Picotamide

Picotamide is an orally active TXA₂ receptor and TXA₂ synthase inhibitor. Picotamide inhibits ADP (HY-W010918)-, Arachidonic acid (HY-109590)-, and Collagen (HY-NP003)-induced platelet aggregation, reduces TXA₂ production during coagulation, and does not inhibit PGI2 synthesis in endothelial cells. Picotamide inhibits contractions induced by α1-adrenergic receptor agonism, TXA2 mediation, and neurogenic (electrical field stimulation-induced) factors in human prostatic smooth muscle, and broadly inhibits agonist-induced contractions of porcine interlobar renal and coronary arteries. Picotamide can be used in research related to thromboembolic diseases, atherosclerosis, and lower urinary tract symptoms^{[1][2][3][4][5]}. In Vitro:Picotamide (10-80 μM; 48 h) dose-dependently decreased the cell viability of L929 cells^[1].
Picotamide (10-100 μM; 48 h) exhibits dose-dependent cytotoxicity in L929 mouse fibroblasts^[4].
Picotamide (3 μM) inhibits α1-adrenergic contractions in human prostatic tissue strips when cyclooxygenase activity is blocked by Indomethacin (HY-14397)^[3].
Picotamide inhibits EFS-induced contraction in human prostate tissue^[3].
Picotamide (0.325-1.3 μM; 2 min) exhibited antiplatelet aggregation activity in rabbit PRP, with an IC₅₀ value of 0.47 μM for ADP-induced aggregation and an IC₅₀ value of 0.34 μM for AA-induced aggregation^[4].
Picotamide (300 μM; 30 min) inhibited U46619-induced contraction of porcine renal interlobar arteries without a rightward shift or a significant increase in EC₅₀ values^[5].
Picotamide (300 μM; 30 min) competitively inhibits Noradrenaline (HY-13715)-, Phenylephrine (HY-B0769)-, and Methoxamine (HY-B1298A)-induced contraction of porcine renal interlobar arteries, increasing EC₅₀ without affecting E_max^[5].
Picotamide (300 μM; 30 min) inhibited Serotonin (HY-B1473A)-induced contraction in porcine renal interlobar arteries, characterized by a rightward shift and an increase in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits α,β-methylene-ATP (HY-134440A)-induced contraction of porcine renal interlobar arteries at high agonist concentrations^[5].
Picotamide (300 μM; 30 min) had minimal effect on weak ATP (HY-B2176)-induced contractions in porcine renal interlobar arteries^[5].
Picotamide (300 μM; 30 min) inhibited Angiotensin-II-induced contraction of porcine renal interlobar arteries without a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits Endothelin-1 (HY-P0202)-induced contraction in porcine renal interlobar arteries^[5].
Picotamide (300 μM; 30 min) inhibited U46619 (HY-108566)-induced contraction of porcine coronary arteries, without a rightward shift or a significant increase in EC₅₀ values^[5].
Picotamide (300 μM; 30 min) inhibited Phenylephrine-induced contraction of porcine coronary arteries, without competitive characteristics or changes in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits Methoxamine-induced contraction of porcine coronary arteries without competitive characteristics or a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibited Methacholine-induced contraction in porcine coronary arteries without causing consistent changes in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits Carbachol (HY-B1208)-induced contraction in porcine coronary arteries, with no consistent change in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibited Serotonin-induced contraction in porcine coronary arteries, manifested as a rightward shift and an increase in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits Angiotensin-II-induced contraction in porcine coronary arteries without a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) inhibits Endothelin-1-induced contraction in porcine coronary arteries^[5].
Picotamide (30-300 μM; 30 min) dose-dependently inhibited EFS-induced contractions in porcine renal interlobar arteries without affecting Ef₅₀^[5].