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BzATP(ammonium salt)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
BzATP(ammonium salt)图片
CAS NO:112898-15-4
包装:1mg
市场价:560元

产品介绍

化学性质

Physical AppearanceA white to off-white solid
StorageStore at -20°C
M.Wt732.42
Cas No.112898-15-4
FormulaC24H27N6O15P3
Solubility≤14 mg/ml in DMSO
Chemical Nameammonium 6-amino-9-((2R,3R,4S,5R)-4-((4-benzoylbenzoyl)oxy)-5-(((((((hydrogenphosphonato)oxy)(hydroxy)phosphoryl)oxy)(hydroxy)phosphoryl)oxy)methyl)-3-hydroxytetrahydrofuran-2-yl)-9H-purine
Canonical SMILESO[C@H]1[C@H](N2C=NC3=C2N=CN=C3N)O[C@H](COP(OP(OP([O-])(O)=O)(O)=O)(O)=O)[C@H]1OC(C4=CC=C(C(C5=CC=CC=C5)=O)C=C4)=O.[NH4+]
运输条件蓝冰运输或根据您的需求运输。
一般建议为了使其更好的溶解,请用37℃加热试管并在超声波水浴中震动片刻。不同厂家不同批次产品溶解度各有差异,仅做参考。若实验所需浓度过大至产品溶解极限,请添加助溶剂助溶或自行调整浓度。溶液形式一般不宜长期储存,请尽快用完。

资料参考

BzATP (ammonium salt) is an agonist of the P2X receptors, exhibiting 5-30-fold higher potency at the P2X7 receptor than ATP. BzATP (ammonium salt) inhibits rat and mouse P2X7 receptors with EC50 values being 3.6 and 285 μM, respectively. However, BzATP (ammonium salt) is not selective for the P2X7 receptor as it can potently activate other P2X receptors, but without the marked superiority to ATP as an agonist. Activation of P2X7 receptors contributes to the proliferation and migration of certain types of tumor, including human glioma, and is involved in sepsis-induced intestinal barrier dysfunction. In addition, BzATP (ammonium salt) can also be used as a photoaffinity probe for exploring adenine nucleotide binding to ATPases.

References:

1. Anderson CM, Nedergaard M. Emerging challenges of assigning P2X7 receptor function and immunoreactivity in neurons. Trends in Neurosciences, 2006, 29(5): 257-262.

2. Young MT, Pelegrin P, Surprenant A. Amino acid residues in the P2X7 receptor that mediate differential sensitivity to ATP and BzATP. Molecular Pharmacology, 2007, 71(1): 92-100.

3. Ji Z, Xie Y, Guan Y, et al. Involvement of P2X7 receptor in proliferation and migration of human glioma cells. BioMed Research International, 2018, 2018: 8591397.

4. Wu X, Ren J, Chen G, et al. Systemic blockade of P2X7 receptor protects against sepsis-induced intestinal barrier disruption. Scientific Reports, 2017, 7(1): 4364.

5. Williams N, Coleman PS. Exploring the adenine nucleotide binding sites on mitochondrial F1-ATPase with a new photoaffinity probe, 3'-O-(4-benzoyl)benzoyl adenosine 5'-triphosphate. Journal of Biological Chemistry, 1982, 257(6): 2834-2841.

试验操作

Cell experiment:[3]

Cell lines

U87 and U251 glioma cells

Reaction Conditions

10 ~ 1000 μM BzATP for 24 h incubation

Applications

BzATP at 10 μM was sufficient to induce the proliferation of glioma cell significantly, while the cell proliferation reached the peak with 100 μM BzATP. Also, the migration of U87 and U251 cells was significantly increased upon BzATP treatment.

Animal experiment:[4]

Animal models

Male 2-month-old C57BL/6 mice, 20 ~ 25 g

Dosage form

5 mg/kg

Intraperitoneal injection

Applications

BzATP significantly promoted P2X7R expression in the intestines compared with intestines in the sham group and the control group after cecal ligation and puncture (CLP) induction.

Note

The technical data provided above is for reference only.

References:

1. Anderson CM, Nedergaard M. Emerging challenges of assigning P2X7 receptor function and immunoreactivity in neurons. Trends in Neurosciences, 2006, 29(5): 257-262.

2. Young MT, Pelegrin P, Surprenant A. Amino acid residues in the P2X7 receptor that mediate differential sensitivity to ATP and BzATP. Molecular Pharmacology, 2007, 71(1): 92-100.

3. Ji Z, Xie Y, Guan Y, et al. Involvement of P2X7 receptor in proliferation and migration of human glioma cells. BioMed Research International, 2018, 2018: 8591397.

4. Wu X, Ren J, Chen G, et al. Systemic blockade of P2X7 receptor protects against sepsis-induced intestinal barrier disruption. Scientific Reports, 2017, 7(1): 4364.

5. Williams N, Coleman PS. Exploring the adenine nucleotide binding sites on mitochondrial F1-ATPase with a new photoaffinity probe, 3'-O-(4-benzoyl)benzoyl adenosine 5'-triphosphate. Journal of Biological Chemistry, 1982, 257(6): 2834-2841.