Picotamide monohydrate

Picotamide (10-80 μM; 48 h) monohydrate decreased the cell viability of L929 cells in a dose-dependent manner^[1].
Picotamide (10-100 μM; 48 h) monohydrate exhibits dose-dependent cytotoxicity against L929 mouse fibroblasts^[4].
Picotamide (3 μM) monohydrate inhibits α1-adrenergic contractions in human prostatic tissue strips when cyclooxygenase activity is blocked by Indomethacin (HY-14397)^[3].
Picotamide monohydrate inhibits EFS-induced contraction in human prostate tissue^[3].
Picotamide (0.325-1.3 μM; 2 min) monohydrate 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) monohydrate 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) monohydrate 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) monohydrate inhibits 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) monohydrate inhibits α,β-methylene-ATP (HY-134440A)-induced contraction of porcine renal interlobar arteries at high agonist concentrations^[5].
Picotamide (300 μM; 30 min) monohydrate has minimal effect on weak ATP (HY-B2176)-induced contraction in porcine renal interlobar arteries^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Angiotensin-II-induced contraction of porcine renal interlobar arteries without a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Endothelin-1 (HY-P0202)-induced contraction in porcine renal interlobar arteries^[5].
Picotamide (300 μM; 30 min) monohydrate 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) monohydrate inhibits Phenylephrine-induced contraction of porcine coronary arteries, without competitive characteristics or changes in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Methoxamine-induced contraction of porcine coronary arteries without competitive characteristics or a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibited Methacholine-induced contraction in porcine coronary arteries without causing consistent changes in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Carbachol (HY-B1208)-induced contraction in porcine coronary arteries, with no consistent change in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Serotonin-induced contraction in porcine coronary arteries, manifested as a rightward shift and an increase in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Angiotensin-II-induced contraction in porcine coronary arteries without a significant change in EC₅₀^[5].
Picotamide (300 μM; 30 min) monohydrate inhibits Endothelin-1-induced contraction in porcine coronary arteries^[5].
Picotamide (30-300 μM; 30 min) monohydrate dose-dependently inhibited EFS-induced contractions in porcine renal interlobar arteries without affecting Ef₅₀^[5].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.