DPO-1

DPO-1 is a potent Kv1.5 and Kv1.3 (EC₅₀ = 3.1 μM) channels inhibitor with potential immunomodulatory and anti-inflammatory effects. DPO-1 reduces Kv1.3 current density, blunts Ca²⁺ influx in Ca²⁺-depleted Jurkat cells, and inhibits IL-2 secretion in activated Jurkat cells. DPO-1 inhibits Uric acid sodium (HY-B2130A) (MSU)-induced NLRP3 inflammasome activation by blocking Kv1.5-mediated K⁺ efflux. DPO-1 can be used for the study of immunologic disorders and atrial fibrillation^[1][2][3]. In Vitro:DPO-1 (1-10 μM) inhibits outward K⁺ currents in mesenteric artery VSMCs from wild-type (Kcna5^+/+) mice, with a more potent inhibitory effect than in VSMCs from Kcna5^-/- mice^[1].
DPO-1 (10 μM, 30 min) induces stable vasocontraction in mesenteric artery rings without PVAT in Kcna5^+/+ and Kcna5^-/- mice^[1].
DPO-1 (0.3-30 μM) blocks Kv1.3 current in a voltage-dependent and concentration-dependent manner in Jurkat cells and human peripheral blood T cells, with IC₅₀ values of 2.58 μM (Jurkat cells) and 3.11 μM (human peripheral blood T cells)^[2].
DPO-1 (1-10 μM, 24 h) decreases Kv1.3 current density at +40 mV in Jurkat cells and reduces Kv1.3 protein expression^[2].
DPO-1 (0.1-3 μM, 24 h) blunts Ca²⁺ influx in Ca²⁺-depleted Jurkat cells induced by Thapsigargin (TG) (HY-13433)^[2].
DPO-1 (3-10 μM, 24 h) inhibits IL-2 secretion in activated Jurkat cells^[2].
DPO-1 (0-100 μM, 6 h) concentration-dependently reduces caspase-1 (p20) and IL-1β (p17) protein levels, prevents intracellular K⁺ concentration decrease, suppresses ASC oligomerization and speck formation in LPS (HY-D1056)-primed J774.1 mouse macrophages^[3].