Amarin Pharma, Inc. v. Hikma Pharm. USA Inc., Case No. 2:16-cv-02525-MMD-NJK

449 F.Supp.3d 967

AMARIN PHARMA, INC., et al., Plaintiffs,

v.HIKMA PHARMACEUTICALS USA INC., et al., Defendants.

Case No. 2:16-cv-02525-MMD-NJK

United States District Court, D. Nevada.

Signed March 30, 2020

Chelsea Latino, Adam Hosmer-Henner, McDonald Carano Wilson LLP, Reno, NV, Daniel Joseph Farnoly, Pro Hac Vice, Jeffrey Elikan, Pro Hac Vice, Jordan Laird Moran, Pro Hac Vice, Megan Patricia Keane, Pro Hac Vice, Michael Kennedy, Pro Hac Vice, Alaina Marie Whitt, Pro Hac Vice, Christopher Neil Sipes, Pro Hac Vice, Einar Stole, Pro Hac Vice, Eric Ritland Sonnenschein, Pro Hac Vice, Han Park, Pro Hac Vice, Covington & Buling LLP, Washington, DC, Jason D. Smith, Nicholas J. Santoro, Las Vegas, NV, for Plaintiffs.

Claire A. Fundakowski, Pro Hac Vice, Charles B. Klein, Winston & Strawn LLP, Washington, DC, Eimeric Reig-Plessis, Pro Hac Vice, San Francisco, CA, Alan Clement, Pro Hac Vice, Locke Lord LLP, New York, NY, George Carter Lombardi, Pro Hac Vice, Alison Michelle Heydorn, Pro Hac Vice, Winston & Strawn, Myoka Kim Goodin, Pro Hac Vice, Nina Vachhani, Pro Hac Vice, Jennifer Marie Coronel, Pro Hac Vice, Locke Lord LLP, Chicago, IL, Justin James Bustos, Dickinson Wright PLLC, Wayne A. Shaffer, Laxalt & Nomura, Ltd., Ryan James Cudnik, Michael D. Rounds, Brownstein Hyatt Farber Schreck, LLC, Reno, NV, Jonathan W. Fountain, W. West Allen, Howard & Howard Attorneys PLLC, Las Vegas, NV, Beth Finkelstein, Pro Hac Vice, Constance S. Huttner, Pro Hac Vice, Frank D. Rodriguez, Pro Hac Vice, James Barabas, Pro Hac Vice, Caroline Sun, Pro Hac Vice, Windels Marx Lane & Mittendorf, LLP, Madison, NJ, for Defendants.

BENCH ORDER

MIRANDA M. DU, CHIEF UNITED STATES DISTRICT JUDGE

I. SUMMARY

This is a consolidated patent infringement case brought under the Hatch-Waxman Act where Plaintiffs Amarin Pharma, Inc. and Amarin Pharmaceuticals Ireland Limited (collectively, "Amarin") seek to prevent Defendants West-Ward Pharmaceuticals International Limited and Hikma Pharmaceuticals USA Inc. (collectively, "Hikma"), and Dr. Reddy's Laboratories, Inc. and Dr. Reddy's Laboratories, Ltd. (collectively, "DRL") from launching generic competitor drugs to Plaintiffs' drug Vascepa®. This order follows a bench trial the Court held in January 2020 (the "Trial"). As further explained below in the Court's findings of fact and conclusions of law, the Court finds that Defendants infringe the asserted claims under Plaintiffs' inducement theory, but the asserted patent claims are all invalid as obvious.

II. CLAIMS

Plaintiffs sued Defendants under the patent laws of the United States, 35 U.S.C. § 100, et seq. , including 35 U.S.C. § 271(e)(2), and the Declaratory Judgment Act, 28 U.S.C. §§ 2201 and 2202, arising from Defendants' filing of Abbreviated New Drug Applications ("ANDAs") under Section 505(j) of the Federal Food, Drug, and Cosmetic Act ("FDCA"), 21 U.S.C. § 355(j), seeking approval from the United States Food and Drug Administration ("FDA") to market generic versions of Plaintiffs' Vascepa product. (ECF No. 324 at 2.)

Plaintiffs specifically assert infringement of U.S. Patent No. 8,293,728 ("the '728 patent"), U.S. Patent No. 8,318,715 ("the '715 patent"), U.S. Patent No. 8,357,677 ("the '677 patent"), U.S. Patent No. 8,367,652 ("the '652 patent"), U.S. Patent No. 8,431,560 ("the '560 patent"), and U.S. Patent No. 8,518,929 ("the '929 patent").¹ (ECF No. 331 at 9.) Each of the Asserted Patents is entitled "METHODS OF TREATING HYPERTRIGLYCERIDEMIA." (Id. ) The U.S. applications that ultimately issued as the Asserted Patents are continuations of U.S. Application No. 12/702,889, filed on February 9, 2010, which ultimately issued as the U.S. Patent No. 8,293,727 ("the '727 patent"). (Id. ) The Asserted Patents further claim priority to U.S. Provisional Application No. 61/151,291, filed on February 10, 2009, and U.S. Provisional Application No. 61/173,755, filed on April 29, 2009. (Id. )

Plaintiffs more specifically assert that Defendants infringe the following ten claims of the Asserted Patents: Claims 1 and 16 of the '728 patent, Claim 14 of the '715 patent, Claims 1 and 8 of the '677 patent, Claim 1 of the '652 patent, Claims 4 and 17 of the '560 patent, and Claims 1 and 5 of the '929 patent.² (ECF Nos. 331 at 9-10, 333 at 13 n.1.) Defendants asserted counterclaims of noninfringement and invalidity. (ECF Nos. 27 at 28-34, 33 at 33-56.)

III. FINDINGS OF FACT

The Court makes the following findings of fact based on the testimony and other evidence admitted during the course of the Trial, along with the pre-trial and post-trial briefing the parties filed in this case.

A. Factual Background

The Asserted Patents are directed to methods of beneficially lowering the levels of certain fats in the bloodstream using drugs made of purified omega-3 fatty acids from fish oil. Fats are natural biological molecules that scientists call "lipids." Triglycerides ("TGs") and cholesterol are two types of lipids that are of major importance in human physiology. TGs are high in calories and are a major source of energy in the diet of humans. (ECF No. 370 at 1561:21-1562:21.) After they are absorbed from the intestine, triglycerides are broken down into their component molecules, resynthesized, and reassembled by the intestine into lipoproteins. Lipoproteins are spherical particles that travel through the bloodstream and contain lipids (such as triglycerides and cholesterol) as well as proteins. (ECF Nos. 366 at 324:5-9, 370 at 1562:12-17.) The major proteins that are in lipoproteins are called apolipoproteins. One type of apolipoprotein is Apo B.

Cholesterol levels measured in a clinical laboratory generally include levels of both free cholesterol and cholesteryl ester. (ECF No. 333 at 8.) The level of cholesterol measured in the blood is generally an indicator for the amount of low-density lipoprotein cholesterol ("LDL-C") in the blood. (Id. ) LDL-C is the "bad" cholesterol that physicians try to reduce in their patients with drugs such as statins. (Id. ) In many patients, there is a strong linear relationship between levels of LDL-C and Apo B. (Id. ) In other words, changes in LDL-C levels occur in parallel with changes in Apo B, reflecting the fact that there is one molecule of Apo B per LDL particle. (Id. )

The Asserted Claims are directed to methods of treating severe hypertriglyceridemia, a condition in which a patient's fasting TG levels rise to very high levels of 500 mg/dL or above. (ECF No. 377 at 33.) The term "hypertriglyceridemia" ("HTG") refers to having elevated TGs, which are the most abundant type of fat in the blood. (ECF No. 373 at 27.) The clinical guidelines that both sides rely on in this case, called "ATP III," define "normal triglycerides" as less than 150 mg/dL, with levels above that considered elevated to various degrees. (Ex. 1526³ (National Institutes of Health, National Heart, Lung, and Blood Institute, "Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), Executive Summary ," May 2001 ("ATP-III Executive Summary")) at 27.) These numbers are referring to the "concentrations of triglycerides in the blood, and [ ] are always taken in the fasting state." (ECF No. 366 at 329:4-17.)

Severe hypertriglyceridemia "has a well-known meaning to doctors who treat the condition." (Id. at 454:6-8.) It "means that a patient has had triglycerides levels greater than or equal to 500 milligrams per deciliter." (ECF No. 365 at 52:24-3; see also ECF No. 366 at 454:9-12.) In other words, "as long as the patients have [TG] levels above 500, regardless of why, they have severe hypertriglyceridemia." (ECF No. 366 at 455:8-11.) This definition is consistent with the ATP-III guidelines as well as the Vascepa indication. (Ex. 1526 at 27; Ex. 2248 at 1.)

For most patients with elevated TGs, "the primary aim of therapy is to achieve the target goal for LDL [-C levels]." (Ex. 1526 at 27.) This is because research has long shown that "elevated LDL cholesterol is a major cause of CHD"—i.e. , coronary heart disease. (Id. at 11.)

The primary aim of therapy is different in patients with severe HTG because they have an elevated risk of acute pancreatitis. Pancreatitis, which involves the inflammation of the pancreas, is an excruciatingly painful and potentially life-threatening condition. (ECF No. 370 at 1567:2-22 ("In the setting of severe hypertriglyceridemia, inflammatory changes [c]an occur within the pancreas that can lead to sudden devastating injury to the pancreas leading to dissolution of pancreatic tissue, resulting in severe pain, inability to eat, to drink, and it constitutes a medical emergency. But even more importantly[,] in some cases[,] it [can] even result in death."); see also ECF Nos. 366 at 331:3-20, 365 at 72:4-13.) In patients with severe hypertriglyceridemia, the primary "aim of therapy is to prevent acute pancreatitis through triglyceride lowering." (ECF No. 366 at 457:11-15; see also Ex. 1526 at 19.) This is the "primary treatment aim [in patients with severe hypertriglyceridemia] regardless of why the patient has triglycerides above 500." (ECF No. 366 at 457:16-18.) This is because "pancreatitis can be a life-threatening condition." (Id. at 473:18-20; see also id. at 568:10-16.)

As noted, the Asserted Claims are directed to methods of treating severe HTG specifically by administering 4 grams ("4 g") per day of purified EPA. Treating patients with severe hypertriglyceridemia with purified EPA reduced TGs in those patients without increasing LDL-C, the bad-cholesterol. (ECF Nos. 367 at 851:15-852:1, 370 at 1574:3-1575:1, 1598:14-17.) Other treatments for severe hypertriglyceridemia dramatically increase LDL-C levels, which then often requires the administration of a separate concurrent cholesterol-lowering drug, such as a statin, just to address that LDL-C increase. (ECF Nos. 367 at 813:8-814:2, 370 at 1598:18-1599:18.) Additionally, purified EPA has now been shown to actually reduce cardiovascular risk in...