Save up -80% on Agalsidase beta
|Note: this is a drug discount program, not an insurance plan.|
|RX BIN: 015558||RX PCN: HT||Group ID: DDN6600||Card Holder ID: DDN6600|
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2019 Price of Fabrazyme
|price without discount in nearest pharmacy. Price may vary.|
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Agalsidase beta volume of distribution
The mean half-life was 56-76 minutes, and the mean volume of distribution at steady state was 17%-18% of body weight, with no significant association between dose and half-life, clearance, or volume of distribution at steady state. The area under the curve was linearly proportional to the dose from 0.1 to 0.4 mg/kg. Baseline average plasma Gb3 was 9.12 +/- 2.61 nmol/mL and after 10 weeks of treatment was significantly reduced by about 50% in each group with no statistically significant differences between groups.
Discount Cards 16,000+
Clients Benefit 29%
Total savings $4,735,080
What is Agalsidase beta
Recombinant human alpha-galactosidase A. The mature protein is composed of 2 subunits of 398 residues. Protein is glycosylated and produced by CHO cells
Agalsidase beta mechanism of action
Alpha-galactosidase A catalyzes the hydrolysis of globotriaosylceramide (GL-3) and other a-galactyl-terminated neutral glycosphingolipids, such as galabiosylceramide and blood group B substances to ceramide dihexoside and galactose.
Dosage forms of Agalsidase beta
|Injection, powder, lyophilized, for solution||intravenous||5 mg/mL|
|Powder for concentrate for solution for infusion||Intravenous use||35 mg|
|Powder for concentrate for solution for infusion||Intravenous use||5 mg|
Agalsidase alfa Alpha-D- galactoside galactohydrolase
Genzyme Canada A Division Of Sanofi Aventis Canada Inc
Humans and other mammals
Indication of Agalsidase beta
For treatment of Fabry’s disease (alpha-galactosidase A deficiency)
Toxicity of Agalsidase beta
Cardiovascular and respiratory toxicity were examined in a cardiac function study in dogs with no indications of any potential safety pharmacological problems. Any further safety pharmacology studies to assess the neurological effects of r-hαGAL were not performed, the argument being that rhα-galactosidase is a protein and is unlikely to cross the blood-brain barrier. Neurological toxicity is therefore not expected.
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