N-(甲基磺酰基)-beta-丙氨酸 | 105611-92-5

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 中文名称: N-(甲基磺酰基)-beta-丙氨酸
• 英文名称: methylsulfonyl-β-alanine
• 英文别名: N-(methylsulfonyl)-beta-alanine；3-(methanesulfonamido)propanoic acid
• CAS: 105611-92-5
• 化学式: C₄H₉NO₄S
• mdl: MFCD06434734
• 分子量: 167.186
• InChiKey: WWQSOJVZBSHWEE-UHFFFAOYSA-N

物化性质

• 沸点：
  353.4±44.0 °C(Predicted)
• 密度：
  1.404±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  -1.2
• 重原子数：
  10
• 可旋转键数：
  4
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.75
• 拓扑面积：
  91.8
• 氢给体数：
  2
• 氢受体数：
  5

安全信息

• 危险等级：
  IRRITANT
• 海关编码：
  2935009090

反应信息

• 作为反应物：
  描述：

  5-[(S)-2-((S)-2-tert-Butoxycarbonylamino-3-phenyl-propionylamino)-2-pentylcarbamoyl-ethyl]-2-methoxycarbonylmethoxy-benzoic acid methyl ester 、 N-(甲基磺酰基)-beta-丙氨酸 在 盐酸 、 三乙胺 、 1-羟基苯并三唑 、 1-(3-二甲基氨基丙基)-3-乙基碳二亚胺 作用下， 生成 5-{(S)-2-[(S)-2-(3-Methanesulfonylamino-propionylamino)-3-phenyl-propionylamino]-2-pentylcarbamoyl-ethyl}-2-methoxycarbonylmethoxy-benzoic acid methyl ester
  参考文献：
  名称：

  Inhibitors of protein tyrosine phosphatase

  摘要：

  本发明涉及小分子量、非肽类的蛋白酪氨酸磷酸酶1（PTP1）的化学式I和II的抑制剂，用于治疗和/或预防非胰岛素依赖型糖尿病（NIDDM）。

  公开号：

  US06353023B1
• 作为产物：
  描述：

  methyl 3-(methylsulfonamido)propanoate 在 lithium hydroxide 作用下， 以 四氢呋喃 、 甲醇 为溶剂， 以82%的产率得到N-(甲基磺酰基)-beta-丙氨酸
  参考文献：
  名称：

  Synthetic Lethality in Pancreatic Cancer: Discovery of a New RAD51-BRCA2 Small Molecule Disruptor That Inhibits Homologous Recombination and Synergizes with Olaparib

  摘要：

  Synthetic lethality is an innovative framework for discovering novel anticancer drug candidates. One example is the use of PARP inhibitors (PARPi) in oncology patients with BRCA mutations. Here, we exploit a new paradigm based on the possibility of triggering synthetic lethality using only small organic molecules (dubbed "fully small-molecule-induced synthetic lethality"). We exploited this paradigm to target pancreatic cancer, one of the major unmet needs in oncology. We discovered a dihydroquinolone pyrazoline-based molecule (35d) that disrupts the RAD51-BRCA2 protein-protein interaction, thus mimicking the effect of BRCA2 mutation. 35d inhibits the homologous recombination in a human pancreatic adenocarcinoma cell line. In addition, it synergizes with olaparib (a PARPi) to trigger synthetic lethality. This strategy aims to widen the use of PARPi in BRCA-competent and olaparib-resistant cancers, making fully small-molecule-induced synthetic lethality an innovative approach toward unmet oncological needs.

  DOI：

  10.1021/acs.jmedchem.9b01526

文献信息

• Discovery of VNRX-7145 (VNRX-5236 Etzadroxil): An Orally Bioavailable β-Lactamase Inhibitor for Enterobacterales Expressing Ambler Class A, C, and D Enzymes
  作者：Robert E. Trout、Allison Zulli、Eugen Mesaros、Randy W. Jackson、Steven Boyd、Bin Liu、Jodie Hamrick、Denis Daigle、Cassandra L. Chatwin、Kaitlyn John、Lisa McLaughlin、Susan M. Cusick、William J. Weiss、Mark E. Pulse、Daniel C. Pevear、Greg Moeck、Luigi Xerri、Christopher J. Burns

  DOI：10.1021/acs.jmedchem.1c00437

  日期：2021.7.22

  acid-containing β-lactamase inhibitor 5 (VNRX-5236). In vitro and in vivo studies demonstrated that 5 restored the activity of the oral cephalosporin antibiotic ceftibuten against Enterobacterales expressing Ambler class A extended-spectrum β-lactamases, class A carbapenemases, class C cephalosporinases, and class D oxacillinases.

  革兰氏阴性菌的主要抗菌素耐药机制是产生 β-内酰胺酶。产生 β-内酰胺酶的多重耐药“超级细菌”的日益出现导致医院急诊科 (ED) 就诊和住院费用增加，因为这些难以治疗的感染需要肠外抗生素治疗细菌。为了解决门诊治疗不足的问题，我们启动了一个迭代计划，将药物化学、生化测试、微生物分析和口服药代动力学评估相结合。先导优化专注于多种更小、更亲脂的活性化合物，然后探索各种其各自前药的口服生物利用度，提供了36(VNRX-7145/VNRX-5236 etzadroxil)，含硼酸的 β-内酰胺酶抑制剂5 (VNRX-5236)的前药。体外和体内研究表明，5恢复了口服头孢菌素抗生素头孢布坦对表达 Ambler A 类超广谱 β-内酰胺酶、A 类碳青霉烯酶、C 类头孢菌素酶和 D 类苯唑西林酶的肠杆菌的活性。
• Novel peptides which are active on the central nervous system and have
  申请人：Hoechst Aktiengesellschaft

  公开号：US04696913A1

  公开（公告）日：1987-09-29

  The invention relates to peptides of the formula I R.sup.4 -A.sup.5 -A.sup.6 -A.sup.7 (I) in which R.sup.4 denotes an acyl group, R.sup.5 denotes D-Lys or Lys, A.sup.6 denotes the radical of phenylalanine, N-methylphenylalanine, 4-alkoxyphenylalanine or 1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid, and R.sup.7 denotes a basic radical, processes for their preparation and their use.

  本发明涉及公式I中的肽，其中R.sup.4表示酰基基团，R.sup.5表示D-Lys或Lys，A.sup.6表示苯丙氨酸基团，N-甲基苯丙氨酸基团，4-烷氧基苯丙氨酸基团或1,2,3,4-四氢异喹啉-3-羧酸基团，R.sup.7表示碱性基团，以及其制备方法和用途。
• NOVEL 3-(INDOL-3-YL)-PYRIDINE DERIVATIVES, PHARMACEUTICAL COMPOSITIONS AND METHODS FOR USE
  申请人：ITEOS THERAPEUTICS

  公开号：US20150225367A1

  公开（公告）日：2015-08-13

  The present invention relates to compound of Formula I or pharmaceutically acceptable enantiomers, salts or solvates thereof. The invention further relates to the use of the compounds of Formula I as TDO2 inhibitors. The invention also relates to the use of the compounds of Formula I for the treatment and/or prevention of cancer, neurodegenerative disorders such as Parkinson's disease, Alzheimer's disease and Huntington's disease, chronic viral infections such as HCV and HIV, depression, and obesity. The invention also relates to a process for manufacturing compounds of Formula I.

  本发明涉及公式I的化合物或其药学上可接受的对映体、盐或溶剂。本发明还涉及将公式I的化合物用作TDO2抑制剂的用途。本发明还涉及将公式I的化合物用于治疗和/或预防癌症、神经退行性疾病，如帕金森病、阿尔茨海默病和亨廷顿病、慢性病毒感染，如丙型肝炎病毒和人类免疫缺陷病毒、抑郁症和肥胖症。本发明还涉及一种制造公式I的化合物的方法。
• Modification of the N-terminus of peptidomimetic protein tyrosine phosphatase 1B (PTP1B) inhibitors: identification of analogues with cellular activity
  作者：Scott D. Larsen、F.Craig Stevens、Thomas J. Lindberg、Paul M. Bodnar、Theresa J. O'Sullivan、Heinrich J. Schostarez、Barbara J. Palazuk、John E. Bleasdale

  DOI：10.1016/s0960-894x(02)01065-x

  日期：2003.3

  Low molecular weight peptidomimetic compounds based on 0-malonyl tyrosine and 0-carboxymethyl salicylic acid are potent inhibitors of PTP1B. Modifications of the N-terminal Boc-Phe moiety were undertaken in an effort to improve physical chemical properties and to achieve cellular activity. Although Phe ultimately proved to be the optimal N-terminal amino acid, several viable replacements for the Boc group were identified, two of which afforded analogues that were effective at enhancing the insulin-stimulated uptake of 2-deoxyglucose by L6 myocytes. (C) 2003 Elsevier Science Ltd. All rights reserved.