3 1.4. In December 1995, the group led by Dr. Mark Stratton announced they had mapped and sequenced the elusive second gene, the BRCA2 gene, which was linked to incidence of ovarian cancer, as well as female and male breast cancer. Partha-sarathy Decl. from AMP Litigation at ¶ 12. The day before the Stratton group published the BRCA2 gene sequence in the scientific journal, Nature, however, Myriad announced that it too had found the BRCA2 gene. Id. Myriad submitted its sequence to GenBank, an international depository of gene sequence information, and applied for patents on the BRCA2 gene in the United States and Europe. Id. The sequencing of the BRCA1 and BRCA2 genes were landmark events in genetics, as mutations in these genes are responsible for many breast and ovarian cancer cases. About 10 percent of breast cancers are inherited genetically, about 5 percent as a result of a BRCA1 or BRCA2 genetic mutation. Swisher Decl. at ¶ 20. Individuals with BRCA1 and BRCA2 mutations have about a 45 to 87 percent risk of developing breast cancer by age 70. Id. Between 20 to 25 percent of ovarian cancers are inherited genetically. For women with inherited ovarian cancer, 75 percent of them can attribute the cancer to either BRCA1 or BRCA2. About 50 percent of inherited ovarian cancers are caused by BRCA1 mutations, about 25 percent are caused by BRCA2 mutations, and the remaining 25 percent are caused by other genes. Women with inherited BRCA1 mutations have a 40 to 52 percent cumulative risk of ovarian cancer by the time they reach 70 years old. For women with inherited BRCA2 mutations, the risk is approximately 15 to 25 percent. Id. at ¶ 22. Very little can be done for patients once diagnosed with ovarian cancer, making preventive care vital. Id. at ¶ 23. D. Myriad’s Testing Products: BRA-CAnalysis, BART, and myRisk Beginning in 1994 and continuing for several years, Myriad obtained numerous patents related to BRCA1 and BRCA2. By 1996, it began to market BRCA1 and BRCA2 molecular testing products. That year, Myriad introduced BRACAnalysis, a molecular diagnostic test used to detect the presence and characterization of ‘point’ or small mutations in the BRCA1 or BRCA2 gene that are responsible for a majority of hereditary breast and ovarian cancers. Ford Decl. at ¶¶ 1, 3; Sept. 12, 2013 Hearing Tr. (Ford) at 312:5-25 (Dkt. 151). The BRACAnalysis test does not include large rearrangement testing for BRCA1 and BRCA 2 — testing that can identify initially false negative results in a BRACAnalysis point mutation test. Myriad offers an additional test that provides large rearrangement testing for the BRCA1 and BRCA2 genes, called BRACAnalysis Rearrangement Test, or “BART.” Sept. 12, 2013 Hearing Tr. (Ford) at 312:19-25. But a patient who obtains Myriad BRACAnalysis testing does not automatically get follow-up BART testing. Id. at 101:22-52:15; Swisher Decl. at ¶¶ 97-98; Matloff Decl. at ¶ 7 (Dkt. 49). If a patient does not satisfy Myriad’s criteria for being at high risk of a large rearrangement mutation in her BRCA1 and BRCA2 genes, or if her insurance does not cover BART, then the patient must pay for the BART test separately. Sept. 12, 2013 Hearing Tr. (Ford) at 314:2-9. According to a 2013 peer-reviewed study in the Journal of Clinical Oncology, Myriad’s criteria for providing BART large rearrangement testing automatically as part of its BRCA testing does not cover half the patients who have large rearrangement mutations: “[f]ewer than half of the large rearrangement carriers in the present study met Myriad Genetics Laboratories’ criteria ... for automatic large rearrangement testing.” Chao Decl. at Exh. P at 212 (Weitzel et al, 31(2) J. Clin. Oncol. 210-06 (2013)). The current list price for BRACAnalysis is $3,340 and the list price for BART is $700. Sept. 12, 2013 Hearing Tr. (Ford) at 313:11-15. Together, the list price for both tests is $4,040. Ford. Decl. at ¶ 11. Those who get BART in addition to BRA-CAnalysis are billed separately for the two tests. Pis.’ Reply Br. at 135. But not all of Myriad’s patients have insurance coverage for BART. Mark C. Capone, President of Myriad Genetic Laboratories, Inc., suggested on May 7, 2013, that approximately 20 percent of patients receiving BRACAn-alysis did not have insurance coverage for BART. Sept. 12, 20Í3 Hearing Exh. 3 at 15 (Dkt. 144-2) (“Our Managed Care team continued to make significant progress on BART reimbursement in the fiscal third quarter and we ended the quarter with reimbursement coverage for approximately 80 percent of patients.”). Because BART is not automatically included as part of Myriad’s BRCA1 and BRCA2 testing, some patients must pay the $700 out-of-pocket for BART if they are to get that testing. On September 5, 2013, Myriad announced a limited launch of myRisk, a new “multi-gene diagnostic test that will provide increased sensitivity by analyzing 25 genes associated with eight major cancers including: breast, colorectal, ovarian, en-dometrial, pancreatic, prostate, gastric and melanoma.” Myriad Press Release, Sept. 5, 2013. This test utilizes the Next-Generation Sequencing used by Defendant and tests for 24 of 25 of the same genes as Defendant’s CancerNext panel. Chao Decl. at ¶¶ 46-47 and Exh. I. In an investor and analyst presentation given on May 9, 2013, Myriad described myRisk as a “significant improvement of BRACAnaly-sis.” Id. at ¶ 45, Exh. I at 19-45. Similarly, in a press release dated May 30, 2013, Myriad stated: “myRisk represents a scientific advancement that will revolutionize hereditary cancer testing for appropriate patients.” Id. at Exh. J at 1. For the time being, it appears that this launch provides limited access to the public, as it is for “a limited number of medical and scientific thought leaders”: myRisk Hereditary Cancer is being launched in a phased approach beginning with an early-access, clinical-experience program to a limited number of medical and scientific thought leaders followed by an expanded access program later in the year. The Company will present extensive clinical validity data for myRisk Hereditary Cancer at The Collaborative Group of the Americas on Inherited Colorectal Cancer (CGA) annual meeting in October and the San Antonio Breast Cancer Symposium in December. Myriad Press Release, Sept. 5, 2013. E. The AMP Litigation 1. Judge Sweet’s Decision — Southern District of New York A group of medical organizations and individuals sued Myriad in 2009, challenging fifteen composition and method claims in seven of Myriad’s BRCA 1 and BRCA2-related patents on the grounds that they were drawn to products of nature and mental processes — subjects that are patent ineligible under 35 U.S.C. § 101. Association for Molecular Pathology v. United States Patent and Trademark Office, 702 F.Supp.2d 181, 186 (S.D.N.Y.2010). These patents were drawn to “(1) isolated DNA containing all or portions of the BRCA1 and BRCA2 gene sequence and (2) methods for ‘comparing’ or ‘analyzing’ BRCA1 and BRCA2 gene sequences to identify the presence of mutations correlating to breast or ovarian cancer.” Id. at 184. United States District Court Judge Robert W. Sweet characterized the overarching issue presented as: “[a]re isolated human genes and the comparison of their sequences patentable?” Id. at 185. Judge Sweet answered that question in the negative and granted summary judgment in favor of the plaintiffs. Id. at 185. Judge Sweet construed “isolated DNA” to mean a “segment of DNA nucleotides existing separate from other cellular components normally associated with native DNA, including proteins and other DNA sequences comprising the remainder of the genome, and includes both DNA originating from a cell as well as DNA synthesized through chemical or heterologous biological means.” Id. at 217. He concluded that neither Myriad’s isolated DNA (composition) claims, nor its method claims were drawn to patent eligible subject matter. The composition claims turned on the issue of “whether or not claims directed to isolated DNA containing naturally-occurring sequences fall within the products of nature exception to § 101.” Id. at 220. As a starting point, Judge Sweet noted that “Supreme Court precedent has established that products of nature do not constitute patentable subject matter absent a change that results in the creation of a fundamentally new product.” Id. at 222. Even “ ‘purification’ of a natural compound, without more, is insufficient to render a product of nature patentable.” Id. at 223. Judge Sweet rejected Myriad’s argument that “purified DNA” is necessarily patent eligible because DNA doesn’t exist in nature in a purified form. Id. at 224. Observing that even a “purified product” must have “‘markedly different characteristics’ in order to satisfy the requirements of § 101,” Judge Sweet analyzed whether ■ Myriad’s “isolated DNA” had ‘“markedly different characteristics’ from a product of nature.” Id. at 227-28 (quoting Diamond v. Chakrabarty, 447 U.S. 303, 310, 100 S.Ct. 2204, 65 L.Ed.2d 144 (1980)). Myriad, citing the “chemical nature of DNA,” argued that isolated DNA “is ‘markedly different’ from DNA found in nature” due to “structural and functional” differences. Id. at 228. For example, Myriad pointed out that there are chromosomal proteins associated with native DNA that are not associated with isolated DNA. Id. at 229-30. But Judge Sweet found that focusing on these differences ignores the reason DNA is unique from other chemical compounds in nature — because it encodes and conveys information: The information encoded in DNA is not information about its own molecular structure incidental to its biological function, as is the case with adrenaline or other chemicals .... Rather, the information encoded by DNA reflects its primary biological function: directing the synthesis of other molecules in the body — namely, proteins.... DNA, and in particular the ordering of its nucleotides, therefore serves as the physical embodiment of laws of nature — those that define the construction of the human body.... Consequently, the use of simple analogies comparing DNA with chemical compounds previously the subject of patents cannot replace consideration of the distinctive characteristics of DNA. Id. at 228-29. It is DNA’s nucleotide sequence that is critical to both its “natural biological function” and “the utility associated with DNA in its isolated form.” Id. at 229. Judge Sweet also rejected Myriad’s argument that isolated DNA is distinct from native DNA insofar as it “may be used in applications for which native DNA is unsuitable, namely, in ‘molecular diagnostic tests (e.g., as probes, primers, templates for sequencing reactions), in biotechnological processes (e.g. production of pure BRCA1 and BRCA2 protein), and even in medical treatments (e.g. gene therapy).’ ” 702 F.Supp.2d at 230-31 (quoting Myriad’s AMP Reply Br. in Support of Motion for Summary Judgment at 9 (other citations omitted)). Judge Sweet noted that the cited applications depend on the single-stranded isolated DNA segment having “the identical sequence as the complementary DNA strand to the DNA strand containing the target DNA sequence.” Id. at 231, n. 54. The BRCA-specific nucleotide sequence is “the defining characteristic of the isolated DNA that will always be required to provide the sequence-specific targeting and protein coding ability that allows isolated DNA to be used for the various applications cited by Myriad.” Id. at 232. Judge Sweet found unpersuasive Myriad’s contention that it “created” the claimed BRCA DNA molecules when it identified the “specific segments of chromosomes 17 and 13 that correlated with breast and ovarian cancer (BRCA1 and BRCA2) and isolated “these sequences away from other genomic DNA and cellular components.”” Id. at 232. Rather than “creating” BRCA, the court concluded that Myriad merely discovered it. While discovery of the “important correlation” was a “valuable scientific achievement” requiring “technical skill and considerable labor,” it was, nevertheless, a “discovery of the handiwork of nature— the natural effect of certain mutations in a particular segment of the human genome.” Id. at 232. For those reasons, Judge Sweet concluded that despite Myriad’s cited structural and functional differences between “native DNA” and “isolated DNA,” the two were not “markedly different” from one another. Myriad’s composition claims were patent ineligible, as they were directed to natural phenomena. Judge Sweet next analyzed Myriad’s method claims, drawn to 1) analyzing and comparing DNA sequences to determine the existence of BRCA1 and BRCA2; and to 2) screening cancer therapeutics by comparing the growth rate of cells when a test compound is added to one cell group. With the law as it was at the time before the Supreme Court’s pronouncements in Mayo Collaborative Services v. Prometheus Laboratories, Inc., — U.S. -, 132 S.Ct. 1289, 182 L.Ed.2d 321 (2012) and Bilski v. Kappos, 561 U.S. 593,