Selected for oral poster tour by the scientific
committee in the gut microbiota section at the International Liver
CongressTM 2019 of EASL
Innovate Biopharmaceuticals, Inc. (Nasdaq: INNT), a clinical stage
biotechnology company focused on developing novel therapeutics for
autoimmune and inflammatory diseases, with its lead drug,
larazotide acetate, comprising a new class of medicines based on
gut-restricted peptides which re-normalize the gut-epithelial
barrier and the gut-liver axis, announced that data
demonstrating proof-of-concept in an established model of
nonalcoholic steatohepatitis (NASH) will be presented at
The International Liver Congress™, the annual meeting of the
European Association for the Study of the Liver (EASL), being
held in Vienna, Austria, April 10-14, 2019. There are
currently no treatments for nonalcoholic fatty liver disease
(NAFLD) or NASH approved by the FDA.
The intestinal epithelium normally forms a tight seal separating
the host from gut contents, via a well-regulated physical barrier.
Tight junctions, one of the most important physiologic and
pathologic structural complexes, regulate the subtle equilibrium
among the gut microbiome, epithelial cells, and the intestinal
mucosa, helping to maintain a delicate homeostasis. A meta-analysis
based on five clinical studies showed that NAFLD and NASH patients
are more likely to have altered gut permeability in comparison with
healthy controls. This association of increased intestinal
permeability was stronger particularly in NASH patients,
demonstrating that the inflammatory changes observed in NASH might
be caused by the increased intestinal permeability.1 On a molecular
level, NAFLD patients are hypothesized to exhibit dysregulated
tight junction molecules, as shown by a genetic model of gut
barrier dysfunction which resulted in more severe steatohepatitis
vs. control mice, when fed a Western diet.2
In the study being presented today, researchers assessed the
effects of larazotide in a preclinical model of NASH that develops
from consumption of a specified diet, the DIAMONDTM mouse
model. The preclinical model recapitulates NAFLD/NASH in
response to a high fat, high sugar Western diet, including
insulin resistance, obesity, and dyslipidemia, which parallels
human disease progression.
The data has been selected as an oral short presentation as part
of the Poster Tour: Gut Microbiota & Liver Disease, Metabolism,
Alcohol & Toxicity section:
Section: Poster Tour - Gut Microbiota and Liver Disease,
Metabolism, Alcohol & Toxicity
Poster Tour No. FRI-267: Serial
measurement of serum dextran absorption by novel competition ELISA
demonstrates larazotide acetate significantly improves "leaky gut"
in a Western diet murine model of metabolic liver
disease.
- Time: April 12, 2019 at 12:30 pm – 1:00 pm Central European
Time (CET)
- Location: Meeting Point 3, Hall B Reed Messe Wien Exhibition
& Congress Center
- Presenter: Rebecca Caffrey, Ph.D.
The paper poster presentation will be displayed in Reed Messe
Wien Exhibition & Congress Center Hall B on Friday, April 12,
2019, from 9:00 am to 5:00 pm, Central European Time (CET). The
research will be presented in the Gut Microbiota & Liver
Disease poster area as Poster FRI-267.
Arun Sanyal, M.D., Professor of Medicine & Executive
Director, Education Core, Clinical Center for Translational
Research at the Virginia Commonwealth University (VCU), stated,
“The demonstration of reduced gut permeability with larazotide,
presented today at the EASL conference, in the setting of
diet-induced obesity opens up the possibility of modulating the
outcomes of metabolic syndrome, including NASH, via this mechanism
and warrants further development for this compound. Increased
intestinal permeability has been linked to many aspects of
metabolic syndrome including type 2 diabetes and nonalcoholic fatty
liver disease.”
About NAFLD/NASH:Nonalcoholic
steatohepatitis (NASH) is a severe disease of the liver caused by
inflammation and a buildup of fat in the organ. In the United
States, NASH affects up to approximately 2-5% of the population. An
additional 10%-30% of Americans have fat in their livers, but no
inflammation or liver damage, a condition called NAFLD or “fatty
liver.” The underlying cause of NASH is unclear, but it most often
occurs in persons who are middle-aged and overweight or obese.
It has been shown that chronic liver diseases, including
NAFLD/NASH, may cause perturbations in the epithelial lining of the
gut, and disrupt barrier integrity, causing a normal intestine to
become more permeable. This “leaky gut” could cause passage of
unwanted toxins and antigenic components to “cross-talk” to the
liver via the blood circulation causing inflammation and damage to
hepatocytes. This gut-liver axis is an emerging area of
research in chronic liver diseases, such as
NAFLD/NASH.
About Larazotide Acetate for Celiac Disease In
celiac disease, larazotide is the only drug which has successfully
met its primary endpoint with statistical significance in a Phase
2b efficacy clinical trial (342 patients). Innovate completed the
End of Phase 2 Meeting with the FDA and is preparing to
launch the Phase 3 registration clinical trials for celiac disease
in the second quarter of 2019. Nearly 600 subjects have been
exposed to larazotide in clinical trials, and a safety profile
comparable to placebo has been demonstrated. Larazotide has
received Fast Track designation from the FDA for celiac
disease
About Innovate Biopharmaceuticals,
Inc. (Nasdaq: INNT) Innovate is a clinical stage
biotechnology company focused on developing novel therapeutics for
autoimmune and inflammatory diseases. Innovate’s lead drug
candidate, larazotide acetate, has a mechanism of action that
renormalizes the dysfunctional intestinal barrier by decreasing
intestinal permeability and reducing antigen trafficking, such as
gliadin fragments in celiac disease, and bacterial toxins and
immunogenic antigens in nonalcoholic steatohepatitis (NASH). In
several diseases, including celiac disease, NASH, Crohn’s
disease, ulcerative colitis, irritable bowel syndrome (IBS), type 1
diabetes mellitus (T1DM), chronic kidney disease (CKD), the
intestinal barrier is dysfunctional with increased
permeability.
Forward Looking Statements This press release
includes forward-looking statements including, but not limited to,
statements related to the development of drug candidates, our
operations and business strategy, our expected financial results,
and corporate updates. The forward-looking statements contained in
this press release are based on management’s current expectations
and are subject to substantial risks, uncertainty and changes in
circumstances. Actual results may differ materially from those
expressed by these expectations due to risks and uncertainties,
including, among others, those related to our ability to obtain
additional capital on favorable terms to us, or at all, including,
without limitation, to fund our current and future preclinical
studies and clinical trials and the success, timing and cost of our
drug development program and our ongoing or future preclinical
studies and clinical trials, including, without limitation, the
possibility of unfavorable new clinical and preclinical data and
additional analyses of existing data, as well as the risks that
prior clinical and preclinical results may not be replicated. These
risks and uncertainties include, but may not be limited to, those
described in our Annual Report on Form 10-K filed with
the SEC on March 18, 2019, and in any subsequent
filings with the SEC. Forward-looking statements speak only as
of the date of this press release, and we undertake no obligation
to review or update any forward-looking statement except as may be
required by applicable law.
SOURCE: Innovate Biopharmaceuticals, Inc.
Innovate Biopharmaceuticals, Inc. Jennifer K.
Zimmons, Ph.D. Investor Relations Tel: +1-917-214-3514
Email: jzimmons@innovatebiopharma.com
www.innovatebiopharma.com
- Luther, J et. al. Hepatic Injury in NASH Contributes to
Altered Intestinal Permeability. CMGH 2015 Vol. 1, Issue 2,
pp. 222-232. (doi: 10.1016/j.cmgh.2015.01.001)
- Rahman, K et. al. Loss of Junctional Adhesion Molecule A
Promotes Severe Steatohepatitis in Mice on a Diet High in Saturated
Fat, Fructose, and Cholesterol. Gastroenterology. 2016 Oct;
151(4): 733-746. (doi: 10/1053/j.gastro.2016.06.022)
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