KRDS

KRDS inhibits the binding of the monoclonal antibody P₂ targeting GP IIb-IIIa to isolated bone marrow megakaryocytes stimulated with 15-20 μM ADP, with mature megakaryocytes (affected proportion 29%) showing higher responsiveness than incompletely matured megakaryocytes (affected proportion 10.9%), whereas lower concentrations of ADP do not trigger this inhibition^[1].

KRDS (450-900 μM; 20-30 min) inhibits the binding of the monoclonal antibodies AP₂ and P₂, which target GP IIb-IIIa, to washed platelets stimulated with 5 μM ADP (the inhibitory effect on P₂ is stronger than on AP₂); at a concentration of 900 μM, it reduces the binding rate of radiolabeled AP₂ by 30%, but has no effect on unstimulated platelets or antibodies targeting other platelet glycoproteins^[1].
KRDS (750 μM) potently inhibits ADP-induced aggregation of washed platelets, with an IC₅₀ of 350 μM^[2].
KRDS (30 min) inhibits the binding of fibrinogen to ADP-activated washed platelets, with an IC₅₀ of 360 μM^[2].
KRDS (75-750 μM) dose-dependently inhibits thrombin-induced aggregation of normal washed platelets, with an inhibition rate of 46% at 750 μM^[2].
KRDS (75-750 μM) dose-dependently inhibits serotonin release from normal washed platelets induced by thrombin (55% inhibition at 750 μM) and from washed platelets of patients with type I Glanzmann thrombasthenia (43% inhibition at 750 μM)^[2].
KRDS does not affect thrombin-induced protein phosphorylation of myosin light chains P20 and P43 in washed platelets^[2].
KRDS (750 μM) does not alter the resting state or thrombin-induced cytoplasmic Ca²⁺ mobilization in Indo-1-AM-loaded washed platelets^[2].