1-amino-9,10-dioxo-9,10-dihydro-anthracene-2-carboxylic acid-(9,10-dioxo-9,10-dihydro-[2]anthrylamide) | 6336-97-6

• 分子结构分类: 有机化合物 - 苯类化合物 - 蒽
• 英文名称: 1-amino-9,10-dioxo-9,10-dihydro-anthracene-2-carboxylic acid-(9,10-dioxo-9,10-dihydro-[2]anthrylamide)
• 英文别名: 1-Amino-9,10-dioxo-9,10-dihydro-anthracen-2-carbonsaeure-(9,10-dioxo-9,10-dihydro-[2]anthrylamid)；1-Amino-9.10-dioxo-N-(9.10-dioxo-9.10-dihydro-anthryl-(2))-9.10-dihydro-anthracencarbamid-(2)；1-Amino-anthrachinon-carbonsaeure-(2)-(anthrachinonyl-(2)-amid)；NCI39914；1-amino-N-(9,10-dioxoanthracen-2-yl)-9,10-dioxoanthracene-2-carboxamide
• CAS: 6336-97-6
• 化学式: C₂₉H₁₆N₂O₅
• 分子量: 472.456
• InChiKey: DTMDZZKQEJZHGP-UHFFFAOYSA-N

物化性质

• 沸点：
  705.7±60.0 °C(Predicted)
• 密度：
  1.524±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  4.5
• 重原子数：
  36
• 可旋转键数：
  2
• 环数：
  6.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  123
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为产物：
  描述：

  2-氨基蒽醌 在 氨 、 苯 作用下， 生成 1-amino-9,10-dioxo-9,10-dihydro-anthracene-2-carboxylic acid-(9,10-dioxo-9,10-dihydro-[2]anthrylamide)
  参考文献：
  名称：

  Rollett, Monatshefte fur Chemie, 1925, vol. 46, p. 133

  摘要：

  DOI：

文献信息

• DE604279
  申请人：——

  公开号：——

  公开（公告）日：——
• DE403395
  申请人：——

  公开号：——

  公开（公告）日：——
• Compositions and methods for bone formation and remodeling
  申请人：Wu Dianqing (Dan)

  公开号：US20100298308A1

  公开（公告）日：2010-11-25

  The mechanism by which the high bone mass (HBM) mutation (G171V) of the Wnt coreceptor LRP5 regulates the canonical Wnt signaling was investigated. The mutation was previously shown to reduce Dkk protein-1-mediated antagonism, suggesting that the first YWTD repeat domain where G171 is located may be responsible for Dkk protein-mediated antagonism. However, we found that the third YWTD repeat, but not the first repeat domain, is required for DKK1-mediated antagonism. Instead, we found that the G171V mutation disrupted the interaction of LRP5 with Mesd, a chaperon protein for LRP5/6 that is required for the coreceptors' transport to cell surfaces, resulting in less LRP5 molecules on the cell surface. Although the reduction in the level of cell surface LRP5 molecules led to a reduction in Wnt signaling in a paracrine paradigm, the mutation did not appear to affect the activity of coexpressed Wnt in an autocrine paradigm. Together with the observation that osteoblast cells produce autocrine canonical Wnt, Wnt7b, and that osteocytes produce paracrine Dkk1, we believe that the G171V mutation may cause an increase in Wnt activity in osteoblasts by reducing the number of targets for paracrine Dkk1 to antagonize without affecting the activity of autocrine Wnt.
• COMPOSITIONS AND METHODS FOR BONE FORMATION AND MODELING
  申请人：ENZO Biochem, Inc.

  公开号：US20130172332A1

  公开（公告）日：2013-07-04

  The present disclosure is directed to methods of identifying a compound that binds to or interacts with a protein receptor involved in bone formation. Specifically, the disclosure is directed to methods of identifying a compound that regulates a Wnt pathway in a cell by binding to or interacting with cavities in proteins such as LRP5, LRP 6 and/or frizzled receptor and interfering with receptor binding to other proteins in a Wnt pathway. The present disclosure is further directed to methods and compositions that comprise an identified compound for treating or preventing a disease in a mammal in which Wnt pathway suppression plays a role.
• US8367822B2
  申请人：——

  公开号：US8367822B2

  公开（公告）日：2013-02-05