Eagle Pharmaceuticals Announces Positive Results of a Study Conducted in Partnership with the U.S. Military to Evaluate Neuroprotective Effects of RYANODEX for the Treatment of Nerve Agent Exposure

— Statistically significant lower incidence of brain damage compared to
control group, demonstrating neuroprotective properties of RYANODEX in
treating nerve agent exposure —

— Statistically significant robust p-values of 0.04 or less were
determined in six cortical areas of the brain —

WOODCLIFF LAKE, N.J.–(BUSINESS WIRE)–Eagle Pharmaceuticals, Inc. (Nasdaq: EGRX) (“Eagle” or the “Company”)
today announced positive results of its study to evaluate the
neuroprotective effects of RYANODEX^® (dantrolene sodium)
secondary to nerve agent (NA) exposure, conducted with the United States
Army Medical Research Institute of Chemical Defense (USAMRICD), the
nation’s leading science and technology laboratory in the area of
medical chemical countermeasures research and development.

The study results show a p-value of 0.04 or less compared to the control
group in six critical areas of the brain. We believe these results
demonstrate the neuroprotective effects of RYANODEX. It has been
hypothesized that nerve agent poisoning triggers intracellular calcium
release in the body. The study data supports the proposed mechanism of
action of RYANODEX, which modulates intracellular calcium in different
organs including the brain.

“We are very pleased that the results of our study support the use of
RYANODEX as a neuroprotective therapy in nerve agent exposure. Current
treatment options do not protect the brain from neurological damage in
the event of exposure. If approved, RYANODEX would represent the first
of its kind agent as a neuroprotective treatment for nerve agent
exposure, serving as an important treatment option for U.S. military
personnel, as part of the U.S. strategic national stockpile for civilian
use, and for our allies abroad,” said Scott Tarriff, Chief Executive
Officer of Eagle.

“We intend to meet with the U.S. Food and Drug Administration (FDA) to
discuss next steps as soon as possible. Given the life-threatening
nature of NA exposure, we believe this indication would be evaluated
under the FDA’s Animal Rule. If approved, this would be an additional
indication for RYANODEX, as we continue to develop additional potential
indications and an intramuscular formulation of the drug,” added Tarriff.

Study Design

Eagle conducted an initial study in 2017 to evaluate the neuroprotective
effects of RYANODEX in a rodent model of NA-induced brain damage.
Positive results of this study led to this GLP study to evaluate the
efficacy of RYANODEX to reduce neuropathology in catheterized rats
exposed to the nerve agent soman. The study was conducted with the
USAMRICD, at their laboratories in Aberdeen, Maryland, under a
Cooperative Research and Development Agreement (CRADA), a written
agreement that allows government laboratories to partner with private
industries or academia on research and development projects.

The animal study was conducted in a rat model of acute nerve agent
(soman) exposure. Animals were randomized into each of the six study
groups, including a positive control and a negative control group. Five
groups received standard treatment with HI-6, atropine and midazolam.
Four of the groups also received RYANODEX. Surviving animals were
evaluated for neuropathology 24 hours post-soman exposure to assess the
neuroprotective effects of RYANODEX in this well-established animal
model.

“We believe the study shows that RYANODEX treatment after soman exposure
decreases free intracellular calcium concentrations, thus lowering
calcium elevations as a result of organophosphate induced status
epilepticus, and, therefore, mitigates neuropathology resulting from
these continuous seizures. The topline results of this GLP study are
strong and confirm our belief in the neuroprotective effects of
RYANODEX,” stated Adrian Hepner, Chief Medical Officer of Eagle.

Mechanism of Action

Scientific evidence indicates that elevated intracellular calcium levels
may have a role in seizure-related brain damage resulting from induced
seizures and status epilepticus secondary to NA exposure. As in other
conditions, including acute hyperthermic and hypermetabolic disorders,
intracellular calcium overload leads to severe brain and other organ
damage. RYANODEX (dantrolene sodium) is a well-characterized ryanodine
receptor antagonist that inhibits intracellular calcium overload
secondary to different triggers. Ryanodine receptors are widely
distributed in the body, including skeletal muscle, heart and brain
tissues. The active ingredient in RYANODEX is the only approved drug
that inhibits the ryanodine receptors, modulating the intracellular
calcium levels.

About Nerve Agents

NAs were first widely used in World War II (WWII); their impact became a
significant public health issue thereafter. NAs acquired their name
because they affect the transmission of nerve impulses in the nervous
system. NAs include compounds such as sarin, VX and soman.

NAs, whether gas, aerosol or liquid, are extremely toxic and have a very
rapid effect. The NA enters the body through inhalation or through the
skin. Poisoning may also occur through consumption of liquids or foods
contaminated with NAs. NA survivors will likely experience severe
symptoms, including neurologic consequences.

NAs produce seizures and seizure-related brain damage. The seizures
quickly develop into status epilepticus and usually become refractory to
standard antiepileptic therapy.

At present, antidotes for nerve agent exposure provide limited
protection, and current treatments do not fully reduce
nerve-agent-induced seizures and subsequent brain injury. Additionally,
medical care for NA casualties is likely to be delayed beyond the
therapeutic window of opportunity to terminate NA-induced seizures,
resulting in seizure-related brain damage that continues along the
pathological cascade. Thus, there is a need for adjunct drug therapy
that is capable of interrupting the pathologic cascade and augmenting
neuroprotection when administered in combination with antiepileptic
drugs during the refractory phase of NA-induced seizures.

Scientific evidence supports a pivotal role of elevated intracellular
calcium levels in seizure-related brain damage resulting from induced
seizures and status epilepticus secondary to NA exposure. In addition,
there are several reports that a neuroprotective approach, aimed at
attenuating delayed calcium overload, combined with antiepileptic
treatment, may lead to greater protection against seizure-related brain
damage than anti-epileptics alone.

About Eagle Pharmaceuticals, Inc.

Eagle is a specialty pharmaceutical company focused on developing and
commercializing injectable products that address the shortcomings, as
identified by physicians, pharmacists and other stakeholders, of
existing commercially successful injectable products. Eagle’s strategy
is to utilize the FDA’s 505(b)(2) regulatory pathway. Additional
information is available on the Company’s website at www.eagleus.com.

Forward-Looking Statements

This press release contains forward-looking information within the
meaning of the Private Securities Litigation Reform Act of 1995, as
amended and other securities laws. Forward-looking statements are
statements that are not historical facts. Words and phrases such as
“will,” “expected,” “we believe,” “committed,” “plan,” “promise,” “may,”
“enables,” “potential,” and similar expressions are intended to identify
forward-looking statements. These statements include, but are not
limited to, statements regarding future events, including: the Company’s
ability to advance RYANODEX, including with USAMRICD or other parties,
in the treatment of nerve agent exposure; the Company’s and USAMRICD’s
ability and willingness to perform their respective obligations under
the Cooperative Research and Development Agreement; the success of the
Company’s commercial relationship with USAMRICD; successful compliance
with the FDA; and the commercial success of the Company’s commercial
portfolio, including RYANODEX, if and when launched. All such statements
are subject to certain risks and uncertainties, many of which are
difficult to predict and generally beyond Eagle’s control, that could
cause actual results to differ materially from those expressed in, or
implied or projected by, the forward-looking information and statements.
Such risks include, but are not limited to: whether the Company can
successfully advance RYANODEX in the treatment of nerve agent exposure;
whether the FDA will ultimately approve RYANODEX for the treatment of
nerve agent exposure and/or other indications; whether Eagle’s studies
will support the safety and efficacy of RYANODEX for the treatment of
nerve agent exposure; whether Eagle will maintain successful compliance
with the FDA and other governmental regulations; whether the Company
will incur unforeseen expenses or liabilities or other market factors;
the effect of competitive factors and Eagle’s reactions to those
factors; the pace and extent of market adoption of Eagle’s products and
technologies; uncertainty in the process of obtaining regulatory
approval or clearance for Eagle’s products; the success of Eagle’s
growth strategies; timing and achievement of product development
milestones; the outcome of ongoing or future litigation; the impact and
benefits of market development; Eagle’s ability to protect its
intellectual property; dependence upon third parties; unexpected new
data, safety and technical issues; market conditions; other risks
inherent to drug development and commercialization; and other risks
described in Eagle’s filings with the U.S. Securities and Exchange
Commission. Readers are cautioned not to place undue reliance on these
forward-looking statements that speak only as of the date hereof, and we
do not undertake any obligation to revise and disseminate
forward-looking statements to reflect events or circumstances after the
date hereof, or to reflect the occurrence of or non-occurrence of any
events.

Contacts

Investor Relations for Eagle Pharmaceuticals, Inc.:
Lisa M.
Wilson
In-Site Communications, Inc.
T: 212-452-2793
E: [email protected]