S-Nitroso-N-acetyl-DL-penicillamine
(Synonyms: N-乙酰基-3-(硫代亚硝基)-DL-缬氨酸,SNAP) 目录号 : GC38849
An S-
Cas No.:67776-06-1
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
SNAP is an S-
1.Butler, A.R., and Rhodes, P.Chemistry, analysis, and biological roles of S-nitrosothiolsAnal. Biochem.249(1)1-9(1997) 2.Gasco, A., Fruttero, R., and Sorba, G.NO-donors: An emerging class of compounds in medicinal chemistryFarmaco51(10)617-635(1996) 3.Cook, J.A., Kim, S.Y., Teague, D., et al.Convenient colorimetric and fluorometric assays for S-nitrosothiolsAnal. Biochem.238(2)150-158(1996) 4.Roy, B., d'Hardemare, A.M., and Fontecave, M.New thionitrites: Synthesis, stability, and nitric oxide generationJ. Org. Chem.597019-7026(1994) 5.Singh, R.J., Hogg, N., Joseph, J., et al.Mechanism of nitric oxide release from S-nitrosothiolsJ. Biol. Chem.27118596-18603(1996)
| Cas No. | 67776-06-1 | SDF | |
| 别名 | N-乙酰基-3-(硫代亚硝基)-DL-缬氨酸,SNAP | ||
| Canonical SMILES | O=NSC(C)(C(C(O)=O)NC(C)=O)C | ||
| 分子式 | C7H12N2O4S | 分子量 | 220.25 |
| 溶解度 | DMSO: 250 mg/mL (1135.07 mM) | 储存条件 | Store at -20°C,unstable in solution, ready to use. |
| 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 | 4.5403 mL | 22.7015 mL | 45.403 mL |
| 5 mM | 0.9081 mL | 4.5403 mL | 9.0806 mL |
| 10 mM | 0.454 mL | 2.2701 mL | 4.5403 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。
Comparative pharmacology of analogues of S-Nitroso-N-acetyl-DL-penicillamine on human platelets
Br J Pharmacol 1994 Aug;112(4):1071-6.PMID:7524991DOI:10.1111/j.1476-5381.1994.tb13192.x.
1. The effects of two new analogues of S-Nitroso-N-acetyl-DL-penicillamine (SNAP), S-nitroso-N-formyl-DL-penicillamine (SNFP) and S-nitroso-DL-penicillamine (SNPL), on platelet function were examined in vitro. 2. SNAP and its analogues were potent inhibitors of platelet aggregation and inducers of disaggregation. 3. All compounds inhibited fibrinogen binding to platelets. 4. They also decreased the release of P-selectin from platelets. 5. Both inhibition of fibrinogen binding and release of P-selectin correlated with an increase in intraplatelet cyclic GMP concentrations. 6. At concentrations sufficient to inhibit platelet function and induce cyclic GMP formation (0.01-3 microM), the release of NO could be detected from SNPL but not from SNAP and SNFP. 7. Release of NO from all compounds was detected at concentrations > or = 10 microM. 8. Thus, the spontaneous release of NO from SNPL explains the actions of this compound on platelet function; however, platelet-mediated mechanisms may be involved in the release of NO from SNAP and SNFP.
Chemical mechanisms underlying the vasodilator and platelet anti-aggregating properties of S-Nitroso-N-acetyl-DL-penicillamine and S-nitrosoglutathione
Bioorg Med Chem 1995 Jan;3(1):1-9.PMID:8612040DOI:10.1016/0968-0896(94)00139-t.
The chemistries of S-nitroso-DL-penicillamine (SNAP) and S-nitrosoglutathione (GSNO) in relation to their ability to relax vascular smooth muscle and prevent platelet aggregation have been investigated. Metal ion catalysis greatly accelerates the decomposition of SNAP, but has little effect on GSNO. Instead, NO release from GSNO is effected either by NO transfer to a free thiol (e.g. cysteine), or by enzymatic cleavage of the glutamyl-cystyl peptide bond. In both cases the resulting nitrosothiol (i.e. S-nitrosocysteine and S-nitrosocystylglycine, respectively) is susceptible to metal ion catalysed NO release. We conclude that transnitrosation or enzymatic cleavage are obligatory steps in the mechanism of NO release from GSNO, whereas SNAP needs only the presence of metal ions to effect this process. The different modes of NO production may go some way towards explaining the different physiological effectiveness of these S-nitrosothiols as vasodilators and inhibitors of platelet aggregation.
Effect of nitric oxide donors S-Nitroso-N-acetyl-DL-penicillamine, spermine NONOate and propylamine propylamine NONOate on intracellular pH in cardiomyocytes
Clin Exp Pharmacol Physiol 2012 Sep;39(9):772-8.PMID:22703333DOI:10.1111/j.1440-1681.2012.05734.x.
1. Previous studies suggest that exogenous nitric oxide (NO) and NO-dependent signalling pathways modulate intracellular pH (pH(i)) in different cell types, but the role of NO in pH(i) regulation in the heart is poorly understood. Therefore, in the present study we investigated the effect of the NO donors S-Nitroso-N-acetyl-DL-penicillamine, spermine NONOate and propylamine propylamine NONOate on pH(i) in rat isolated ventricular myocytes. 2. Cells were isolated from the hearts of adult Wistar rats and pH(i) was monitored using the pH-sensitive fluorescent indicator 5-(and-6)-carboxy seminaphtharhodafluor (SNARF)-1 (10 μmol/L) and a confocal microscope. To test the effect of NO donors on the Na⁺/H⁺ exchanger (NHE), basal pH(i) in Na⁺-free buffer and pH(i) recovery from intracellular acidosis after an ammonium chloride (10 mmol/L) prepulse were monitored. The role of carbonic anhydrase was tested using acetazolamide (50 μmol/L). 4,4-Diisothiocyanatostilbene-2,2'-disulphonic acid (0.5 mmol/L; DIDS) was used to inhibit the Cl⁻/OH⁻ and Cl⁻/HCO₃-exchangers. Acetazolamide and DIDS were applied via the superfusion system 1 and 5 min before the NO donors. 3. All three NO donors acutely decreased pH(i) and this effect persisted until the NO donor was removed. In Na⁺-free buffer, the decrease in basal pH(i) was increased, whereas inhibition of carbonic anhydrase and Cl⁻/OH⁻ and Cl⁻/HCO₃⁻ exchangers did not alter the effects of the NO donors on pH(i). After an ammonium preload, pH(i) recovery was accelerated in the presence of the NO donors. 4. In conclusion, exogenous NO decreases basal pH(i), leading to increased NHE activity. Carbonic anhydrase and chloride-dependent sarcolemmal HCO₃⁻ and OH⁻ transporters are not involved in the NO-induced decrease in pH(i) in rat isolated ventricular myocytes.
Modulation of acetylcholine release in the guinea-pig trachea by the nitric oxide donor, S-Nitroso-N-acetyl-DL-penicillamine (SNAP)
Br J Pharmacol 2000 Sep;131(1):94-8.PMID:10960074DOI:10.1038/sj.bjp.0703531.
The effects of the nitric oxide (NO) donor S-Nitroso-N-acetyl-DL-penicillamine (SNAP) and the NO synthase inhibitor L-N(G)-nitroarginine (L-NOARG) on the electrically evoked [(3)H]-acetylcholine release were studied in an epithelium-free preparation of guinea-pig trachea that had been preincubated with [(3)H]-choline. SNAP (100 and 300 microM) caused small but significant increases of the electrically evoked [(3)H]-acetylcholine release (121+/-4% and 124+/-10% of control). Resting outflow of [(3)H]-ACh was not affected by SNAP. The increase by SNAP was abolished by the specific inhibitor of soluble guanylyl cyclase, 1H-[1,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ, 1 microM). The facilitatory effect of SNAP (100 and 300 microM) was reversed into inhibition of release (to 74+/-4% and to 78+/-2%) after pretreatment of the trachea with capsaicin (3 microM). ODQ prevented the inhibition. Capsaicin pretreatment alone did not significantly alter the release of [(3)H]-acetylcholine. A significant inhibition by SNAP (100 microM) of [(3)H]-acetylcholine release (78+/-3%) was also seen in the presence of the NK(2) receptor antagonist SR 48968 (30 nM). L-NOARG (10 and 100 microM) significantly enhanced the electrically-evoked smooth muscle contractions, but caused no significant increases of the evoked release from capsaicin pretreated trachea strips. This might indicate that the inhibitory effect of endogenous NO on acetylcholine release is too small to be detected by overflow studies. It is concluded that NO has dual effects on the evoked acetylcholine release. NO enhances release in the absence of modifying drugs, but NO inhibits acetylcholine release after blockade of the NK(2) receptor or after sensory nerve depletion with capsaicin. This suggests that NO and endogenous tachykinins act in series to produce an increase in acetylcholine release.
A Novel Nitric Oxide Donor, S-Nitroso-NPivaloyl-D-Penicillamine, Activates a Non-Neuronal Cardiac Cholinergic System to Synthesize Acetylcholine and Augments Cardiac Function
Cell Physiol Biochem 2019;52(4):922-934.PMID:30964609DOI:10.33594/000000064.
Background/aims: In a previous study, we reported that cardiomyocytes were equipped with non-neuronal cardiac cholinergic system (NNCCS) to synthesize acetylcholine (ACh), which is indispensable for maintaining the basic physiological cardiac functions. The aim of this study was to identify and characterize a pharmacological inducer of NNCCS. Methods: To identify a pharmacological inducer of NNCCS, we screened several chemical compounds with chemical structures similar to the structure of S-Nitroso-N-acetyl-DL-penicillamine (SNAP). Preliminary investigation revealed that SNAP is an inducer of non-neuronal ACh synthesis. We screened potential pharmacological inducers in H9c2 and HEK293 cells using western blot analysis, luciferase assay, and measurements of intracellular cGMP, NO₂ and ACh levels. The effects of the screened compound on cardiac function of male C57BL6 mice were also evaluated using cardiac catheter system. Results: Among the tested compounds, we selected S-nitroso-Npivaloyl-D-penicillamine (SNPiP), which gradually elevated the intracellular cGMP levels and nitric oxide (NO) levels in H9c2 and HEK293 cells. These elevated levels resulted in the gradual transactivation and translation of the choline acetyltransferase gene. Additionally, in vitro and in vivo SNPiP treatment elevated ACh levels for 72 h. SNPiP-treated mice upregulated their cardiac function without tachycardia but with enhanced diastolic function resulting in improved cardiac output. The effect of SNPiP was dependent on SNPiP nitroso group as verified by the ineffectiveness of N-pivaloyl-D-penicillamine (PiP), which lacks the nitroso group. Conclusion: SNPiP is identified to be one of the important pharmacological candidates for induction of NNCCS.