Galectin Therapeutics Inc. (NASDAQ:GALT), the leading developer of
therapeutics that target galectin proteins, today provided
highlights from a late-breaker oral presentation at The
International Liver Congress™ 2018, European Association for
the Study of the Liver (EASL) in Paris, France on Saturday, April
14, 2018.
Naga P. Chalasani, M.D., Associate Dean for
Clinical Research; Director, Division of Gastroenterology and
Hepatology at Indiana University School of Medicine, and co-lead
principal investigator on Galectin Therapeutics’ recent Phase 2b
NASH-CX trial, delivered a late-breaker presentation entitled “A
multicenter, randomized, double-blind, PLB-controlled trial of
Galectin-3 inhibitor (GR-MD-02) in patients with NASH cirrhosis and
portal hypertension” (click for presentation). The session focused
on the Company’s recent Phase 2b NASH-CX trial results and the
innovative work the Company is doing for patients with
non-alcoholic steatohepatitis (NASH) cirrhosis and portal
hypertension.
Dr. Chalasani’s late-breaker presentation highlighted and
extended the study’s primary findings in patients without
esophageal varices and those with mild portal hypertension. Most
importantly, in patients with NASH cirrhosis without esophageal
varices, Galectin Therapeutics’ lead compound, GR-MD-02,
demonstrated a statistically significant improvement in portal
pressure, an improvement in liver cell death (hepatocyte
ballooning) on biopsy for the total population, and a reduction in
the development of new esophageal varices at the end of the
one-year study. This subgroup is large and commercially relevant as
it comprises about half of all patients with NASH cirrhosis.
Since reporting these initial findings in December 2017,
continued analysis of the data has led to two additional findings
that reinforce the positive effects of GR-MD-02. First, a
statistically significant (p=0.04) correlation was identified
between the decrease in portal pressure (HVPG, or hepatic venous
pressure gradient) and the improvement in hepatocyte ballooning
(viz., representing a decrease in liver cell death) upon treatment
with GR-MD-02 at 2 mg/Kg. This suggests an important
pathophysiological link between the improvement in liver biopsy and
reductions in HVPG. To our knowledge, this is the first time that
such a correlation has been demonstrated in a human clinical trial
in patients with NASH cirrhosis.
Secondly, an evaluation of GR-MD-02 blood levels provided an
explanation for the reduced efficacy response observed in the
higher GR8 (8 mg/Kg) dose group. In the GR2 (2 mg/Kg) dose
group, the blood levels (or total exposure to the drug as measured
by area under the concentration-time curve) were tightly grouped.
In contrast, there was a broad distribution of higher drug
exposures in the GR8 group. Approximately half of the patients who
received GR8 had GR-MD-02 blood concentration levels that had risen
to a range where a reduced efficacy effect in the liver had been
noted at very high doses in the NASH animal models.
When the GR8 group was divided, based on pharmacokinetic
analysis of drug levels, into separate low (<12K µg*hr./mL) and
high (>12K µg*hr./mL) drug exposure ranges, a statistically
significant effect (p=0.03) of GR8 on both HVPG and hepatocyte
ballooning was observed in those patients with drug levels in the
lower drug exposure range. There was no corresponding statistically
significant effect in the higher drug exposure range group of
patients receiving GR8 in analogy to what was observed in the NASH
animal studies. Therefore, the GR8 dose, in cirrhotic patients,
seems to be at the upper range of efficacy. Importantly, this not
only provides an explanation of the dose ranging results but also
more clearly defines the upper range of human drug dosing for
GR-MD-02 in patients with NASH cirrhosis. Further, these
results suggest it might be useful to explore intermediate doses
between 2mg/kg and 8mg/Kg in future clinical studies.
“The findings presented by Dr. Chalasani reinforce how the
NASH-CX trial has demonstrated clinically meaningful improvement
for those patients with NASH cirrhosis without esophageal varices
with a drug that was well tolerated over one year of therapy,” said
Dr. Peter Traber, CEO and Chief Medical Officer of Galectin
Therapeutics. “Since about 50 percent of the total population of
patients with NASH cirrhosis do not have esophageal varices and
endoscopy to evaluate for varices is part of the standard of care
for patients with NASH cirrhosis, there is a large and easily
identifiable population of patients that might benefit from
GR-MD-02. We look forward to presenting our findings to the FDA
next month and to continuing advanced clinical studies to progress
GR-MD-02 toward approval for the treatment of NASH cirrhosis in an
appropriate patient group.”
About NASH Cirrhosis NASH cirrhosis is the
final stage in the progression of non-alcoholic steatohepatitis
(NASH), a disease of the liver which affects millions of people in
the U.S. and worldwide. The liver cell death and inflammation seen
in NASH eventually causes progressive scarring of the liver, that
eventually can result in liver cirrhosis. While the early stages of
NASH can be treated by changes in lifestyle, such as losing weight
and exercising, once the disease progresses to NASH cirrhosis there
is no treatment available short of a liver transplant. Of the total
number of individuals in the world felt to presently have NASH, it
is predicted that NASH cirrhosis will eventually kill 20 million of
those people.
One of the results of NASH cirrhosis is an increase in blood
pressure in the portal vein that brings blood and nutrients from
the digestive tract through the liver and then out to the rest of
the body. As the scarring effect of cirrhosis on the liver
progresses, blood flow through the liver becomes more difficult,
increasing the blood pressure in the portal vein, creating varying
degrees of portal hypertension. Eventually, this increase in blood
pressure causes the veins connected to the liver to dilate and form
esophageal varices, in which are dilated veins that divert blood
through the esophagus, bypassing flow through the liver. These
dilated veins in the esophagus are prone to bleeding, which is a
major cause of morbidity and mortality in patients with NASH
cirrhosis.
About the NASH-CX Trial The NASH-CX trial was a
randomized, double-blind, placebo-controlled Phase 2b clinical
trial which enrolled 162 NASH cirrhosis patients; NASH-cirrhosis
was confirmed both by liver biopsy and by confirmation of an
elevated hepatic venous pressure gradient (HVPG). Enrolled patients
received either 8 mg/kg or 2 mg/kg of GR-MD-02 or placebo every
other week for 52 weeks, for a total of 26 doses. The aim of the
NASH-CX clinical trial was to evaluate the safety and efficacy of
GR-MD-02 in patients with well-compensated NASH cirrhosis. The
primary study endpoint was a reduction in HVPG. Patients treated
with GR-MD-02 were evaluated to determine the change in HVPG as
compared to patients treated with placebo. Secondary end-points
include NASH fibrosis stage and percent of fibrotic tissue based on
liver biopsy and other non-invasive measures (see:
www.clinicaltrials.gov for further details).
About GR-MD-02 GR-MD-02 is a non-biologic
complex carbohydrate drug that targets galectin-3, a critical
protein in the pathogenesis of fatty liver disease and fibrosis.
Galectin-3 plays a major role in diseases that involve scarring of
organs including fibrotic disorders of the liver, lung, kidney,
heart and vascular system. The drug binds to galectin-3 proteins
and disrupts its function. Preclinical data in animals have shown
that GR-MD-02 has robust treatment effects in reversing liver
fibrosis and cirrhosis.
About Galectin Therapeutics Galectin
Therapeutics is dedicated to developing novel therapies to improve
the lives of patients with chronic liver and skin diseases and
cancer. Galectin's lead drug (GR-MD-02) is a carbohydrate-based
drug that inhibits the galectin-3 protein that is directly involved
in multiple inflammatory, fibrotic, and malignant diseases. The
lead development program is in non-alcoholic steatohepatitis (NASH)
with cirrhosis, the most advanced form of NASH related fibrosis.
This is the most common liver disease and one of the largest drug
development opportunities available today. Additional development
programs are for treatment of severe atopic dermatitis,
moderate-to-severe plaque psoriasis, and in combination
immunotherapy for advanced melanoma and other malignancies.
Galectin seeks to leverage extensive scientific and development
expertise as well as established relationships with external
sources to achieve cost-effective and efficient development.
Additional information is available at
www.galectintherapeutics.com.
Forward looking statements
This press release contains forward-looking statements within
the meaning of the Private Securities Litigation Reform Act of
1995. These statements relate to future events or future financial
performance, and use words such as “may,” “estimate,” “could,”
“expect” and others. They are based on management’s current
expectations and are subject to factors and uncertainties that
could cause actual results to differ materially from those
described in the statements. These statements include those
regarding the hope that Galectin’s development program for GR-MD-02
will lead to the first therapy for the treatment of NASH with
cirrhosis, and those regarding the hope that our lead compounds
will be successful in connection with the treatment of skin disease
and cancer immunotherapy. Factors that could cause actual
performance to differ materially from those discussed in the
forward-looking statements include, among others, that Galectin may
not be successful in developing effective treatments and/or
obtaining the requisite approvals for the use of GR-MD-02 or any of
its other drugs in development; the Company’s future clinical
studies may not produce positive results in a timely fashion, if at
all, and could prove time consuming and costly; plans regarding
development, approval and marketing of any of Galectin’s drugs are
subject to change at any time based on the changing needs of the
Company as determined by management and regulatory agencies; the
Company may find that its patents does not offer the protection
anticipated, and regardless of the results of any of its
development programs, Galectin may be unsuccessful in developing
partnerships with other companies or raising additional capital
that would allow it to further develop and/or fund any studies or
trials. Galectin has incurred operating losses since
inception, and its ability to successfully develop and market drugs
may be impacted by its ability to manage costs and finance
continuing operations. For a discussion of additional factors
impacting Galectin’s business, see the Company’s Annual Report on
Form 10-K for the year ended December 31, 2017, and subsequent
filings with the SEC. You should not place undue reliance on
forward-looking statements. Although subsequent events may cause
its views to change, management disclaims any obligation to update
forward-looking statements.
Investor Contact:Galectin Therapeutics,
Inc.Jack Callicutt, Chief Financial Officer(678)
620-3186ir@galectintherapeutics.com
Media Contact:Gregory FCALeigh Minnier, Vice
President610-228-2108leigh@gregoryfca.com
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