Ward v. Schaefer
| Decision Date | 29 March 2021 |
| Docket Number | Civil Action No. 16-12543-FDS |
| Parties | EDMUND EDWARD WARD, Plaintiff, v. ERNST J. SCHAEFER, M.D., Defendant. |
| Court | U.S. District Court — District of Massachusetts |
MEMORANDUM AND ORDER ON DEFENDANT'S MOTION FOR SUMMARY JUDGMENT
This is an action arising out of the use of a drug in a compassionate-use protocol. Plaintiff Edmund Edward Ward suffers from a rare genetic deficiency that has resulted in, among other things, severe kidney disease. He alleges that he was fraudulently induced by defendant Ernst Schaefer, M.D., to participate in what he contends was a non-therapeutic, experimental drug trial. He further contends that he was led to believe that the drug, ACP-501, would reverse his kidney disease, but that Dr. Schaefer's true purpose in treating him was to gain data for research and commercial benefit.
Ward initially filed suit against Dr. Schaefer; the company that originally produced the drug (AlphaCore Pharma, LLC); one of its officers (Bruce Auerbach); the company that later purchased AlphaCore (MedImmune, LLC); a related company (AstraZeneca Biopharmaceuticals, Inc.); and the doctors at the National Institutes of Health involved in the compassionate-use protocol (Robert Shamburek, M.D., and Alan Remaley, M.D.). All claims against parties other than Dr. Schaefer have previously been dismissed.
Dr. Schaefer has moved for summary judgment. For the following reasons, the motion will be granted as to all of the claims except those based, in substance, on a lack of informed consent. The evidence as those claims, while hardly free from doubt, is sufficient to establish an issue of disputed material fact. Accordingly, the motion will be granted in part and denied in part.
The following facts are as set forth in the record and are undisputed except as noted.
Edmund Edward Ward was born with an extremely rare genetic deficiency of a bloodstream enzyme, called lecithin-cholesterol acyltransferase ("LCAT"). (Def. Ex. 2 at ¶ 2; Def. Ex. 6 ("Ward Dep.") at 19; Def. Ex. 5 at 493). LCAT is associated with high-density lipoprotein cholesterol ("HDL-C"), often referred to as the "good cholesterol." (See Def. Ex. 3 ("Schaefer Dep. Vol. 1") at 42; Def. Ex. 5 at 496-97). As a result of his deficiency, referred to as "familial LCAT deficiency" or "FLD," Ward produces virtually no cholesterol. (See Schaefer Dep. Vol. 1 at 42-43; Def. Ex. 5 at 496-97; Def. Ex. 8 ("Shamburek Dep.") at 18-19). He also suffers from associated health conditions, including kidney disease and a history of atrial fibrillation. (Def. Ex. 2 at ¶ 5; Def. Ex. 5 at 493). He is in stage-five kidney failure and receives dialysis treatment several times a week. (Ward Dep. at 44-45; Pl. Ex. 43).
Ernst J. Schaefer, M.D., is a physician at the Tufts University School of Medicine. (Schaefer Dep. Vol. 1 at 23). He is the founder of the Dyslipidemia Foundation of Boston, which "supports research awards, research, education, and patient care in the area of dyslipidemia." (Pl. Ex. 2 at 2). At all relevant times, he was also one of Ward's regular treatingphysicians. (Ward Dep. at 19-20).
Dr. Schaefer is also the founder and chief medical officer of Boston Heart Diagnostics ("BHD"), a company that provides, among other things, laboratory and diagnostic services, focusing on heart-disease prevention. (Schaefer Dep. Vol. 1 at 26-27). Since 2007, BHD has used the HDL Map—a test co-developed and patented by Dr. Schaefer—to examine HDL particles by two-dimensional gel electrophoresis. (Def. Ex. 4 ("Schaefer Dep. Vol. 2") at 283, 306-08; Def. SMF ¶ 90).1
On October 21, 2003, U.S. Patent Number 6,635,614 ("the '614 Patent") was issued to three scientists associated with the National Institutes of Health ("NIH") within the Department of Health and Human Services. (Pl. Ex. 6). The claims for the patent involve "[a] method for decreasing accumulation of cholesterol in arteries in a human subject not suffering from [LCAT] deficiency syndrome." ). The patent was assigned to the NIH. (Id. at 1; Pl. Ex. 7 at 52803). Dr. Schaefer was not listed as an inventor, nor does it appear that he had any involvement in obtaining the patent. (Pl. Ex. 6 at 1; see Schaefer Dep. Vol. 1 at 207).
Alan Remaley, M.D., and Robert Shamburek, M.D., are physicians associated with the NIH. (Def. Ex. 7 ("Remaley Dep.") at 15; Shamburek Dep. at 15). They study "lipid and lipoprotein metabolism," including disorders such as LCAT deficiency. (See Remaley Dep. at 15-16, 20-21; Shamburek Dep. at 12-15). Dr. Remaley leads the same laboratory that was previously led by the inventors of the '614 Patent. (Remaley Dep. at 41-42).
In approximately 2007 or 2008, Bruce Auerbach and Brian Krause approached Dr. Remaley about the '614 Patent. (Id. at 41; Pl. Ex. 8). Auerbach and Krause had founded AlphaCore Pharma, LLC, and they were "interested in licensing the patent and potentially trying to develop [it] into a drug." (Remaley Dep. at 41). Dr. Remaley agreed to collaborate, and in 2008 the NIH entered into a research agreement with AlphaCore. (Id. at 43-45; Pl. Ex. 12 at 2).2 Around the same time, AlphaCore licensed the '614 Patent from the NIH. (See Shamburek Dep. at 43). The NIH provided a grant of $240,129 to AlphaCore to produce recombinant LCAT enzyme and to conduct animal testing. (Pl. Ex. 9 at 168). AlphaCore then started to make recombinant human LCAT, which it called ACP-501. (Remaley Dep. at 19; Shamburek Dep. at 43).
In approximately 2012, AlphaCore and the NIH conducted a Phase 1 clinical trial of ACP-501 in 16 patients with cardiovascular disease. (See Remaley Dep. at 50-52; Def. Ex. 12).3 That study indicated that ACP-501 was safe for use in humans and could "raise[] HDL" levels. (Remaley Dep. at 52). The NIH shared the study's results with the Food and Drug Administration. (Id. at 60-61).
After the Phase 1 study, "a limited supply" of ACP-501 remained. (Id. at 70). The parties dispute whether there were plans at one point to use that leftover ACP-501 in another study. (Def. SMF ¶ 33; Pl. Resp. to Def. SMF ¶ 33; compare Remaley Dep. at 70, with id. at 171). In any event, AlphaCore ultimately donated the leftover ACP-501 so that the NIH coulduse it to treat Ward. (First Auerbach Aff. (Dkt. No. 20) ¶ 18).
In May 2010, Ward saw Dr. Om Ganda for a consultation about a lipid disorder. (See Pl. Ex. 5). Dr. Ganda concluded that Ward had an LCAT deficiency and referred him to Dr. Schaefer. (Id. at 3; Def. Ex. 14). After genetic sequencing performed at BHD in June 2010 confirmed that Ward had FLD, he made an appointment with Dr. Schaefer to "discuss therapeutic options." (Def. Ex. 14 at 1).
Ward and Dr. Schaefer first met on July 1, 2010. (Ward Dep. at 19). Over the next two years, they met "on a monthly basis" to discuss Ward's condition. (Id.).
Shortly after Ward was diagnosed with FLD in June 2010, Dr. Schaefer attended a medical conference, where he discussed Ward's condition with Dr. Remaley and Brian Krause of AlphaCore. (See Def. Ex. 14 at 1). Dr. Remaley offered to help, and shared the fact that the NIH and AlphaCore were "developing recombinant LCAT as a therapy," presumably for cardiovascular disease, and hoped "to start a clinical trial sometime" in 2011. (Id.).
Sometime later, Dr. Schaefer called Dr. Remaley to discuss Ward and ask whether he had plans to use ACP-501 to treat LCAT-deficient patients. (Remaley Dep. at 78-80). Ward was also on the call, but Dr. Remaley "had very limited conversation with him." (Id. at 78). Dr. Remaley told them that at the time, AlphaCore and the NIH "had no plan to design a study to systematically treat" LCAT deficiency using ACP-501. (Id. at 79).
Over the next year or so, Dr. Schaefer, Ward, and Dr. Remaley continued to correspond about LCAT therapy. In November 2011, Ward told his nephrologist, Bijan Roshan, M.D., that he "may be one of the first to receive an IV injection with the LCAT enzyme." (Def. Ex. 15). In December 2011, he sent an e-mail to Dr. Remaley to thank him for keeping him informed about "the progress of the LCAT enzyme" and to "reiterate [his] desire and willingness to have theenzyme administered as soon as feasible." (Def. Ex. 16).
In December 2011, Dr. Roshan, Dr. Ganda, Dr. Schaefer, and others published an article about LCAT deficiency in the Journal of Clinical Lipidology, which included Ward's data and information concerning his diagnosis. .4 The article listed Ward as a co-author. (Def. Ex. 5 at 493). It concluded that "[i]n the future, the use of recombinant LCAT may be of value in patients who develop significant renal impairment." (Id. at 498). The article included a disclosure that Dr. Schaefer "[is] supported by research grants to the Lipid Metabolism Laboratory at Tufts University from the National Institutes of Health, Bethesda, MD." (Id.).
On February 29, 2012, Dr. Schaefer e-mailed Dr. Remaley to inquire "about the status of recombinant LCAT in LCAT deficiency." (Pl. Ex. 16 at 1). Dr. Remaley replied that he needed to collect more safety data before he could obtain the FDA's approval to use ACP-501 in a trial to treat LCAT-deficient patients. (See id.). Dr. Schaefer indicated that Ward wanted to participate in such a trial once Dr. Remaley had obtained the FDA's approval. (See id.).
In March 2012, Dr. Schaefer and Dr. Remaley again e-mailed about having Ward participate in a trial involving ACP-501. (See Pl. Ex. 17). Dr. Remaley indicated that Ward could likely participate in such a trial. (Id.). Dr. Schaefer replied that Ward was "ready when you are," copied Ward, and shared Ward's phone numbers and home address. (Id.).
On April 10, 2012, Dr. Schaefer sent an e-mail to Dr. Remaley and copied Ward and Dr. Roshan. (Def. Ex. 18). The e-mail stated that due to changes in Ward's condition, Dr. Roshan had "recommended the placement of a...
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