United States District Court, D. Massachusetts
MEMORANDUM AND ORDER ON DEFENDANTS' MOTIONS TO
DISMISS FOR FAILURE TO STATE A CLAIM AND FOR LACK OF PERSONAL
Dennis Saylor IV United States District Judge.
a tort 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 to participate in what he contends
was a non-therapeutic, experimental drug trial. He alleges
that he was led to believe that the drug, ACP-501, would
reverse his kidney disease, but that defendants' true
purpose in treating him was to gain data that would be
beneficial in selling the company that produced the drug.
has filed suit against the company that originally produced
the drug (AlphaCore Pharma, LLC), as well as one of its
officers (Bruce Auerbach); the company that later purchased
AlphaCore (Medimmune, LLC); a related company (AstraZeneca
Biopharmaceuticals, Inc.); and the doctors involved in his
treatment (Ernst Schaefer, Robert Shamburek, and Alan
MedImmune, LLC and AstraZeneca Biopharmaceuticals, Inc., have
moved to dismiss the claims against them for the failure to
state a claim upon which relief can be granted. Defendants
AlphaCore Pharma, LLC and Auerbach have moved to dismiss the
claims against them for lack of personal jurisdiction. For
the reasons stated below, both motions will be granted.
Edward Ward is a Massachusetts resident and a lawyer. (Compl.
¶ 1; 2d Auerbach Aff. Ex. A at 498). Ward was born with
an extremely rare genetic deficiency of a bloodstream enzyme,
called lecithin-cholesterol acyltransferase
(“LCAT”). (Id. ¶ 9). LCAT is
associated with high-density lipoprotein cholesterol
(“HDL-C”), often referred to as the “good
cholesterol.” (Id. ¶ 11). As a result of
his deficiency, referred to as “familial LCAT
deficiency” or “FLD, ” Ward produces
virtually no cholesterol. (Id. ¶ 9). Ward also
suffers from other associated health conditions, including
kidney disease. (Id.). He is in stage 5 kidney
failure, and receives dialysis treatment three times a week.
Auerbach is a Michigan resident. He is an officer and
principal of defendant AlphaCore Pharma, LLC
(“AlphaCore”), a limited liability company based
in Ann Arbor, Michigan. (Id. ¶ 2). As of 2012,
AlphaCore was the sole patent licensee of a form of
recombinant human LCAT (“rhLCAT”) called ACP-501.
(Id. ¶ 13). The relevant patent, concerning the
“Use of Lecithin-Cholesterol Acytransferase [sic] LCAT)
to Reduce Accumulation of Cholesterol, ” is owned by
the United States. (Id. ¶ 14).
Ernst Schaefer is a Massachusetts resident. He is a physician
at the Tufts University School of Medicine and Boston Heart
Diagnostics. (Id. ¶ 3). Dr. Schaefer is one of
Ward's regular treating physicians. (Id. ¶
Robert Shamburek and Alan Remaley are physicians employed by
the United States Department of Health and Human Services,
National Institutes of Health (“NIH”), in
Bethesda, Maryland. (Id. ¶ 4).
AstraZeneca Biopharmaceuticals, Inc.
(“AstraZeneca”) is a corporation with a usual
place of business in Delaware. (Id. ¶ 7).
MedImmune, LLC is a limited liability company and a
subsidiary of AstraZeneca. (Id.).
claims of the patent for ACP-501 involve “a method for
decreasing accumulation of cholesterol in arteries in a human
subject not suffering from . . . LCAT . . . deficiency
syndrome.” (Id. ¶ 14). In 2011, Dr.
Schaefer and several other physicians published a paper in
the Journal of Clinical Lipidology about LCAT deficiency. (2d
Auerbach Aff Ex. A at 498).The paper concluded that
“[i]n the future, the use of recombinant LCAT may be of
value in patients who develop significant renal
2012, in collaboration with the NIH, AlphaCore conducted a
clinical trial of ACP-501 to determine the safety and
tolerability of a single injection of the drug in 16 to 18
patients with stable coronary artery disease. (Compl. ¶
15). Defendants Shamburek and Remaley collaborated with
Auerbach in running the trial, and reported that a single
injection of ACP-501 was safe and tolerated by the subjects.
(Id. ¶ 16).
The Proposal to Ward
to the complaint, sometime in 2012, Ward was introduced to
Shamburek, Remaley, and Auerbach by his treating physician,
Dr. Schaefer, as a potential “ideal research subject
for ACP-501.” (Id. ¶ 18).
complaint alleges that the individual defendants induced Ward
to participate as the only subject in a long-term trial of
ACP-501 by misrepresenting that the drug would reverse his
advanced kidney disease. (Id. ¶¶ 22, 46).
According to the complaint, the individual defendants
withheld their true motivation for the study, which was to
test the effect of ACP-501 on the production of HDL-C in an
LCAT-deficient patient, “hoping the drug would be
considered a potential breakthrough in the prevention of
cardiovascular disease, ” as well as to acquire
long-term safety data, in order to accelerate the sale of
AlphaCore to a large pharmaceutical company. (Id.
¶¶ 23, 46-47).
was granted an “orphan drug” designation for
ACP-501 and a “compassionate use” protocol was
approved. (Id. ¶ 20). AlphaCore donated to the
NIH the ACP-501 needed for the trial. (Id. ¶
January 2013, Ward travelled from Massachusetts to the NIH in
Maryland to begin treatment. (Id. ¶ 27). At the
outset of the trial, Auerbach met with Ward and allegedly
told him that the process of using ACP-501 to reverse his
kidney failure would take a long time, and that he should
remain in the trial for the full course of treatment because
he would “get out of it what [he puts] into it.”
the beginning of 2013, Ward “was considered by his
physicians to be in kidney failure, ” and he was about
to receive regular dialysis. (Id. ¶ 21). Ward
postponed dialysis in order to participate in the trial.
(Id. ¶¶ 21, 41).
point (the complaint does not specify when), the NIH created
a Clinical Protocol for Ward's treatment. The protocol
was titled “Expanded access use of intravenous ACP-501
in one subject with Familial lecithin:cholesterol
acyltransferase [rhLCAT] Deficiency.” (Id.
¶ 36). It appears that AlphaCore and Auerbach played
some role in the creation of the protocol, although the
details of their roles are unclear. (See Pl. Ex. G).
Under the protocol, Dr. Shamburek was the principal
investigator, Dr. Remaley was the safety-review investigator,
and Dr. Schaefer was the medical monitor. (Id.
of the protocol provided for two study sites: one at the NIH
facility in Maryland, and another in Massachusetts where Ward
would be treated by his regular physician, Dr. Schaefer. (Pl.
Ex. E at 23). Under that draft of the protocol, Ward would
receive an initial phase of treatment at NIH in Maryland;
later, during phase two, he would receive treatments every
few weeks in Massachusetts with additional treatments at NIH
every few months. (Id. at 26-27).
parties dispute whether that draft became the final operative
protocol or whether a later draft, which provided for only
one test site in Maryland, was in fact the final approved
protocol. (See 2d Auerbach Aff. Ex. B at 21; Pl.
Surreply at 6-7). It is undisputed that the protocol,
whichever version was adopted, did call for Dr. Schaefer to
monitor Ward while he was home in Massachusetts. (2d Auerbach
Aff. Ex. B at 21 (stating that Dr. Schaefer would
“monitor and treat [Ward's] renal dysfunction and
other disorders associated with his FLD” while in
Massachusetts); Pl Ex. E at 21 (stating that Dr. Schaefer
would monitor Ward)).
appears that in June and July 2013 there was some discussion
between Dr. Schaefer and Dr. Remaley concerning the
possibility of having ACP-501 sent to Massachusetts so that
Ward could be treated there. (Pl. Ex. H). However, it does
not appear that any ACP-501 treatments took place in
was admitted to the NIH facility in Maryland on January 6,
2013. (Id. ¶ 28). According to the complaint,
Ward did not receive and sign the NIH's Consent to
Participate in a Clinical Research Study until January 24,
after he had already been subjected to several days of study.
(Id. ¶ 29). The complaint further alleges that
the consent form was inadequate, because it failed to fully
disclose defendants' financial interests in ACP-501.
(Id. ¶ 35).
regimen which Ward underwent was “painful, grueling,
and confining.” (Id. ¶ 28). For example,
from January 24 to February 27, 2013, Ward remained in one
NIH hospital room for 24 hours a day. (Id.). He had
two intravenous lines continuously inserted, one to
administer ACP-501 for one hour in the morning, and the other
to draw blood as many as 32 times per day. (Id.).
From February 27 to June 28, Ward travelled from
Massachusetts to Maryland every Tuesday. At NIH, he would
check into a hospital room, and Dr. Shamburek would
administer ACP-501 on Wednesday morning and then draw his
blood six times on Wednesday and another six times on
Thursday. (Id. ¶ 38).
to the complaint, Drs. Shamburek and Remaley both told Ward
that the ACP-501 was materially improving his kidney
function, even though the data as to the drug's effects
was at best ambiguous. (Id. ¶¶ 39-40).
Throughout the trial, at the counseling of Drs. Shamburek and
Remaley, Ward did not receive dialysis. (Id. ¶
April or May 2013, Ward's nephrologist, Dr. Valerie
Price, told him that he could no longer go without dialysis.
(Id. ¶ 50). Nonetheless, he continued with the
2013, the supply of ACP-501 at NIH was running low.
(Id. ¶ 52). Drs. Shamburek and Remaley
convinced Ward to continue the trial at a lower dose.
(Id.). That lower dose caused Ward's HDL-C to
plummet. (Id. ¶ 53). He expressed a desire to
drop out of the trial if he could not continue to receive the
higher dose. (Id.). According to the complaint, Drs.
Shamburek and Remaley induced him to remain in the trial with
false promises of a new shipment of ACP-501, meaning a return
to the higher dose, and reversing his kidney disease.
(Id. ¶¶ 54, 56).
July to September 2013, Ward again travelled from
Massachusetts to Maryland every Tuesday for treatment with
the lower dose of ACP-501. (Id. ¶ 58).
According to the complaint, his kidney function deteriorated
on the lower dose. (Id. ¶ 59). In September, at
the urging of Drs. Price and Schaefer, Ward decided to
withdraw from the trial in order to receive needed dialysis.
(Id. ¶¶ 59, 61). The complaint alleges
that Dr. Shamburek then tried to convince Ward to remain in
the trial by telling him he had “interesting new
information” and that the lower dose was working to
improve kidney function. (Id. ¶ 60). In
October, Dr. Shamburek allegedly called Ward and told him
that he could not “just leave the program” and
that he had to “come back to the NIH.”
(Id. ¶ 61). According to the complaint, in
early fall 2013, Ward “learned that the only effect of
the ACP-501 experimentation on his kidney condition was to
delay, for many months, critical dialysis treatment.”
(Id. ¶ 41).
appears that AlphaCore reimbursed Ward for his travels to and
from Maryland, as well as for any lab work conducted in
Massachusetts in connection with the trial. (Pl. Ex. D).
The Sale of AlphaCore
April 2013, during the course of the trial, MedImmune
purchased AlphaCore for $20, 000, 000. (Id. ¶
43). According to the complaint, the sale was
“based” principally on . . . Ward's HDL-C
results.” (Id.). It further alleges that Ward
was not made aware of sale until 2014, almost a year after he
had withdrawn from the trial. (Id. ¶ 43, 49).
complaint alleges that the individual defendants,
“acting in concert, ” were AlphaCore
shareholders, owned AlphaCore options or warrants, or
“otherwise benefitted materially from the sale of
[AlphaCore] to [AstraZeneca] in secret.” (Id.
Allegations as to MedImmune and Astra
allegations of the complaint as to the involvement of