Molecular Weight(MW): 508.61
PD 123319 is a potent, selective AT2 angiotensin II receptor antagonist with IC50 of 34 nM.
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Ang II-induced MMP-2 protein expression through AT1 receptor in ex vivo cultured IAAA aortic walls (A) Ex vivo cultured aortic pieces from IAAA patients (n = 5) were incubated in the presence of different concentrations of Ang II for 48 h. (B) Ex vivo cultured aneurysmal aorta walls were pre-treated with either candesartan (10 µM, AT1R inhibitor) or PD123319 (10 µM, AT2R antagonist) for 48 h, followed by 1 µM Ang II treatment for 48 h. The group without Ang II incubation was used as control. **P < 0.01 vs. untreated control group; ##P < 0.01 vs. treated with Ang II alone. CA, candesartan; PD, PD123319.
Acta Biochim Biophys Sin (Shanghai), 2015, 47(7):539-47.. PD123319 purchased from Selleck.
Ang II induces MMP-2 protein expression and ERK phosphorylation ASMCs via AT1R. (a) ASMCs were pretreated with 0.1 μM candesartan (CA, selective AT1R inhibitor, 30 min) or 1 μM PD123319 (PD, selective AT2R inhibitor, 30 min) followed by stimulation with 0.1 μM Ang II for 2 min six-well plates. Western blot was performed to assess the levels of ERK phosphorylation in cell lysates. Top panel: Graphs show the relative p-ERK1/2 protein levels, respectively, normalized to total ERK1/2 relative to control. Bottom panel: Ratio of p-ERK1/2/t-ERK1/2 protein expression, respectively, evaluated using Western blot analysis from a representative experiment. Shown are mean±SEM of three individual experiments. **P < 0.01 vs. untreated control cells; ##P < 0.01 vs. cells treated with Ang II. (b) ASMCs were incubated with 1 μM candesartan or 10 μM PD123319 for 60 min before stimulation with 0.1 μM Ang II for 24 h in six-well plates. Western blot was used for analyses of the levels of MMP-2 expression in cell lysates. Top panel: Graphs show the relative MMP-2 protein levels normalized to GAPDH relative to control. Bottom panel: Ratio of MMP-2/GAPDH protein expression from a representative Western blot experiment. Shown are mean±SEM of three individual experiments. **P < 0.01 vs. untreated control cells; ##P < 0.01 vs. cells treated with Ang II.
Exp Biol Med (Maywood), 2015, 240(12):1564-71. . PD123319 purchased from Selleck.
Effect of PD123319 treatment on sodium current (INa). Typical recordings of INa in cells from control (a), non-PD123319 (b), and PD123319 (c). x-axis: time (ms mini-second); y-axis: current volume (pA). The voltage clamp protocol is shown in (d). e Average I-V relationships of INa density (pA/pF) as a function of step potential (mV), obtained in control (filled squares), non-PD123319 (empty squares), and PD123319 (empty circles)
Naunyn Schmiedebergs Arch Pharmacol, 2016, 389(12):1333-1340. PD123319 purchased from Selleck.
Purity & Quality Control
Choose Selective RAAS Inhibitors
|Description||PD 123319 is a potent, selective AT2 angiotensin II receptor antagonist with IC50 of 34 nM.|
PD 123319 is shown to discriminate between two subclasses of AII receptors in many different tissues. 125I-AII specifically labeled two classes of binding sites for AII in a membrane preparation of bovine adrenal glomerulosa cells. The first class (DuP-753 sensitive) represents approximately 85% of the total binding sites for AII and possesses a high affinity (IC50 of 92.9 nM) for DuP-753. PD-123319 does not have any effect on 125I-AII binding to this site. The second class of binding sites is more sensitive to PD-123319, with an IC50 of 6.9 nM, and has a much lower affinity for DuP-753 (IC50 around 10 microM). 
|In vivo||PD 123319 has no effect on cerebral blood flow autoregulation. Acute AT2-receptor blockade does not influence CBF autoregulation. Intravenous administration of PD 123319 to conscious hypertensive rats elicites an immediate dose-dependent increase in MAP that is sustained for approximately 7.4 min with 3 mg/kg PD 123319. |
|In vitro||DMSO||100 mg/mL (196.61 mM)|
|Water||100 mg/mL (196.61 mM)|
|Ethanol||100 mg/mL (196.61 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
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