3-hydroxy-N'-(3-methylbenzylidene)-2-naphthohydrazide

• 分子结构分类: 有机化合物 - 苯类化合物 - 萘
• 英文名称: 3-hydroxy-N'-(3-methylbenzylidene)-2-naphthohydrazide
• 英文别名: 3-hydroxy-N-[(E)-(3-methylphenyl)methylideneamino]naphthalene-2-carboxamide
• 化学式: C₁₉H₁₆N₂O₂
• 分子量: 304.3
• InChiKey: IJQJPPVQFKWAPJ-UDWIEESQSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.6
• 重原子数：
  23
• 可旋转键数：
  3
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.05
• 拓扑面积：
  61.7
• 氢给体数：
  2
• 氢受体数：
  3

文献信息

• BATE-LACTAMASE INHIBITORS
  申请人：Dmitrienko Gary I.

  公开号：US20110046101A1

  公开（公告）日：2011-02-24

  The present invention relates to broad spectrum β-lactamase inhibitors. More particularly, the invention relates to inhibitors of Class B metallo (MBL) and Class D (OXA) β-lactamases. A method of treating a bacterial infection is provided, wherein the method comprises administering to a mammalian patient in need of such treatment a compound of formula (I) wherein R 1 is selected from R 2 is selected from with certain provisos as herein defined; in combination with a pharmaceutically acceptable β-lactam antibiotic in an amount which is effective for treating the bacterial infection.

  本发明涉及广谱β-内酰胺酶抑制剂。更具体地，本发明涉及类B金属酶(MBL)和类D（OXA）β-内酰胺酶的抑制剂。提供了一种治疗细菌感染的方法，其中该方法包括向需要此类治疗的哺乳动物患者施用具有以下结构的化合物（I）其中R1从中选择R2从中选择与此处定义的某些条件一起；与一种对治疗细菌感染有效的药用β-内酰胺抗生素结合在一起。
• ANDROGEN RECEPTOR LIGANDS
  申请人：Lloyd David George

  公开号：US20140357682A1

  公开（公告）日：2014-12-04

  Non ligand binding pocket antagonists for the human androgen receptor. The androgen receptor (AR) is a member of the Nuclear Receptor (NR) family and its role is to modulate the biological effects of the endogenous androgens, testosterone (tes) and dihydrotestosterone (DHT). Synthetic androgens and anti-androgens have therapeutic value in the treatment of various androgen dependent conditions, from regulation of male fertility to prostate cancer. Current treatment of prostate cancer (PCa) typically involves administration of ‘classical’ antiandrogens, competitive inhibitors of natural AR ligands, DHT and tes, for the ligand binding pocket (LBP) in the C-terminal ligand binding domain (LBD) of the AR. However, prolonged LBP-targeting can often lead to androgen resistance and alternative therapies and therapeutic strategies are urgently required. Disclosed herein are a class of non-steroidal, small molecule AR antagonists which inhibit the transcriptional activity of the AR by non LBP-mediated modulation. The novel class reported demonstrates full (‘true’) antagonism in AR with low micromolar potency, high selectivity over both the Estrogen Receptors alpha and beta (ERα and ERβ) and the Glucocorticoid Receptor (GR) and only micromolar partial antagonism in the Progesterone Receptor (PR). Data provide compelling evidence for such non-LBP intervention as an alternative approach to classical PCa therapy. (Formula I).
• US9296716B2
  申请人：——

  公开号：US9296716B2

  公开（公告）日：2016-03-29
• [EN] ANDROGEN RECEPTOR LIGANDS<br/>[FR] LIGANDS DU RÉCEPTEUR DES ANDROGÈNES
  申请人：PROVOST FELLOWS & SCHOLARS COLLEGE OF THE HOLY UNDIVIDED TRINITY OF QUEEN ELIZABETH NEAR DUBLIN

  公开号：WO2013076275A1

  公开（公告）日：2013-05-30

  Non ligand binding pocket antagonists for the human androgen receptor. The androgen receptor (AR) is a member of the Nuclear Receptor (NR) family and its role is to modulate the biological effects of the endogenous androgens, testosterone (tes) and dihydrotestosterone (DHT). Synthetic androgens and anti-androgens have therapeutic value in the treatment of various androgen dependent conditions, from regulation of male fertility to prostate cancer. Current treatment of prostate cancer (PCa) typically involves administration of 'classical' antiandrogens, competitive inhibitors of natural AR ligands, DHT and tes, for the ligand binding pocket (LBP) in the C-terminal ligand binding domain (LBD) of the AR. However, prolonged LBP-targeting can often lead to androgen resistance and alternative therapies and therapeutic strategies are urgently required. Disclosed herein are a class of non-steroidal, small molecule AR antagonists which inhibit the transcriptional activity of the AR by non LBP-mediated modulation. The novel class reported demonstrates full ('true') antagonism in AR with low micromolar potency, high selectivity over both the Estrogen Receptors alpha and beta (ERα and ERβ) and the Glucocorticoid Receptor (GR) and only micromolar partial antagonism in the Progesterone Receptor (PR). Data provide compelling evidence for such non-LBP intervention as an alternative approach to classical PCa therapy. (Formula I).