Trial reportBMC clinical pharmacology2010
Pharmacokinetic comparability of Prolastin®-C to Prolastin® in alpha₁-antitrypsin deficiency: a randomized study.
Trial report in BMC clinical pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00295061 (Multi-center, Randomized, Double-blind, Crossover Trial to Evaluate the Pharmacokinetic Comparability of Alpha-1 MP to Prolastin in Subjects With Alpha1-antitrypsin Deficiency.), which is not on this map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Multi-center, Randomized, Double-blind, Crossover Trial to Evaluate the Pharmacokinetic Comparability of Alpha-1 MP to Prolastin in Subjects With Alpha1-antitrypsin Deficiency.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Treatment of lung disease in alpha-1 antitrypsin deficiency: a systematic review.International journal of chronic obstructive pulmonary disease · 2017Pooled it
- Alpha-1 Antitrypsin Deficiency and Bronchial Asthma: Current Challenges.Biomolecules · 2025Review
- Recombinant Alpha-1 Antitrypsin-Fc Fusion Protein INBRX-101 in Adults With Alpha-1 Antitrypsin Deficiency: A Phase 1 Study.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2024Article
- Alpha 1 "Hereditary Emphysema" Experience: A Patient-Physician Perspective.Pulmonary therapy · 2020Review
- Alpha-1 Antitrypsin Deficiency: a Rare Disease?Current allergy and asthma reports · 2020Review
- Alpha-1 Antitrypsin Deficiency and Accelerated Aging: A New Model for an Old Disease?Drugs & aging · 2019Review
- Article
- Alpha 1-antitrypsin deficiency in patients with chronic obstructive pulmonary disease patients: is systematic screening necessary?BMC research notes · 2019Article
- Clinical utility of alpha-1 proteinase inhibitor in the management of adult patients with severe alpha-1 antitrypsin deficiency: a review of the current literature.Drug design, development and therapy · 2017Review
- Alpha-1 proteinase inhibitors for the treatment of alpha-1 antitrypsin deficiency: safety, tolerability, and patient outcomes.Therapeutics and clinical risk management · 2015Review
- Expression and Purification of Functionally Active Recombinant Human Alpha 1-Antitrypsin in Methylotrophic Yeast Pichia pastoris.Avicenna journal of medical biotechnology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlpha1-antitrypsin (AAT) deficiency is characterized by low blood levels of alpha1-proteinase inhibitor (alpha₁-PI) and may lead to emphysema. Alpha₁-PI protects pulmonary tissue from damage caused by the action of proteolytic enzymes. Augmentation therapy with Prolastin® (Alpha₁-Proteinase Inhibitor [Human]) to increase the levels of alpha₁-PI has been used to treat individuals with AAT deficiency for over 20 years. Modifications to the Prolastin manufacturing process, incorporating additional purification and pathogen-reduction steps, have led to the development of an alpha₁-PI product, designated Prolastin®-C (Alpha₁-Proteinase inhibitor [Human]). The pharmacokinetic comparability of Prolastin-C to Prolastin was assessed in subjects with AAT deficiency.
methodsIn total, 24 subjects were randomized to receive 60 mg/kg of functionally active Prolastin-C or Prolastin by weekly intravenous infusion for 8 weeks before crossover to the alternate treatment for another 8 weeks. Pharmacokinetic plasma samples were drawn over 7 days following last dose in the first treatment period and over 10 days following the last dose in the second period. The primary end point for pharmacokinetic comparability was area under the plasma concentration versus time curve over 7 days post dose (AUC₀₋₇ (days)) of alpha₁-PI determined by potency (functional activity) assay. The crossover phase was followed by an 8-week open-label treatment phase with Prolastin-C only.
resultsMean AUC₀₋₇ (days) was 155.9 versus 152.4 mg*h/mL for Prolastin-C and Prolastin, respectively. The geometric least squares mean ratio of AUC₀₋₇ (days) for Prolastin-C versus Prolastin had a point estimate of 1.03 and a 90% confidence interval of 0.97-1.09, demonstrating pharmacokinetic equivalence between the 2 products. Adverse events were similar for both treatments and occurred at a rate of 0.117 and 0.078 per infusion for Prolastin-C (double-blind treatment phase only) and Prolastin, respectively (p = 0.744). There were no treatment-emergent viral infections in any subject for human immunodeficiency virus, hepatitis B or C, or parvovirus B19 during the course of the study.
conclusionProlastin-C demonstrated pharmacokinetic equivalence and a comparable safety profile to Prolastin.
trial registrationClinicalTrials.gov Identifier: NCT00295061.
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