PKB/Akt激酶小分子抑制剂研究进展
摘 要
PKB/Akt激酶，也称为蛋白激酶B，是一种在细胞信号传导中起关键作用的酶。它属于丝氨酸/苏氨酸激酶家族，是PI3K-Akt信号通路的重要组成部分。这一信号通路在调节细胞生长、增殖、存活和代谢等多个生理过程中发挥着核心作用。PKB/Akt激酶作为肿瘤治疗的重要靶点，其小分子抑制剂在抗肿瘤机制方面展现出了独特的优势。通过特异性地抑制PKB/Akt激酶的活性，这些抑制剂可以有效地阻断肿瘤细胞的生长和增殖，从而达到抗肿瘤的目的。在临床试验中，PKB/Akt激酶小分子抑制剂已经展现出了良好的疗效和安全性。特别是在与其他抗肿瘤药物的联合应用中，这些抑制剂能够发挥协同作用，进一步提高抗肿瘤效果。基于患者特征的个体化治疗也成为了PKB/Akt激酶小分子抑制剂临床应用的新趋势。抑制剂的选择性、耐受性、代谢动力学和药代动力学等方面的问题需要进一步优化和改进。
关键词：PKB/Akt激酶；抗肿瘤机制；个体化治疗
Abstract
The PKB / Akt kinase, also known as protein kinase B, is an enzyme that plays a key role in cell signaling. It belongs to the serine / threonine kinase family and is an important component of the PI3K-Akt signaling pathway. This signaling pathway plays a central role in regulating multiple physiological processes, including cell growth, proliferation, survival, and me tabolism. As an important target of PKB / Akt kinase, its small kinase-molecule inhibitors show unique advantages in anti-tumor mechanisms. By specifically inhibiting PKB / Akt kinase activity, these inhibitors can effectively block the growth and proliferation of tumor cells, thus achieving anti-tumor purposes. PKB / Akt kinases have shown good efficacy and safety in clinical trials. Especially in combination with other antitumor agents, these inhibitors are able to exert synergistic effects to further improve the antitumor effect. Individualized therapy based on patient characteristics has also become a new trend in the clinical application of small-molecule inhibitors of PKB / Akt kinase. Problems concerning the selectivity, tolerability, me tabolic kinetics of the inhibitors require further optimization and improvement.
Key words: PKB / Akt kinase; antitumor mechanisms; individualized therapy
目 录
中文摘要 I
英文摘要 II
目 录 III
引 言 1
第1章、PKB/Akt激酶概述 2
1.1、PKB/Akt激酶的基本结构 2
1.2、PKB/Akt激酶在肿瘤中的作用 2
1.3、PKB/Akt激酶小分子抑制剂的作用机理 3
第2章、PKB/Akt激酶小分子抑制剂的研究进展 4
2.1、已有的PKB/Akt激酶小分子抑制剂 4
2.2、PKB/Akt激酶小分子抑制剂的设计与优化 4
2.3、PKB/Akt激酶小分子抑制剂的体外与体内活性研究 5
第3章、PKB/Akt激酶小分子抑制剂的临床应用前景 6
3.1、肿瘤治疗中的新选择 6
3.2、与其他抗肿瘤药物的联合应用 6
3.3、基于患者特征的个体化治疗 7
3.4、市场前景与竞争格局 7
结 论 9
参考文献 10
摘 要
PKB/Akt激酶，也称为蛋白激酶B，是一种在细胞信号传导中起关键作用的酶。它属于丝氨酸/苏氨酸激酶家族，是PI3K-Akt信号通路的重要组成部分。这一信号通路在调节细胞生长、增殖、存活和代谢等多个生理过程中发挥着核心作用。PKB/Akt激酶作为肿瘤治疗的重要靶点，其小分子抑制剂在抗肿瘤机制方面展现出了独特的优势。通过特异性地抑制PKB/Akt激酶的活性，这些抑制剂可以有效地阻断肿瘤细胞的生长和增殖，从而达到抗肿瘤的目的。在临床试验中，PKB/Akt激酶小分子抑制剂已经展现出了良好的疗效和安全性。特别是在与其他抗肿瘤药物的联合应用中，这些抑制剂能够发挥协同作用，进一步提高抗肿瘤效果。基于患者特征的个体化治疗也成为了PKB/Akt激酶小分子抑制剂临床应用的新趋势。抑制剂的选择性、耐受性、代谢动力学和药代动力学等方面的问题需要进一步优化和改进。
关键词：PKB/Akt激酶；抗肿瘤机制；个体化治疗
Abstract
The PKB / Akt kinase, also known as protein kinase B, is an enzyme that plays a key role in cell signaling. It belongs to the serine / threonine kinase family and is an important component of the PI3K-Akt signaling pathway. This signaling pathway plays a central role in regulating multiple physiological processes, including cell growth, proliferation, survival, and me tabolism. As an important target of PKB / Akt kinase, its small kinase-molecule inhibitors show unique advantages in anti-tumor mechanisms. By specifically inhibiting PKB / Akt kinase activity, these inhibitors can effectively block the growth and proliferation of tumor cells, thus achieving anti-tumor purposes. PKB / Akt kinases have shown good efficacy and safety in clinical trials. Especially in combination with other antitumor agents, these inhibitors are able to exert synergistic effects to further improve the antitumor effect. Individualized therapy based on patient characteristics has also become a new trend in the clinical application of small-molecule inhibitors of PKB / Akt kinase. Problems concerning the selectivity, tolerability, me tabolic kinetics of the inhibitors require further optimization and improvement.
Key words: PKB / Akt kinase; antitumor mechanisms; individualized therapy
目 录
中文摘要 I
英文摘要 II
目 录 III
引 言 1
第1章、PKB/Akt激酶概述 2
1.1、PKB/Akt激酶的基本结构 2
1.2、PKB/Akt激酶在肿瘤中的作用 2
1.3、PKB/Akt激酶小分子抑制剂的作用机理 3
第2章、PKB/Akt激酶小分子抑制剂的研究进展 4
2.1、已有的PKB/Akt激酶小分子抑制剂 4
2.2、PKB/Akt激酶小分子抑制剂的设计与优化 4
2.3、PKB/Akt激酶小分子抑制剂的体外与体内活性研究 5
第3章、PKB/Akt激酶小分子抑制剂的临床应用前景 6
3.1、肿瘤治疗中的新选择 6
3.2、与其他抗肿瘤药物的联合应用 6
3.3、基于患者特征的个体化治疗 7
3.4、市场前景与竞争格局 7
结 论 9
参考文献 10
