1,3-bis(3,5-dichlorophenyl)urea | 73439-19-7

• 分子结构分类: 有机化合物 - 苯类化合物 - 苯和取代衍生物
• 英文名称: 1,3-bis(3,5-dichlorophenyl)urea
• CAS: 73439-19-7
• 化学式: C₁₃H₈Cl₄N₂O
• mdl: MFCD01566238
• 分子量: 350.031
• InChiKey: VKVJIWVUYNTBEZ-UHFFFAOYSA-N

物化性质

• 熔点：
  298-300 °C
• 沸点：
  363.2±42.0 °C(Predicted)
• 密度：
  1.608±0.06 g/cm3(Predicted)
• 溶解度：
  DMSO：125 mg/mL（357.11 mM；需要超声波）

计算性质

• 辛醇/水分配系数(LogP)：
  5
• 重原子数：
  20
• 可旋转键数：
  2
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  41.1
• 氢给体数：
  2
• 氢受体数：
  1

安全信息

• 危险性防范说明：
  P261,P280,P301+P312,P302+P352,P305+P351+P338
• 危险性描述：
  H302,H315,H319,H335

反应信息

• 作为反应物：
  描述：

  谷胱甘肽 、 1,3-bis(3,5-dichlorophenyl)urea 在 GSTP enzyme 作用下， 以 aq. phosphate buffer 、 二甲基亚砜 为溶剂， 生成
  参考文献：
  名称：

  COMPOUND FOR TREATING CANCER AND DIABETES

  摘要：

  披露的一个方面涉及使用二氯苯基脲衍生物治疗癌症。

  公开号：

  US20160354327A1
• 作为产物：
  描述：

  3,5-二氯苯异氰酸酯 、 3,5-二氯苯胺 以 四氢呋喃 为溶剂， 反应 2.0h， 以88%的产率得到1,3-bis(3,5-dichlorophenyl)urea
  参考文献：
  名称：

  [EN] SUBSTITUTED 1,3-DIPHENYLUREA DERIVATIVES AND 1-PHENYL-3-PYRIDYLUREA DERIVATIVES FOR PLANT BIOTECHNOLOGY, PREPARATIONS CONTAINING THESE COMPOUNDS AND USE THEREOF
  [FR] DÉRIVÉS 1,3-DIPHÉNYLURÉE SUBSTITUÉS ET DÉRIVÉS 1-PHÉNYL-3-PYRIDYLURÉE POUR LA BIOTECHNOLOGIE VÉGÉTALE, PRÉPARATIONS CONTENANT CES COMPOSÉS ET LEUR UTILISATION

  摘要：

  本发明涉及通式（I）的取代1-苯基-3-基脲衍生物以及含有这些衍生物的制剂，其中Y为氮或碳；R1为卤素、甲氧基、甲基硫基，可选地，甲氧基和甲基硫基的氢可以被卤素取代，R2和R4分别为氢、氟、氯、溴或甲基，R3为氢或R1，但当Y为氮时，R1为卤素或甲氧基。本发明还涉及通式（I）的1-苯基-3-基脲衍生物在植物生物技术中的使用，用于增加新植物的再生和生存能力，特别是在有用植物的生产中，以及含有这些衍生物的制剂。

  公开号：

  WO2022078533A1

文献信息

• NICOTINYL RIBOSIDE COMPOUNDS AND THEIR USES
  申请人：MitoPower, LLC

  公开号：US20200397807A1

  公开（公告）日：2020-12-24

  The disclosure provides nicotinamide riboside (NR), the reduced form of NR (NRH), nicotinic acid riboside (NAR), the reduced form of NAR (NARH), derivatives thereof, compositions thereof and uses thereof. The NR and NAR derivatives have improved stability and bioavailability compared to NR and NAR. NR, NRH, NAR, NARH, and derivatives thereof can increase cellular NAD + levels and enhance mitochondrial and cellular function and cell viability. Therefore, NR, NRH, NAR, NARH, and derivatives thereof, whether alone or in combination with one or more additional therapeutic agents (e.g., a mitochondrial uncoupler or/and a PARP inhibitor), are useful for treating mitochondrial diseases, mitochondria-related diseases and conditions, metabolic disorders, and other disorders and conditions.

  该披露提供烟酰胺核糖苷（NR）、烟酰胺核糖苷的还原形式（NRH）、烟酸核糖苷（NAR）、烟酸核糖苷的还原形式（NARH）、以及它们的衍生物、组合物和用途。与NR和NAR相比，NR和NAR的衍生物具有更好的稳定性和生物利用度。NR、NRH、NAR、NARH和它们的衍生物可以增加细胞NAD+水平，增强线粒体和细胞功能以及细胞存活能力。因此，NR、NRH、NAR、NARH和它们的衍生物，无论是单独使用还是与一个或多个额外治疗剂（例如线粒体解耦蛋白抑制剂和/或PARP抑制剂）结合使用，都可用于治疗线粒体疾病、与线粒体相关的疾病和症状、代谢紊乱以及其他疾病和症状。
• Preparation of oxazolidine-2,4-diones
  申请人：BASF Aktiengesellschaft

  公开号：US04233450A1

  公开（公告）日：1980-11-11

  A novel process for the preparation of oxazolidine-2,4-diones by reaction of ureas with 2-hydroxycarboxylic acid esters.

  一种新型的制备噁唑烷二酮的方法，通过尿素与2-羟基羧酸酯反应。
• Structure–Activity Relationship and Mechanistic Studies of Bisaryl Urea Anticancer Agents Indicate Mitochondrial Uncoupling by a Fatty Acid-Activated Mechanism
  作者：Edward York、Daniel A. McNaughton、Ariane Roseblade、Charles G. Cranfield、Philip A. Gale、Tristan Rawling

  DOI：10.1021/acschembio.1c00807

  日期：2022.8.19

  mitochondria through the fatty acid-activated mechanism. This mechanistic insight was used to develop a library of substituted bisaryl ureas for structure–activity relationship studies and subsequent cell testing. It was found that lipophilic electron-withdrawing groups on bisaryl ureas enhanced electrogenic proton transport via the fatty acid-activated mechanism and had the capacity to depolarize mitochondria

  靶向癌细胞线粒体是开发新型抗癌药物的一种很有前途的方法。实验性抗癌剂N , N'-双 (3,5-二氯苯基) 脲 ( SR4 ) 通过使用无蛋白机制解偶联线粒体氧化磷酸化 (OxPhos)，在多种癌细胞系中诱导细胞凋亡。然而， SR4使线粒体去极化的确切机制尚不清楚，因为SR4缺乏通常在蛋白质非依赖性解偶联剂中发现的酸性官能团。最近，研究表明，结构相关的硫脲可以通过脂肪酸激活机制促进质子跨脂质双层的传输，其中脂肪酸充当质子化/去质子化位点，硫脲充当穿梭于去质子化脂肪酸的阴离子转运体穿过磷脂双分子层以实现质子泄漏。在本文中，我们表明SR4介导的质子传输因脂质双层中游离脂肪酸的存在而增强，表明SR4通过脂肪酸激活机制解偶联线粒体。这种机制洞察力被用于开发取代双芳基脲库，用于结构-活性关系研究和随后的细胞测试。研究发现，双芳基脲上的亲脂性吸电子基团通过脂肪酸激活机制增强了生电质子传输，并具有使线粒体去极化和降低
• Polymer implants for treatment of metabolic disorders
  申请人：UNIVERSITY OF SOUTH CAROLINA

  公开号：US10092508B2

  公开（公告）日：2018-10-09

  Implantable devices including a biocompatible matrix configured for long term location in adipose tissue and a biologically active agent that can be carried by the matrix and delivered to the adipose tissue following implant therein. The biologically active agent can include a modulator or a precursor thereof that can directly or indirectly modify the gene expression of adipose cells, e.g., adipocytes, and thereby modify the presence or quantity of one or more expression products of the adipose tissue that may act locally on distant from the implant site in an endocrine fashion. Modulators can include small molecules (e.g., resveratrol), polynucleotides (e.g., RNAi), or polypeptides (e.g., antibodies or functional fragments thereof).

  可植入装置包括用于长期植入脂肪组织的生物相容性基质，以及可由基质携带并在植入脂肪组织后输送到脂肪组织的生物活性剂。生物活性剂可包括调制剂或其前体，可直接或间接改变脂肪细胞（如脂肪细胞）的基因表达，从而改变脂肪组织中一种或多种表达产物的存在或数量，这些产物可在局部以内分泌方式作用于远离植入部位的地方。调节剂可包括小分子（如白藜芦醇）、多核苷酸（如 RNAi）或多肽（如抗体或其功能片段）。
• 1,3-Bis(3,5-dichlorophenyl) urea compound ‘COH-SR4’ inhibits proliferation and activates apoptosis in melanoma
  作者：Sharad S. Singhal、James Figarola、Jyotsana Singhal、Kathryn Leake、Lokesh Nagaprashantha、Christopher Lincoln、B. Gabriel Gugiu、David Horne、Richard Jove、Sanjay Awasthi、Samuel Rahbar

  DOI：10.1016/j.bcp.2012.08.020

  日期：2012.12

  The current clinical interventions in malignant melanomas are met with poor response to therapy due to dynamic regulation of multiple melanoma signaling pathways consequent to administration of single target agents. In this context of limited response to single target agents, novel candidate molecules capable of effectively inducing tumor inhibition along with targeting multiple critical nodes of melanoma signaling assume translational significance. In this regard, we investigated the anti-cancer effects of a novel dichlorophenyl urea compound called COH-SR4 in melanoma. The SR4 treatment decreased the survival and inhibited the clonogenic potential of melanomas along with inducing apoptosis in vitro cultures. SR4 treatments lead to inhibition of GST activity along with causing G2/M phase cell cycle arrest. Oral administration of 4 mg/kg SR4 leads to effective inhibition of tumor burdens in both syngeneic and nude mouse models of melanoma. The SR4 treatment was well tolerated and no overt toxicity was observed. The histopathological examination of resected tumor sections revealed decreased blood vessels, decrease in the levels of angiogenesis marker, CD31, and proliferation marker, Ki67, along with an increase in pAMPK levels. Western blot analyses of resected tumor lysates revealed increased PARP cleavage, Him, pAMPK along with decreased pAkt, vimentin, fibronectin, CDK4 and cyclin B1. Thus, SR4 represents a novel candidate for the further development of mono and combinatorial therapies to effectively target aggressive and therapeutically refractory melanomas. (C) 2012 Elsevier Inc. All rights reserved.