InChI
1S/C5H4N4O/c10-5-3-1-8-9-4(3)6-2-7-5/h1-2H,(H2,6,7,8,9,10)
SMILES string
O=C1NC=Nc2[nH]ncc12
InChI key
OFCNXPDARWKPPY-UHFFFAOYSA-N
grade
pharmaceutical primary standard
API family
allopurinol
manufacturer/tradename
USP
mp
>300 °C (lit.)
application(s)
pharmaceutical (small molecule)
format
neat
storage temp.
15-25°C
Gene Information
human ... XDH(7498)
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General description
This product is provided as delivered and specified by the issuing Pharmacopoeia. All information provided in support of this product, including SDS and any product information leaflets have been developed and issued under the Authority of the issuing Pharmacopoeia.For further information and support please go to the website of the issuing Pharmacopoeia.
Application
Allopurinol USP reference standard, intended for use in specified quality tests and assays as specified in the USP compendia. Also, for use with USP monographs such as:
- Allopurinol Compounded Oral Suspension
- Allopurinol Tablets
Biochem/physiol Actions
黄嘌呤氧化酶和初始嘧啶生物合成的抑制剂。治疗高尿酸血症和痛风的经典药物。
Analysis Note
These products are for test and assay use only. They are not meant for administration to humans or animals and cannot be used to diagnose, treat, or cure diseases of any kind.
Other Notes
Sales restrictions may apply.
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral - Skin Sens. 1
存储类别
6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
Dino Premilovac et al.
Diabetologia, 57(12), 2586-2595 (2014-09-13)
High sodium (HS) effects on hypertension are well established. Recent evidence implicates a relationship between HS intake and insulin resistance, even in the absence of hypertension. The aim of the current study was to determine whether loss of the vascular
Jennifer J DuPont et al.
American journal of physiology. Renal physiology, 306(12), F1499-F1506 (2014-04-25)
Oxidative stress promotes vascular dysfunction in chronic kidney disease (CKD). We utilized the cutaneous circulation to test the hypothesis that reactive oxygen species derived from NADPH oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation in CKD. Twenty subjects
C C Wen et al.
Clinical pharmacology and therapeutics, 97(5), 518-525 (2015-02-14)
The first-line treatment of hyperuricemia, which causes gout, is allopurinol. The allopurinol response is highly variable, with many users failing to achieve target serum uric acid (SUA) levels. No genome-wide association study (GWAS) has examined the genetic factors affecting allopurinol
Zhao-Qing Meng et al.
The American journal of Chinese medicine, 42(6), 1471-1483 (2014-11-12)
Gout is a metabolic disorder associated with hyperuricemia resulting in the deposition of monosodium urate (MSU) crystals in joints and tissues. Lowering serum uric acid (Sur) levels and anti-inflammation are highly essential in treating gout. Chlorogenic acid (CA), as one
Veit M Stoecklein et al.
Journal of immunology (Baltimore, Md. : 1950), 194(3), 1178-1189 (2014-12-30)
Radiation exposure induces cell and tissue damage, causing local and systemic inflammatory responses. Because the inflammasome pathway is triggered by cell death and danger-associated molecular patterns, we hypothesized that the inflammasome may signal acute and chronic immune responses to radiation.
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