Alpha-2 Antiplasmin Deficient Plasma

Affinity’s Alpha-2 Antiplasmin Deficient Plasma is manufactured from pooled normal human plasma depleted of Alpha-2 Antiplasmin using antibodies directed to A2AP. Only the highest quality citrated plasma is used as starting material. Our Frozen Deficient or Depleted Plasma products are typically buffered with the addition of HEPES to 20mM final concentration and our Lyophilized Deficient Plasma products are typically buffered with the addition of HEPES to 50mM final concentration.

All Alpha-2 Antiplasmin Deficient or Depleted Plasma from Affinity Biologicals are for Research Use Only and must not be used for diagnostic applications.

Factoro XIII Deficient Plasma - Frozen and Lyophilized

Alpha-2-Antiplasmin Deficient – Depleted Plasma

Alpha-2-Antiplasmin Deficient – Depleted Plasma is manufactured from normal citrated human plasma that has been depleted of Alpha-2-Antiplasmin by selective affinity immuno-adsorption using antibodies directed towards A2AP. Available in two different formats – Frozen and Lyophilized

Only the highest quality citrated plasma is used as starting material and in many cases the parent plasma is available as control material. Our Alpha-2-Antiplasmin Deficient – Depleted Plasma can be used for further manufacturing or research use only applications

Frozen A2AP Deficient Plasma

Product Code: A2AP-DP

Presentation: Frozen Alpha-2-Antiplasmin Deficient – Depleted Plasma

Preparation/Handling: Thaw 1 ml vials in 37^oC water bath for 5 minutes; for bulk volumes, thawing time will be dependent on bottle size.

Storage and Stability: Plasma is shipped frozen and should be stored below -60^oC. Product is stable until date stated on vial label when stored at -60^oC. Once thawed, plasma is stable for 4 hours at 2-8^oC in original vial.

Certificate of Analysis: available upon request

Lyophilized A2AP Deficient Plasma

Product Code: A2AP-LDP

Presentation: Freeze Dried Alpha-2-Antiplasmin Deficient – Depleted Plasma containing 50 mM HEPES and stabalizers.

Reconstitution: Reconstitute with 1 mL of reagent grade water. Allow contents to dissolve for 15 minutes at room temperature with occasional swirling. Stability after reconstitution is 4 hours at ambient (18-25^oC), or 30 days at –20^oC.

Storage and Stability: Prior to reconstitution, dried plasma should be stored at 2-8°C. Product is stable until date stated on vial label when stored at 2-8^oC. Stability after reconstitution is 4 hours at ambient (18-25^oC), or 30 days at –20^oC.

Certificate of Analysis: available upon request

Description of Alpha 2-Antiplasmin

Alpha 2-Antiplasmin (A2AP), also known as Alpha 2-Plasmin Inhibitor (A2PI), is a member of the SERPIN family of proteinase inhibitors and the primary inhibitor of the enzyme plasmin in blood. It is produced in the liver and circulates in plasma at ~70 μg/ml (~1 μM). α₂AP is a single chain molecule with a mass of 67 kDa as determined by SDS-PAGE. The primary target enzyme for A2AP is plasmin, but A2AP also acts as secondary or “backup” inhibitor of activated FXI, activated Protein C and trypsin. Inhibition of these enzymes by A2AP occurs through proteolytic cleavage after Arg₃₆₄ with subsequent rapid formation of a stable, inactive 1:1 enzyme-α₂AP complex. A2AP also acts to regulate fibrinolysis by binding to the lysine binding sites on plasminogen thus competitively inhibiting plasminogen binding to fibrin. About 30% of A2AP present in plasma is partially degraded and lacks a peptide in the carboxyl region that contains the plasminogen-binding site. This form of A2AP (~65 kDa) has a reduced rate of plasmin inhibition and has been referred to as the “slow form” of A2AP. During fibrin formation, a portion of circulating A2AP is cross-linked to the α-chain of fibrin by activated factor XIII, and this linking of plasmin inhibitor to the plasmin substrate provides an additional measure of protection to the fibrin clot from proteolysis by plasmin^1-4.

References and Reviews

Aoki N, Suni Y, Miura O, Hirosawa S; Human α₂Plasmin Inhibitor; Methods in Enzymology, 223, pp 185-197, 1993.
Shieh BH, Travis J; The Reactive Site of Human α2-Plasmin Inhibitor ; JBC 262, pp 6055-6059, 1987.
Moroi M, Aoki N; Isolation and Characterization of α₂-Plasmin Inhibitor from Human Plasma; JBC 251, pp 5956-5965, 1976.
Harpel PC; Blood Proteolytic Enzyme Inhibitors: Their Role in Modulating Blood Coagulation and Fibrinolytic Enzyme Pathways; in Hemostasis and Thrombosis, eds. RW Colman, J Hirsh, VJ Marder and EW Salzman, pp. 738-747, J.B. Lippincott Co., Philadelphia PA, USA, 1982.

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