A2P5P

A2P5P (2',5'-ADP) (100 μM) strongly inhibits hypotonicity-induced elevation of [Ca²⁺]_i in HTC rat hepatoma cells^[1].
A2P5P (100 μM) strongly inhibits ADP-induced Ca²⁺ mobilization in HTC rat hepatoma cells^[1].
A2P5P (30 s) does not significantly modulate IP₃ accumulation in 1321N1 cells expressing human P2Y11, whether tested alone or together with 100 μM ATP^[2].
A2P5P (15 min) does not significantly modulate Cyclic AMP (HY-B1511)
accumulation in CHO-K1 cells expressing human P2Y11, whether tested alone or together with 100 μM ATP^[2].
A2P5P (1 mM) abolishes ADP-induced aggregation in washed human platelets and strongly inhibits aggregation and secretion induced by low concentrations of U46619 (HY-108566) or low concentrations of thrombin, while having no effect on high concentrations of U46619 or high concentrations of thrombin^[4].
A2P5P (1 mM; 10-45 s) prevents ADP-induced shape change and granule centralization in washed human platelets, inhibits filopodia formation induced by low concentrations of U46619, and partially prevents shape change induced by low concentrations of thrombin^[4].
A2P5P (1 mM) eliminates ADP-induced F-actin assembly in washed human platelets and reduces the F-actin increase triggered by low concentrations of U46619 or low concentrations of thrombin^[4].
A2P5P (1 mM; 2-30 s) abolishes ADP- and low-concentration U46619-induced cytoskeletal translocation of cdc42, rac1, and rhoA in washed human platelets^[4].
A2P5P (1 mM; 3 s) abolishes ADP-induced early activation of αIIbβ3 in washed human platelets^[4].
A2P5P (100 µM; 24 h) blocks 2-MeSADP-induced AChE promoter activity in 10 DIV rat cortical neurons^[5].
A2P5P (1 mM; 3 min) reduces ADP-induced platelet aggregation in human platelet-rich plasma by 58.3%^[6].
A2P5P (1 mM; 3 min) inhibits ADP-induced calcium influx in human platelet-rich plasma^[6].
A2P5P (at a 30-fold molar excess relative to 10 µM ADP) inhibits P2Y1-mediated intracellular calcium mobilization in human platelets, with complete inhibition at a 30-fold molar excess relative to 10 µM ADP^[7].
A2P5P (300 µM) inhibits ADP- and 2-MeSADP (HY-108648A)-induced morphological changes in Aspirin (HY-14654)-treated human platelets, with complete inhibition at 300 µM^[7].
A2P5P (200 µM; 0.5 min before ADP) does not block ADP-induced inhibition of adenylyl cyclase in human platelets, indicating that P2Y1 antagonism does not prevent this P2T_AC-mediated response^[7].
A2P5P (100 µM) inhibits ADP-induced rat platelet aggregation and morphological changes, with a pA value of 5.6 and a Schild slope of 0.74^[8].
A2P5P (100 µM) eliminates ADP-induced elevation of [Ca²⁺]_i in rat platelets^[8].
A2P5P (100 µM) does not affect basal or PGE1-stimulated cAMP, nor does it reverse ADP-induced adenylyl cyclase inhibition in rat platelets^[8].
A2P5P (5 min) displaces residual [³³P]2MeSADP binding on rat platelets treated with Clopidogrel (HY-15283) with a K_i of 9.5 µM^[8].
A2P5P (50 mM; at least 4 h) binds to bovine pancreatic RNase A within the asymmetric unit in two different modes, with its 2′- or 5′-phosphate group anchored at the P1 subsite, while the adenine occupies different B2 positions^[9].