DPTA NONOate
(Synonyms: 3,3'-(羟基亚硝基肼)二-1-丙胺,Dipropylenetriamine NONOate) 目录号 : GC43570A nitric oxide donor
Cas No.:146724-95-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
DPTA NONOate is a NO donor. It spontaneously dissociates in a pH-dependent, first-order process with a half-life of three hours and five hours at 37°C and 22-25°C, pH 7.4, respectively, to liberate 2 moles of NO per mole of parent compound. [1][2]
Reference:
[1]. Hrabie, J.A., Klose, J.R., Wink, D.A., et al. New nitric oxide-releasing zwitterions derived from polyamines. The Journal of Organic Chemistry 58, 1472-1476 (1993).
[2]. Keefer, L.K., Nims, R.W., Davies, K.M., et al. “NONOates” (1-substituted diazen-1-ium-1,2-diolates) as nitric oxide donors: Convenient nitric oxide dosage forms. Methods in Enzymology 268, 281-293 (1996).
| Cas No. | 146724-95-0 | SDF | |
| 别名 | 3,3'-(羟基亚硝基肼)二-1-丙胺,Dipropylenetriamine NONOate | ||
| 化学名 | (Z)-1-[N-(3-aminopropyl)-N-(3-ammoniopropyl)amino]diazen-1-ium-1,2-diolate | ||
| Canonical SMILES | [NH3+]CCCN(N(N=O)[O-])CCCN | ||
| 分子式 | C6H17N5O2 | 分子量 | 191.2 |
| 溶解度 | Highly soluble in water | 储存条件 | Store at -80°C sealed under nitrogen,protect from light |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.2301 mL | 26.1506 mL | 52.3013 mL |
| 5 mM | 1.046 mL | 5.2301 mL | 10.4603 mL |
| 10 mM | 0.523 mL | 2.6151 mL | 5.2301 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Photoinduced release of nitroxyl and nitric oxide from diazeniumdiolates
J Phys Chem B 2007 Jun 21;111(24):6861-7.PMID:17488001DOI:10.1021/jp070959+.
Aqueous photochemistry of diazen-1-ium-1,2,2-triolate (Angeli's anion) and (Z)-1[N-(3-aminopropyl)-N-(3-aminopropyl)amino]diazen-1-ium-1,2-diolate (DPTA NONOate) has been investigated by laser kinetic spectroscopy. In neutral aqueous solutions, 266 nm photolysis of these diazeniumdiolates generates a unique spectrum of primary products including the ground-state triplet (3NO-) and singlet (1HNO) nitroxyl species and nitric oxide (NO*). Formation of these spectrophotometrically invisible products is revealed and quantitatively assayed by analyzing a complex set of their cross-reactions leading to the formation of colored intermediates, the N2O2*- radical and N3O3- anion. The experimental design employed takes advantage of the extremely slow spin-forbidden protic equilibration between 3NO- and 1HNO and the vast difference in their reactivity toward NO*. To account for the kinetic data, a novel combination reaction, 3NO-+1HNO, is introduced, and its rate constant of 6.6x10(9) M-1 s-1 is measured by competition with the reduction of methyl viologen by 3NO-. The latter reaction occurring with 2.1x10(9) M-1 s-1 rate constant and leading to the stable, colored methyl viologen radical cation is useful for detection of 3NO-. The distributions of the primary photolysis products (Angeli's anion: 22% 3NO-, 58% 1HNO, and 20% NO*; DPTA NONOate: 3% 3NO-, 12% 1HNO, and 85% NO*) show that neither diazeniumdiolate is a highly selective photochemical generator of nitroxyl species or nitric oxide, although the selectivity of DPTA NONOate for NO* generation is clearly greater.
Nitric oxide sustains IL-1β expression in human dendritic cells enhancing their capacity to induce IL-17-producing T-cells
PLoS One 2015 Apr 8;10(4):e0120134.PMID:25853810DOI:10.1371/journal.pone.0120134.
The role played by lung dendritic cells (DCs) which are influenced by external antigens and by their redox state in controlling inflammation is unclear. We studied the role played by nitric oxide (NO) in DC maturation and function. Human DCs were stimulated with a long-acting NO donor, DPTA NONOate, prior to exposure to lipopolysaccharide (LPS). Dose-and time-dependent experiments were performed with DCs with the aim of measuring the release and gene expression of inflammatory cytokines capable of modifying T-cell differentiation, towardsTh1, Th2 and Th17 cells. NO changed the pattern of cytokine release by LPS-matured DCs, dependent on the concentration of NO, as well as on the timing of its addition to the cells during maturation. Addition of NO before LPS-induced maturation strongly inhibited the release of IL-12, while increasing the expression and release of IL-23, IL-1β and IL-6, which are all involved in Th17 polarization. Indeed, DCs treated with NO efficiently induced the release of IL-17 by T-cells through IL-1β. Our work highlights the important role that NO may play in sustaining inflammation during an infection through the preferential differentiation of the Th17 lineage.
Endothelial nitric oxide synthase is a site of superoxide synthesis in endothelial cells treated with glyceryl trinitrate
Br J Pharmacol 2000 Nov;131(5):1019-23.PMID:11053225DOI:10.1038/sj.bjp.0703665.
Tolerance to glyceryl trinitrate (GTN) involves superoxide (O(2)(*-)) production by endothelial cells. Nitric oxide synthase (NOS) produces O(2)(*-) when L-arginine (L-arg) is limited. The purpose of this study was to test the hypothesis that GTN stimulates NOS to increase O(2)(*-) synthesis in endothelial cells when L-arg is limited. Production of O(2)(*-) by bovine aortic endothelial cells (BAEC, passages 3 - 5) was determined by spectrophotometrically measuring superoxide dismutase-inhibited reduction of ferricytochrome C to ferrocytochrome C. Cells were incubated in buffer without L-arg. O(2)(*-) production was measured using BAEC either untreated or treated with L-NAME or L-arg alone or following treatment with GTN (10(-9) to 10(-6) M) for 30 min or DPTA NONOate (10(-7) and 10(-6) M) alone or with GTN or DPTA NONOate after pretreatment with nitro-L-arginine methyl ester (L-NAME), L-arg or their inactive enantiomers, D-NAME or D-arg (all 5 x 10(-4) M) (n=6 - 7/group). L-NAME alone produced a 69% reduction in O(2)(*-) levels. Treatment with L-arg alone had no effect. Cells treated with GTN alone exhibited an increase in O(2)(*-). This effect was prevented by pretreatment with either L-NAME or L-arg, and was unaffected by D-NAME or D-arg. We observed a dose-response relationship in O(2)(*-) production to GTN over a range of 10(-9) to 10(-7) M. The NO donor, DPTA-NONOate, unlike GTN, did not have a significant effect on O(2)(*-) production. In conclusion, endothelial NOS is a site of O(2)(*-) synthesis in endothelial cells activated by GTN.
In vitro cytotoxicity of the nitric oxide donor, S-nitroso-N-acetyl-penicillamine, towards cells from human oral tissue
Pharmacol Toxicol 1999 May;84(5):218-25.PMID:10361978DOI:10.1111/j.1600-0773.1999.tb01486.x.
The cytotoxicity of the nitric oxide donor, S-nitroso-N-acetyl-penicillamine (SNAP), towards cultured human cells from oral tissue was evaluated. The toxicity of SNAP to Smulow-Glickman gingival epithelial cells was correlated with the liberation of nitric oxide, as N-acetyl-D,L-penicillamine, the SNAP metabolites, N-acetyl-D,L-penicillamine disulfide and nitrite, and preincubated (denitrosylated) SNAP did not affect viability. Comparing equimolar concentrations of various nitric oxide donors, cytotoxicity appeared to be inversely related to the relative stability (i.e., half-life) of the test compound; the sequence of cytotoxicity for a 4 hr exposure was S-nitrosoglutathione>>spermine NONOate> SNAP>DPTA NONOate>>DETA NONOate. Intracellular reduced glutathione (GSH) was lowered in S-G cells exposed to SNAP. Pretreatment of the cells with the GSH depleter, 1,3-bis-(chloroethyl)-1-nitrosourea (BCNU), enhanced the toxicity of SNAP Similar findings of enhanced sensitivity to SNAP were noted with gingival fibroblasts and periodontal ligament cells pretreated with BCNU. The toxicity of SNAP towards the gingival epithelial cells was decreased by cotreatment with the antioxidants, N-acetyl-L-cysteine, L-ascorbic acid, and (+)-catechin. Cells exposed to SNAP exhibited nuclear aberrations, including multilobed nuclei and multinucleation. SNAP-induced cell death was apparently by apoptosis, as noted by fluorescence microscopy and DNA agarose gel electrophoresis.