产品
编 号：F612259
分子式：C30H57N7O8S
分子量：675.88
分子式：C30H57N7O8S
分子量：675.88
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CAS No: 533902-29-3
产品详情
生物活性：
LCKLSL is a N-terminal hexapeptide and a competitive annexin A2 (AnxA2) inhibitor. LCKLSL potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2. LCKLSL also inhibits the generation of plasmin and has anti-angiogenic roles.
体内研究：
Application of LCKLSL in two in vivo models (in chicken chorioallantoic membrane and murine Matrigel plug assays) of angiogenesis demonstrates suppression of the angiogenic responses. Treatment with the LCKLSL peptide significantly decreases the vascular length. At a dose of 5 μg/mL, the LCKLSL peptide significantly decreases the number of vascular branches, junctions and end-points.
体外研究：
In human retinal microvascular endothelial cells (RMVECs), treatment with LCKLSL (0-2 mg) inhibits the generation of plasmin and suppresses the VEGF-induced activity of tPA under hypoxic conditions.
LCKLSL is a N-terminal hexapeptide and a competitive annexin A2 (AnxA2) inhibitor. LCKLSL potently inhibits the binding of tissue plasminogen activator (tPA) to AnxA2. LCKLSL also inhibits the generation of plasmin and has anti-angiogenic roles.
体内研究：
Application of LCKLSL in two in vivo models (in chicken chorioallantoic membrane and murine Matrigel plug assays) of angiogenesis demonstrates suppression of the angiogenic responses. Treatment with the LCKLSL peptide significantly decreases the vascular length. At a dose of 5 μg/mL, the LCKLSL peptide significantly decreases the number of vascular branches, junctions and end-points.
体外研究：
In human retinal microvascular endothelial cells (RMVECs), treatment with LCKLSL (0-2 mg) inhibits the generation of plasmin and suppresses the VEGF-induced activity of tPA under hypoxic conditions.
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