Purification and characterization of Cc-Lec, C-type lactose-binding lectin: A platelet aggregation and blood-clotting inhibitor from Cerastes cerastes venom

Purification and Characterization of a Novel Antiplatelet Peptide from Deinagkistrodon acutus Venom

“…Rhodocetin from Calloselasma rhodostoma [ 14 , 15 ] and Flavocetin-A from Trimeresurus flavoviridis [ 16 , 17 ] inhibited platelet aggregation by targeting α2β1 integrin, while kistomin from C. rhodostoma inhibited CVX (specific for GPVI)-induced platelet aggregation at a dose of 1.2 µM [ 18 ]. Furthermore, Cc-Lec (34,271.59 Da) from Cerastescerastes inhibited platelet aggregation induced by ADP, arachidonic acid, or fibrinogen at a minimal dose of 10 µM [ 19 ].…”

State-of-the-art review - A review on snake venom-derived antithrombotics: Potential therapeutics for COVID-19-associated thrombosis?

“…It has been observed that the anticoagulant action of many venom toxins is through targeting factor Xa and/or thrombin, the key components of the blood coagulation cascade. The tenase complex consisting of tissue factor, factor VIIa, and Ca 2+ (extrinsic pathway), or factor IXa and factor VIIa (intrinsic pathways) converts the inactivated factor X to Xa [102] , and several venom toxins primarily from the PLA 2 (Daboxin P), snaclec (Cc-Lec), protease (Atrase B, VaaSPH-1), and three-finger toxin (Exactin, Ringhalexin) families attenuate this activation [103] , [104] , [105] , [106] , [107] , [108] . As a result, the coagulation cascade is stalled, and the formation of the prothrombinase complex is abrogated, resulting in blood anticoagulation.…”

“…Similarly, the prothrombinase complex that comprises the serine protease, factor Xa, a cofactor Va, and Ca 2+ converts the inactive zymogen prothrombin (factor II) to thrombin (factor IIa) [109] . This first committed step is very critical in the blood coagulation cascade for thrombus formation, and venom proteins from PLA 2 (Cc1-PLA 2 , Cc2-PLA 2 , Daboxin P, Nk-PLA 2 α, RVVA-PLA 2 -I), Kunitz-type serine protease inhibitors (KSPI; Rusvikunin II), and snaclec (ACF isoforms, Cc-Lec, RVsnaclec) families, and a few peptides (ACH-11, Ruviprase) inhibit the catalytic activation of prothrombin [94] , [103] , [104] , [110] , [111] , [112] , [113] , [114] , [115] , [116] , [117] . Consequently, thrombin, which catalyzes fibrin clot formation from fibrinogen, is hindered, resulting in inhibition of thrombus formation.…”

Antiplatelet and anticoagulant activities of two phospholipase A2s purified from Cerastes cerastes venom: Structure‐function relationship

“…cerastes ‐5′Nucleotidase), and Cc‐Lec ( C. cerastes ‐Lectin) . However, only two previous studies have reported the characterization of two PLA 2 s in this venom, acting as potential blockers of platelet aggregation, and/or blood clotting called Cc 1 ‐PLA 2 and Cc 2 ‐PLA 2 .…”