Fenoldopam (mesylate)

Fenoldopam (SKF-82526) mesylate is a selective dopamine D₁ receptor agonist. Fenoldopam mesylate binds to rat D₁B dopamine receptors (K_d = 11 nM) and human D₁A receptors (K_d = 17 nM) in COS-7 cell membranes expressing the cloned receptors. Fenoldopam mesylate modulates dopamine receptor expression, induces vasorelaxation in vascular tissues, reverses glomerular hyperfiltration in rat models, increases intracellular cAMP levels, promotes DARPP-32 phosphorylation in small cell lung cancer (SCLC) cells, inhibits cytokine secretion, and downregulates T cell activation markers in activated human T cells. Fenoldopam mesylate can be used for research on hypertension, acute kidney injury, psoriasis, and small cell lung cancer^{[1][2][3][4][5][6][7][8]}. IC50 & Target:IC50: 0.8974 μM (LSD1)^[2] In Vitro:Fenoldopam (SKF-82526) (40 min) mesylate competes for specific 125I-Sch 23982 binding sites in rat renal cortical membranes with a K_i of 1,975 nM (Tris-HCl buffer) and 1,895 nM (Dulbecco's buffer)^[1].
Fenoldopam (1 nM-6 μM; 72 h) mesylate does not inhibit the proliferation of CD3/CD28-stimulated Jurkat leukemic T cells, in contrast to its inhibitory effect on normal activated T cells^[2].
Fenoldopam (1 μM; 5 h) mesylate co-treated Theophylline (HY-B0809) increases intracellular cAMP levels in CD3/CD28-stimulated Jurkat cells^[2].
Fenoldopam (1 μM; 10-30 min) mesylate increases DARPP-32 phosphorylation in small cell lung cancer (SCLC) H-69 cells and primary SCLC cultures^[3].
Fenoldopam (1 μM; 30 180 min) mesylate induces cAMP accumulation in SCLC cells and increases BrdU incorporation in SCLC H-69 cells as well as primary SCLC cultures (SCLC H-3)^[3].
Fenoldopam (0.1 μM; 48 h) mesylate reduces the secretion of TNF-α, IFN-γ, IL-1β, IL-2, IL-4, IL-6, IL-8 and IL-10 by IL-2 activated PBMCs, and downregulates the expression of T cell activation markers CD69, CD28 and intracellular IL-2 in CD3⁺ T cells from psoriasis patients^[4].
Fenoldopam (0.1 μM; 1 h) mesylate reduces the chemotactic migration of CD3/CD28-activated normal human T cells towards SDF-1/CXCL12 by 27-55%^[4].
Fenoldopam (0.1 μM; 15 sec) mesylate induces depolarization of resting and activated normal human T cells^[4].
Fenoldopam (10 pM-1 μM; 24 h) increases D₁ and D₃ receptor protein expression in a concentration- and time-dependent manner in rat aortic smooth muscle A10 cells^[6].
Fenoldopam (0.1 μM; 24 h) mesylate increases D1/D3 receptor coimmunoprecipitation in A10 cells^[6].
Fenoldopam (100 pM-1 mM) mesylate induces vasorelaxation in rat mesenteric arterial rings preconstricted with KCl (E_max = 83%, pED₅₀ = 5.0)^[6].
Fenoldopam mesylate binds to rat D₁B dopamine receptors with a Kd of 11 nM and human D₁A receptors with a Kd of 17 nM in COS-7 cell membranes expressing the cloned receptors^[7].
Fenoldopam (1 nM-100 μM; cumulative) mesylate has minimal effect on mouse ductus arteriosus tone, and does not impair O₂-or indomethacin-induced ductus constriction^[8]. In Vivo:Fenoldopam (SKF-82526) (1 μg/kg; i.v.; during glycine infusion) mesylate reverses glycine-induced glomerular hyperfiltration in conscious male Sprague-Dawley rats (320-360 g), reducing GFR from 1.30 to 1.17 mL/100 g/min^[5].
Fenoldopam (1, 3, 10 μg/kg; i.v.; 40 min per dose) mesylate increases effective renal plasma flow (ERPF) in a dose-dependent manner in conscious rats, with no significant change in GFR, resulting in a decreased filtration fraction^[5].
Fenoldopam (1 mg/kg; i.p.; once hourly for 4 doses) mesylate does not impair postnatal ductus arteriosus closure in newborn CD-1 mice^[8].