Morpholine substituted quinazoline derivatives as anticancer agents against MCF-7, A549 and SHSY-5Y cancer cell lines and mechanistic studies

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dc.contributor.authorDwivedi, Ashish Ranjan
dc.contributor.authorKumar, Vijay
dc.contributor.authorPrashar, Vikash
dc.contributor.authorVerma, Akash
dc.contributor.authorKumar, Naveen
dc.contributor.authorParkash, Jyoti
dc.contributor.authorKumar, Vinod
dc.date.accessioned2024-01-21T10:38:20Z
dc.date.accessioned2024-08-13T12:05:15Z
dc.date.available2024-01-21T10:38:20Z
dc.date.available2024-08-13T12:05:15Z
dc.date.issued2022-04-05T00:00:00
dc.description.abstractA series of morpholine substituted quinazoline derivatives have been synthesized and evaluated for cytotoxic potential against A549, MCF-7 and SHSY-5Y cancer cell lines. These compounds were found to be non-toxic against HEK293 cells at 25 ?M and hence display anticancer potential. In these series compounds, AK-3 and AK-10 displayed significant cytotoxic activity against all the three cell lines. AK-3 displayed IC50 values of 10.38 � 0.27 ?M, 6.44 � 0.29 ?M and 9.54 � 0.15 ?M against A549, MCF-7 and SHSY-5Y cancer cell lines. Similarly, AK-10 showed IC50 values of 8.55 � 0.67 ?M, 3.15 � 0.23 ?M and 3.36 � 0.29 ?M against A549, MCF-7 and SHSY-5Y, respectively. In the mechanistic studies, it was found that AK-3 and AK-10 inhibit the cell proliferation in the G1 phase of the cell cycle and the primary cause of death of the cells was found to be through apoptosis. Thus, morpholine based quinazoline derivatives have the potential to be developed as potent anticancer drug molecules. � 2022 RSCen_US
dc.identifier.doi10.1039/d2md00023g
dc.identifier.issn26328682
dc.identifier.urihttp://10.2.3.109/handle/32116/3537
dc.identifier.urlhttp://xlink.rsc.org/?DOI=D2MD00023G
dc.language.isoen_USen_US
dc.publisherRoyal Society of Chemistryen_US
dc.titleMorpholine substituted quinazoline derivatives as anticancer agents against MCF-7, A549 and SHSY-5Y cancer cell lines and mechanistic studiesen_US
dc.title.journalRSC Medicinal Chemistryen_US
dc.typeArticleen_US
dc.type.accesstypeOpen Accessen_US

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