4-(1H-pyrazolo[4,3-d]pyrimidin-3-yl)morpholine

• 分子结构分类: 有机化合物 - 有机杂环化合物 - 吡唑并嘧啶类
• 英文名称: 4-(1H-pyrazolo[4,3-d]pyrimidin-3-yl)morpholine
• 化学式: C₉H₁₁N₅O
• 分子量: 205.22
• InChiKey: XWQAZHGVGYUFNK-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0
• 重原子数：
  15
• 可旋转键数：
  1
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.44
• 拓扑面积：
  66.9
• 氢给体数：
  1
• 氢受体数：
  5

文献信息

• Biomarkers for response to rapamycin analogs
  申请人：MEMORIAL SLOAN-KETTERING CANCER CENTER

  公开号：US10610521B2

  公开（公告）日：2020-04-07

  The present invention relates to the use of one or more biomarkers to evaluate the likelihood that a rapamycin analog would produce an anti-cancer effect in a subject. It is based, at least in part, on the results of experiments employing an integrated next-generation sequencing approach to interrogate spatially separated tumor specimens from the same individuals to decipher intra-tumor and intertumor heterogeneity and determine the oncogenomic basis of exceptional therapeutic benefit to rapalogs in kidney cancer patients. These experiments implicated loss of function mutations in TSC1 and/or TSC2 and/or gain-of-function of mTOR in therapeutic responsiveness to rapamycin analogs. Accordingly, in non-limiting embodiments, the present invention provides for assay methods and kits for determining the presence of loss of function mutations in TSC1 and/or TSC2 and/or gain-of-function of mTOR, and methods of using such determinations in selecting a therapeutic regimen for a cancer patient and in methods of treating cancer patients. In particular non-limiting embodiments, a plurality of tumor sites are evaluated and the composite effect of the genetic background on mTOR function is assessed.

  本发明涉及使用一种或多种生物标志物来评估雷帕霉素类似物对受试者产生抗癌效果的可能性。本发明至少部分基于采用综合下一代测序方法的实验结果，该方法可对来自同一个体的空间上分离的肿瘤标本进行检测，以破译肿瘤内和肿瘤间的异质性，并确定雷帕霉素类似物对肾癌患者产生特殊疗效的肿瘤基因组学基础。这些实验表明，TSC1和/或TSC2的功能缺失突变和/或mTOR的功能增益与雷帕霉素类似物的治疗反应性有关。因此，在非限制性实施方案中，本发明提供了用于确定 TSC1 和/或 TSC2 和/或 mTOR 功能增益中是否存在功能缺失突变的检测方法和试剂盒，以及在为癌症患者选择治疗方案和治疗癌症患者的方法中使用这种确定方法的方法。在特定的非限制性实施方案中，对多个肿瘤部位进行评估，并评估遗传背景对 mTOR 功能的综合影响。
• BIOMARKERS FOR RESPONSE TO RAPAMYCIN ANALOGS
  申请人：Memorial Sloan Kettering Cancer Center

  公开号：EP2971122B1

  公开（公告）日：2020-08-26
• SYSTEM AND METHOD FOR PROSTRATE TREATMENT
  申请人：RESURGE THERAPEUTICS, INC.

  公开号：US20220031606A1

  公开（公告）日：2022-02-03

  A minimally invasive treatment of benign prostatic hyperplasia (BPH) tissue. A system includes a sustained release formulation comprising a cytostatic or cytotoxic drug, and an applicator or delivery system for local delivery of a composition comprising or consisting essentially of the sustained release formulation to the prostate. A method includes introducing a composition into the prostate to achieve a sustained release of the cytostatic or cytotoxic drug over a period of between about 14 days and 12 months.
• [EN] BIOMARKERS FOR RESPONSE TO RAPAMYCIN ANALOGS<br/>[FR] BIOMARQUEURS POUR RÉPONSE À DES ANALOGUES DE RAPAMYCINE
  申请人：SLOAN KETTERING INST CANCER

  公开号：WO2014144451A2

  公开（公告）日：2014-09-18

  The present invention relates to the use of one or more biomarkers to evaluate the likelihood that a rapamycin analog would produce an anti-cancer effect in a subject. It is based, at least in part, on the results of experiments employing an integrated next-generation sequencing approach to interrogate spatially separated tumor specimens from the same individuals to decipher intra-tumor and intertumor heterogeneity and determine the oncogenomic basis of exceptional therapeutic benefit to rapalogs in kidney cancer patients. These experiments implicated loss of function mutations in TSC1 and/or TSC2 and/or gain-of- function of mTOR in therapeutic responsiveness to rapamycin analogs. Accordingly, in non-limiting embodiments, the present invention provides for assay methods and kits for determining the presence of loss of function mutations in TSC1 and/or TSC2 and/or gain-of- function of mTOR, and methods of using such determinations in selecting a therapeutic regimen for a cancer patient and in methods of treating cancer patients. In particular non-limiting embodiments, a plurality of tumor sites are evaluated and the composite effect of the genetic background on mTOR function is assessed.