| ResorcinolnaphthaleinACE2 activator |
Sample solution is provided at 25 µL, 10mM.
Nature.2017 Jan 19;541(7637):417-420.
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- Purity = 98.00%
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Chemical structure
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| Cas No. | 41307-63-5 | SDF | Download SDF |
| Synonyms | NSC 354317 | ||
| Chemical Name | 3",6"-dihydroxy-spiro[1H,3H-naphtho[1,8-cd]pyran-1,9"-[9H]xanthen-3-one | ||
| Canonical SMILES | Oc1ccc2c(c1)Oc1cc(O)ccc1C12OC(=O)c2cccc3cccc1c23 | ||
| Formula | C24H14O5 | M.Wt | 382.4 |
| Solubility | ≤20mg/ml in ethanol;20mg/ml in DMSO;20mg/ml in dimethyl formamide | Storage | Store at -20°C |
| Physical Appearance | A crystalline solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
| 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. | ||
Resorcinolnaphthalein is an Angiotensin-converting enzyme 2 (ACE2) activator [1].
Angiotensin-converting enzyme 2 (ACE2) has been involved in hydrolyzing angiotensin II and opposing its actions, and plays a protective role in the pathogenesis of pulmonary arterial hypertension (PAH) [2]. Targeted disruption of ACE2 in mice results in a severe cardiac contractility defect, increased angiotensin II levels, and upregulation of hypoxia-induced genes in the heart [2].
In vitro: Resorcinolnaphthalein enhanced ACE2 activity in a dose-dependent manner [1].
In vivo: Resorcinolnaphthalein caused significant activation of ACE2 in both normal and diseased rats in 7 days after treatment. Treatment with resorcinolnaphthalein prevented high PAP, right ventricular hypertrophy and neointimal formation. Resorcinolnaphthalein caused an improved endothelia-dependent vasorelaxation and decreased in proinflammatory cytokines, such as TNF-α, MCp-1, IL-6, and increased in anti-inflammatory cytokine IL-10 in the early stage of the pathogenesis [3]. Resorcinolnaphthalein can specifically and effectively enhanced ACE2 activity in rats [4]. ACE2 activation by resorcinolnaphthalein showed effects on pulmonary endothelial dysfunction and neointimal formation during the development of severe PAH in rats [4].
References:[1] Prada J A H, Ferreira A J, Katovich M J, et al. Structure-based identification of small-molecule angiotensin-converting enzyme 2 activators as novel antihypertensive agents[J]. Hypertension, 2008, 51(5): 1312-1317.[2] Crackower M A, Sarao R, Oudit G Y, et al. Angiotensin-converting enzyme 2 is an essential regulator of heart function[J]. Nature, 2002, 417(6891): 822-828.[3] Haber P K, Ye M, Wysocki J, et al. Angiotensin-converting enzyme 2–independent action of presumed angiotensin-converting enzyme 2 activatorsNovelty and significance[J]. Hypertension, 2014, 63(4): 774-782.[4] Li G, Liu Y, Zhu Y, et al. ACE2 activation confers endothelial protection and attenuates neointimal lesions in prevention of severe pulmonary arterial hypertension in rats[J]. Lung, 2013, 191(4): 327-336.
