Diphenylamine
(Synonyms: NSC 215210) 目录号 : GC43473
Diphenylamine is an antioxidant that has been found in a variety of plants, including black and green tea plants, onion, and citrus.
Cas No.:122-39-4
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
Diphenylamine is an antioxidant that has been found in a variety of plants, including black and green tea plants, onion, and citrus. It inhibits the oxidation of α-farnesene in solution as well as in the coating of Granny Smith apples. Diphenylamine (1,000 ppm) prevents superficial scald in several varieties of apples when applied by dipping or wrapping post-harvest. It induces toxicity in the aquatic organisms D. magna, P. phosphoreum, and V. fischeri (EC50s = 2.3, ~4.75, and ~5.5 mg/L, respectively). Diphenylamine has been used in colorimetric assays for the quantification of DNA. Formulations containing diphenylamine have been used to prevent deterioration of apple and pear crops post-harvest.
| Cas No. | 122-39-4 | SDF | |
| 别名 | NSC 215210 | ||
| Canonical SMILES | C1(NC2=CC=CC=C2)=CC=CC=C1 | ||
| 分子式 | C12H11N | 分子量 | 169.2 |
| 溶解度 | Chloroform: Slightly Soluble,Methanol: Slightly Soluble | 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 | 5.9102 mL | 29.5508 mL | 59.1017 mL |
| 5 mM | 1.182 mL | 5.9102 mL | 11.8203 mL |
| 10 mM | 0.591 mL | 2.9551 mL | 5.9102 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。
Diphenylamine and derivatives in the environment: a review
Chemosphere 2003 Dec;53(8):809-18.PMID:14505701DOI:10.1016/S0045-6535(03)00613-1.
Diphenylamine (DPA) is a compound from the third European Union (EU) list of priority pollutants. It was assigned by the EU to Germany to assess and control its environmental risks. DPA and derivatives are most commonly used as stabilizers in nitrocellulose-containing explosives and propellants, in the perfumery, and as antioxidants in the rubber and elastomer industry. DPA is also widely used to prevent post-harvest deterioration of apple and pear crops. DPA is a parent compound of many derivatives, which are used for the production of dyes, pharmaceuticals, photography chemicals and further small-scale applications. Diphenylamines are still produced worldwide by the chemical industries. First reports showed that DPA was found in soil and groundwater. Some ecotoxicological studies demonstrated the potential hazard of various diphenylamines to the aquatic environment and to bacteria and animals. Studies on the biodegradability of DPA and its derivatives are very sparse. Therefore, further investigation is required to determine the complete dimension of the potential environmental hazard and to introduce possible (bio)remediation techniques for sites that are contaminated with this class of compounds. This is the first detailed review on DPA and some derivatives summarizing their environmental relevance as it is published in the literature so far and this review will recommend conducting further research in the future.
Impacts of Diphenylamine NSAID halogenation on bioactivation risks
Toxicology 2021 Jun 30;458:152832.PMID:34107285DOI:10.1016/j.tox.2021.152832.
Diphenylamine NSAIDs are highly prescribed therapeutics for chronic pain despite causing symptomatic hepatotoxicity through mitochondrial damage in five percent of patients taking them. Differences in toxicity are attributed to structural modifications to the Diphenylamine scaffold rather than its inherent toxicity. We hypothesize that marketed Diphenylamine NSAID substituents affect preference and efficiency of bioactivation pathways and clearance. We parsed the FDA DILIrank hepatotoxicity database and modeled marketed drug bioactivation into quinone-species metabolites to identify a family of seven clinically relevant Diphenylamine NSAIDs. These drugs fell into two subgroups, i.e., acetic acid and propionic acid diphenylamines, varying in hepatotoxicity risks and modeled bioactivation propensities. We carried out steady-state kinetic studies to assess bioactivation pathways by trapping quinone-species metabolites with dansyl glutathione. Analysis of the glutathione adducts by mass spectrometry characterized structures while dansyl fluorescence provided quantitative yields for their formation. Resulting kinetics identified four possible bioactivation pathways among the drugs, but reaction preference and efficiency depended upon structural modifications to the Diphenylamine scaffold. Strikingly, Diphenylamine dihalogenation promotes formation of quinone metabolites through four distinct metabolic pathways with high efficiency, whereas those without aromatic halogen atoms were metabolized less efficiently through two or fewer metabolic pathways. Overall metabolism of the drugs was comparable with bioactivation accounting for 4-13% of clearance. Lastly, we calculated daily bioload exposure of quinone-species metabolites based on bioactivation efficiency, bioavailability, and maximal daily dose. The results revealed stratification into the two subgroups; propionic acid diphenylamines had an average four-fold greater daily bioload compared to acetic acid diphenylamines. However, the lack of sufficient study on the hepatotoxicity for all drugs prevents further correlative analyses. These findings provide critical insights on the impact of Diphenylamine bioactivation as a precursor to hepatotoxicity and thus, provide a foundation for better risk assessment in drug discovery and development.
Proliferation inhibition of novel Diphenylamine derivatives
Bioorg Chem 2019 Mar;83:487-499.PMID:30453141DOI:10.1016/j.bioorg.2018.10.063.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most widely used drugs in the world but some NSAIDs such as diclofenac and tolfenamic acid display levels of cytotoxicity, an effect which has been attributed to the presence of Diphenylamine contained in their structures. A novel series of Diphenylamine derivatives were synthetised and evaluated for their cytotoxic activities and proliferation inhibition. The most active compounds in the cytotoxicity tests were derivative 6g with an IC50 value of 2.5 ± 1.1 × 10-6 M and derivative 6f with an IC50 value of 6.0 ± 3.0 × 10-6 M (L1210 cell line) after 48 h incubation. The results demonstrate that leukemic L1210 cells were much more sensitive to compounds 6f and 6g than the HEK293T cells (IC50 = 35 × 10-6 M for 6f and IC50 > 50 × 10-6 M for 6g) and NIH-3T3 (IC50 > 50 × 10-6 M for both derivatives). The IC50 values show that these substances may selectively kill leukemic cells over non-cancer cells. Cell cycle analysis revealed that a primary trend of the Diphenylamine derivatives was to arrest the cells in the G1-phase of the cell cycle within the first 24 h. UV-visible, fluorescence spectroscopy and circular dichroism were used in order to study the binding mode of the novel compounds with DNA. The binding constants determined by UV-visible spectroscopy were found to be in the range of 2.1-8.7 × 104 M-1. We suggest that the observed trend for binding constant K is likely to be a result of different binding thermodynamics accompanying the formation of the complexes.
Characterization of Novel Diphenylamine Compounds as Ferroptosis Inhibitors
J Pharmacol Exp Ther 2021 Aug;378(2):184-196.PMID:34011530DOI:10.1124/jpet.121.000534.
Ferroptosis is a form of oxidative cell death that is increasingly recognized as a key mechanism not only in neurodegeneration but also in regulated cell death, causing disease in other tissues. In neurons, major hallmarks of ferroptosis involve the accumulation of lipid reactive oxygen species (ROS) and impairment of mitochondrial morphology and function. Compounds that interfere with ferroptosis could provide novel treatment options for neurodegenerative disorders and other diseases involving ferroptosis. In the present study, we developed new compounds by refining structural elements of the BH3 interacting-domain death agonist inhibitor BI-6c9, which was previously demonstrated to block ferroptosis signaling at the level of mitochondria. Here, we inserted an antioxidative Diphenylamine (DPA) structure to the BI-6c9 structure. These DPA compounds were then tested in models of erastin, and Ras-selective lethal small molecule 3 induced ferroptosis in neuronal HT22 cells. The DPA compounds showed an increased protective potency against ferroptotic cell death compared with the scaffold molecule BI-6c9. Moreover, hallmarks of ferroptosis such as lipid, cytosolic, and mitochondrial ROS formation were abrogated in a concentration- and time-dependent manner. Additionally, mitochondrial parameters such as mitochondrial morphology, mitochondrial membrane potential, and mitochondrial respiration were preserved by the DPA compounds, supporting the conclusion that lipid ROS toxicity and mitochondrial impairment are closely related in ferroptosis. Our findings confirm that the DPA compounds are very effective agents in preventing ferroptotic cell death by blocking ROS production and, in particular, via mitochondrial protection. SIGNIFICANCE STATEMENT: Preventing neuronal cells from different forms of oxidative cell death was previously described as a promising strategy for treatment against several neurodegenerative diseases. This study reports novel compounds based on a Diphenylamine structure that strongly protects neuronal HT22 cells from ferroptotic cell death upon erastin and Ras-selective lethal small molecule 3 induction by preventing the development of different reactive oxygen species and by protecting mitochondria from ferroptotic impairments.
[Deaths due to Poisoning with Diphenylamine Hydrochloride Tablets：Four Case Reports]
Fa Yi Xue Za Zhi 2022 Jun 25;38(3):420-422.PMID:36221841DOI:10.12116/j.issn.1004-5619.2020.400205.
某女，20岁，本科，某年7月30日09：00许前往某快餐店，10：30许通过手机外卖购买药物送至店内，11：00许将9盒盐酸地芬尼多片包装丢弃至店内垃圾桶，13：30许突然倒地，后“120”到场抢救无效死亡。于14：00许采集心血。.