24-Week Phase 3 Study Found Investigational Drug Dapagliflozin Improved Glycosylated Hemoglobin (HbA1c) When Added to Glimepiride in Adults With Type 2 Diabetes Mellitus

STOCKHOLM, September 20, 2010 - Bristol-Myers Squibb Company (NYSE: BMY)(www.bms.com) and
AstraZeneca (NYSE: AZN)(www.astrazeneca-us.com)
today announced results from a randomized, double blind Phase 3 clinical
study, which demonstrated that the addition of the investigational drug
dapagliflozin to existing glimepiride (sulphonylurea) therapy produced
significant reductions in glycosylated hemoglobin levels (HbA1c) in adult
patients with type 2 diabetes compared to glimepiride alone. The study also
demonstrated that dapagliflozin plus glimepiride achieved reductions in the
secondary efficacy endpoints of change in total body weight, oral glucose
tolerance test (OGTT) and fasting plasma glucose (FPG) levels from baseline
at week 24 compared to placebo plus glimepiride. More people taking
dapagliflozin and glimepiride were able to achieve a target HbA1c of less
than 7% compared to patients taking glimepiride alone. Results from the study
were presented at the 46th European Association for the Study of Diabetes
(EASD) Annual Meeting.

Overall, the frequency of drug-related adverse events was reported at a
similar rate between treatment groups, although signs, symptoms and other
reports suggestive of genital tract infections, but not urinary tract
infections, were more frequently reported in dapagliflozin treated subjects.

Dapagliflozin, an investigational compound, is a first-in-class
sodium-glucose cotransporter-2 (SGLT2) inhibitor and is currently in Phase 3
trials under joint development by Bristol-Myers Squibb and AstraZeneca as a
once-daily oral therapy for the treatment of adult patients with type 2
diabetes. SGLT2 inhibitors, which act independently of insulin mechanisms,
facilitate the excretion of glucose and associated calories in the urine,
thereby lowering blood glucose levels.

"With type 2 diabetes, we often see a progressive deterioration of
glycemic control in patients, which may require treatment intensification
with additional drug therapy," said Krzysztof Strojek, Professor, Department
of Internal Diseases Diabetology & Nephrology Silesian Medical University,
Zabrze (Poland), principal investigator of the study. "This study, which adds
to the Phase 3 data available for this investigational compound, demonstrated
that dapagliflozin improved glycemic control, as measured by HbA1c, FPG and
PPG, in adult patients with type 2 diabetes when added to the commonly used
oral diabetic agent - glimepiride."

About The Study

The study was a 24-week, multicenter, international, randomized,
parallel-group, double-blind, placebo-controlled Phase 3 study, which was
designed to assess the efficacy of dapagliflozin (2.5 mg, 5 mg or 10 mg per
day) compared to placebo as add-on therapy to glimepiride (4 mg/day) in
improving glycemic control in adult patients with type 2 diabetes, as
determined by the change in HbA1c levels from baseline at week 24, and
includes a 24-week double-blind extension. The study included 597 type 2
diabetes patients (aged greater than or equal to 18 years) with inadequate
glycemic control (HbA1c greater or equal to 7.0% and less than or equal to
10% at baseline) on at least half maximal recommended dose of glimepiride
alone. Individuals were equally randomized to one of four treatment groups:
dapagliflozin 2.5 mg plus glimepiride, dapagliflozin 5 mg plus glimepiride,
dapagliflozin 10 mg plus glimepiride or placebo plus glimepiride.

The primary endpoint of the study was to assess the change from baseline
in HbA1c at 24 weeks. Key secondary endpoints included the change from
baseline in body weight, change in oral glucose tolerance test (OGTT),
proportion of patients achieving an HbA1c of less than 7% and reduction in
fasting plasma glucose (FPG) levels at week 24.

Study Results

Individuals taking dapagliflozin plus glimepiride achieved significant
dose-dependent reductions from baseline in HbA1c of -0.58%, -0.63% and -0.82%
for dapagliflozin 2.5 mg, 5 mg and 10 mg, respectively compared to -0.13% for
placebo plus glimepiride (p-value of less than 0.0001 for all three treatment
arms).

Patients treated with dapagliflozin plus glimepiride achieved greater
weight loss compared to those treated with placebo plus glimepiride: -1.18
kg, -1.56 kg, -2.26 kg for dapagliflozin 2.5 mg, 5 mg and 10 mg, respectively
compared to -0.72 kg for glimepiride plus placebo at week 24 (p-value less
than 0.01 and less than 0.0001 for dapagliflozin 5 mg and 10 mg,
respectively; p-value of dapagliflozin 2.5 mg was not statistically
significant).

Individuals treated with dapagliflozin plus glimepiride achieved
significant reductions from baseline in the OGTT of -32.0 mg/dL and -34.9
mg/dL for dapagliflozin 5 mg and 10 mg, respectively compared to -6.0 mg/dL
for placebo plus glimepiride (p-value less than 0.01 and less than 0.0001 for
dapagliflozin 5 mg and 10 mg, respectively). Dapagliflozin 2.5 mg reduced
OGTT by 37.5 mg/dL.

The study demonstrated that more patients taking dapagliflozin plus
glimepiride achieved an HbA1c level of less than 7% compared to placebo plus
glimepiride at week 24: 30.3% and 31.7% for dapagliflozin 5 mg and 10 mg,
respectively compared to 13.0% for glimepiride plus placebo (p-value less
than 0.01 and less than 0.0001 for dapagliflozin 5 mg and 10 mg,
respectively). For patients treated with dapagliflozin 2.5 mg, 26.8% achieved
HbA1c <7%.

Individuals treated with dapagliflozin 5 mg and 10 mg plus glimepiride
demonstrated significant improvements in FPG from baseline at week 24:
-21.2 mg/dL for dapagliflozin 5 mg and -28.5 mg/dL for dapagliflozin 10 mg,
compared to -2.0 mg/dL for placebo plus glimepiride (p-value less than 0.0001
for both treatment arms). Dapagliflozin 2.5 mg reduced FPG by -16.8 mg/dL.

The number of individuals experiencing adverse events after 24 weeks was
51.9%, 48.3% and 50.3% for dapagliflozin 2.5 mg, 5 mg, and 10 mg plus
glimepiride, respectively compared to 47.3% for glimepiride plus placebo. The
percentage of patients experiencing the most common adverse events for
dapagliflozin 2.5 mg, 5 mg, 10 mg and placebo when added to glimepiride,
respectively was as follows: back pain (1.9%, 2.1%, 4.6% vs. 2.7%), upper
respiratory tract infection (3.2%, 4.1%, 4.6% vs. 2.7%) and bronchitis (1.3%,
2.1%, 3.3% vs. 0.7%). Most cases of adverse events were mild to moderate.
Discontinuations due to adverse events were 3.2%, 3.4%, 2.6% for
dapagliflozin 2.5 mg, 5 mg, and 10 mg plus glimepiride vs. 2.1% for
glimepiride plus placebo.

Adverse events suggestive of urinary tract infection and genital
infection were analyzed based on predefined groupings of preferred terms for
each of these two categories. The percentage of patients with signs, symptoms
and other reports suggestive of urinary tract infection was similar across
treatment groups: 3.9%, 6.9% and 5.3% for dapagliflozin 2.5 mg, 5 mg, and 10
mg, respectively compared to 6.2% for glimepiride plus placebo. One patient
discontinued due to a urinary tract infection. Signs, symptoms and other
reports suggestive of genital infection were higher for the dapagliflozin 2.5
mg, 5 mg, and 10 mg plus glimepiride treatment groups compared to the
glimepiride plus placebo group: 3.9%, 6.2% and 6.6% vs. 0.7%, respectively.

Serious adverse events were 7.1%, 6.9% and 6.0% for dapagliflozin 2.5 mg,
5 mg, and 10 mg plus glimepiride, respectively compared to 4.8% for
glimepiride plus placebo.

The percentage of individuals with any hypoglycemic event at week 24 for
patients treated with dapagliflozin 2.5 mg, 5 mg, and 10 mg plus glimepiride
was 7.1%, 6.9% and 7.9%, respectively compared to 4.8% for those treated with
placebo plus glimepiride.

Effects upon blood pressure were examined as exploratory endpoints.
Changes in seated systolic blood pressure were -4.7 mmHg, -4.0 mmHg and -5.0
mmHg and in seated diastolic blood pressure were -1.1 mmHg, -1.7 mmHg and
-2.8 mmHg in the dapagliflozin 2.5, 5 and 10 mg treatment groups respectively
compared to changes in seated systolic blood pressure of -1.2 mmHg and seated
diastolic blood pressure -1.4 mmHg for those treated with placebo plus
glimepiride.

About Type 2 Diabetes

Type 2 diabetes (diabetes mellitus) is a chronic, progressive disease
that is characterized by dysfunction of beta cells in the pancreas, which
decreases insulin secretion and leads to elevated glucose levels. Over time,
this sustained hyperglycemia contributes to worsening insulin resistance and
further beta cell dysfunction.

Many patients with type 2 diabetes have co-morbidities such as obesity
and hypertension. Significant unmet needs exist as nearly half of treated
patients remain uncontrolled on their current glucose-lowering regimen and
even fewer are controlled across multiple parameters. In the past, treatments
for type 2 diabetes have focused primarily on insulin-dependent mechanisms.
An approach that acts independently of insulin may provide an option for
adults with type 2 diabetes in helping manage their glucose levels.

About SGLT2 Inhibition

The renal SGLT system plays a major role in overall glucose balance in
the body. Normally, the kidney filters ~180g of glucose each day, and
virtually all is reabsorbed back into circulation. Glucose reabsorbtion
occurs in the proximal tubule of the kidney via the SGLT system. Selective
inhibition of SGLT2 by an insulin independent mechanism of action facilitates
the excretion of glucose and associated calories in the urine, thereby
lowering blood glucose levels.

Bristol-Myers Squibb and AstraZeneca Collaboration

Bristol-Myers Squibb and AstraZeneca entered into a collaboration in
January 2007 to enable the companies to research, develop and commercialize
select investigational drugs for type 2 diabetes. The Bristol-Myers
Squibb/AstraZeneca Diabetes collaboration is dedicated to global patient
care, improving patient outcomes and creating a new vision for the treatment
of type 2 diabetes.

About Bristol-Myers Squibb

Bristol-Myers Squibb is a global biopharmaceutical company whose mission
is to discover, develop and deliver innovative medicines that help patients
prevail over serious diseases. For more information about Bristol-Myers
Squibb, visit www.bms.com or follow us on Twitter at
twitter.com/bmsnews.

This press release contains "forward-looking statements" as that term is
defined in the Private Securities Litigation Reform Act of 1995 regarding
product development. Such forward-looking statements are based on current
expectations and involve inherent risks and uncertainties, including factors
that could delay, divert or change any of them, and could cause actual
outcomes and results to differ materially from current expectations. No
forward-looking statement can be guaranteed. Among other risks, there can be
no guarantee that dapagliflozin will receive regulatory approval or, if
approved, that it will become a commercially successful product.
Forward-looking statements in this press release should be evaluated together
with the many uncertainties that affect Bristol-Myers Squibb's business,
particularly those identified in the cautionary factors discussion in
Bristol-Myers Squibb's Annual Report on Form 10-K for the year ended December
31, 2009, in our Quarterly Reports on Form 10-Q and our Current Reports on
Form 8-K. Bristol-Myers Squibb undertakes no obligation to publicly update
any forward-looking statement, whether as a result of new information, future
events or otherwise.

About AstraZeneca

AstraZeneca is a global, innovation-driven biopharmaceutical business
with a primary focus on the discovery, development and commercialisation of
prescription medicines. As a leader in gastrointestinal, cardiovascular,
neuroscience, respiratory and inflammation, oncology and infectious disease
medicines, AstraZeneca generated global revenues of US $32.8 billion in 2009.
For more information please visit: www.astrazeneca.com

Contacts: Media: Ken Dominski, Bristol-Myers Squibb, +1-609-252-5251, ken.dominski at bms.com; Jim Minnick, AstraZeneca, +1-302-885-5135, jim.minnick at astrazeneca.com; Investors: John Elicker, Bristol-Myers Squibb, +1-609-252-4611,
john.elicker at bms.com; Karl Hard, AstraZeneca, +44-20-7304-5322, karl.hard at astrazeneca.com; Clive Morris, AstraZeneca, +44-20-7304-5084, clive.morris at astrazeneca.com