VUF 5574Potent, selective hA3 antagonist CAS# 280570-45-8 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 280570-45-8 | SDF | Download SDF |
PubChem ID | 4046493 | Appearance | Powder |
Formula | C21H17N5O2 | M.Wt | 371.39 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 4 mM in DMSO | ||
Chemical Name | 1-(2-methoxyphenyl)-3-(2-pyridin-3-ylquinazolin-4-yl)urea | ||
SMILES | COC1=CC=CC=C1NC(=O)NC2=NC(=NC3=CC=CC=C32)C4=CN=CC=C4 | ||
Standard InChIKey | YRAFEJSZTVWUMD-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C21H17N5O2/c1-28-18-11-5-4-10-17(18)24-21(27)26-20-15-8-2-3-9-16(15)23-19(25-20)14-7-6-12-22-13-14/h2-13H,1H3,(H2,23,24,25,26,27) | ||
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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | Potent, selective, competitive antagonist for the human adenosine A3 receptor (Ki = 4 nM). Displays ≥ 2500-fold selectivity over A1 and A2A receptors. |
VUF 5574 Dilution Calculator
VUF 5574 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.6926 mL | 13.4629 mL | 26.9259 mL | 53.8517 mL | 67.3147 mL |
5 mM | 0.5385 mL | 2.6926 mL | 5.3852 mL | 10.7703 mL | 13.4629 mL |
10 mM | 0.2693 mL | 1.3463 mL | 2.6926 mL | 5.3852 mL | 6.7315 mL |
50 mM | 0.0539 mL | 0.2693 mL | 0.5385 mL | 1.077 mL | 1.3463 mL |
100 mM | 0.0269 mL | 0.1346 mL | 0.2693 mL | 0.5385 mL | 0.6731 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Nitric oxide synthase/K+ channel cascade triggers the adenosine A(2B) receptor-sensitive renal vasodilation in female rats.[Pubmed:23396225]
Eur J Pharmacol. 2013 Feb 28;702(1-3):116-25.
Adenosine A2B-receptors mediate the adenosine-evoked renal vasodilations in male rats. Here, we tested whether this finding could be replicated in female renal vasculature and whether K(+) hyperpolarization induced by nitric oxide synthase (NOS) and/or heme oxygenase (HO) accounts for adenosine A2B receptor-sensitive renal vasodilations. In phenylephrine-preconstricted perfused kidneys, vasodilations caused by the adenosine analog 5'-N-ethylcarboxamidoadenosine (NECA, 1.6-50 nmol) were attenuated after blockade of adenosine A2B (alloxazine) but not A2A [8-(3-Chlorostyryl) caffeine, CSC] or A3 receptors (N-(2-methoxyphenyl)-N'-[2-(3-pyridinyl)-4-quinazolinyl]-urea, VUF 5574), confirming the preferential involvement of A2B receptors in NECA responses. NOS activation mediated the A2B receptor-mediated NECA response because: (i) NOS inhibition (N(omega)-nitro-L-arginine-methyl ester, L-NAME) attenuated NECA vasodilations, (ii) concurrent L-NAME/alloxazine exposure caused more inhibition of NECA responses, and (iii) inhibition of NECA responses by alloxazine disappeared in L-arginine-supplemented preparations. Although HO inhibition (zinc protoporphyrin) failed to modify NECA responses, the attenuation of these responses by alloxazine disappeared in hemin (HO inducer)-treated preparations. NECA vasodilations were also attenuated after exposure to BaCl2, glibenclamide but not tetraethylammonium (blockers of inward rectifier, ATP-sensitive, and Ca(2+)-dependent K(+)-channels, respectively). The combined alloxazine/BaCl2/glibenclamide infusion caused no additional attenuation of NECA vasodilations. Vasodilations caused by minoxidil (K(+)-channel opener) were reduced by L-NAME or BaCl2/glibenclamide, supporting the importance of NOS signaling in K(+) hyperpolarization. NECA or minoxidil vasodilations were attenuated by ouabain, Na(+)/K(+)-ATPase inhibitor, and in KCl-preconstricted preparations. Overall, facilitation of adenosine A2B receptor/NOS/K(+) channel/Na(+)/K(+)-ATPase cascade underlies NECA vasodilations in female rats. Enhancing HO activity, albeit not causally related to NECA vasodilations, improves the pharmacologically compromised (alloxazine) NECA response.
Adenosine A(3) receptor-induced proliferation of primary human coronary smooth muscle cells involving the induction of early growth response genes.[Pubmed:22906537]
J Mol Cell Cardiol. 2012 Nov;53(5):639-45.
In human coronary smooth muscle cells adenosine A(2B) receptors mediate the inhibition of platelet-derived growth factor (PDGF)-induced proliferation via induction of the transcription factor nuclear receptor subfamily 4, group A, member 1 (NR4A1). In the absence of PDGF, adenosine analogues increased proliferation. In the present study we characterised the adenosine receptor mediating the increase in proliferation of these cells and identified involved transcription factors. Cultured human coronary smooth muscle cells were treated with selective A(3) receptor ligands. Effects on proliferation were determined by counting cells and measuring changes in impedance. The induction of transcription factors was assessed by qPCR. The A(3) receptor agonist 2-chloro-IB-MECA (2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide) enhanced the number of human coronary smooth muscle cells with a half-maximal concentration of only 1 nM. 2-chloro-IB-MECA also increased the expression of the transcription factors early growth response protein (EGR)2 and EGR3, but not of EGR1, NR4A1, NR4A2 and NR4A3. The responses to 2-chloro-IB-MECA were blocked by two A(3) receptor antagonists, MRS1523 (3-propyl-6-ethyl-5[(ethylthio)carbonyl]-2-phenyl-4-propyl-3-pyridine-carboxylate ; 10-300 muM) and VUF 5574 (N-(2-methoxyphenyl)-N'-[2-(3-pyridinyl)-4-quinazolinyl]-urea; 1-100 nM, as well as by the phospholipase C-inhibitor U73343 (0.2 muM). Small interfering RNA directed against EGR2 and EGR3 abolished the increases in proliferation induced by 2-chloro-IB-MECA. In summary, this is the first report demonstrating a coupling of smooth muscle adenosine A(3) receptors to increases in proliferation of human coronary smooth cells by the activation of phospholipase C and an induction of the transcriptions factors EGR2 and EGR3. The results facilitate the understanding of the role of adenosine A(3) receptors in the cardiovascular system.
A3 adenosine receptor antagonists delay irreversible synaptic failure caused by oxygen and glucose deprivation in the rat CA1 hippocampus in vitro.[Pubmed:16415905]
Br J Pharmacol. 2006 Mar;147(5):524-32.
The role of adenosine A3 receptor activation during ischaemia-like conditions produced by oxygen and glucose deprivation (OGD) was evaluated with extracellular recordings from the CA1 region of rat hippocampal slices. In all, 7 min of OGD evoked tissue anoxic depolarisation (AD, peak at approximately 7 min from OGD start, n=20) and were invariably followed by irreversible loss of electrically evoked field epsps (fepsps, n=42).The selective adenosine A3 antagonists 3-propyl-6-ethyl-5[(ethylthio)carbonyl]-2-phenyl-4-propyl-3-pyridinecarboxylate (MRS 1523, 1-100 nM, n=31), N-[9-chloro-2-(2-furanyl)[1,2,4]-triazolo[1,5-c]quinazolin-5-yl]benzeneacetamide (MRS 1220, 100 nM, n=7), N-(2-methoxyphenyl)-N'-[2-(3-pyrindinyl)-4-quinazolinyl]-urea, (VUF 5574, 100 nM, n=3) and 5-[[(4-pyridyl)amino]carbonyl]amino-8-methyl-2-(2-furyl)-pyrazolo[4,3-e]1,2,4-tri azolo[1,5-c]pyrimidine hydrochloride (1 nM, n=4), prevented the irreversible failure of neurotransmission induced by 7 min OGD (n=45) and the development of AD in 20 out of 22 monitored slices. When tested on OGD episodes of longer duration (8-10 min, n=18), 100 nM MRS 1523 prevented or delayed the appearance of AD and exerted a protective effect on neurotransmission for episodes of up to 9 min duration. In the absence of AD, the fepsp recovery was almost total, regardless of OGD episode duration. These findings support the notion that A3 receptor stimulation is deleterious during ischaemia and suggest that selective A3 receptor block may substantially increase the resistance of the CA1 hippocampal region to ischaemic damage.
Isoquinoline and quinazoline urea analogues as antagonists for the human adenosine A(3) receptor.[Pubmed:10841801]
J Med Chem. 2000 Jun 1;43(11):2227-38.
Isoquinoline and quinazoline urea derivatives were found to bind to human adenosine A(3) receptors. Series of N-phenyl-N'-quinazolin-4-ylurea derivatives and N-phenyl-N'-isoquinolin-1-ylurea derivatives were synthesized and tested in radioligand binding assays on their adenosine receptor affinities. A structure-affinity analysis indicated that on the 2-position of the quinazoline ring or the equivalent 3-position of the isoquinoline ring a phenyl or heteroaryl substituent increased the adenosine A(3) receptor affinity in comparison to unsubstituted or aliphatic derivatives. Furthermore, the structure-affinity relationship of substituted phenylurea analogues was investigated. Substituents such as electron-withdrawing or electron-donating groups were introduced at different positions of the benzene ring to probe electronic and positional effects of substitution. Substitution on the 3- or 4-position of the phenyl ring decreased the adenosine A(3) receptor affinity. Substitution at position 2 with an electron-donating substituent, such as methyl or methoxy, increased human adenosine A(3) receptor affinity, whereas substitution on the 2-position with an electron-withdrawing substituent did not influence affinity. Combination of the optimal substituents in the two series had an additive effect, which led to the potent human adenosine A(3) receptor antagonist N-(2-methoxyphenyl)-N'-(2-(3-pyridyl)quinazolin-4-yl)urea (VUF5574, 10a) showing a K(i) value of 4 nM and being at least 2500-fold selective vs A(1) and A(2A) receptors. Compound 10a competitively antagonized the effect of an agonist in a functional A(3) receptor assay, i.e., inhibition of cAMP production in cells expressing the human adenosine A(3) receptor; a pA(2) value of 8.1 was derived from a Schild plot. In conclusion, compound 10a is a potent and selective human adenosine A(3) receptor antagonist and might be a useful tool in further characterization of the human A(3) receptor.