Integrated Analysis Demonstrates Alpha(1)-Augmentation Therapy Significantly Reduces Loss of Lung Tissue in Patients with AAT-deficiency-related Emphysema

RESEARCH TRIANGLE PARK, North Carolina, November 15, 2010 - Talecris Biotherapeutics announced today the publication of combined data
from two studies demonstrating that augmentation therapy with Alpha(1)
-Proteinase Inhibitor (Human) (A1PI) significantly reduces lung tissue loss
in patients with emphysema related to Alpha(1)-antitrypsin (AAT) deficiency.
Results of the studies, published as an integrated analysis of the raw data
from two similar pilot trials, were published in the journal Respiratory
Research. (respiratory-research.com/content/11/1/136)

AAT deficiency is a rare, genetic disease in which low levels of the AAT
protein circulating in the lungs can increase an individual's risk of
developing emphysema. Treatment with A1PI therapy augments or increases the
levels of this protein in the lungs.

Two randomized, double-blind, placebo-controlled clinical trials
investigated the effect of A1PI therapy on emphysema progression using change
in lung density as a measure. Lung density is a validated and specific
measure of emphysema that relates well to physiological and clinical features
of the disease. Lung density has also been shown to be the best independent
predictor of mortality from emphysema.

An analysis of the data from both studies was conducted by Professor
Robert A Stockley, Birmingham, UK, and Professor Asger Dirksen, Hellerup,
Denmark. The two studies were comparable in design, treatment duration,
patient characteristics and the use of computed tomography (CT) to study lung
density. The similar characteristics of the studies allowed the pooling of
the individual patient data, which increased the robustness of the analysis.

The results of the integrated analysis demonstrated a mean change in lung
density from baseline to the final CT scan of -4.082 g/L for the AAT
treatment group and -6.379g/L for the placebo group, a statistically
significant difference of 2.297 (95% CI, 0.669 to 3.926; p = 0.006).

"The mean data demonstrate a deceleration of lung tissue loss with AAT
augmentation therapy with a high degree of statistical significance," said
Stockley. "This indicates that AAT augmentation therapy reduces decline in
lung density and may therefore reduce the future risk of mortality in
patients with AAT-deficiency-related emphysema."

The two clinical trials included in the integrated analysis were a
three-year Danish-Dutch study of 56 patients
(ajrccm.atsjournals.org/cgi/content/full/160/5/1468) and the
EXAcerbations and CT scan as Lung Endpoints (EXACTLE) trial of 77 patients
over 24 to 30 months (erj.ersjournals.com/content/33/6/1345.full). In
both trials, patients were randomized to receive infusions of A1PI or a
placebo. The results for each trial individually suggested a trend toward
reduction in emphysema progression with A1PI therapy, as measured by CT
densitometry. The trials were not powered to show efficacy; thus neither
trial reached statistical significance on its own. Pooling the data increased
the number of patients and the statistical power of the analysis.

Talecris Biotherapeutics, manufacturer of PROLASTIN(R)/PROLASTINA(R)
/PULMOLAST(R) (Alpha(1)-Proteinase Inhibitor [Human]), funded the integrated
analysis and the EXACTLE trial included in the analysis.

About PROLASTIN/PROLASTINA/PULMOLAST

Prolastin(R) Prolastina(R) Pulmolast(R)

Active ingredient: Human Alpha(1)-proteinase inhibitor. Powder and
solvent for reconstituting an infusion solution. One ml of the reconstituted
solution contains 25 mg human Alpha(1)-proteinase inhibitor. Composition: 1
bottle contains 1000 mg human Alpha(1)-proteinase inhibitor. Other
ingredients: Powder: Sodium chloride and sodium dihydrogen phosphate;
solvent: water for injection. Indications: For long-term augmentation therapy
in patients with Alpha(1)-proteinase inhibitor deficiency (genotype PiZZ,
PiZ-Null, PiNull-Null, and PiSZ) within the limits of moderate airflow
obstruction (FEV1 35-60%) and the evaluation of the clinical condition
(disability). Contraindications: Prolastin(R) must not be used in patients
with selective IgA deficiency who are known to have antibodies against IgA,
as allergic reactions to the point of anaphylactic shock may occur in such
cases and in patients known to be hypersensitive to Alpha(1)-proteinase
inhibitors or any of the excipients. Since Prolastin(R) can cause a transient
increase in blood volume, particular caution is necessary in patients with
severe heart failure and in patients at risk of circulatory overload. Use
during pregnancy and lactation: No clinical data are available on exposure to
Prolastin(R) during pregnancy. Animal studies have not been conducted.
Caution is advised if used during pregnancy. It is not known if
Alpha(1)-proteinase inhibitor is excreted into human breast milk. No animal
studies are available that investigated whether Alpha(1)-proteinase
inhibitors enter the maternal milk. When deciding whether treatment with
Prolastin(R) should be continued or stopped, the benefit of breast-feeding
for the child and the benefit of Prolastin(R) therapy for the mother should
be considered. Undesirable effects: Uncommon: Chills, fever, flu-like
symptoms, chest pain, urticaria, dizziness /drowsiness, headache, dyspnea,
rash, nausea, arthralgia; rare: hypersensitivity reactions, back pain,
tachycardia, hypotension, hypertension; very rare: anaphylactic shock.
Infectious diseases due to pathogen transmission via the administration of
drugs derived from human blood or plasma cannot be fully ruled out. Available
on prescription only. Date of information: D/2 (Sept 2007) Talecris
Biotherapeutics GmbH, 60528 Frankfurt, Germany. Prolastin(R) is licensed in
14 European countries (Austria, Belgium, Denmark, Finland, Germany, Greece,
Ireland, Italy, The Netherlands, Norway, Poland, Portugal, Spain, Sweden),
and Switzerland [Status: Feb 2010]

About Alpha(1)-Antitrypsin Deficiency

Alpha(1)-antitrypsin deficiency, also known as AAT deficiency or Alpha-1,
is an inherited disorder that causes significant reduction in the naturally
occurring protein Alpha(1)-proteinase inhibitor. It is most common in the
Caucasian population of northern Europe and North America. AAT deficiency is
also the most common cause of genetic liver disease in children, and genetic
emphysema (shortness of breath) in adults. Individuals suffering from AAT
deficiency often develop severe chronic obstructive pulmonary disease (COPD)
causing disability and premature death. AAT deficiency is estimated to affect
200,000 people in North America and Europe combined, although greater than
90% remain undiagnosed.

About Talecris Biotherapeutics: Inspiration. Dedication. Innovation.

Talecris Biotherapeutics (Nasdaq: TLCR) is a global biotherapeutic and
biotechnology company that discovers, develops and produces critical care
treatments for people with life-threatening disorders in a variety of
therapeutic areas including immunology, pulmonology, neurology and
hemostasis. (www.talecris.com)

Cautionary statement regarding forward-looking statements

This press release contains forward-looking statements within the meaning
of the safe harbor provisions of the U.S. Private Securities Litigation
Reform Act of 1995. These statements include, but are not limited to,
quotations from management in this press release, statements regarding
strategic and operation plans, and statements regarding the development or
commercialization of therapies. Forward-looking statements are based on
current beliefs and expectations and are subject to inherent risks and
uncertainties. You are cautioned not to place undue reliance on
forward-looking statements. Although Talecris believes that the
forward-looking statements contained in this press release are reasonable,
there is no assurance that expectations will be fulfilled.

The following factors, among others, could cause actual results to differ
materially from those expressed or implied in forward-looking statements:
possible U.S. legislation or regulatory action affecting, among other things,
the U.S. healthcare system, pharmaceutical pricing and reimbursement,
including Medicaid and Medicare; our ability to procure adequate quantities
of plasma and other materials which are acceptable for use in our
manufacturing processes from our own plasma collection centers or from
third-party vendors; our ability to maintain compliance with government
regulations and licenses, including those related to plasma collection,
production and marketing; our ability to identify growth opportunities for
existing products and our ability to identify and develop new product
candidates through our research and development activities; and the timing
of, and our ability to, obtain and/or maintain regulatory approvals for new
product candidates, the rate and degree of market acceptance, and the
clinical utility of our products. Additional information about factors that
could affect the business and financial results of Talecris is contained in
its final Prospectus filed pursuant to Rule 424(b)(1) with the Securities and
Exchange Commission on October 1, 2009. Talecris undertakes no duty to update
any forward-looking statement.

Becky Levine, +1-919-316-6316, or Fax: +1-919-316-6377, or becky.levine at talecris.com