Eagle Pharmaceuticals Announces Positive Results of Study Conducted to Evaluate Neuroprotective Effects of RYANODEX Secondary...
September 05 2017 - 10:00AM
Business Wire
Eagle Pharmaceuticals, Inc. (Nasdaq: EGRX) (“Eagle” or “the
Company”) today announced positive results of an initial study in
over 50 rodents to evaluate the neuroprotective effects of
RYANODEX® (dantrolene sodium) in an established rodent model of
Nerve Agent-(NA) induced seizures and seizure-related brain
damage.
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.
Animals treated with RYANODEX in combination with nerve gas
antidotes and anti-epileptic drugs (AEDs) after exposure to NAs had
better performance in neurobehavioral testing compared to animals
treated with AEDs alone, as well as substantially less brain
damage.
“We believe these study data support further investigation of
RYANODEX as a neuroprotective therapy in Nerve Agent casualties, a
potential new indication for the drug,” said Scott Tarriff, Chief
Executive Officer of Eagle. “Our next steps are to continue to
engage with the military and meet with the FDA. We will continue to
develop our animal research with the expectation that indications
like these are approved under the Animal Rule1.”
In this study, animals were exposed to a high dose of the NA
soman and treated with the known antidote for acute poisoning
(atropine and HI-6). All surviving study animals developed severe
status epilepticus and were treated with standard AEDs according to
protocol. Study animals were randomly assigned to receive RYANODEX
or control vehicle as added treatment.
Neurobehavioral testing (NBT) was conducted between two and four
weeks after exposure to soman, at which time brain neuropathology
(NP) was also evaluated. NBT included Forced Swim Test and Sucrose
Preference Test.
Animals treated with RYANODEX + AEDs had better performance in
NBT, compared to animals treated with AEDs only. Analysis of NP
showed a substantially lower level of brain cell necrosis in
animals treated with RYANODEX + AEDs, compared to AEDs alone.
Animals treated with standard therapy showed a mean necrosis score
of 2.6 in fronto-parietal cortex, compared to a group of RYANODEX
treated animals showing a score of 0.6 in the same anatomical
region. The scoring system for cell necrosis ranges between 0
(normal, no necrosis) to 5 (cellular necrosis greater than 80%) In
addition, no safety issues were observed in animals treated with
RYANODEX.
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. NA 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.
Medical care for NA casualties will likely be delayed beyond the
therapeutic window of opportunity to terminate NA-induced seizures,
and seizure-related brain damage will continue 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 such
as “will,” “may,” “can,” “could be,” “believe,” “intends,”
“anticipate(s),” “plan,” “enables,” “potentially,” “entitles,” and
similar expressions are intended to identify forward-looking
statements. These statements include statements regarding future
events including, but not limited to: the ability of Eagle to
generate data sufficient to support the grant of an indication from
the FDA for the use of Ryanodex as a neuroprotective therapy in
treating the effects of NA exposure; the willingness of the FDA to
grant approval for such an indication; and the ability of the
Company to develop and sustain a market for such indication; and
other factors that are discussed in Eagle’s Annual Report on Form
10-K for the year ended December 31, 2016, and its other filings
with the U.S. Securities and Exchange Commission (“SEC”). All of
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 Eagle’s management and/or board of directors will be
effective in managing Eagle’s business and future growth, whether
Eagle will maintain successful compliance with FDA and other
governmental regulations applicable to manufacturing facilities,
products and/or businesses, as well as the other risks described in
Eagle’s filings with the SEC. 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.
1 FDA Guidance for Industry ‘Product Development Under the
Animal Rule’ (October
2015).https://www.fda.gov/downloads/Drugs/GuidanceComplianceRegulatoryInformation/Guidances/UCM399217.pdf
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Investor Relations for Eagle Pharmaceuticals,
Inc.:In-Site Communications, Inc.Lisa M. Wilson,
212-452-2793lwilson@insitecony.com
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