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Form 8-K

 

 

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

 

 

FORM 8-K

 

 

CURRENT REPORT

Pursuant to Section 13 or 15(d) of the

Securities Exchange Act of 1934

April 11, 2012

Date of Report (Date of earliest event reported)

 

 

GALECTIN THERAPEUTICS INC.

(Exact Name of Registrant as Specified in Charter)

 

 

 

NEVADA   000-32877   04-3562325

(State or Other Jurisdiction

of Incorporation)

  

(Commission

File Number)

  

(IRS Employer

Identification No.)

7 WELLS AVENUE

NEWTON, MASSACHUSETTS

02459

(Address of Principal Executive Offices) (Zip Code)

(617) 559-0033

(Registrant’s telephone number, including area code)

 

 

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions (see General Instruction A.2. below):

 

¨ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

 

¨ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

 

¨ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

 

¨ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

 

 

 

Item 7.01. Regulation FD Disclosure.

Executives of Galectin Therapeutics Inc. are presenting a corporate update in April contained in the slide presentation attached as Exhibit 99.1 to this Current Report on Form 8-K (this “Report”).

The information in this Report is being furnished pursuant to this Item 7.01 and shall not be deemed “filed” for purposes of Section 18 of the Securities Exchange Act of 1934 (the “Exchange Act”) or otherwise subject to the liabilities of that section, and it shall not be deemed incorporated by reference in any filing under the Securities Act of 1933 or under the Exchange Act, whether made before or after the date hereof, except as expressly set forth by specific reference in such filing to this Report.

 

Item 9.01. Financial Statements and Exhibits.

 

(d) Exhibits  

99.1        Corporate Update Presentation Slides - dated April 2012.

SIGNATURES

Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

 

GALECTIN THERAPEUTICS INC.

By:

  

/s/ Thomas A. McGauley

  Thomas A. McGauley
  Chief Financial Officer
  Date: April 11, 2012

Exhibit Index

 

Exhibit

Number

     
99.1    Corporate Update Presentation Slides dated April 2012.
Corporate Update Presentation Slides
Corporate Summary
April 2012
NASDAQ: GALT
Exhibit 99.1

Forward Looking Statements
This presentation contains, in addition to historical information, 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 our current expectations
and are subject to factors and uncertainties which could cause actual results to differ
materially from those described in the statements. Factors that could cause our actual
performance to differ materially from those discussed in the forward-looking statements
include, among others: incurrence of operating losses since our inception, uncertainty as to
adequate financing of our operations, extensive and costly regulatory oversight that could
restrict or prevent product commercialization, inability to achieve commercial product
acceptance, inability to protect our intellectual property, dependence on strategic
partnerships, product competition, and others stated in risk factors contained in our SEC
filings. We cannot assure that we have identified all risks or that others may emerge which
we do not anticipate. You should not place undue reliance on forward-looking statements.
Although subsequent events may cause our views to change, we disclaim any obligation to
update forward-looking statements.
©
2012 Galectin Therapeutics  
GALT
2

Proprietary
Compounds
•
First in class, proprietary compounds that inhibit galectin proteins
•
Complex carbohydrate drugs with highly favorable safety profile
•
•
GR-MD-02: Preclinical: Non-alcoholic steatohepatitis (NASH, fatty
liver disease) and other causes of liver fibrosis
Validated Science
•
Pre-clinical models show galectins are critical targets for intended
diseases with mechanisms that would be novel in the market
Large Market
Opportunities
•
Enhancing the ability of immune system to kill cancer cells is
synergistic with many current and experimental therapies
•
NASH and liver fibrosis indications would be first therapies for
completely unmet medical needs, representing a multi-billion dollar
market
Intellectual Property
•
Sole ownership, no licenses granted
•
GM-CT-01: Matter and methods granted (expire 2023)
•
GR-MD-02: Matter and methods pending (priorities of 2006-2011)
Experienced
Management Team
•
Management
team
has
collective
experience
in
multiple
biotech
and
Pharma companies and relevant scientific areas
©
2012 Galectin Therapeutics  
GALT
3
Investment Highlights
GM-CT-01:
Phase
II:
Melanoma;
Enhances
ability
of
immune
cells
to kill cancer cells

Experienced Management Team
4
Peter G. Traber, MD
President, CEO, CMO
•
Over 25 years experience in biomedicine and pharmaceutical industries in research
and development, clinical medicine, management and leadership, and business
development. Medical expertise in liver disease
•
GlaxoSmithKline (CMO), Un of Pennsylvania (CEO), Baylor College of Medicine (CEO)
Anatole Klyosov, PhD
Chief Scientist
•
Over 35 years experience in biochemical reactions and their mechanisms,
biotechnology, and carbohydrate research
•
Moscow
University,
Russian
Academy
of
Sciences,
Harvard
Medical
School
Eliezer Zomer, PhD
EVP, Product
Development
•
Over 30 years
experience in biotechnology engineering  and regulatory
in
pharmaceuticals and
diagnostics.
•
Koor
Biotechnologies,
Charm
Sciences,
Glycogenesis,
HU
Medical
School
(Jerusalem), Harvard University
Thomas A. McGauley
CFO (acting)
•
Over 10 years in accounting and finance with life science and technology companies
•
PricewaterhouseCoopers, Pro-Pharmaceuticals, deCode Genetics
Maureen Foley
COO
•
Over 30 years’
experience in business and operations management for public and
private scientific, and biotech corporations and startup companies
•
eHealthDirect, Signatron, ArsDigita and Thermo Fibergen
Elena Chekhova, PhD
Program Manager
•
Over10 years of experience working in the biotech and life sciences industries, project
management, manufacturing and business development.
•
Regis Tech., Decode, Zafgen, Boston College, Tokai Pharma, MIT, University of
Dortmund, Harvard University
©
2012 Galectin Therapeutics  
GALT

•
Science of Galectins
•
Galectin Function
•
Galectin Inhibitors
•
Intellectual Property
•
Immune Enhancement in Cancer Therapy
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Liver Fibrosis
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Milestones
5
©
2012 Galectin Therapeutics  
GALT

Galectin Proteins Are Critical Participants In
Pathogenesis of Many Fibrotic and Neoplastic
Diseases
6
©
2012 Galectin Therapeutics  
GALT
Bind to cell surface
and matrix
glycoproteins
(galactose residues)
•
Modulate cell
signaling
•
Promote cell-cell
interactions
•
Promote cell-
matrix interactions
Markedly Increased in:
1.
Inflammation
2.
Fibrosis
3.
Cancer
Galectin-3 is most
prominent galectin
secreted in disease
*Secreted in small amounts normally
by a number of cells, predominantly
macrophages
Secreted
Galectin
Proteins*
GALECTINS
PROMOTE
PATHOLOGY

Galectin Inhibitors: A New Class of
Pathology Modulators
7
•
Novel complex carbohydrate drugs that target
secreted and membrane-associated galectins by
virtue of high molecular weight
•
Strongest binding to galectin-3, most prominent
galectin in disease processes
•
Binding to galectins disrupts function and
modulates multiple
cellular pathways in
pathology representing a potential new class of
therapeutic agents
•
Low toxicity potential as a carbohydrate
with no toxic metabolites
•
Two classes of compounds under development
•
GM-CT
•
GR-MD
•
Low manufacturing costs; abundant natural
plant product starting materials
©
2012 Galectin Therapeutics  
GALT
Galectin
Proteins
Galectin
Inhibitor

Intellectual Property
•
GM-CT Class (current NCE is GM-CT-01)
•
US Composition of matter patent Issued 2011 (priority 2003)
•
Five US issued method of use patents in combination with cancer therapy for
increased efficacy and reduced side effects
•
International Patents:  13 granted and 5 pending
•
Method of use in liver fibrosis patent pending (priority 2006)
•
Method of use in NASH patent pending (priority 2011)
•
GR-MD Class (current NCE is GR-MD-02)
•
Composition of matter patent pending (priority 2011)
•
Method of use in liver fibrosis patent pending (priority 2006)
•
Method of use in NASH patent pending (priority 2011)
•
All intellectual property generated in house with no encumbrances
•
No established generic pathway for such complex carbohydrate drugs
8
©
2012 Galectin Therapeutics  
GALT

•
Science of Galectins
•
Galectin Function
•
Galectin Inhibitors
•
Intellectual Property
•
Immune Enhancement in Cancer Therapy
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Liver Fibrosis
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Milestones
9
©
2012 Galectin Therapeutics  
GALT

The Vast Majority of Cancers Secrete Large Amounts
of Galectins Which Have Multiple Roles in Tumor
Pathogenesis
•
Tumor cell invasion:
extracellular matrix
adhesion & detachment
•
Metastasis:
cell invasion and migration
•
Angiogenesis
•
Tumor immunity has
recently been shown to be
critically affected by
galectins
10
The “Galectin Effect”
protects tumors from
immune system
©
2012 Galectin Therapeutics  
GALT

11
Experiments performed by Dr. Pierre van der Bruggen of the Ludwig Institute in
Brussels, Belgium in collaboration with Galectin Therapeutics
Tumors Evade the Immune System Using the
“Galectin Effect”
and GM-CT-01 Reverses This Effect
©
2012 Galectin Therapeutics  
GALT
Galectin-3
Cytokines
Kill tumor cells
GM-CT-01
Galectin-3 secreted by
tumor cells binds to surface
of T-cells and inhibits
cytokine secretion
Treatment with GM-CT-01
blocks Galectin-3 and
restores  T-cell cytokine
secretion and tumor killing
Tumor
Cells
T-Cells
Tumor
Cells
Cytokines
T-Cells

GM-CT-01 Activates Secretion of INF-
in a Dose-
Dependent Manner In Tumor Infiltrating CD8+ T-
Cells From Human Patients
12
©
2012 Galectin Therapeutics  
GALT
GM-CT-01 in
g/ml

GM-CT-01 Restores Ability of Human CD8
T-Cells to Kill Tumor Cells Through Inhibition of
“Galectin Effect”
13
Effectors: CD8+ T Cells
Target:  Tumor Cells
©
2012 Galectin Therapeutics  
GALT

GM-CT-01 Has Demonstrated Safety  in over 100
Human Subjects in Phase I and Partially Completed
Phase II Clinical Trials with Some Evidence of
Efficacy
•
Phase  I trial (DAVFU-001) in 40 subjects with end stage cancer showed GM-CT-01
was safe alone and in combination with the chemotherapy 5-FU
•
Three Phase II trials were conducted, but only partially completed
•
One Phase II trial (DAVFU-001) of 5-FU plus GM-CT-01 in line 3/4 therapy of metastatic
colorectal cancer
showed
6.7
months
median
survival.
In
similar
patients,
Erbitux
®*
had
a
6.1
month survival compared to 4.6 months with no therapy
•
When
the
data
from
the
three
partially
completed
Phase
II
trials
were
pooled
,
the
serious
adverse
events
associated
with
5-FU
were
reduced
when
compared
to
historical
controls
•
The company is seeking partners with significant chemotherapy business for pursuing
an indication for reduction in side effects for 5-FU and leucovorin containing
chemotherapy regimens. 
•
Our preclinical efficacy and clinical safety data were strong enough to obtain an IMPD 
for Phase I/II trial in metastatic melanoma with a combination of a tumor
vaccine
and
GM-CT-01
to
test
the
efficacy
of
blocking
the
“Galectin
Effect”
[Study
not being conducted under FDA IND, but there is open IND for GM-]CT-01
14
*“Erbitux®
is a registered trademark of ImClone LLC, a wholly-owned subsidiary of Eli Lilly and Company.“
©
2012 Galectin Therapeutics  
GALT

Preclinical efficacy and clinical safety data sufficient to
obtain an IMPD for treatment of metastatic melanoma to test
the efficacy of blocking the “Galectin Effect”
15
Melanoma “Proof of Concept”
Trial:
Patients: 
Advanced metastatic melanoma
Design:
Two Stage (12 in stage 1 and 46 in stage 2)
Regimen: 
Prime with melanoma specific peptide vaccine
Treat with GM-CT-01 to block “Galectin Effect”
Endpoint:
Partial or complete response by imaging
Group 2 patients have additional injection of GM-CT-01 in cutaneous tumors
©
2012 Galectin Therapeutics  
GALT

Tumor Immune Enhancement Development Program
16
Q1
Q2
Q3
Q4
Q1
Q2
Q3
Q4
Q1
Q2
Q3
Q4
2012
2013
2014
Preclinical Efficacy
Studies
GM-CT-01
Phase I/II Melanoma Trial*
*Conducted in Belgium under an IMPD.  Not conducted under FDA IND, but there is an open IND for GM-CT-01
At conclusion of Stage 1 of study:
•
•
•
•
©
2012 Galectin Therapeutics  
GALT
Pursue Partnering
Discussions
Efficacy in immune
competent mice with
syngeneic tumors
Top line
results in
Stage 1
Top line
results in
Stage 2
Seek partnership with company with marketed or
late stage cancer immunotherapy
Consider Phase IIb controlled trial with strong
efficacy
Continue to Stage 2 with some efficacy
Stop for lack of efficacy

Immune Enhancement by Blocking “Galectin
Effect”
is Synergistic With Many Emerging
Cancer Immunotherapies
•
Enhancing
the
ability
of
the
immune
system
to
recognize
and
kill
tumor
cells is a very active area in the personalized approach to cancer therapy. 
The “Galectin Effect”
inhibits the immune system
•
Two agents have been approved for use to date
•
Dendritic cell vaccine: Provenge®
(Dendreon)
•
T-cell activator (CTLA4 receptor mAb): Yervoy®
(Ipilimumab, BMS)
•
Many more vaccines and activators in development
•
Our drugs reverse the “Galectin Effect”
by which tumors inhibit the
immune
system
and
may
be
synergistic
with
all
tumor
immunotherapies.
May be effective with unaltered immune system
•
While
tumor
vaccines
are
patient
and
tumor
specific,
reversal
of
the
“Galectin Effect”
appears to be universal.  Initial Phase I/II clinical trial in
Belgium in combination with a vaccine to treat metastatic melanoma
•
The tumor vaccine market is forecast to be over $7 billion by 2015
17
©
2012 Galectin Therapeutics  
GALT

Best Positioned to Advance Tumor
Immunotherapy with Galectin Inhibitor
•
Market for tumor vaccines is expected to grow to $7B by 2015.  If
ipilimumab (Yervoy ®, BMS) is included, market is even larger
•
Blocking the “Galectin Effect”
would be synergistic with all types of tumor
vaccines or immune stimulatory approaches
•
In this regard, competition will come from other galectin-inhibitors
•
Galecto Biotech AG (Sweden):  Discovery phase focusing on small molecule inhibitors
•
LaJolla Pharmaceuticals (CA):  In Jan. 2012, they purchased GCS-100 from Solana
Therapeutics (formally Prospect Therapeutics, formally Glycogenesis).  GCS-100 is a
natural product compound with claims for binding galectins; focused on blood cancers;
significant side effects reported.
•
Mandel Med (Oakland, CA):  Truncated galectin-3 protein.  Not progressed into human
trials and no active program currently.
•
Stelic Institute (Japan): Pre-clinical RNAi approach in inflammatory bowel disease
•
Galectin Therapeutics is best positioned with a human trial in cancer
immunotherapy; GM-CT-01 has proved safe in Phase I and three partially
completed Phase II trials.
18
©
2012 Galectin Therapeutics  
GALT

•
Science of Galectins
•
Galectin Function
•
Galectin Inhibitors
•
Intellectual Property
•
Immune Enhancement in Cancer Therapy
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Liver Fibrosis
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Milestones
19
©
2012 Galectin Therapeutics  
GALT

NASH and Liver Fibrosis are Multi-
Billion Dollar Markets In US Alone
* Performed in US in 2010  (UNOS)
* * Prevalence in US 2010 (UNOS)
20
#
Deaths in 1998 (AASLD Workshop, 2001)
##
Prevalence in US 1976-1980 (NIDDK)
&
Prevalence in US 2011 (NIH)
©
2012 Galectin Therapeutics  
GALT
•
The ONLY current therapy for advanced fibrosis (cirrhosis) is liver transplantation
•
No approved medical therapy for fibrosis
•
While there are treatments for some underlying etiologies (Hepatitis C and B), there is
no approved therapy for NASH
Transplants
(6,291*)
Wait List
(17,000**)
Death From Cirrhosis
(44,677
#
)
Cirrhosis
(400,000
##
)
NASH: 9-15 Million
&
Hepatitis C, Hepatitis B, Alcohol

Galectin-3 Is A Critical Protein Target
For Therapy of Liver Fibrosis
Galectin-3 is produced in large amounts by fibrotic liver (animal and
human)
Galectin-3 is essential in mice for the development of liver fibrosis
Fibrosis due to toxin exposure or fatty liver does not
occur in mice
that lack the galectin-3 gene
Galectin inhibitors block production of fibrogenic markers in the key
human cell (stellate cells) responsible for liver fibrosis
Galectin inhibitors reverse experimental fibrosis in rats induced by both
fibrosis and fatty liver
21
Key Evidence: 
Key Evidence: 
©
2012 Galectin Therapeutics  
GALT

Galectin Inhibitor GR-MD-02 Effectively
Treats Toxin-Induced Liver Fibrosis in Rats
22
Galectin Therapeutics Data
Liver fibrosis induced in all rats by injection of chemical
toxin (thioacetimide) for 8 weeks
©
2012 Galectin Therapeutics  
GALT
Treatment with vehicle alone for
four weeks (Control) shows
robust fibrosis
Treatment with GR-MD-02 for four
weeks shows dramatic regression
of fibrosis

GR-MD-02 Markedly Improved NASH (Non-Alcoholic
Steatohepatitis) in a Mouse Model
Vehicle
GR-MD-02
NASH was induced in mice by rendering them diabetic and
feeding them a high fat diet
©
2012 Galectin Therapeutics  
GALT

GR-MD-02 Prevented and Completely Reversed
Fibrosis in NASH Mouse Model
24
Early Treatment
Late Treatment
normal
mouse 0.33
©
2012 Galectin Therapeutics  
GALT

Treatment with GR-MD-02 Markedly
Reduces Galectin-3 in NASH Mice
25
Vehicle
GR-MD-02
Immunohistochemistry for detection of Galectin-3
©
2012 Galectin Therapeutics  
GALT

Inhibition of Gal-3 May Have Multiple Sites
of Action in Therapy of NASH
26
Cause of
Liver Injury
Mediators
Inflammation
Fibrosis
Resolution
Metabolic Syndrome
Glucose
Intolerance
Fat
Accumulation
Impaired Lipid
Metabolism
Hyperglycemia
Adipocytokines
Free Fatty Acids
Extracellular
Matrix
Cytokines
ECM Dissolution
MMPs
Inflammation
ceases
Stellate Cells
Macrophages
Gal-3
Gal-3
Gal-3
Gal-3
Stellate Cell
Release of multiple inflammatory
cytokines, including TGF-
1, a critical
mediator of fibrosis
Quiescent
Activated
Hepatocyte
Macrophage
(Kupffer Cell)
T-Cell
Bile Duct Cell
Lipo-peroxidation Products
Scavenger receptor increases
cellular uptake of toxic products
Inhibit scavenger mechanism
and reduce cellular toxicity
Galectin Functions
GR-MD-02 Putative
Mechanisms
Increases TGF-
receptor
signaling
Reduce cell membrane TGF-
receptor activity
Promotes cell-cell and cell
matrix interactions which
enable inflammatory networks
Disrupt cell-cell signaling to
reduce inflammatory cascade
Enhance interactions between
matrix protein components to
stabilize matrix
Destabilize matrix to make
more available for degradation
Increase expression of MMPs
Modulate expression of
Metaloproteases (MMPs)
©
2012 Galectin Therapeutics  
GALT

27
Q1
Q2
Q3
Q4
Q1
Q2
Q3
Q4
Q1
Q2
Q3
Q4
2012
2013
2014
Phase I1
NASH
NASH
NASH Development Program: GR-MD-02
Phase 2 NASH Trial
File Fast Track Designation
Jan
Jul
Sep
IND
©
2012 Galectin Therapeutics  
GALT
Phase I Trial:
Patient Inclusion:
Design:
Primary Endpoint:
Secondary Endpoints:
Biopsy proven NASH with fibrosis
Single dose escalation to target dose and then additional 10
patient extension for two months of therapy
Patient safety
Serum markers; MR-fat and elastography
Phase II Trial:
Patient Inclusion:
Design:
Primary Endpoint:
Secondary Endpoints:
Biopsy proven NASH with fibrosis
Randomized, controlled, double blinded study with six
months of therapy
Liver biopsy NASH score and percent area collagen
Safety; Serum markers; MR-fat and elastography
Pre-Clinical (Target SQ)
Top line
results
First patient
enrolled
Top line
results

Among Competition Company is Best Positioned
For a Successful Development Program in NASH
General Mechanism
Examples
Comments
Treat Diabetes and
Insulin Resistance
•
Pioglitazone
•
Failed to achieve significant endpoints in phase II and
phase III clinical trials
Inhibit Lipid
Metabolism
•
Aramchol
•
Colesevelam
•
Cholesterol inhibition, no clinical results; weak
mechanism
•
Intestinal bile salt binder, no clinical results, weak
mechanism
Modulate the
Immune System
•
EGS21 (Enzo)
•
Pentoxifylline
•
Abandoned after phase II trial
•
Non significant phase III results
Protease Inhibition
•
GS-9450 (Gilead)
•
Liver Toxicity: abandoned  (caspase inhibitor)
Anti-Oxidant
•
MND-21 (Mochida)
•
Cysteamine (Raptor)
•
Omega-3 fatty acid (phase II trial)
•
Increase glutathione in liver cells, single point of action
(phase II)
•
GR-MD-02 is well positioned with respect to competition
•
Most attractive mechanism: multiple sites of action in disease
•
Independent of hyperglycemia or hyperlipidemia
•
May reverse established fibrosis
•
Low toxicity potential as a carbohydrate with no toxic metabolites
28
©
2012 Galectin Therapeutics  
GALT

•
Science of Galectins
•
Galectin Function
•
Galectin Inhibitors
•
Intellectual Property
•
Immune Enhancement in Cancer Therapy
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Liver Fibrosis
•
Mechanism of Action
•
Regulatory and Clinical Plan
•
Competitive Positioning
•
Milestones
29
©
2012 Galectin Therapeutics  
GALT

Company Milestones
•
General
•
09/12: Host Global Conference on Galectins in Disease and Therapy;
planned second edition of book on Galectins
•
Cancer
•
03/12: Operational start of Phase I/II melanoma trial
•
04/12: First patient infusedPhase I/II melanoma trial
•
01/13: Stage 1 top line results (12 patients)
•
01/14: Stage 2 top line results (46 patients)
•
Fibrosis
•
05/12: NASH Presentation at DDW (Digestive Disease Week)
•
12/12:  NASH FDA IND
•
01/13:  Initiate Phase I NASH trial
•
07/13:  Phase I NASH trial results
•
09/13:  Initiate Phase II NASH trial
•
10/14:  Phase II NASH top line results
30
©
2012 Galectin Therapeutics  
GALT

Proprietary
Compounds
•
First in class, proprietary compounds that inhibit galectin proteins
•
Complex carbohydrate drugs with highly favorable safety profile
•
GM-CT-01: Enhanced ability of immune cells to kill of cancer cells
•
GR-MD-02: Potential to treat non-alcoholic steatohepatitis (NASH)
and other causes of liver fibrosis
Validated Science
•
Pre-clinical models show galectins are critical targets for intended
diseases with mechanisms that would be novel in the market
Large Market
Opportunities
•
Enhancing the ability of immune system to kill cancer cells is
synergistic with many current and experimental therapies
•
NASH and liver fibrosis indications would be first therapies for
completely unmet medical needs, representing a multi-billion
dollar market
Intellectual Property
•
Sole ownership, no licenses granted
•
GM-CT-01: Matter and methods granted (expire 2023)
•
GR-MD-02: Matter and methods pending (priorities of 2006-2011)
Experienced
Management Team
•
Management team has collective experience in multiple biotech
and Pharma companies and relevant scientific areas
31
Investment Highlights
©
2012 Galectin Therapeutics  
GALT