ARC 239

ARC 239 (0.1 nM-1 mM; 30 min) shows the highest binding affinity at rat kidney α₂B and human recombinant α₂C sites (pK_i 7.06 and 6.95, respectively), whereas its affinity at the human platelet α₂A site is much lower (pK_i 5.45)^[1].
ARC 239 (0.3-1 µM; 60 min) competitively antagonizes Norepinephrine (HY-13715)-induced contraction of human saphenous vein rings with a pK_B of 7.19^[1].
ARC 239 (0.1 nM-0.1 mM; incubated at 37°C for 30 min) recognizes rat cortical 5-HT₁A receptors in a [³H]8-OH-DPAT competitive binding assay with a K_i of 63.1 nM^[2].
ARC 239 (0.1 nM-0.1 mM; incubated at 25°C for 30 min) displaces the binding of [³H]RX 821002 to rat hippocampal 5-HT₁A receptors under conditions where α₂-adrenoceptors are masked, with a K_i of 136 nM^[2].
ARC 239 dihydrochloride (30 μM; pretreatment for 30 min + co-incubation for 48 h) prevents Norepinephrine bitartrate monohydrate (HY-13715B) (5 µM)-induced RhoA activation, ROCK-dependent MYPT1 phosphorylation, and loss of Claudin-5 tight junctions in HUVECs^[3].
ARC 239 (50 nM; 30 min) does not inhibit α2-AR-mediated vasoconstriction in isolated distal mouse tail arteries at 37°C or 28°C, which is consistent with its K_D of 4.6 nM for α_2B-AR and K_D >50 nM for mouse tail arteries^[5].