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Catalog No.GC16394

PD123319 Chemical Structure

PD123319 is a non-peptide inhibitor of angiotensin II receptor with IC50 value of 34nM .

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10mM (in 1mL DMSO)
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Cell experiment [1]:

Cell lines

Neuro-2aneuroblastoma cells

Preparation Method

Neuro-2a cells were incubated for 24-h in a 37 °C incubator, and then treated for another 24-h with designed concentrations of PD123319. Optical density (OD) was measured at 570 nm.

Reaction Conditions

100μM PD123319 for 24 hours


Significant reduction in cell viability was observed when Neuro-2a cells were treated with the concentration of PD123319 (100 μM).

Animal experiment [2]:

Animal models

LDL receptor -/- mice that were either wild type or deficient for AT2 receptors

Preparation Method

Osmotic minipumps were implanted subcutaneously to deliver saline, AngII (500 ng/kg/min), or PD123319 (3 mg/kg/d )

Dosage form

Osmotic minipump, 3 mg/kg/d


PD123319 acts through an angiotensin type 2(AT2) receptor-independent mechanism in angiotensin II -induced vasoconstriction in mice. PD123319 significantly increased Ang II-induced suprarenal aortic (AAAs) independent of AT2 receptors.


[1]. Y.J. Chen, Z.M. Qian, Y. Sheng, J. Zheng, Y. Liu. Angiotensin II down-regulates transferrin receptor 1 and ferroportin 1 expression in neuro-2a cells via activation of type-1 receptor. Neurosci. Lett., 716 (2020), p. 134684, 10.1016/j.neulet.2019.134684

[2]. Daugherty A, Rateri DL, Howatt DA, Charnigo R, Cassis LA. PD123319 augments angiotensin II-induced abdominal aortic aneurysms through an AT2 receptor-independent mechanism. PLoS One. 2013; 8:e61849. doi: 10.1371/journal.pone.0061849.


PD123319 is a non-peptide inhibitor of angiotensin II receptor with IC50 value of 34nM [1].

PD123319 is an antagonist of angiotensin II receptor, unlike previous drugs act as inhibitors of the formation of Ang II. PD123319 shows inhibition potency in both rat adrenal and brain binding assay with IC50 values of 34nM and 210nM, respectively. It is found to prevent Ang II from binding the bovine zona glomerulosa microsomal preparation with IC50 value of 6.9nM in the binding assay using microsome. [2,3]. PD123319 inhibited AT2 amplification product from rat pheochromocytoma cells (PC12w) binding to 0.5 nM 125I-[Sar1, Ile8]-Ang II with IC50 values of 1.7±0.2 nM [4] .In addition, it is reported that administration of PD123319 can suppress the generation of cyclic guanosine monophosphate and increase the production of prostaglandin E2[2,3].

PD123319 was transfused intra-brachial arterial in healthy young volunteers to investigated forearm vascular responses and systemic blood pressure responses. There are significant increases in mean arterial pressure were observed during intra-brachial arterial infusions of PD123319 (p = 0.003) during both placebo (80±9 to 92±17 mmHg) and telmisartan (80±11 to 90±14 mmHg) therapy, possibly in locations other than the forearm resistance vessels. Intra-brachial arterial infusion of PD123319 (10 μg/min) has significant systemic effects on rising mean arterial pressure [5].

[1] Blankley C J, Hodges J C, Klutchko S R, et al.  Synthesis and structure-activity relationships of a novel series of non-peptide angiotensin II receptor binding inhibitors specific for the AT2 subtype. Journal of medicinal chemistry, 1991, 34(11): 3248-3260.
[2] Boulay G, Servant G, Luong T T, et al.  Modulation of angiotensin II binding affinity by allosteric interaction of polyvinyl sulfate with an intracellular domain of the DuP-753-sensitive angiotensin II receptor of bovine adrenal glomerulosa. Molecular pharmacology, 1992, 41(4): 809-815.
[3] Siragy H.  Angiotensin II receptor blockers: review of the binding characteristics. The American journal of cardiology, 1999, 84(10): 3-8.
[4] Kambayashi, Y., Takahashi, K., Bardhan, S. et al. Molecular structure and function of angiotensin type2 receptor, Kidney Inr, 1994, 46, 1502- 1504.
[5] Daugherty A, Rateri DL, Howatt DA, Charnigo R, Cassis LA. PD123319 augments angiotensin II-induced abdominal aortic aneurysms through an AT2 receptor-independent mechanism. PLoS One. 2013; 8:e61849. doi: 10.1371/journal.pone.0061849.

Chemical Properties

Cas No. 130663-39-7 SDF
Synonyms N/A
Chemical Name (6S)-1-[[4-(dimethylamino)-3-methylphenyl]methyl]-5-(2,2-diphenylacetyl)-6,7-dihydro-4H-imidazo[4,5-c]pyridine-6-carboxylic acid
Canonical SMILES CC1=C(C=CC(=C1)CN2C=NC3=C2CC(N(C3)C(=O)C(C4=CC=CC=C4)C5=CC=CC=C5)C(=O)O)N(C)C
Formula C31H32N4O3 M.Wt 508.61
Solubility ≥ 22.4mg/mL in DMSO, ≥ 140 mg/mL in EtOH, ≥ 104.2 mg/mL in H2O Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

PD123319, angiotensin II type II receptor antagonist, inhibits oxidative stress and inflammation in 2, 4-dinitrobenzene sulfonic acid-induced colitis in rat and ameliorates colonic contractility

Inflammopharmacology2020 Feb;28(1):187-199.PMID: 31321575DOI: 10.1007/s10787-019-00619-z

Angiotensin II, the main effector of renin angiotensin system, plays an important role in the inflammatory process and most of its effects are mediated through the AT1 receptor activation. However, the knowledge about the AT2 receptor involvement in this process is still evolving. We previously found that in an experimental model of colitis, AT2 receptor activation can contribute to the impairment of the muscle contractility in vitro in the course of inflammation. Here, we investigated the potential alleviating effects of the in vivo treatment of PD123319 (1-[[4-(Dimethylamino)-3-methylphenyl]methyl]-5-(diphenylacetyl)-4,5,6,7- tetrahydro-1H-imidazo[4,5-c]pyridine-6-carboxylic acid ditrifluoroacetate), AT2 receptor antagonist, in 2,4-dinitrobenzene sulfonic acid (DNBS)-induced rat model of colitis. The effects of i.p PD123319 (0.3, 3 and 10 mg/kg) administration to rats subjected to intra-rectal DNBS instillation were investigated. The study revealed that the colon injury and the inflammatory signs were ameliorated by PD123319 when visualized by the histopathological examination. The colon shortening, myeloperoxidase activity, and colonic expression of IL-1β, IL-6 and iNOS were downregulated in a dose-dependent manner in DNBS-induced colitis rats treated with PD123319 and the anti-oxidant defense machinery was also improved. The mechanism of these beneficial effects was found in the ability of PD123319 to inhibit NF-κB activation induced by DNBS. The colonic contractility in inflamed tissues was also improved by PD123319 treatment. In conclusion, our data have demonstrated previously that undescribed proinflammatory effects for the AT2 receptors in DNBS-induced colitis in rats in which they are mediated likely by NF-κB activation and reactive oxygen species generation. Moreover, when the inflammatory process is mitigated by the AT2 receptor antagonist treatment, the smooth muscle is able to recover its functionality.

PD123319 augments angiotensin II-induced abdominal aortic aneurysms through an AT2 receptor-independent mechanism

PLoS One2013 Apr 12;8(4):e61849.PMID: 23593499DOI: 10.1371/journal.pone.0061849

Background: AT2 receptors have an unclear function on development of abdominal aortic aneurysms (AAAs), although a pharmacological approach using the AT2 receptor antagonist PD123319 has implicated a role. The purpose of the present study was to determine the role of AT2 receptors in AngII-induced AAAs using a combination of genetic and pharmacological approaches. We also defined effects of AT2 receptors in AngII-induced atherosclerosis and thoracic aortic aneurysms.
Methods and results: Male AT2 receptor wild type (AT2 +/y) and deficient (AT2 -/y) mice in an LDL receptor -/- background were fed a saturated-fat enriched diet, and infused with either saline or AngII (500 ng/kg/min). AT2 receptor deficiency had no significant effect on systolic blood pressure during AngII-infusion. While AngII infusion induced AAAs, AT2 receptor deficiency did not significantly affect either maximal width of the suprarenal aorta or incidence of AAAs. The AT2 receptor antagonist PD123319 (3 mg/kg/day) and AngII were co-infused into male LDL receptor -/- mice that were either AT2 +/y or -/y. PD123319 had no significant effect on systolic blood pressure in either wild type or AT2 receptor deficient mice. Consistent with our previous findings, PD123319 increased AngII-induced AAAs. However, this effect of PD123319 occurred irrespective of AT2 receptor genotype. Neither AT2 receptor deficiency nor PD123319 had any significant effect on AngII-induced thoracic aortic aneurysms or atherosclerosis.
Conclusions: AT2 receptor deficiency does not affect AngII-induced AAAs, thoracic aortic aneurysms and atherosclerosis. PD123319 augments AngII-induced AAAs through an AT2 receptor-independent mechanism.

Angiotensin II type 2 receptor blocker PD123319 has more beneficial effects than losartan on ischemia-reperfusion injury and oxidative damage in isolated rat heart

Can J Physiol Pharmacol2019 Dec;97(12):1124-1131.PMID: 31361968DOI: 10.1139/cjpp-2019-0076

Our study aimed to determine the effects of losartan and PD123319 in ischemia-reperfusion (IR) injury in isolated perfused rat heart. The study used 40 male Wistar albino rats that were grouped as Control, IR, and IR treatment groups that received losartan (20 mg/kg), PD123319 (20 mg/kg), and losartan+PD123319. The hearts were attached to Langendorff isolated heart system by employing in situ cannulation method, and cardiodynamic parameters were recorded during the experiment. At the end of experiment, hearts were retained for biochemical analysis and all data were statistically evaluated. A partial recovery of cardiodynamic parameters was observed in all treatment groups. A significant increase in oxidative stress parameters were seen in the IR group, whereas all treatment groups exhibited lower increase. Furthermore, levels of all antioxidant parameters were significantly lower in the IR group, but higher in the treatment groups. Effects on all parameters were much more remarkable in the PD123319 group. Levels of angiotensin II and renin were increased (P < 0.001) with IR application and decreased (P < 0.001) with the treatment of both antagonists. In conclusion, treatment of losartan and PD123319 played a cardioprotective role against IR injury, PD123319 being more effective in this protection.

Long-term treatment of spontaneously hypertensive rats with PD123319 and electrophysiological remodeling of left ventricular myocardium

Naunyn Schmiedebergs Arch Pharmacol2016 Dec;389(12):1333-1340.PMID: 27629578DOI: 10.1007/s00210-016-1300-0

To investigate the effects of PD123319, an antagonist of angiotensin II subtype-2 receptor (AT2R), on the electrophysiological characteristics of the left ventricular hypertrophic myocardium in spontaneously hypertensive rats (SHR). A total of twenty-four 10-week-old male SHR were divided into two groups: PD123319 and non-PD123319 groups (n = 12 in each). Twelve 10-week-old Wistar-Kyoto rats served as the control group. Systolic blood pressure, left ventricular mass index (LVMI), ventricular effective refractory period, and ventricular fibrillation threshold were also measured after 8 weeks. I Na, I CaL, I to, and membrane capacitance were measured in the left ventricular myocytes after 8 weeks by whole-cell patch clamp. PD123319 increased LVMI compared with the non-PD123319 group (PD123319 vs. non-PD123319, 3.83 ± 0.11 vs. 3.60 ± 0.19 mg/g; P < 0.01). PD123319 also decreased the ventricular fibrillation threshold compared with the non-PD123319 group (PD123319 vs. non-PD123319, 14.75 ± 0.65 vs. 16.0 ± 0.86 mA; P < 0.01). PD123319 enhanced membrane capacitance compared with the non-PD123319 group (PD123319 vs. non-PD123319, 283.63 ± 5.80 vs. 276.50 ± 4.28 pF; P < 0.05). PD123319 increased the density of I CaL compared with the non-PD123319 group (PD123319 vs. non-PD123319, -6.76 ± 0.48 vs. -6.13 ± 0.30 pA/pF; P < 0.05). PD123319 decreased the density of I to compared with the non-PD123319 group (PD123319 vs. non-PD123319, 11.49 ± 0.50 vs. 12.23 ± 0.36 pA/pF; P < 0.05). Long-term treatment with PD123319 worsened the development of myocyte hypertrophy and associated electrophysiological alterations in spontaneously hypertensive rat.

Angiotensin II type 2 receptor ligand PD123319 attenuates hyperoxia-induced lung and heart injury at a low dose in newborn rats

Am J Physiol Lung Cell Mol Physiol2014 Aug 1;307(3):L261-72.PMID: 24951776DOI: 10.1152/ajplung.00345.2013

Intervening in angiotensin (Ang)-II type 2 receptor (AT2) signaling may have therapeutic potential for bronchopulmonary dysplasia (BPD) by attenuating lung inflammation and preventing arterial hypertension (PAH)-induced right ventricular hypertrophy (RVH). We first investigated the role of AT2 inhibition with PD123319 (0.5 and 2 mg·kg(-1)·day(-1)) on the beneficial effect of AT2 agonist LP2-3 (5 μg/kg twice a day) on RVH in newborn rats with hyperoxia-induced BPD. Next we determined the cardiopulmonary effects of PD123319 (0.1 mg·kg(-1)·day(-1)) in two models: early treatment during continuous exposure to hyperoxia for 10 days and late treatment starting on day 6 in rat pups exposed postnatally to hyperoxia for 9 days, followed by a 9-day recovery period in room air. Parameters investigated included lung and heart histopathology, fibrin deposition, vascular leakage, and differential mRNA expression. Ten days of coadministration of LP2-3 and PD123319 abolished the beneficial effects of LP2-3 on RVH in experimental BPD. In the early treatment model PD123319 attenuated cardiopulmonary injury by reducing alveolar septal thickness, pulmonary influx of inflammatory cells, including macrophages and neutrophils, medial wall thickness of small arterioles, and extravascular collagen III deposition, and by preventing RVH. In the late treatment model PD123319 diminished PAH and RVH, demonstrating that PAH is reversible in the neonatal period. At high concentrations PD123319 blocks the beneficial effects of the AT2-agonist LP2-3 on RVH. At low concentrations PD123319 attenuates cardiopulmonary injury by reducing pulmonary inflammation and fibrosis and preventing PAH-induced RVH but does not affect alveolar and vascular development in newborn rats with experimental BPD.


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