“Molecular Modeling, Synthesis and Anticancer Activity of Fused Triazine Derivatives”
Khulood Hayal Oudah;
Abstract
Cancer is the uncontrolled growth of abnormal cells in the body. Cancer develops when the body’s normal control mechanism stops working. Old cells do not die and instead grow out of control, forming new, abnormal cells. Cell division and cell death are the two predominant physiological processes that regulate normal tissue homeostasis. Alteration of these two physiological processes has a pivotal role in the pathogenesis of cancer. Great efforts to a certain components of the cell cycle are guiding to novel approaches for the treatment of cancer.
CDKs are overactive in some cancers depending on cyclin overexpression or down regulation of endogenous CDKIs. According to this data, researchers focus on whether the strategy of CDK inhibition is able to render cancer treatment more successful
.S ome studies suggest that inhibiting CDKs may be an effective therapy in many cancers.
CDK2-cyclin A complex predominantly control the G1 to S-phase check point, therefore represents an attractive target for therapeutics designed to arrest or recover control of the cell cycle in abnormally dividing cells. CDK2 hyper activation in human cancers is most often associated with amplification and/or overexpression of its partner cyclins A and E in a wide variety of human cancers, but in particular in breast cancer, ovarian and endometrial carcinomas, lung and thyroid carcinoma, melanoma and osteosarcoma and clinically, it often confers a poor prognosis.
The current study aim to design novel pyrazolo[1,5-a][1,3,5]triazine derivatives targeting CDK2. The design focused on exploration of the previously revealed SAR studies and bioisosteric modifications of the lead compound. Synthesis of the designed compounds was then accomplished and their structures were confirmed by various spectral and microanalytical data.
This study involved the synthesis of the following unavailable reported intermediates
1) Ethyl 5-amino-1H-pyrazole-4-carboxylate (II)
2) Benzoyl chloride (IVa)
CDKs are overactive in some cancers depending on cyclin overexpression or down regulation of endogenous CDKIs. According to this data, researchers focus on whether the strategy of CDK inhibition is able to render cancer treatment more successful
.S ome studies suggest that inhibiting CDKs may be an effective therapy in many cancers.
CDK2-cyclin A complex predominantly control the G1 to S-phase check point, therefore represents an attractive target for therapeutics designed to arrest or recover control of the cell cycle in abnormally dividing cells. CDK2 hyper activation in human cancers is most often associated with amplification and/or overexpression of its partner cyclins A and E in a wide variety of human cancers, but in particular in breast cancer, ovarian and endometrial carcinomas, lung and thyroid carcinoma, melanoma and osteosarcoma and clinically, it often confers a poor prognosis.
The current study aim to design novel pyrazolo[1,5-a][1,3,5]triazine derivatives targeting CDK2. The design focused on exploration of the previously revealed SAR studies and bioisosteric modifications of the lead compound. Synthesis of the designed compounds was then accomplished and their structures were confirmed by various spectral and microanalytical data.
This study involved the synthesis of the following unavailable reported intermediates
1) Ethyl 5-amino-1H-pyrazole-4-carboxylate (II)
2) Benzoyl chloride (IVa)
Other data
| Title | “Molecular Modeling, Synthesis and Anticancer Activity of Fused Triazine Derivatives” | Other Titles | " النمذجة الجزيئية والتشييد والفاعلية ضد السرطان لمشتقات الترايزين الملتحمة " | Authors | Khulood Hayal Oudah | Issue Date | 2017 |
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