Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.1/4230
Título: Artemisinin-polypyrrole conjugates: synthesis, DNA binding studies and preliminary antiproliferative evaluation
Autor: La Pensée, Louise
Sabbani, Sunil
Sharma, Raman
Bhamra, Inder
Shore, Emma
Chadwick, Amy E.
Berry, Neil
Firman, J.
Araújo, Nuna C.
Cabral, L. I. L.
Cristiano, Maria Lurdes Santos
Bateman, Cerys
Janneh, Omar
Gavrila, Adelina
Wu, Yi Hang
Hussain, Afthab
Ward, Stephen A.
Stocks, Paul A.
Cosstick, Rick
O'Neill, Paul M.
Palavras-chave: Artemisinin
Molecular modelling
Binding studies
Data: 2013
Editora: Wiley
Citação: La Pensée, Louise; Sabbani, Sunil; Sharma, Raman; Bhamra, Inder; Shore, Emma; Chadwick, Amy E.; Berry, Neil G.; Firman, James; Araujo, Nuna C.; Cabral, Lília; Cristiano, Maria L. S.; Bateman, Cerys; Janneh, Omar; Gavrila, Adelina; Wu, Yi Hang; Hussain, Afthab; Ward, Stephen A.; Stocks, Paul A.; Cosstick, Rick; O’Neill, Paul M. Artemisinin-Polypyrrole Conjugates: Synthesis, DNA Binding Studies and Preliminary Antiproliferative Evaluation, ChemMedChem, 8, 5, 709-718, 2013.
Resumo: Artemisinin-based combination therapies (ACTs) are currently the recommended treatment for uncomplicated and severe cases of malaria.[1] Additionally, artemisinins, as well as a number of other sesquiterpene lactones (SLs), are currently in phase I–II clinical trials against breast, colorectal and nonsmall-cell lung cancers.[2] As outlined by the iron-dependent activation hypothesis,[3] the activity of artemisinin (ART) is dependent on the endoperoxide bridge.[4] The peroxide is cleaved by endogenous sources of FeII to generate highly reactive carbon-centred radicals (CCRs), which are believed to react with critical cellular targets.[3] ART demonstrates selectivity towards rapidly proliferating cancer cell lines that possess a high intracellular iron content required to sustain their characteristic high rates of multiplication.[5] Iron activation links this particular potency of ART towards rapidly proliferating cancer cell lines; differentiation between healthy and cancerous cells by variation of iron concentration provides a strategy for selective cytotoxicity by ART and its derivatives.[4] The mechanism by which ART exerts its cytotoxic activity still remains elusive. ART acts by disruption of proliferation,[6, 7] oxidative stress,[8] anti-angiogenesis,[9] NF-kB signalling,[10] apoptosis[4] and interfering with iron uptake and metabolism.[6] ART also induces DNA breakage,[11] and it has been reported that artesunate-mediated DNA damage contributes to its therapeutic efficacy.
Peer review: yes
URI: http://hdl.handle.net/10400.1/4230
DOI: http://dx.doi.org/10.1002/cmdc.201200536
ISSN: 1860-7179
Aparece nas colecções:CCM2-Artigos (em revistas ou actas indexadas)

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