Please use this identifier to cite or link to this item: https://hdl.handle.net/10216/82041
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dc.creatorNuno Vale
dc.creatorPaula Gomes
dc.creatorHelder A Santos
dc.date.accessioned2022-09-12T06:41:52Z-
dc.date.available2022-09-12T06:41:52Z-
dc.date.issued2013
dc.identifier.issn1389-2002
dc.identifier.othersigarra:89175
dc.identifier.urihttps://hdl.handle.net/10216/82041-
dc.description.abstractEthionamide (ETH) is an important second-line antituberculosis drug used for the treatment of patients infected with multidrug-resistant Mycobacterium. Although ETH is a structural analogue of isoniazid (INH), both are pro-drugs that need to be activated by mycobacterial enzymes to exert their antimicrobial activity. ETH mechanism of action is thought to be identical to INH although the pathway of activation is distinct from that of INH. ETH is activated by an EthA enzyme, leading to the formation of an S-oxide metabolite that has considerably better activity than the parent drug. This review comprehensively examines the aspects related with the metabolism of ETH since its discovery up to today.
dc.language.isoeng
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/
dc.subjectMedicina básica
dc.subjectBasic medicine
dc.titleMetabolism of the Antituberculosis Drug Ethionamide
dc.typeArtigo em Revista Científica Internacional
dc.contributor.uportoFaculdade de Ciências
dc.identifier.authenticusP-002-246
dc.subject.fosCiências médicas e da saúde::Medicina básica
dc.subject.fosMedical and Health sciences::Basic medicine
Appears in Collections:FCUP - Artigo em Revista Científica Internacional

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