Allopurinol Sodium - CAS 17795-21-0
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
Allopurinol Sodium
Catalog Number:
17795-21-0
CAS Number:
17795-21-0
Description:
Allopurinol Sodium is a xanthine oxidase inhibitor with an IC50 of 7.82±0.12 μM.
Molecular Weight:
159.1
Molecular Formula:
C5H4N4NaO
COA:
Inquire
MSDS:
Inquire
Chemical Structure
CAS 17795-21-0 Allopurinol Sodium

Reference Reading


1.A pilot study on the impact of a low fructose diet and allopurinol on clinic blood pressure among overweight and prehypertensive subjects: a randomized placebo controlled trial.
Madero M1, Rodríguez Castellanos FE2, Jalal D3, Villalobos-Martín M2, Salazar J2, Vazquez-Rangel A2, Johnson RJ3, Sanchez-Lozada LG2. J Am Soc Hypertens. 2015 Nov;9(11):837-44. doi: 10.1016/j.jash.2015.07.008. Epub 2015 Jul 30.
Fructose and sodium intake have been associated with hypertension and metabolic syndrome. Although various mechanisms are involved, fructose causes hypertension partly through rising intracellular and serum uric acid. To date, there are no studies in adults that have evaluated the impact of low fructose diets and allopurinol on prehypertensive and overweight subjects. The objective of this study was to compare the effect of low fructose diet and allopurinol or placebo on blood pressure (BP) and metabolic syndrome components The study was a controlled clinical trial and consisted of two phases; in the first phase of intervention (4 weeks), patients were randomized to either low fructose diet (34 patients) or control diet (38 patients). In the second phase of intervention (weeks 4-8), the same groups continued with the same diet prescriptions but were further randomized to receive placebo or allopurinol (300 mg/d). Clinic and 24-hour ambulatory BP, anthropometric measures, and laboratory data were determined at baseline, weeks 4 and 8.
2.Role of xanthine oxidoreductase in the anti-thrombotic effects of nitrite in rats in vivo.
Kramkowski K1, Leszczynska A1, Przyborowski K2, Kaminski T3, Rykaczewska U1, Sitek B2, Zakrzewska A2, Proniewski B2, Smolenski RT4, Chabielska E1, Buczko W3, Chlopicki S2,5. Platelets. 2016 May;27(3):245-53. doi: 10.3109/09537104.2015.1083545. Epub 2015 Sep 16.
The mechanisms underlying nitrite-induced effects on thrombosis and hemostasis in vivo are not clear. The goal of the work described here was to investigate the role of xanthine oxidoreductase (XOR) in the anti-platelet and anti-thrombotic activities of nitrite in rats in vivo. Arterial thrombosis was induced electrically in rats with renovascular hypertension by partial ligation of the left renal artery. Sodium nitrite (NaNO2, 0.17 mmol/kg twice daily for 3 days, p.o) was administered with or without one of the XOR-inhibitors: allopurinol (ALLO) and febuxostat (FEB) (100 and 5 mg/kg, p.o., for 3 days). Nitrite treatment (0.17 mmol/kg), which was associated with a significant increase in NOHb, nitrite/nitrate plasma concentration, resulted in a substantial decrease in thrombus weight (TW) (0.48 ± 0.03 mg vs. vehicle [VEH] 0.88 ± 0.08 mg, p < 0.001) without a significant hypotensive effect. The anti-thrombotic effect of nitrite was partially reversed by FEB (TW = 0.
3.Use of cinacalcet in nephrolithiasis associated with normocalcemic or hypercalcemic primary hyperparathyroidism: results of a prospective randomized pilot study.
Brardi S1, Cevenini G, Verdacchi T, Romano G, Ponchietti R. Arch Ital Urol Androl. 2015 Mar 31;87(1):66-71. doi: 10.4081/aiua.2015.1.66.
OBJECTIVES: To evaluate, by means of a prospective randomized study, the efficacy of cinacalcet in the forms of nephrolithiasis associated with primary hyperparathyroidism in both the hypercalcemic and normocalcemic variant.
4.Zinc oxide nanoparticles induce lipoxygenase-mediated apoptosis and necrosis in human neuroblastoma SH-SY5Y cells.
Kim JH1, Jeong MS2, Kim DY1, Her S2, Wie MB3. Neurochem Int. 2015 Nov;90:204-14. doi: 10.1016/j.neuint.2015.09.002. Epub 2015 Sep 11.
Zinc oxide nanoparticles (ZnO NPs) are known to induce oxidative stress and modulate an inflammatory process in various cell types. Although the cytotoxic effects of ZnO NPs in various cell types have been evaluated, few neurotoxic surveys on ZnO NPs as well as rescue studies have been reported. This study was designed to examine the neurotoxic ZnO NP concentration according to exposure time and dose, and the mechanisms that underlie ZnO NP-induced neurotoxicity in the SH-SY5Y human neuroblastoma cell line. A significant reduction in neuronal viability as well as distinct morphological findings resulted from application of 15 μM ZnO NPs. Apoptotic injury-as measured by annexin V and caspase 3/7 activities-was significantly elevated at 12 h and 24 h, but not 6 h, after ZnO NP exposure. However, electron microscopy revealed typical necrotic characteristics, such as swelling or loss of cell organelles and rupture of the cytosolic or nuclear membrane at 12 h and 24 h after ZnO NP exposure.