plasmin

Plasminogen is a zymogen secreted as a precursor protein that, when cleaved by urokinase plasminogen activator (uPA) or tissue plasminogen activator (tPA), is converted into plasmin. Plasmin is a protease with broad specificity, capable of degrading fibrin and various extracellular matrix (ECM) components. Additionally, plasminogen functions as a proinflammatory regulator, promoting the healing of both acute and diabetic wounds. It is utilized in research related to wound healing, inflammation, and hypoplasminogenemia [1] [2].

Leupeptin is a competitive protease inhibitor produced by actinomycetes. Leupeptin can inhibit cysteine, serine and threonine peptidases. Leupeptin inhibits serine proteinases (trypsin (Ki=3.5 nM), plasmin (Ki= 3.4 nM), porcine kallikrein), and cysteine p

LCKLSL, an N-terminal hexapeptide, acts as a competitive inhibitor of annexin A2 (AnxA2), effectively preventing the binding of tissue plasminogen activator (tPA) to AnxA2 while also inhibiting the generation of plasmin. In addition, LCKLSL exhibits anti-angiogenic properties.

N-CBZ-Phe-Arg-AMC (Z-FR-AMC) is a substrate for serine proteases, including cathepsins, kallikrein, and plasmin. The substrate exhibits absorption emission at 330 390 nm (weak fluorescence), while the end product (AMC) shows absorption emission at 342 441 nm (strong fluorescence).

KKI 5 is a serine protease inhibitor that inhibits kallikrein and plasmin. KKI 5 may exhibit anticancer chemotherapeutic benefit and may also be used as a treatment for angioedema.

KKI-5 acetate is a serine protease inhibitor that inhibits kallikrein and plasmin. KKI 5 may exhibit anticancer chemotherapeutic benefit and may also be used as a treatment for angioedema.

LCKLSL acetate is a competitive annexin A2 (AnxA2) inhibitor. LCKLSL acetate potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2 and the generation of plasmin. LCKLSL acetate has anti-angiogenic roles.