Incyte Annual Report 2006

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FY2006 Annual Report · Incyte

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Incyte Corporation

Experimental Station

Route 141 & Henry Clay Road, Building E336

Wilmington, DE 19880

www.incyte.com

THE DRIVE TO DISCOVER.

THE EXPERIENCE TO DELIVER.

Annual Report 2006

“With six INDs ﬁ led in the last 15 months,

we have the potential for multiple clinical proof-of-

concept results in 2007.”

Richard Levy, M.D., Senior Vice President, Drug Development, Incyte

Incyte’s vision is to become a leading drug discovery and development

company by building a proprietary product pipeline of novel small

molecule drugs. We have an experienced team with prior success in

bringing important new drugs to market. We believe we have the

resources, experience and drive to improve the lives of patients and

build sustainable value for our shareholders.

INCYTE PIPELINE

Preclinical

Phase I

Phase II

HIV

Diabetes

Oncology

CCR5 Antagonists
INCB9471
INCB15050

11beta-HSD1
INCB13739

Sheddase Inhibitor
INCB7839: Solid Tumors
JAK2

Inflammation

CCR2 Antagonists
INCB8696: MS/Lupus Nephritis
Pfizer Collaboration (as of 11/2005)
JAK2

BO ARD OF DIRECTORS

EXE CUTIV E MAN AGEME NT

Richard U. De Schutter
Chairman of the Board
Formerly Chairman
and Chief Executive Ofﬁ cer
DuPont Pharmaceuticals Company

Paul A. Friedman, M.D.
President and Chief Executive Ofﬁ cer
Incyte Corporation

Barry M. Ariko
President, Chief Executive Ofﬁ cer
and Chairman
Mirapoint, Inc.

Julian C. Baker
Managing Member
Baker Bros. Advisors, LLC

Paul A. Brooke
Chairman and Chief Executive Ofﬁ cer
Ithaka Acquisition Corp.
Managing Member, PMSV Holdings, LLC
Senior Advisor, Morgan Stanley

Matthew W. Emmens
Chief Executive Ofﬁ cer
Shire plc

John F. Niblack, Ph.D.
Formerly Vice Chairman
and President of Global Research
and Development
Pﬁ zer Inc.

Roy A. Whitﬁ eld
Formerly Chairman of the Board
and Chief Executive Ofﬁ cer
Incyte Corporation

Paul A. Friedman, M.D.
President and Chief Executive Ofﬁ cer

David C. Hastings
Executive Vice President
and Chief Financial Ofﬁ cer

John A. Keller, Ph.D.
Executive Vice President
and Chief Business Ofﬁ cer

Brian W. Metcalf, Ph.D.
Executive Vice President
and Chief Drug Discovery Scientist

Patricia A. Schreck
Executive Vice President
and General Counsel

Paula J. Swain
Executive Vice President,
Human Resources

Transfer Agent and Registrar
Mellon Investor Services LLC
PO Box 3315
South Hackensack, New Jersey 07606
or
480 Washington Boulevard
Jersey City, New Jersey 07310
Phone: 800/522-6645
TDD for Hearing Impaired:
800/231-5469
Foreign Shareholders:
201/680-6610
TDD Foreign Shareholders:
201/680-6578
www.mellon-investor.com/isd

Annual Meeting
The Annual Meeting of Stockholders
will be held May 22, 2007, at 10:00 a.m.,
Eastern Daylight Time, at the
Hotel du Pont, 11th and Market Streets,
Wilmington, Delaware.

Outside Counsel
Pillsbury Winthrop Shaw Pittman LLP

Independent Registered Public
Accounting Firm
Ernst & Young LLP

Market Information
Incyte’s Common Stock is listed on
the NASDAQ Global Market under the
symbol INCY.

Investor Relations
You can obtain recent press releases
and other publicly available information
on Incyte by visiting our web site at
www.incyte.com.

Contact
Pamela Murphy
Vice President, Investor Relations and
Corporate Communications
Email: pmurphy@incyte.com

Corporate Headquarters
Incyte Corporation
Experimental Station
Route 141 & Henry Clay Road
Building E336
Wilmington, Delaware 19880
302/498-6700

Forward-looking Statements

Except for the historical statements contained herein, the statements contained in this annual report, including without limitation, statements as to the

anticipated advancement and composition of our pipeline, the expected timing, progress and other information regarding our preclinical and clinical trials,

our development plans and goals for 2007 and 2008, plans to present and disclose data from our clinical trials, the potential beneﬁ ts and effectiveness of our

compounds in treating disease, and the ability of our cash position to advance our pipeline and continue our operations for a stated period of time, are forward-

looking statements within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. The forward-looking statements

are based on our current intent, belief and expectations, using information currently available to us, and are therefore subject to certain risks, uncertainties,

and assumptions that may cause actual results to differ materially, including the results of further scientiﬁ c research, the impact of technological advances and

competition, unanticipated delays or uses of capital, and other risks discussed in our Annual Report on Form 10-K for the year ended December 31, 2006, which

is contained herein, and in our ﬁ lings with the Securities and Exchange Commission. These forward-looking statements speak only as of the date hereof. Incyte

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disclaims any intent or obligation to update these forward-looking statements.

In 2002, we set out to develop a broad pipeline
of potential new therapeutics by:

Building a powerful discovery research team

120 biologists and chemists, supported by a
core team of clinical and regulatory professionals,
working seamlessly to advance multiple programs.

Identifying and validating promising drug targets

Programs focused on some of the most promising
new mechanisms in their therapeutic area: CCR5
for HIV,11beta-HSD1 for diabetes, sheddase for
oncology and JAK for inﬂ ammation and oncology.

Moving rapidly into lead optimization and
preclinical development

8 INDs ﬁ led to date; several more expected in 2007.

Creating a diversiﬁ ed portfolio of high-quality drug
candidates for important medical markets

Working in four therapeutic areas: HIV, diabetes,
oncology and inﬂ ammation. Clinical trials in 2007
expected to generate multiple proof-of-concept results.

Pursuing partnerships and acquisitions
to accelerate pipeline growth

Pﬁ zer collaboration in CCR2 antagonist program.

To Our Shareholders:

We are working intensively to build a diverse pipeline of products capable of creating signiﬁ cant and sustainable
value. With encouraging Phase IIa clinical data for our HIV and diabetes compounds, and with excellent
progress in new programs for inﬂ ammatory diseases and oncology, we moved closer to this goal in 2006.

2006 Accomplishments

Important measures of our success in 2006 were the ﬁ lings of Investigational New Drug (IND) applications
for four novel compounds:

• Our lead CCR5 antagonist for HIV, INCB9471, now in Phase IIa clinical trials. In the ﬁ rst

seven HIV patients treated, the compound was well-tolerated and achieved a mean 1.9 log
viral load reduction by day 14 of therapy.

• Our lead 11-beta hydroxysteroid dehydrogenase type 1 (11beta-HSD1) inhibitor, INCB13739,

for type 2 diabetes, also in Phase IIa development. Clinical results showed that a single oral dose

of INCB13739 completely inhibited 11beta-HSD1 activity in both adipose tissue and liver
of obese insulin-resistant individuals over a 24 hour period.

• Our follow-on CCR5 antagonist, INCB15050, for HIV.

• Our CCR2 antagonist, INCB8696, for multiple sclerosis, one of the indications we retained in

the CCR2 license agreement with Pﬁ zer established in January 2006.

In refractory cancer patients with solid tumors, we continued the testing of our lead sheddase inhibitor,
INCB7839, a compound that interferes with signaling through all four of the epidermal growth factor
receptors (HER1, HER2, HER3 and HER4). In 2006, there were an increasing number of scientiﬁ c publications
and presentations indicating the importance, in particular, of HER3-driven signaling in maintaining tumor cell
growth in the presence of inhibitors of HER1 and HER2. As INCB7839 can inhibit the production of heregulin,
the activating ligand for HER3, these publications further support the rationale for this mechanism.

The discovery team also successfully advanced compounds from a new program involving inhibitors of Janus-
associated kinases (JAK) into IND-enabling trials. Several INDs have recently been ﬁ led and we expect to begin
a series of Phase I clinical trials in the ﬁ rst half of this year. I believe these orally available JAK inhibitors could
have signiﬁ cant therapeutic potential in a number of areas including inﬂ ammatory diseases, myeloproliferative
disorders and certain cancers.

2007 Program Objectives

In 2007, we expect to make signiﬁ cant and visible pipeline progress in the following programs:

HIV: At a scientiﬁ c meeting later this year, we plan to present the full viral-load reduction and safety data from
the Phase IIa trial of our lead CCR5 antagonist, INCB9471. Once we’ve completed a series of required drug-
interaction studies, we plan to initiate Phase IIb trials. Top-line data from the Phase IIa trial reveal the potential
for our compound to be differentiated from others in this important new class of drugs. In particular, its long
half-life allows once-daily dosing without boosting with ritonavir; its long half-life could also improve the
efﬁ cacy and sustainability of combination treatment regimens by maintaining drug levels sufﬁ cient to block
viral replication even when patients occasionally miss doses.

Every year is important, but 2007 has the
potential to be transforming for Incyte.

Diabetes: For our lead 11beta-HSD1 inhibitor, INCB13739, we are currently enrolling patients in a 28-day Phase
IIa trial in type 2 diabetics. This trial will utilize a sensitive technique to measure the ability of INCB13739 to
improve the body’s response to insulin. Positive results would constitute proof-of-concept for this compound
and for the mechanism itself, and are expected to be predictive of long-term improvements in glycemic
control. The next step would be a three-month trial to assess the longer-term effects of INCB13739 using the
well established primary endpoint of improvement in hemoglobin A1c levels.

Oncology: Once the maximum tolerated dose of our oral sheddase inhibitor, INCB7839, has been deﬁ ned
in the ongoing Phase Ib/IIa dose-escalation trial, we plan to initiate Phase II trials in breast cancer and
possibly one other solid tumor type. We also plan to disclose relevant biomarker data generated in the Phase
Ib/IIa trial.

Inﬂ ammation: We intend to begin the development of our lead CCR2 antagonist, INCB8696, as a treatment
for multiple sclerosis, with a Phase I trial in healthy volunteers.

We also expect to begin clinical trials in the JAK program this year. Therapeutic areas of interest include chronic
inﬂ ammation, myeloproliferative disorders and cancer. For competitive reasons, we have not disclosed speciﬁ c
details of our clinical plans; however, we expect to produce proof-of-concept results for at least one indication
this year.

Importantly, our year-end 2006 cash position of approximately $330 million is expected to carry us into 2010,
providing a strong foundation to advance our pipeline and build value for our stakeholders.

Next Steps in Value Creation

Every year is important, but 2007 has the potential to be transforming for Incyte. We anticipate results from
clinical proof-of-concept studies with lead compounds from four of our programs: CCR5 antagonists for HIV,
11beta-HSD1 inhibitors for diabetes, sheddase inhibitors for solid cancers, and JAK2 inhibitors. With this
high level of clinical activity, driven by our focused and determined team, I remain very optimistic about our
prospects for 2007 and beyond.

Sincerely,

Paul A. Friedman, M.D.
President and Chief Executive Ofﬁ cer
April 2007

CCR5 Antagonists:
A Next Generation in HIV Therapy

“As part of the original Sustiva team, I was able to
see ﬁ rsthand how a promising product candidate can
fundamentally change the treatment of HIV. To once again
have the opportunity with INCB9471, which looks like it
could be best-in-class among this important new class of
CCR5 antagonists, is very exciting.”

Sue Erickson-Viitanen, Ph.D.

Senior Director, Virology Drug Development, Incyte

Mechanism of Action

Human immunodeﬁ ciency virus (HIV)
enters T-cells by binding to CD4 and one
of two obligate co-receptors:
CCR5 or CXCR4

• CCR5 antagonists block entry of
HIV that binds exclusively to CCR5

(R5 tropic virus).

• Over 85% of patients starting HIV
therapy have only R5 tropic virus

detectable in blood.
• About 50 to 60% of highly treat-
ment-experienced patients still
have only R5 tropic virus detectable

in blood.

Potential Beneﬁ ts

• Safe addition to therapy, comple-
mentary to drugs with other
modes of action.
• Less risk of developing drug

resistance.

Our lead compound: INCB9471

• Potential to be best-in-class.
• Potent antiviral compound with
excellent pharmacokinetics.
• Allows for once daily use without
boosting with ritonavir, a compound
associated with cardiovascular risk.
• Potential for use in ﬁ rst and second

line regimens.

• Long half-life expected to provide
more effective anti-viral activity even
if doses are occasionally missed.

CCR5 antagonists in HIV regimens
may provide

Clinical Status

10-Day Phase I studies in healthy
volunteers completed

• Substantial beneﬁ t in patients with
R5 tropic virus.
• Immunologic beneﬁ t in all subjects
based on increasing CD4 cell counts.

• Multiple doses up to 200 mg once
daily for 10 days of dosing.
• Very well-tolerated with no dose-

limiting toxicity identiﬁ ed.

14-Day Phase IIa study ongoing

• Includes treatment-naïve and

treatment-experienced patients not
currently on HIV therapy.
• R5 tropic HIV/naïve to CCR5
antagonists with viral load >
10,000 copies/ml.
• Impressive and sustained antiviral
effect demonstrated with 200
mg once daily dose of INCB9471
as monotherapy.
• Additional cohorts planned to
examine higher and lower doses.
• Full results expected to be presented
at scientiﬁ c meetings this year.

Required drug interaction studies to be
completed in 2007

• Single doses of INCB9471 studied
up to 300 mg.

Phase IIb clinical studies expected to
follow in late 2007 and early 2008

“I believe that current data show that
the best time to use a CCR5 antagonist
may be early on in the course of
treatment where R5-tropic HIV virus
dominates. Additionally, because these
compounds work differently than
existing HIV therapies and can be easily
combined with other treatments, this
new class represents the potential for
an important advance for how we treat
HIV patients.”

Calvin Cohen, M.D.
Research Director of the Community Research Initiative of
New England and HIV Clinical Management Consultant at
Harvard Vanguard Medical Associates

11beta-HSD1 Inhibitors:
An Emerging New Class of Drugs for
Metabolic Disease

“While other companies are pursuing this target, Incyte
may well be the ﬁ rst to conﬁ rm the clinical relevance
of 11beta-HSD1. The fact that our chemists have built
such a broad and diverse portfolio of proprietary oral
HSD1 inhibitors puts us in an ideal position to generate
signiﬁ cant value from this program.”

Project Leader 11beta-HSD1/Director, Applied Technology, Incyte

Reid Huber, Ph.D.

Mechanism of Action

11beta-HSD1 is an enzyme that converts
the biologically inactive steroid cortisone
into the potent biologically active
hormone cortisol, which is known to
act as a functional antagonist of insulin
action in multiple target tissues

• Liver: cortisol reduces insulin’s ability

to suppress glucose production.

• Muscle: cortisol reduces insulin’s ability

to promote glucose uptake.

• Adipose: cortisol blocks insulin’s ability

to suppress free fatty acid release.

Several additional lines of evidence
implicate 11beta-HSD1 activity as a
primary driver of insulin resistance and a
critical point for disease intervention

• 11beta-HSD1 is upregulated 3-5 fold

in obese humans.

• Adipose-speciﬁ c overexpression of
11beta-HSD1 by 2-3 fold in transgenic
mice produces a phenotype closely
resembling human type 2 diabetes.

• Reduction of intracellular cortisol levels
in the rodent as a result of pharma-
cologic inhibition of 11beta-HSD1
can reverse manifestations of the

metabolic syndrome including obesity,
diabetes, dyslipidemia and
atherosclerosis.

Clinical Status

Very well-tolerated in single- and
multiple-dose-ranging Phase I studies

Phase IIa adipose and liver pharmaco-
dynamic activity study in obese/insulin
resistant subjects completed

Potential Beneﬁ ts

By reducing the insulin resistance caused
by intracellular cortisol, an 11beta-
HSD1 inhibitor may be useful as a
treatment for type 2 diabetes and also
in allied conditions such as dyslipidemia,
cardiovascular disease, obesity and
hypertension.

Our lead compound: INCB13739

• Potent, selective oral compound with
excellent pharmacokinetic proﬁ le.
• Completely inhibits the production of

intra-adipose and intra-hepatic cortisol

by 11beta-HSD1, while maintaining
normal systemic cortisol levels, which
are essential for immune function
and response to stress.

• First compound publicly shown to
completely inhibit 11beta-HSD1

activity in both adipose tissue and liver;
a required characteristic to truly

test the clinical value of 11beta-HSD1
inhibition.

Twenty-eight day study including two-
step insulin clamp in type 2 diabetics
initiated 1Q2007

• Sensitive and accurate measure of
hepatic and peripheral insulin

sensitivity; expected to be predictive
of long-term improvements in insulin

resistance and glycemic control.

Three-month efﬁ cacy study in patients
with Type 2 diabetes expected to follow

“11beta-HSD1 is a signiﬁ cant and
promising new therapeutic target for
the metabolic syndrome. Current
therapies, particularly for diabetes,
fail to prevent disease progression
long term, demonstrating a clear need
for more effective, broad spectrum
approaches to treatment. By inhibiting
cortisol production in key tissues,
inhibitors of 11beta-HSD1 have the
potential to directly and profoundly
improve insulin resistance, thus
targeting the fundamental underlying
cause of type 2 diabetes and
cardiovascular disease.”

Jonathan Seckl, M.D., Ph.D.
Moncrieff-Arnott Professor of Molecular Medicine
Centre for Cardiovascular Science
The Queen’s Medical Research Institute, Edinburgh

Sheddase Inhibitors:
Novel Intervention in a Proven Pathway

“There is compelling evidence suggesting that elevated levels of
EGFR/HER ligands as well as increased levels of circulating HER2
extracellular domain (ECD) correlate with poor patient outcomes.
As early pharmacodynamic data clearly demonstrate that INCB7839
is impacting both ligand and HER2 shedding, we remain conﬁ dent
that sheddase inhibition could well represent an important and
novel approach to treating cancers.”

Steve Friedman, M.D.

Senior Vice President, Drug Discovery, Incyte

Mechanism of Action

Potential Beneﬁ ts

Epidermal growth factor receptor (EGFR)
signaling pathways consist of four
known cellular receptors: HER1 (also
known as EGFR), HER2, HER3, and HER4.
Normally, these HER pathways are tightly
regulated. In cancer, signaling through
these pathways can increase, resulting
in growth, proliferation, migration, and
survival of cancer cells. This correlates
with disease progression and poor
prognosis.

Sheddases are enzymes, speciﬁ cally ADAM
enzymes 10 and 17, that promote growth
activity through all four HER pathways.
Several marketed therapies that target
individual EGFR family members have
demonstrated that inhibition of HER
signaling is an effective mechanism for
treating certain solid tumors.

Sheddase inhibition blocks two different
pro-oncogenic mechanisms, generation of
active EGFR ligands and generation of a
constitutively active HER2 kinase.

• Inhibition of additional and/or common
HER pathways is expected to be

synergistic with currently approved
EGFR inhibitors and improve patient
outcomes.
• Sheddase can activate HER3 through
generation of the HER3 ligand,
heregulin. As this pathway is involved
in resistance to current EGFR targeted
therapies, decreasing the activity of this

pathway with inhibitors of sheddase
may be beneﬁ cial.

Our lead compound: INCB7839

• Novel, potent, orally bioavailable.

• In preclinical models: single agent
efﬁ cacy; synergistic with other
EGFR therapies; and synergistic with

chemotherapy.

Clinical Status

Phase I completed in healthy volunteers

• INCB7839 was well-tolerated.
• In a dose-dependent manner,

INCB7839 decreased HER2 ECD levels,

a clinically relevant biomarker.

Phase Ib/IIa trial in refractory cancer
patients (breast, colorectal, head and
neck, prostate, non-small cell lung) is
ongoing

Phase II trials in HER2+ breast cancer
planned for the second half of 2007

Phase II trial in an additional solid tumor
expected to follow in late 2007 or early
2008

“Currently approved agents that
target the EGFR/HER pathway have
shown limited activity in treating solid
tumors. While the reasons for this are
still emerging, this limited efﬁ cacy in
metastatic disease may relate to the
fact that existing treatments inhibit
only one or two of the HER pathways.
I believe new agents in development
that target multiple HER pathways or
target these pathways through novel
mechanisms such as inhibition of
ligand shedding and receptor cleavage
are likely to lead to superior clinical
outcomes, especially when used in
combination with current therapies.”

Allan Lipton, M.D.
Medical Oncology and Hematology
Milton S. Hershey Medical Center
Penn State University College of Medicine

JAK Inhibitors:
Compelling Approach to Treat Inﬂ ammation,
Myeloproliferative Disorders and Cancer

“Multiple activating mutations in JAK2 have recently been identiﬁ ed in
the majority of myeloproliferative disorders, including polycythemia vera,
essential thrombocythemia and primary myeloﬁ brosis. Research results
suggesting a causal role for these mutations in the pathogenesis of
myeloproliferative disorders strongly support the development of
JAK2 inhibitors as targeted drugs for these disorders - many of which
can be life threatening and for which we lack effective therapies.”

Professor in Hematology and Internal Medicine
Mayo Clinic College of Medicine, Division of Hematology in the Department of Medicine

Ayalew Tefferi, M.D.

Mechanism of Action

Potential Beneﬁ ts

Program Status

Janus-associated kinases (JAK) are
enzymes that mediate signaling of
several important drivers of inﬂ ammatory
diseases, myeloproliferative disorders
(MPDs) and malignancies. There are four
known JAK enzymes: JAK1, 2, 3 and TYK2

• Known inﬂ ammatory cytokines, such
as IL-6, IL-12, and IL-23, signal
through JAKs to promote
inﬂ ammation.

• Activating mutations of JAK2 are
present in >90% of polycythemia
vera and ~50% of essential

thrombocythemia and myeloid
metaplasia with myeloﬁ brosis.
• Aberrant activation of the JAK-STAT
pathway has been documented in a
variety of cancers.

• Convenient oral dosing - current
best-of-care therapies are injectable.
• Expected to be effective in patients
refractory to anti-TNF therapies.
• Rapid onset of action based on data

from early clinical studies.

• Potential to be ﬁ rst targeted therapy

for MPDs.

• Broad applicability in a number of
autoimmune diseases and malignant

conditions.

Multiple potent, selective, orally
bioavailable candidates currently in
preclinical development

• >100x selectivity against a broad
panel of kinases.
• 10 – 40x selectivity over the JAK3
enzyme.

GLP-safety studies successfully completed

Multiple IND applications expected to be
ﬁ led in 2007

Multiple clinical trials planned in 2007

“Recent clinical data with an oral JAK
inhibitor demonstrating dramatic
efﬁ cacy and rapid onset of action in
both rheumatoid arthritis and psoriasis
represent a signiﬁ cant development in
our approach to treat these diseases.
While the data are still early, I believe
that JAK inhibition is one of the most
exciting new therapeutic approaches for
chronic inﬂ ammatory diseases.”

Larry Moreland, M.D.
Professor of Medicine, University of Alabama
Director of the UAB Arthritis Clinical Intervention Program
Director of the UAB Pittman General Clinical Research Center

“In preclinical studies, INCB8696 has demonstrated a favorable safety
proﬁ le at doses sufﬁ cient to completely inhibit CCR2 function.
Given the critical role the CCR2 chemokine receptor is thought to play
in the formation of MS lesions, we believe our CCR2 antagonist could
provide a safe and effective approach to treating this chronic and
debilitating disease. Preclinical data also suggest that autoimmune
nephritides are additional indications for this mechanism.”

William Williams, M.D.

Vice President, Exploratory Develpment, Incyte

CCR2 Antagonists:
A Promising Target for Inﬂ ammatory Diseases

“CCR2 is a chemokine receptor that is involved in

the trafﬁ cking of inﬂ ammatory monocytes. These

monocytes are believed to play critical roles in the

pathogenesis of inﬂ ammatory diseases, including

multiple sclerosis. Based on the published preclinical

data on CCR2, an oral CCR2 antagonist may have

the potential to provide signiﬁ cant therapeutic effects

in MS, and not cause overt immunosuppression.”

Israel F. Charo, M.D., Ph.D.

Professor of Medicine, University of California, San Francisco

Mechanism of Action

CCR2 antagonists prevent blood
monocytes from entering tissue and
becoming inﬂ ammatory macrophages:

• The severity of inﬂ ammation in a
number of disease states correlates
with the number of macrophages

in tissue.

• In multiple sclerosis (MS), activated

macrophages accumulate in the lesions
and are associated with destruction of

the myelin sheath.

• In autoimmune nephritides,
macrophages are implicated in lupus

Our lead compound: INCB8696

• Selective compound with excellent
pharmacokinetic properties.
• Convenient oral dosing.

renal pathology.

Potential Beneﬁ ts

• Novel mechanism.
• Potential for efﬁ cacy with minimal

immunosuppression.

Clinical Status

• IND ﬁ led for MS with Phase I trials in
healthy volunteers planned in 2007.