H2S Donor 5a
(Synonyms: N-(苯甲酰基硫基)苯甲酰胺,N-(Benzoylthio)benzamide) 目录号 : GC41630
H2S（硫化氢）供体 5a 作为稳定的半胱氨酸活化硫化氢供体，可以与半胱氨酸和还原型谷胱甘肽等含有巯基的还原剂反应，释放出 H2S。
Cas No.:134861-13-5
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
H2S (Hydrogen sulfide) Donor 5a, as a stable, cysteine activated hydrogen sulfide donor, can react with reducing agents containing sulfhydryl groups such as cysteine and reduced glutathione to release H2S. H2S Donor 5a is very stable in aqueous solution, however, it will degrade and release H2S in biological samples containing thiols such as blood, tissues or cells.[1]
H2S exerts cytoprotective and anticancer effects, promotes wound healing, inhibits platelet aggregation and protects against myocardial ischemia, etc.[2]
In vitro experiment it shown that 0.5 mg/mL and 2 mg/mL of the most promising material (5A@Chi) was loaded with H2S and added to the HeLa cells. Both concentrations, which correspond to a H2S release of 0.49 μM and 2.20 μM, respectively, indicated no toxicity after 48 h to the cells.[3]
References:
[1]Zhao Y, et al. Cysteine-activated hydrogen sulfide (H2S) donors. J Am Chem Soc. 2011 Jan 12;133(1):15-7.
[2]Zheng Y., et al. Toward hydrogen sulfide based therapeutics: Critical drug delivery and developability issues. Med. Res. Rev. 2018;38:57–100.
[3]Batista M, et al. Chitosan Biocomposites for the Adsorption and Release of H2S. Materials (Basel). 2021 Nov 7;14(21):6701.
H2S（硫化氢）供体 5a 作为稳定的半胱氨酸活化硫化氢供体,可以与半胱氨酸和还原型谷胱甘肽等含有巯基的还原剂反应,释放出 H2S。 H2S Donor 5a 在水溶液中非常稳定,但在血液、组织或细胞等含有硫醇的生物样品中会降解并释放 H2S。[1]
H2S具有细胞保护和抗癌作用,促进伤口愈合,抑制血小板聚集,防止心肌缺血等。[2]
体外实验表明,0.5 mg/mL 和 2 mg/mL 最有前途的材料 (5A@Chi) 负载 H2S 并添加到 HeLa 细胞中。这两个浓度分别对应于 0.49 μM 和 2.20 μM 的 H2S 释放,表明 48 小时后对细胞没有毒性。[3]
| Cas No. | 134861-13-5 | SDF | |
| 别名 | N-(苯甲酰基硫基)苯甲酰胺,N-(Benzoylthio)benzamide | ||
| Canonical SMILES | O=C(SNC(C1=CC=CC=C1)=O)C2=CC=CC=C2 | ||
| 分子式 | C14H11NO2S | 分子量 | 257.3 |
| 溶解度 | DMSO : 100 mg/mL (388.64 mM; Need ultrasonic) | 储存条件 | Store at -20°C |
| 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 | 3.8865 mL | 19.4326 mL | 38.8651 mL |
| 5 mM | 0.7773 mL | 3.8865 mL | 7.773 mL |
| 10 mM | 0.3887 mL | 1.9433 mL | 3.8865 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。
Chitosan Biocomposites for the Adsorption and Release of H 2 S
Materials (Basel)2021 Nov 7;14(21):6701.PMID: 34772227DOI: 10.3390/ma14216701
The search for H2S donors has been increasing due to the multiple therapeutic effects of the gas. However, the use of nanoporous materials has not been investigated despite their potential. Zeolites and activated carbons are known as good gas adsorbents and their modification with chitosan may increase the material biocompatibility and simultaneously its release time in aqueous solution, thus making them good H2S donors. Herein, we modified with chitosan a series of A zeolites (3A, 4A and 5A) with different pore sizes and an activated carbon obtained from glycerin. The amount of H2S adsorbed was evaluated by a volumetric method and their release capacity in aqueous solution was measured. These studies aimed to verify which of the materials had appropriate H2S adsorption/release properties to be considered a potential H2S donor. Additionally, cytotoxicity assays using HeLa cells were performed. Considering the obtained results, the chitosan composite with the A zeolite with the larger pore opening was the most promising material to be used as a H2S donor so a further cytotoxicity assay using H2S loaded was conducted and no toxicity was observed.
Hydrogen sulfide-mediated endothelial function and the interaction with eNOS and PDE5A activity in human internal mammary arteries
J Int Med Res2019 Aug;47(8):3778-3791.PMID: 31155983DOI: 10.1177/0300060519847386
Objective: To investigate the role of hydrogen sulfide (H2S) in human internal mammary arteries (IMA) and its interaction with endothelial nitric oxide synthase (eNOS) and phosphodiesterase (PDE)5A activity.
Methods: Human IMA segments from patients undergoing coronary artery bypass grafting (CABG) were studied by myography for acetylcholine and sodium hydrosulfide (NaHS)-induced relaxation. Locations of 3-mercaptopyruvate sulfurtransferase (3-MPST) and cysteine aminotransferase (CAT) were examined immunohistochemically. Levels of H2S, eNOS, phosphorylated-eNOSser1177, and PDE5A were measured.
Results: In IMA segments from 47 patients, acetylcholine-induced relaxation (resistant to NG-nitro-L-arginine and indomethacin) was significantly attenuated by aminooxyacetic acid or L-aspartate (CAT inhibitors), iberiotoxin (large-conductance calcium-activated K+ channel blocker), TRAM-34 plus apamin (intermediate- and small-conductance Ca2+-activated K+ channel blockers) or glibenclamide (ATP-sensitive K+ channel blocker). 3-MPST and mitochondrial CAT were found in endothelial and smooth muscle cells while cytosolic CAT was located only in endothelial cells. Acetylcholine significantly increased the H2S levels. The H2S donor, NaHS, increased eNOS phosphorylation and down-regulated PDE5A.
Conclusions: Human conduit artery endothelium releases H2S under basal and stimulated conditions, involving the 3-MPST/CAT pathway, eNOS phosphorylation, PDE5A activity, and potassium channels. These findings may provide new therapeutic targets for treating vasospasm in CABG grafts and facilitate the development of new vasodilator drugs.
Regulation of the Heme Oxygenase-1/carbon monoxide system by hydrogen sulfide in murine coxsackievirus B3-induced myocarditis
Cell Mol Biol (Noisy-le-grand)2015 May 28;61(2):69-73.PMID: 26025406DOI: 10.1152/ajpgi.00556.2010
To explore the impact of hydrogen sulfide (H2S) on the heme oxygenase—1 (HO—1)/carbon monoxide (CO) system in coxsackie virus B3 (CVB3)—induced myocarditis. A total of 80 Balb/c mice were divided randomly into four groups designated N, C, P and S. Group N served as the negative control while groups C, P, and S were infected with CVB3 to induce myocarditis. Group P was additionally treated with DL—propargylglycine (PAG) to inhibit the generation of H2S while Group S was treated with NaHS, an H2S donor. Ten days after infection, heart sections were scored for histopathology. We also measured carboxyhemoglobin (COHb) levels in the blood and HO—1 expression by immunohistochemistry. 1. Each CVB3—infected group (C, P, and S) exhibited increased pathology, COHb levels, and HO—1 expression compared to uninfected controls. 2. Regarding histopathology, the score of group P was worse, while that of group S was better, than that of group C. 3. The P group COHb level was lower than group C, while the S group COHb level was higher than group C. 4. Positive HO—1 expression was seen in group C with reduced expression in group P and increased expression in group S. 5. A positive correlation was observed between the COHb concentration and HO—1expression; alternatively, a negative correlation was found between the histopathologic scores and both the concentration of COHb and the expression level of HO—1. Modulation of H2S can play a regulatory role in the pathogenesis of VMC by impacting the HO—1/CO pathway.