Factor XIII (human)

Specification

• Cat#: THP-0069
• Product Name: Factor XIII (human)
• Description: The product is a heat-treated, lyophilized concentrate of coagulation factor XIII, an endogenous enzyme responsible for the crosslinking of fibrin and an essential component of the coagulation cascade. Also known as Fibrin Stabilizing Factor (FSF), Factor XIII is an endogenously produced coagulation factor and the final enzyme within the blood coagulation cascade. Within the body, FXIII circulates as a heterotetramer composed of 2 A-subunits and 2 B-subunits (A2B2). Other products with similar structure and function to the product include Coagulation Factor XIII A-Subunit (Recombinant), which is a recombinant form of the A subunit of human coagulation factor XIII. Compared to the product , which is purified from pooled human plasma, Coagulation Factor XIII A-Subunit (Recombinant) is produced through recombinant DNA technology where the target protein is grown in yeast and then isolated.
• Sequences: Not Available
• Species: Human
• Molecular Weight: Not Available
• Cas No: 9013-56-3
• Formula: Not Available
• Endotoxin Level: <0.001 EU per 1 μg of the protein by the LAL method
• Biological Activity: 250U

Pharmaceutical Information

• Pharmaceutical Application: Factor XIII (human)
• Applications: The product, available as the commercially available product, is approved by the Food and Drug Administration for routine prophylactic treatment and peri-operative management of surgical bleeding in adult and pediatric patients with congenital FXIII deficiency.
• Examples of Clinical Use: Surgical bleeding
• Pharmacodynamics: Not Available
• Mechanism of action: Also known as Fibrin Stabilizing Factor (FSF), Factor XIII is an endogenously produced coagulation factor and the final enzyme within the blood coagulation cascade. Within the body, FXIII circulates as a heterotetramer composed of 2 A-subunits and 2 B-subunits (A2B2). When activated by thrombin at the site of injury, the FXIII pro-enzyme is cleaved resulting in activation of the catalytic A-subunit and dissociation from its carrier B-subunit. As a result, the active transglutaminase from subunit A cross-links fibrin and other proteins resulting in increased mechanical strength and resistance to fibrinolysis of the fibrin clot. This contributes to enhanced platelet and clot adhesion to injured tissue, thereby improving blood coagulation and maintenance of hemostasis. Exogenous replacement of Factor XIII is a cornerstone of treatment for bleeding associated with congenital Factor XIII deficiency.
• Affected organisms: Not Available