1,2-Bis-n-pentylcyclopenten-3-on | 57374-42-2

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: 1,2-Bis-n-pentylcyclopenten-3-on
• 英文别名: 2,3-Dipentylcyclopent-2-en-1-one
• CAS: 57374-42-2
• 化学式: C₁₅H₂₆O
• 分子量: 222.371
• InChiKey: QYZHFVLPSHAADR-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  4.9
• 重原子数：
  16
• 可旋转键数：
  8
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.8
• 拓扑面积：
  17.1
• 氢给体数：
  0
• 氢受体数：
  1

反应信息

• 作为产物：
  描述：

  Acetic acid 2,3-dipentyl-cyclopent-1-enyl ester 在 四乙基对甲苯磺酸铵 、 溶剂黄146 作用下， 生成 1,2-Bis-n-pentylcyclopenten-3-on
  参考文献：
  名称：

  Electroorganic chemistry. XXI. Selective formation of .alpha.-acetoxy ketones and general synthesis of 2,3-disubstituted 2-cyclopentenones through the anodic oxidation of enol acetates

  摘要：

  DOI：

  10.1021/ja00854a030

文献信息

• Prevention of insulin-dependent diabetes, complications thereof, or allograft rejection by inhibition of cyclooxygenase-2 activity
  申请人：Oklahoma Medical Research Foundation

  公开号：US20030017148A1

  公开（公告）日：2003-01-23

  Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease believed to be caused by an inflammatory process in the pancreas leading to selective destruction of the &bgr; cells. Inducible cyclooxygenase (COX-2) is expressed under inflammatory conditions and its product prostaglandin E 2 (PGE 2 ) is an important inflammation mediator. Administration of the selective COX-2 inhibitor such as, e.g., NS-398 prevents the onset of diabetes in mice brought on by multiple low-doses of streptozotocin (STZ). Histological observations indicated that STZ-mediated destruction of &bgr; cells was prevented by NS-398 treatment. Delayed (day 3) administration of NS-398 was also protective in this model. These results demonstrate the critical importance of COX-2 activity in autoimmune destruction of &bgr; cells, and point to the fact that COX-2 inhibition should provide a preventive therapy against IDDM or other autoimmune problems, including allograft rejection. Inhibitors of NF-&kgr;B activation may also be used to prevent IDDM and allograft rejection.

  胰岛素依赖型糖尿病（IDDM）是一种自身免疫性疾病，据信是由胰腺炎症过程导致&bgr;细胞选择性破坏引起的。诱导环氧化酶（COX-2）在炎症条件下表达，其产物前列腺素 E 2 (PGE 2 是一种重要的炎症介质。服用选择性 COX-2 抑制剂（如 NS-398）可防止小鼠因多次服用低剂量链脲佐菌素（STZ）而引发糖尿病。组织学观察表明，NS-398 能防止 STZ 介导的 &bgr; 细胞破坏。延迟（第 3 天）服用 NS-398 对该模型也有保护作用。这些结果表明，COX-2 的活性在 &bgr; 细胞的自身免疫性破坏中至关重要，并指出抑制 COX-2 可为 IDDM 或其他自身免疫性问题（包括异体移植排斥反应）提供预防性疗法。NF-&kgr;B激活抑制剂也可用于预防IDDM和异体移植排斥反应。
• PREVENTION OF INSULIN-DEPENDENT DIABETES, COMPLICATIONS THEREOF, OR ALLOGRAFT REJECTION BY INHIBITION OF CYCLOOXYGENASE-2 ACTIVITY WITH NS398 OR PDTC
  申请人：Oklahoma Medical Research Foundation

  公开号：EP1282423A2

  公开（公告）日：2003-02-12
• BIOPHOTONIC COMPOSITIONS COMPRISING A FUNGAL-DERIVED CHROMOPHORE
  申请人：Orphaderm Limited

  公开号：EP3463467A1

  公开（公告）日：2019-04-10
• US4005153A
  申请人：——

  公开号：US4005153A

  公开（公告）日：1977-01-25
• [EN] PREVENTION OF INSULIN-DEPENDENT DIABETES, COMPLICATIONS THEREOF, OR ALLOGRAFT REJECTION BY INHIBITION OF CYCLOOXYGENASE-2 ACTIVITY<br/>[FR] PREVENTION DU DIABETE INSULINO-DEPENDANT, DES COMPLICATIONS, OU DU REJET DE GREFFE ALLOGENIQUE PAR INHIBITION DE L'ACTIVITE DE LA CYCLOOXYGENASE DE TYPE 2
  申请人：OKLAHOMA MED RES FOUND

  公开号：WO2001085175A2

  公开（公告）日：2001-11-15

  Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease believed to be caused by an inflammatory process in the pancreas leading to selective destruction of the β cells. Inducible cyclooxygenase (COX-2) is expressed under inflammatory conditions and its product prostaglandin E2(PGE2) is an important inflammation mediator. Administration of the selective COX-2 inhibitor such as, e.g., NS-398 prevents the onset of diabetes in mice brought on by multiple low-doses of streptozotocin (STZ). Histological observations indicated that STZ-mediated destruction of β cells was prevented by NS-398 treatment. Delayed (day 3) administration of NS-398 was also protective in this model. These results demonstrate the critical importance of COX-2 activity in autoimmune destruction of β cells, and point to the fact that COX-2 inhibition should provide a preventive therapy against IDDM or other autoimmune problems, including allograft rejection. Inhibitors of NF-λB activation may also be used to prevent IDDM and allograft rejection.