Generic Name: alpha-1-proteinase inhibitor human
Dosage Form: injection
Medically reviewed on Sep 3, 2018
Alpha1-Proteinase Inhibitor (Human), Zemaira®, is a sterile, stable, lyophilized preparation of highly purified human alpha1-proteinase inhibitor (A1-PI), also known as alpha1-antitrypsin, derived from human plasma. Zemaira® is manufactured from large pools of human plasma by cold ethanol fractionation according to a modified Cohn process followed by additional purification steps.
Zemaira® is supplied as a sterile, white, lyophilized powder to be administered by the intravenous route. The specific activity of Zemaira® is ≥0.7 mg of functional A1-PI per milligram of total protein. The purity is ≥90% A1-PI. Following reconstitution with 20 mL of Sterile Water for Injection, USP, each vial contains approximately 1000 mg of functionally active A1-PI, 81 mM sodium, 38 mM chloride, 17 mM phosphate, and 144 mM mannitol. Hydrochloric acid and/or sodium hydroxide may have been added to adjust the pH. Zemaira® contains no preservatives.
Each vial of Zemaira® contains the labeled amount of functionally active A1-PI in milligrams as stated on the vial label as determined by its capacity to neutralize human neutrophil elastase.
All Source Plasma used in the manufacture of this product was tested by FDA-licensed Nucleic Acid Tests (NAT) for HCV and HIV-1 and found to be nonreactive (negative).
An investigational NAT for HBV was also performed on all Source Plasma used in the manufacture of this product and found to be nonreactive (negative). The aim of the HBV test is to detect low levels of viral material, however, the significance of a nonreactive (negative) result has not been established.
Two viral reduction steps are employed in the manufacture of Zemaira®: pasteurization at 60°C for 10 hours in an aqueous solution with stabilizers and nanofiltration. These viral reduction steps have been validated in a series of in vitro experiments for their capacity to inactivate/remove a wide range of viruses of diverse physicochemical characteristics including: Human Immunodeficiency Virus (HIV), West Nile Virus (WNV), Hepatitis A Virus (HAV), Parvovirus B19, and the following model viruses: Bovine Viral Diarrhea Virus (BVDV) as a model virus for HCV, Pseudorabies Virus (PRV) as a non-specific model virus for large DNA viruses, e.g. herpes, and Canine Parvovirus (CPV) as a model virus for Parvovirus B19. Total log10 reductions range from ≥ 6.4 to ≥ 16.7 log10 as shown in Table 1.
|Cumulative Reduction Factor [log10]|
|N.A.: Not applicable|
|HIV-1||≥ 6.8||≥ 5.5||≥ 12.3|
|WNV||≥ 8.3||≥ 8.4||≥ 16.7|
|BVDV||≥ 5.2||≥ 5.4||≥ 10.6|
|PRV||4.4||≥ 6.3||≥ 10.7|
|HAV||≥ 5.4||≥ 5.3||≥ 10.7|
|CPV||N.A.||≥ 6.4||≥ 6.4|
Zemaira - Clinical Pharmacology
Alpha1-proteinase inhibitor (A1-PI) deficiency is a chronic, hereditary, autosomal, co-dominant disorder that is usually fatal in its severe form. Low blood levels of A1-PI (i.e., below 11 µM) are most commonly associated with progressive, severe emphysema that becomes clinically apparent by the third to fourth decade of life. In addition, PiSZ individuals, whose serum A1-PI levels range from approximately 9 to 23 µM are considered to have moderately increased risk for developing emphysema, regardless of whether their serum A1-PI levels are above or below 11 µM.1 Not all individuals with severe genetic variants of A1-PI deficiency have emphysema. Augmentation therapy with Alpha1-Proteinase Inhibitor (Human) is indicated only in patients with severe congenital A1-PI deficiency who have clinically evident emphysema. A recent registry study showed 54% of A1-PI deficient subjects had emphysema.2 Another registry study showed 72% of A1-PI deficient subjects had pulmonary symptoms.3 Smoking is an important risk factor for the development of emphysema in patients with A1-PI deficiency.
Approximately 100 genetic variants of A1-PI deficiency can be identified electrophoretically, only some of which are associated with the clinical disease.4,5 Ninety-five percent of A1-PI deficient individuals are of the severe PiZZ phenotype. Up to 39% of A1-PI deficient patients may have an asthmatic component to their lung disease, as evidenced by symptoms and/or bronchial hyperreactivity.2 Pulmonary infections, including pneumonia and acute bronchitis, are common in A1-PI deficient patients and contribute significantly to the morbidity of the disease.
Augmenting the levels of functional protease inhibitor by intravenous infusion is an approach to therapy for patients with A1-PI deficiency. However, the efficacy of augmentation therapy in affecting the progression of emphysema has not been demonstrated in randomized, controlled clinical trials. The intended theoretical goal is to provide protection to the lower respiratory tract by correcting the imbalance between neutrophil elastase and protease inhibitors. Whether augmentation therapy with Zemaira® or any A1-PI product actually protects the lower respiratory tract from progressive emphysematous changes has not been evaluated. Individuals with endogenous levels of A1-PI below 11 µM, in general, manifest a significantly increased risk for development of emphysema above the general population background risk.5,6,7,8 Although the maintenance of blood serum levels of A1-PI (antigenically measured) above 11 µM has been historically postulated to provide therapeutically relevant anti-neutrophil elastase protection9, this has not been proven. Individuals with severe A1-PI deficiency have been shown to have increased neutrophil and neutrophil elastase concentrations in lung epithelial lining fluid compared to normal PiMM individuals, and some PiSZ individuals with A1-PI above 11 µM have emphysema attributed to A1-PI deficiency.1 These observations underscore the uncertainty regarding the appropriate therapeutic target serum level of A1-PI during augmentation therapy.
Mechanism of Action
Pulmonary disease, particularly emphysema, is the most frequent manifestation of A1-PI deficiency.5 The pathogenesis of emphysema is understood to evolve as described in the "protease-antiprotease imbalance" model. A1-PI is now understood to be the primary antiprotease in the lower respiratory tract, where it inhibits neutrophil elastase (NE).10 Normal healthy individuals produce sufficient A1-PI to control the NE produced by activated neutrophils and are thus able to prevent inappropriate proteolysis of lung tissue by NE. Conditions that increase neutrophil accumulation and activation in the lung, such as respiratory infection and smoking, will in turn increase levels of NE. However, individuals who are severely deficient in endogenous A1-PI are unable to maintain an appropriate antiprotease defense and are thereby subject to more rapid proteolysis of the alveolar walls leading to chronic lung disease. Zemaira® serves as A1-PI augmentation therapy in this patient population, acting to increase and maintain serum levels and lung epithelial lining fluid (ELF) levels of A1-PI.
In 18 subjects treated with a single dose (60 mg/kg) of Zemaira®, the mean area under the curve (AUC) and standard deviation (SD) were 144 µM × day (SD 27), maximum serum concentration was 44.1 µM (SD 10.8), clearance was 603 mL per day (SD 129), and terminal half-life was 5.1 days (SD 2.4).
Weekly repeated infusions of A1-PI at a dose of 60 mg/kg lead to serum A1-PI levels above the historical target threshold of 11 µM.
The clinical benefit of the increased blood levels of A1-PI at the recommended dose for any A1-PI product has not been established.
Clinical studies were conducted with Zemaira® in 89 subjects (59 males and 30 females). The subjects ranged in age from 29 to 68 years (median age 49 years). Ninety-seven percent of the treated subjects had the PiZZ phenotype of A1-PI deficiency, and 3% had the MMALTON phenotype. At screening, serum A1-PI levels were between 3.2 and 10.1 µM (mean of 5.6 µM). The objectives of the clinical studies were to demonstrate that Zemaira® augments and maintains serum levels of A1-PI above 11 µM and increases A1-PI levels in ELF of the lower lung.
In a double-blind, controlled clinical study to evaluate the safety and efficacy of Zemaira®, 44 subjects were randomized to receive 60 mg/kg of either Zemaira® or Prolastin® (a commercially available Alpha1-Proteinase Inhibitor [Human] product) once weekly for 10 weeks. After 10 weeks, all subjects received Zemaira® for an additional 14 weeks. All subjects were followed for a total of 24 weeks to complete the safety evaluation. The mean trough serum A1-PI levels at steady state (Weeks 7-11) in the Zemaira®-treated subjects were statistically equivalent to those in the Prolastin®-treated subjects. Both groups were maintained above 11 µM (80 mg/dL). The mean (range and standard deviation) of the steady state trough serum antigenic A1-PI level for Zemaira®-treated subjects was 17.7 µM (range 13.9 to 23.2, SD 2.5) and for Prolastin®-treated subjects was 19.1 µM (range 14.7 to 23.1, SD 2.2). The difference between the Zemaira® and the Prolastin® groups was not considered clinically significant and may be related to the higher specific activity of Zemaira®.
In a subgroup of subjects enrolled in the study (10 Zemaira®-treated subjects and 5 Prolastin®-treated subjects), bronchoalveolar lavage was performed at baseline and at Week 11. Four A1-PI related analytes in ELF were measured: antigenic A1-PI, A1-PI:NE complexes, free NE, and functional A1-PI (anti-neutrophil elastase capacity, ANEC). A blinded retrospective analysis, which revised the prospectively established acceptance criteria showed that within each treatment group, ELF levels of antigenic A1-PI and A1-PI:NE complexes increased from baseline to Week 11. Free elastase was immeasurably low in all samples. The post-treatment ANEC values in ELF were not significantly different between the Zemaira®-treated and Prolastin®-treated subjects (mean 1725 nM vs. 1418 nM). No conclusions can be drawn about changes of ANEC values in ELF during the study period as baseline values in the Zemaira®-treated subjects were unexpectedly high. No A1-PI analytes showed any clinically significant differences between the Zemaira® and Prolastin® treatment groups.
|Analyte||Treatment||Mean change from baseline||90% CI|
|A1-PI (nM)||Zemaira®||1358.3||822.6 to 1894.0|
|Prolastin®||949.9||460.0 to 1439.7|
|ANEC (nM)||Zemaira®||-588.1||-2032.3 to 856.1|
|Prolastin®||497.5||-392.3 to 1387.2|
|A1-PI:NE Complexes (nM)||Zemaira®||118.0||39.9 to 196.1|
|Prolastin®||287.1||49.8 to 524.5|
The clinical efficacy of Zemaira® or any A1-PI product in influencing the course of pulmonary emphysema or pulmonary exacerbations has not been demonstrated in adequately powered, randomized, controlled clinical trials.
Subjects were also monitored for the presence of antibodies to HIV and markers for viral hepatitis (HAV, HBV, and HCV). Subjects who were negative for Hepatitis B surface antigen (HBsAg) at screening were vaccinated against Hepatitis B. Zemaira®-treated subjects were tested six months after the end of treatment for HAV, HBV, HCV, HIV, and Parvovirus B19, and no evidence of viral transmission was observed. No subjects developed detectable antibodies to Zemaira®.
Indications and Usage for Zemaira
Zemaira® is indicated for chronic augmentation and maintenance therapy in individuals with alpha1-proteinase inhibitor (A1-PI) deficiency and clinical evidence of emphysema.
Zemaira® increases antigenic and functional (ANEC) serum levels and lung epithelial lining fluid levels of A1-PI.
Clinical data demonstrating the long-term effects of chronic augmentation therapy of individuals with Zemaira® are not available.
Safety and effectiveness in pediatric patients have not been established.
The effect of augmentation therapy with Zemaira® or any A1-PI product on pulmonary exacerbations and on the progression of emphysema in A1-PI deficiency has not been demonstrated in randomized, controlled clinical trials. Zemaira® is not indicated as therapy for lung disease patients in whom severe A1-PI deficiency has not been established.
Zemaira® is contraindicated in individuals with a known hypersensitivity to any of its components. Zemaira® is also contraindicated in individuals with a history of anaphylaxis or severe systemic response to A1-PI products.
Zemaira® is contraindicated in IgA deficient patients with antibodies against IgA, due to the risk of severe hypersensitivity.
Zemaira® may contain trace amounts of IgA. Patients with known antibodies to IgA, which can be present in patients with selective or severe IgA deficiency, have a greater risk of developing potentially severe hypersensitivity and anaphylactic reactions. Zemaira® is contraindicated in patients with antibodies against IgA due to risk of severe hypersensitivity.
Zemaira® is made from human plasma. Products made from human plasma may contain infectious agents, such as viruses, that can cause disease. Because Zemaira® is made from human blood, it may carry a risk of transmitting infectious agents, e.g., viruses, and theoretically the Creutzfeldt-Jakob disease (CJD) agent. The risk that such products will transmit an infectious agent has been reduced by screening plasma donors for prior exposure to certain viruses, by testing for the presence of certain current virus infections, and by inactivating and/or removing certain viruses during manufacture. (See DESCRIPTION section for viral reduction measures.) The manufacturing procedure for Zemaira® includes processing steps designed to reduce further the risk of viral transmission. Stringent procedures utilized at plasma collection centers, plasma testing laboratories, and fractionation facilities are designed to reduce the risk of viral transmission. The primary viral reduction steps of the Zemaira® manufacturing process are pasteurization (60°C for 10 hours) and nanofiltration. Additional purification procedures used in the manufacture of Zemaira® also potentially provide viral reduction. Despite these measures, such products may still potentially contain human pathogenic agents, including those not yet known or identified. Thus, the risk of transmission of infectious agents can not be totally eliminated. Any infections thought by a physician possibly to have been transmitted by this product should be reported by the physician or other healthcare provider to CSL Behring at 1-866-915-6958. The physician should discuss the risks and benefits of this product with the patient.
Individuals who receive infusions of blood or plasma products may develop signs and/or symptoms of some viral infections (see Information For Patients).
During clinical studies, no cases of hepatitis A, B, C, or HIV viral infections were reported with the use of Zemaira®.
Infusion rates and the patient's clinical state should be monitored closely during infusion. The patient should be observed for signs of infusion-related reactions.
As with any colloid solution, there may be an increase in plasma volume following intravenous administration of Zemaira®. Use caution in patients at risk for circulatory overload.
Information For Patients
Patients should be informed of the early signs of hypersensitivity reactions including hives, generalized urticaria, tightness of the chest, dyspnea, wheezing, faintness, hypotension, and anaphylaxis. Patients should be advised to discontinue use of the product and contact their physician and/or seek immediate emergency care, depending on the severity of the reaction, if these symptoms occur.
As with all plasma-derived products, some viruses, such as parvovirus B19, are particularly difficult to remove or inactivate at this time. Parvovirus B19 may most seriously affect pregnant women and immune-compromised individuals. Symptoms of parvovirus B19 include fever, drowsiness, chills, and runny nose followed two weeks later by a rash and joint pain. Patients should be encouraged to consult their physician if such symptoms occur.
Inform patients that administration of Zemaira® has been demonstrated to raise the plasma level of A1-PI, but that the effect of this augmentation on the frequency of pulmonary exacerbations and on the rate of progression of emphysema has not been established by clinical trials.
Pregnancy Category C
Animal reproduction studies have not been conducted with Zemaira®. It is also not known whether Zemaira® can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Zemaira® should be given to a pregnant woman only if clearly needed.
It is not known whether Zemaira® is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Zemaira® is administered to a nursing woman.
Safety and effectiveness in the pediatric population have not been established.
Clinical studies of Zemaira® did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects. As for all patients, dosing for geriatric patients should be appropriate to their overall situation.
In clinical studies, the following adverse reactions considered treatment-related by the investigator were reported following intravenous administration of Zemaira®, 60 mg/kg weekly: asthenia, injection site pain, dizziness, headache, paresthesia, and pruritus. Each of these related adverse events was observed in 1 of 89 subjects (1%). The adverse reactions were mild.
Should evidence of an acute hypersensitivity reaction be observed, the infusion should be stopped promptly and appropriate countermeasures and supportive therapy should be administered.
Table 3 summarizes the adverse event data obtained with single and multiple doses during clinical trials with Zemaira® and Prolastin®. No clinically significant differences were detected between the two treatment groups.
|No. of subjects treated||89||32|
|No. of subjects with adverse events regardless of causality (%)||69 (78%)||20 (63%)|
|No. of subjects with related adverse events (%)||5 (6%)||4 (13%)|
|No. of subjects with related serious adverse events||0||0|
|No. of infusions||1296||160|
|No. of adverse events regardless of causality (rates per infusion)||298 (0.230)||83 (0.519)|
|No. of related adverse events
(rates per infusion)
|6 (0.005)||5 (0.031)|
The frequencies of adverse events per infusion that were ≥0.4% in Zemaira®-treated subjects, regardless of causality, were: headache (33 events per 1296 infusions, 2.5%), upper respiratory infection (1.6%), sinusitis (1.5%), injection site hemorrhage (0.9%), sore throat (0.9%), bronchitis (0.8%), asthenia (0.6%), fever (0.6%), pain (0.5%), rhinitis (0.5%), bronchospasm (0.5%), chest pain (0.5%), increased cough (0.4%), rash (0.4%), and infection (0.4%).
The following adverse events, regardless of causality, occurred at a rate of 0.2% to <0.4% per infusion: abdominal pain, diarrhea, dizziness, ecchymosis, myalgia, pruritus, vasodilation, accidental injury, back pain, dyspepsia, dyspnea, hemorrhage, injection site reaction, lung disorder, migraine, nausea, and paresthesia.
Diffuse interstitial lung disease was noted on a routine chest x-ray of one subject at Week 24. Causality could not be determined.
In a retrospective analysis, during the 10-week blinded portion of the 24-week clinical study, 6 subjects (20%) of the 30 treated with Zemaira® had a total of 7 exacerbations of their chronic obstructive pulmonary disease (COPD). Nine subjects (64%) of the 14 treated with Prolastin® had a total of 11 exacerbations of their COPD. The observed difference between groups was 44% (95% confidence interval from 8% to 70%). Over the entire 24-week treatment period, of the 30 subjects in the Zemaira® treatment group, 7 subjects (23%) had a total of 11 exacerbations of their COPD.
Zemaira Dosage and Administration
Each vial of Zemaira® contains the labeled amount of functionally active A1-PI in milligrams as stated on the vial label as determined by capacity to neutralize human neutrophil elastase. The recommended dose of Zemaira® is 60 mg/kg body weight administered once weekly. Dose ranging studies using efficacy endpoints have not been performed with any A1-PI product.
When reconstituted as directed, Zemaira® may be administered intravenously at a rate of approximately 0.08 mL/kg/min as determined by the response and comfort of the patient. The recommended dosage of 60 mg/kg body weight will take approximately 15 minutes to infuse.
Each product package contains one Zemaira® single use vial, one 20 mL vial of Sterile Water for Injection, USP (diluent) and one color-coded vented transfer device with air inlet filter. Administer within three hours after reconstitution.
- Bring both product (green cap) vial and diluent (white cap) vial to room temperature prior to reconstitution.
- Remove the plastic flip-top caps from the vials. Aseptically cleanse the rubber stoppers with antiseptic solution and allow them to dry.
|NOTE:||The transfer device (Fig. 1) provided in the package is comprised of a white (diluent) end, which has a double orifice, and a green (product) end, which has a single orifice. Incorrect use of the transfer device will result in loss of vacuum and prevent transfer of the diluent, thereby preventing reconstitution of the product.
|The transfer device is sterile. Do not touch the exposed ends of the spike after removing the protective covers.|
- Remove the protective cover from the white (diluent) end of the transfer device. Insert the white end of the transfer device into the center of the stopper of the upright diluent vial first. (Fig. 2)
- Remove the protective cover from the green (product) end of the transfer device. Invert the diluent vial with the attached transfer device and, using minimum force, insert the green end of the transfer device into the center of the rubber stopper of the upright Zemaira® vial (green top). (Fig. 3) The flange of the transfer device should rest on the surface of the stopper so that the diluent flows into the Zemaira® vial.
- Allow the vacuum in the Zemaira® vial to pull the diluent into the Zemaira® vial.
- During diluent transfer, wet the lyophilized cake completely by gently tilting the Zemaira® vial. (Fig. 4) Do not allow the air inlet filter to face downward. Care should be taken not to lose the vacuum, as this will prolong reconstitution of the product.
- After diluent transfer is complete, the transfer device will allow filtered air into the Zemaira® vial through the air filter. Additional venting of the product vial after diluent transfer is complete is not required. When diluent transfer is complete, withdraw the transfer device and diluent vial and properly discard in accordance with biohazard procedures.
- Gently swirl the Zemaira® vial until the powder is completely dissolved. (Fig. 5) DO NOT SHAKE.
- Inspect parenteral drug products visually for particulate matter and discoloration prior to administration. Administer at room temperature within three hours after reconstitution.
Pooling Reconstituted Vials
If more than one vial of Zemaira® is needed to achieve the required dose, use an aseptic technique to transfer the reconstituted solution from the vials into the administration container (e.g., empty I.V. bag or glass bottle).
Parenteral drug preparations should be inspected visually for particulate matter and discoloration prior to administration. Administer at room temperature within three hours after reconstitution.
Filter the reconstituted solution during administration. To ensure proper filtration of Zemaira®, use an I.V. administration set with a suitable 5 micron infusion filter (not supplied). Follow the appropriate procedure for I.V. administration.
After administration, any unused solution and administration equipment should be discarded in accordance with biohazard procedures.
How is Zemaira Supplied
Zemaira® is supplied in a single use vial containing the labeled amount of functionally active A1-PI, as stated on the label. Each carton contains one single use vial of Zemaira®, one 20 mL vial of Sterile Water for Injection, USP (diluent) and one vented transfer device.
Each product package consists of the following:
|0053-7201-02||Carton (kit) containing one vial of Zemaira® [NDC 0053-7211-01], one 20 mL vial of Sterile Water for Injection, USP (diluent) [NDC 0053-7653-20] and one vented transfer device.|
When stored up to 25°C (77°F), Zemaira® is stable for the period indicated by the expiration date on its label. Avoid freezing which may damage container for the diluent.
- Turino GM, Barker AF, Brantly ML, et al: Clinical Features of Individuals with PI*SZ Phenotype of α1-Antitrypsin Deficiency. Am J Respir Crit Care Med 154:1718-1725, 1996.
- Stoller JK, Brantly M, et al. Formation and current results of a patient-organized registry for α1-antitrypsin deficiency. Chest 118(3):843-848, 2000.
- McElvaney NG, Stoller JK, et al. Baseline Characteristics of Enrollees in the National Heart, Lung, and Blood Institute Registry of α1-Antitrypsin Deficiency. Chest 111:394-403, 1997.
- Crystal RG. α1-Antitrypsin Deficiency, Emphysema, and Liver Disease; Genetic Basis and Strategies for Therapy. J Clin Invest 85:1343-1352, 1990.
- World Health Organization. Alpha-1-Antitrypsin Deficiency; Report of a WHO Meeting. Geneva. 18-20 March 1996.
- Eriksson S. Pulmonary Emphysema and Alpha1-Antitrypsin Deficiency. ACTA Med Scand 175(2):197-205, 1964.
- Eriksson S. Studies in α1-antitrypsin deficiency. ACTA Med Scan Suppl. 432:1-85, 1965.
- Gadek JE, Crystal RG. α1-Antitrypsin Deficiency. In: The Metabolic Basis of Inherited Disease 5th ed. Stanbury JB, Wyngaarden JB, Frederickson DS, et al., eds: New York, McGraw-Hill. 1983; pp. 1450-1467.
- American Thoracic Society. Guidelines for the Approach to the Patient with Severe Hereditary Alpha-1-Antitrypsin Deficiency. Am Rev Respir Dis 140:1494-1497, 1989.
- Gadek JE, Fells GA, Zimmerman RL, Rennard SI, Crystal RG. Antielastases of the Human Alveolar Structures; Implications for the Protease-Antiprotease Theory of Emphysema. J Clin Invest 68:889-898, 1981.
Prolastin® is a registered trademark of Talecris Biotherapeutics, Inc.
CSL Behring LLC
Kankakee, IL 60901 USA
US License No. 1767
Revised: August, 2010
PRINCIPAL DISPLAY PANEL - Vial Label
Store up to 25°C (77°F).
I.V. use only
CSL Behring LLC
Kankakee, IL 60901 USA
US License No. 1767
PRINCIPAL DISPLAY PANEL - Carton
One single dose vial
For Intravenous Administration Only.
This package contains one vial of Zemaira®, one vial of Sterile Water for Injection, USP and
one vented transfer device for reconstitution.
Storage: Zemaira® stored up to 25°C (77°F) is stable for the period indicated by the
expiration date on the label. Avoid freezing.
CSL Behring LLC
Kankakee, IL 60901 USA
US License No. 1767
alpha-1-proteinase inhibitor human kit
|Labeler - CSL Behring LLC (931896963)|
|CSL Behring LLC||931896963||MANUFACTURE|
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