γ-aminovaleric acid methyl ester hydrochloride | 58620-99-8

• 分子结构分类: 有机化合物 - 有机酸及其衍生物 - 羧酸及其衍生物
• 英文名称: γ-aminovaleric acid methyl ester hydrochloride
• 英文别名: Methyl 4-aminopentanoate hydrochloride；methyl 4-aminopentanoate;hydrochloride
• CAS: 58620-99-8
• 化学式: C₆H₁₃NO₂*ClH
• 分子量: 167.636
• InChiKey: GLGDQRWTKGJGRE-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0.71
• 重原子数：
  10
• 可旋转键数：
  4
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.83
• 拓扑面积：
  52.3
• 氢给体数：
  2
• 氢受体数：
  3

反应信息

• 作为反应物：
  描述：

  (R)-methoxytrifluoromethylphenylacetyl chloride 、 γ-aminovaleric acid methyl ester hydrochloride 在 吡啶 作用下， 生成 methyl (RS)-4-amino>pentanoate
  参考文献：
  名称：

  Synthetic studies on antitumor antibiotic, bleomycin. 27. Man-designed bleomycin with altered sequence specificity in DNA cleavage

  摘要：

  DOI：

  10.1021/ja00158a052
• 作为产物：
  描述：

  4-aminopentanoic acid 在 氯化亚砜 作用下， 以 甲醇 为溶剂， 反应 72.0h， 以100%的产率得到γ-aminovaleric acid methyl ester hydrochloride
  参考文献：
  名称：

  Synthetic studies on antitumor antibiotic, bleomycin. 27. Man-designed bleomycin with altered sequence specificity in DNA cleavage

  摘要：

  DOI：

  10.1021/ja00158a052

文献信息

• Michael additions of hydrazones for carbon–carbon bond formation
  作者：Jack E. Baldwin、Robert M. Adlington、Jeffrey C. Bottaro、Ashok U. Jain、Jayant N. Kolhe、Matthew W. D. Perry、Ian M. Newington

  DOI：10.1039/c39840001095

  日期：——

  The lithium salts of t-butyl-and trityl-hydrazones react with methyl crotonate to form C-trapped azo-esters and similar products were observed from a thermal ene-reaction of aldehyde t-butylhydrazones with methyl acrylate or acrylonitrile, and aldehyde phenylhydrazones with methyl acrylate; these products can be diverted into synthetically useful γ-keto-esters, γ-keto-nitriles, saturated esters, γ

  叔丁基hydr和三苯甲基-的锂盐与巴豆酸甲酯反应形成C捕获的偶氮酯，并且通过醛叔丁基hydr与丙烯酸甲酯或丙烯腈的热烯反应，以及醛苯hydr与丙烯的热烯反应观察到类似的产物。丙烯酸甲酯 这些产品可以分为合成有用的γ-酮酯，γ-酮腈，饱和酯，γ-烷基-2-吡咯烷酮和γ-氨基酯。
• [EN] NOVEL CYCLIC CATIONIC LIPIDS AND METHODS OF USE<br/>[FR] NOUVEAUX LIPIDES CATIONIQUES CYCLIQUES ET PROCÉDÉS D'UTILISATION
  申请人：PROTIVA BIOTHERAPEUTICS INC

  公开号：WO2011141704A1

  公开（公告）日：2011-11-17

  The present invention provides compositions and methods for the delivery of therapeutic agents to cells. In particular, these include novel cationic lipids and nucleic acid- lipid particles that provide efficient encapsulation of nucleic acids and efficient delivery of the encapsulated nucleic acid to cells in vivo. The compositions of the present invention are highly potent, thereby allowing effective knock-down of a specific target protein at relatively low doses. In addition, the compositions and methods of the present invention are less toxic and provide a greater therapeutic index compared to compositions and methods previously known in the art.

  本发明提供了用于将治疗剂传递至细胞的组合物和方法。具体包括新型阳离子脂质和核酸-脂质颗粒，能够有效地封装核酸并有效地将封装的核酸传递至体内细胞。本发明的组合物非常强效，因此能够以相对较低的剂量有效地降低特定靶蛋白的表达。此外，与先前已知的组合物和方法相比，本发明的组合物和方法毒性较低，提供更大的治疗指数。
• Pharmaceutical preparations having psychotropic activity and process for
  申请人：Hoechst Aktiengesellschaft

  公开号：US04053588A1

  公开（公告）日：1977-10-11

  Pharmaceutical preparations containing an L-pyroglutamic acid amide, processes for their preparation and methods of treating psychotic diseases with them.

  含有L-吡咯環戊二酸酰胺的制药制剂，其制备方法以及用它们治疗精神疾病的方法。
• Role of Lysine 411 in Substrate Carboxyl Group Binding to the Human Reduced Folate Carrier, as Determined by Site-Directed Mutagenesis and Affinity Inhibition
  作者：Yijun Deng、Zhanjun Hou、Lei Wang、Christina Cherian、Jianmei Wu、Aleem Gangjee、Larry H. Matherly

  DOI：10.1124/mol.107.043190

  日期：2008.4

  Reduced folate carrier (RFC) is the major membrane transporter for folates and antifolates in mammalian tissues. Recent studies used radioaffinity labeling with N -hydroxysuccinimide (NHS)-[3H]methotrexate (MTX) to localize substrate binding to residues in transmembrane domain (TMD) 11 of human RFC. To identify the modified residue(s), seven nucleophilic residues in TMD11 were mutated to Val or Ala and mutant constructs expressed in RFC-null HeLa cells. Only K411A RFC was not inhibited by NHS-MTX. By radioaffinity labeling with NHS-[3H]MTX, wild-type (wt) RFC was labeled; for K411A RFC, radiolabeling was abolished. When Lys411 was replaced with Ala, Arg, Gln, Glu, Leu, and Met, only K411E RFC showed substantially decreased transport. Nine classic diamino furo[2,3- d ]pyrimidine antifolates with unsubstituted α- and γ-carboxylates (1), hydrogen- or methyl-substituted α-(2,3) or γ-(4,5) carboxylates, or substitutions of both α- and γ-carboxylates (6-9) were used to inhibit [3H]MTX transport with RFC-null K562 cells expressing wt and K411A RFCs. For wt and K411A RFCs, inhibitory potencies were in the order 4 > 5 > 1 > 3 > 2; 6 to 9 were poor inhibitors. Inhibitions decreased in the presence of physiologic anions. When NHS esters of 1, 2, and 4 were used to covalently modify wt RFC, inhibitory potencies were in the order 2 > 1 > 4; inhibition was abolished for K411A RFC. These results establish that Lys411 participates in substrate binding via an ionic association with the substrate γ-carboxylate; however, this is not essential for transport. An unmodified α-carboxylate is required for high-affinity substrate binding to RFC, whereas the γ-carboxyl is not essential.

  还原型叶酸载体（RFC）是哺乳动物组织中叶酸和抗叶酸剂的主要膜转运蛋白。最近的研究使用 N-羟基琥珀酰亚胺 (NHS)-[3H]甲氨蝶呤 (MTX) 的放射性亲和标记来定位与人 RFC 跨膜结构域 (TMD) 11 残基结合的底物。为了鉴定修饰的残基，TMD11 中的七个亲核残基被突变为 Val 或 Ala，并在 RFC 无效的 HeLa 细胞中表达突变构建体。只有 K411A RFC 不被 NHS-MTX 抑制。通过用 NHS-[3H]MTX 进行放射亲和标记，标记野生型 (wt) RFC；对于 K411A RFC，放射性标记已被废除。当 Lys411 被 Ala、Arg、Gln、Glu、Leu 和 Met 取代时，只有 K411E RFC 显示运输量显着下降。九种经典的二氨基呋喃并[2,3-d]嘧啶抗叶酸剂，具有未取代的 α- 和 γ- 羧酸盐 (1)、氢或甲基取代的 α-(2,3) 或 γ-(4,5) 羧酸盐或取代基使用 α- 和 γ- 羧酸盐 (6-9) 来抑制表达 wt 和 K411A RFC 的 RFC-null K562 细胞的 [3H]MTX 转运。对于 wt 和 K411A RFC，抑制效力的顺序为 4 > 5 > 1 > 3 > 2； 6至9是较差的抑制剂。存在生理阴离子时抑制作用减弱。当NHS酯1、2和4用于共价修饰wt RFC时，抑制效力的顺序为2>1>4； K411A RFC 的抑制被取消。这些结果证实 Lys411 通过与底物 γ-羧酸盐的离子缔合参与底物结合；然而，这对于运输来说并不是必需的。高亲和力底物与 RFC 结合需要未修饰的 α-羧酸酯，而 γ-羧基不是必需的。
• VASILEVA, O. S.;USIK, N. V.;SINILINA, I. P.;SMIRNOVA, A. A., METODY SINTEZA, STROENIE I XIM. PREVRASHCHENIYA NITROSOED. I AMINOKISLOT,+
  作者：VASILEVA, O. S.、USIK, N. V.、SINILINA, I. P.、SMIRNOVA, A. A.

  DOI：——

  日期：——