Agalsidase Beta Suppliers & Bulk Manufacturers

Available Forms: Injection

Available Strengths: 35 mg

Reference Brands: Fabrazyme (USA/EU)

Category: Orphan Drugs

Agalsidase beta is a recombinant form of the human enzyme alpha-galactosidase A, used in enzyme replacement therapy for Fabry disease. It helps break down globotriaosylceramide (GL-3), a fatty substance that accumulates in the cells of patients with this inherited lysosomal storage disorder. By reducing GL-3 buildup, Agalsidase beta helps alleviate symptoms such as pain, kidney dysfunction, and cardiovascular complications associated with Fabry disease. Agalsidase beta is available in Injection and strengths such as 35 mg. Sourced from GMP-certified and ISO-compliant manufacturers, this API meets global pharmacopeia standards (USP/EP/JP as applicable). Ideal for pharmaceutical formulation and commercial manufacturing, Agalsidase beta is supplied in bulk quantities with complete regulatory support including DMF, COA, and MSDS.

Agalsidase beta can be exported to over 30 countries across Asia, Africa, Europe, and Latin America. Flexible packaging, competitive pricing, and a verified supplier network make Pharmatradz a trusted sourcing partner for pharmaceutical companies and contract manufacturers worldwide.

Product Description:

Agalsidase beta is a recombinant human alpha-galactosidase A enzyme designed for intravenous administration and approved for the treatment of Fabry disease, a rare, progressive, multisystemic, and potentially life-threatening lysosomal storage disorder. Fabry disease results from a deficiency of the alpha-galactosidase A enzyme, which leads to the accumulation of glycosphingolipids—particularly globotriaosylceramide (GL-3)—within lysosomes across various tissues. This accumulation is a key driver of the disease’s progression, affecting organs such as the kidneys, heart, and nervous system.

Agalsidase beta provides an exogenous source of alpha-galactosidase A, facilitating the breakdown of accumulated GL-3. Clinical studies have demonstrated that intravenous administration of agalsidase beta effectively clears GL-3 from target cells and prevents its reaccumulation over long-term therapy. In post-approval trials, treatment with agalsidase beta was associated with a reduced risk of major clinical events and improved patient outcomes. The therapy is generally well tolerated and represents a significant advancement in the management of Fabry disease. Agalsidase beta therapy is strongly recommended for patients with confirmed Fabry disease who are appropriate candidates for enzyme replacement therapy.