diethyl 3,5-dihydroxyhomophthalate | 6121-80-8

• 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: diethyl 3,5-dihydroxyhomophthalate
• 英文别名: ethyl 2-(2'-ethoxyoxoethyl)-4,6-dihydroxybenzoate；diethyl 4,6-dihydroxy homophthalate；(2-Aethoxycarbonyl-3,5-dihydroxy-phenyl)-essigsaeure-aethylester；2-Ethoxycarbonyl-3,5-dihydroxy-phenylessigsaeure-ethylester；(3.5-Dihydroxy-2-aethoxycarbonyl-phenyl)-essigsaeure-aethylester；(2-ethoxycarbonyl-3,5-dihydroxy-phenyl)-acetic acid ethyl ester；Ethyl-3,5-dihydroxy-2-ethoxycarbonylphenylacetat；Ethyl 2-(2-ethoxy-2-oxoethyl)-4,6-dihydroxybenzoate
• CAS: 6121-80-8
• 化学式: C₁₃H₁₆O₆
• 分子量: 268.266
• InChiKey: GJSUFRTVYKVTTB-UHFFFAOYSA-N

物化性质

• 熔点：
  108 °C
• 沸点：
  448.6±24.0 °C(Predicted)
• 密度：
  1.277±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.1
• 重原子数：
  19
• 可旋转键数：
  7
• 环数：
  1.0
• sp3杂化的碳原子比例：
  0.38
• 拓扑面积：
  93.1
• 氢给体数：
  2
• 氢受体数：
  6

反应信息

• 作为反应物：
  描述：

  diethyl 3,5-dihydroxyhomophthalate 在 磺酰氯 作用下， 以 四氢呋喃 为溶剂， 生成
  参考文献：
  名称：

  靶向Hsp90伴侣：Hsp90的新型间苯二酸大内酯抑制剂的合成

  摘要：

  已经通过化学合成制备了一系列的苯并马甲内酯，并被评估为热休克蛋白90（Hsp90）的抑制剂，HSP90是新型癌症治疗剂的新兴靶标。描述了天然产物radicicol的这些间苯二酸大内酯类似物的新合成，其中关键步骤是酰化和开裂高邻苯二甲酸酐以生成异香豆素，然后进行开环易位以形成大环。该方法已扩展到一系列新的结合了1,2,3-三唑环的内酯。

  DOI：

  10.1002/chem.200902766
• 作为产物：
  描述：

  生成 diethyl 3,5-dihydroxyhomophthalate
  参考文献：
  名称：

  Improved synthesis of 5-alkylresorcinols

  摘要：

  DOI：

  10.1021/jo00983a025

文献信息

• An Improved Synthesis of Resorcylic Acid Macrolactone Inhibitors of Hsp90
  作者：Christopher Moody、James Day、Alexander Blake

  DOI：10.1055/s-0029-1217329

  日期：——

  A synthesis of resorcylic acid macrolactone analogues of the natural product radicicol is described in which the key steps are the acylation and ring opening of a homophthalic anhydride to give an isocoumarin, followed by a ring-closing metathesis to form the macrocycle.

  本文介绍了天然产物根赤壳菌素类化合物中，一种含有间苯二甲酸酐衍生物的合成方法，关键步骤包括酰化反应和环打开以生成异香豆素，随后通过环闭合的交叉复分解反应形成大环结构。
• Protection of all cleavable sites of DNA with the multiple CGCG or continuous CGG sites from the restriction enzyme, indicative of simultaneous binding of small ligands
  作者：Hirotaka Murase、Gentaro Wakisaka、Tomoharu Noguchi、Shigeki Sasaki

  DOI：10.1016/j.bmc.2020.115730

  日期：2020.10

  synthesized and evaluated by a restriction enzyme inhibition assay. DNA substrates composed of multiple CGCG or CGG sites are fully hydrolyzed by a restriction enzyme that is selective for each sequence. Under such conditions, the full-length DNA substrate remains only when the ligand binds to all binding sites and protects it from hydrolysis by the restriction enzymes. In the assay using AccII and the

  合成了具有酮酚和异羟肟酸单元的蒽酮配体（1 – 12），并通过限制酶抑制试验进行了评估。由多个CGCG或CGG位点组成的DNA底物被对每个序列具有选择性的限制酶完全水解。在这种条件下，全长DNA底物仅在配体结合所有结合位点并保护其不受限制酶水解时保留。在使用Acc II和以不同的非结合AT碱基对间隔包含不同数量CGCG位点的50-mer DNA底物的测定中，CGCG位点越多，全长DNA越增加。即同时结合配体（5）到CGCG的位置按（CGCG）5 >（CGCG）2 >（CGCG）1的顺序增加。此外，异羟肟酸与蒽酮骨架的间隔长度在CGCG位点之间的d（A / T）碱基对数目的偏爱中起着重要作用。长的间隔配体（5）相对于具有五个AT对的CGCG位点优先，而短的间隔配体（10）相对于具有两个AT对的CGCG位点优先。在使用限制性内切酶Fnu的测定中，间隔最短的配体（12）在同时结合由16个连续CGG位点组成的54-mer
• 一种从仙鹤草中提取的天然产物Agrimonolide（Ⅰ）消旋体的合成工艺
  申请人：中国药科大学

  公开号：CN108794446A

  公开（公告）日：2018-11-13

  本发明属于化学合成领域，具体涉及植物仙鹤草中提取的天然产物6，8‑二羟基‑3‑(4’‑甲氧基苯乙基)异色满‑1‑酮(dl‑Agrimonolide(I))的全合成方法。该方法由商业途径购买的4‑氯间苯二酚经七步反应合成植物仙鹤草中提取的天然产物6，8‑二羟基‑3‑(4’‑甲氧基苯乙基)异色满‑1‑酮(dl‑Agrimonolide(I))。
• Stereoselective synthesis of (+)-2-deoxyolivin based on cycloaddition reaction between the homophthalic anhydride and the chiral cyclohexenone derivative
  作者：Yoshinari Haruta、Kazumitsu Onizuka、Kyouichi Watanabe、Kyoko Kono、Akihiro Nohara、Kenichi Kubota、Shuhei Imoto、Shigeki Sasaki

  DOI：10.1016/j.tet.2008.05.080

  日期：2008.7

  tricyclic aglycon core, olivin. In this study, we established the efficient synthesis of the anthracenone core skeleton based on a cycloaddition reaction between the homophthalic anhydride and the chiral cyclohexenone derivatives, which is promoted by the combined use of molecular sieves, proton sponge, and a Lewis acid. The cyclohexenone with four chiral centers was synthesized by asymmetric and diastereoselective

  olivomycins是该化合物的aureolic家族中的代表性抗肿瘤抗生素，其包含三环糖苷配基核心olivin。在这项研究中，我们建立了基于间苯二甲酸酐与手性环己烯酮衍生物之间的环加成反应的蒽环核心骨架的有效合成方法，该反应可通过分子筛，质子海绵和路易斯酸的组合使用而得到促进。通过不对称和非对映选择性反应合成具有四个手性中心的环己烯酮，并使其与高邻苯二甲酸酐进行环加成反应，然后进行一系列反应以完成（+）-2-脱氧低聚香醇的立体选择性合成。
• Loss of heterozygosity of the MEN1 gene in a large series of TSH-secreting pituitary adenomas
  作者：C. Asteria、M. Anagni、L. Persani、Paolo Beck-Peccoz

  DOI：10.1007/bf03343929

  日期：2001.11

  Thyrotropin-secreting pituitary adenomas (TSH-omas) are rare tumors (0.5% of all pituitary adenomas) showing an invasive behavior and usually sporadic, although a few cases are associated with multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant inherited syndrome. This disorder is linked to loss of heterozygosity (LOH) on 11q13 and inactivating mutations of MEN1 gene, which is located in the same chromosomal region. As other types of anterior pituitary adenomas, TSH-omas are the result of a monoclonal outgrowth where the intrinsic genetic defects involving oncogenes or tumor suppressor genes occur in a progenitor cell. However, so far no activating mutations of particular oncogenes or inactivating mutations of tumor suppressor genes have been identified. Starting from the observation that 3-30% of sporadic pituitary adenomas show LOH on 11q13, and that allelic losses on the long arms of chromosome 11, beside 10 and 13, are significantly associated with the transition from the non-invasive to the invasive phenotype, we decided to investigate LOH on 11q13 and mutations of menin in a large series of TSH-omas. Thirteen tumors were evaluated. DNA was extracted from tumors by standard methods and genomic DNA from peripheral blood leukocytes was used as control. LOH was screened by using 3 polymorphic markers on 11q13: D11S956, PYGM, INT-2. In 3 out of 15 cases we could demonstrate LOH on 11q13, but none of the tumors showed menin mutation after sequence analysis. These data strongly suggest that menin does not play a causative role in the development of TSH-omas, and are in agreement with other studies demonstrating a limited role of menin in pituitary sporadic tumorigenesis. (C) 2001, Editrice Kurtis.