antimicobacterianos la isioniazida rifampicina priazinamida, etambutol estreptomicina son los cinco fármacos de primera línea para el tratamiento de la. En determinadas situaciones debe añadirse un cuarto fármaco, etambutol en adultos y estreptomicina en niños, en quienes no puede Antimicobacterianos. Antibióticos beta-lactámicos y otros antibióticos de amplio espectro. Fármacos antimicobacterianos y antifúngicos. Fármacos antivirales.
|Published (Last):||28 December 2017|
|PDF File Size:||4.44 Mb|
|ePub File Size:||3.33 Mb|
|Price:||Free* [*Free Regsitration Required]|
Rational approach in the new antituberculosis agent design: In conjunction with the spread of HIV infection, tuberculosis TB has been among the worldwide health threats. Mycobacteria resistance to farmacoa drugs currently used in the therapeutics is the main cause of TB resurgence.
In view of this severe situation, the new and selective anti-TB design is of utmost importance. Fatty acid biosynthesis is a prokariontes and eucariontes biochemical process that supplies essential precursors for the assembly of important cellular components, such as phospholipids, lipoproteins, lipopolysaccharides, mycolic acids and cellular envelope. However, the biochemical and functional differences between the bacterial and mammals’ fatty acid synthetic pathway have endowed the mycobacterial enzymes with distinct properties.
These provide valuable opportunities for structure- or catalytic mechanism-based design of selective inhibitors as novel anti-TB drugs with improved properties. The enoyl-reductases are essential enzymes in the fatty acids elongation pathway towards the mycolic acids, the main mycobacteria cell wall constituents, biosynthesis and so they are potential targets to the rational new antimycobacteria drug design.
Antimicobacterianos by Ragde Avoch on Prezi
This paper highlights recent approaches regarding the design of new anti-TB agents, particularly, the enoyl-ACP reductase inhibitors. Em geral, as tiofeno-diazoborinas foram os inibidores mais potentes, seguidos pelas benzo-diazoborinas e furano-diazoborinas, enquanto que as pirrol-diazoborinas foram totalmente inativas. Estes pesquisadores isolaram cepas de E. Mechanism of action of diazaborines. A mechanism of drug action revealed by structural studies of enoyl reductase.
The mabA gene from the inhA operon of Mycobacterium tuberculosis encodes a 3-ketoacyl reductase that fails to confer isoniazid resistance. Drug sensitivity antimicobacteianos environmental adaptation of mycobacterial cell wall components.
Chemotherapy of experimental tuberculosis – V. Isonicotinic acid hydrazide nydrazid and related compounds. Chemotherapy of experimental tuberculosis – VI. Chemotherapy of experimental tuberculosis – VII. Heterocyclic acid hydrazides and derivatives. The envelope of mycobacteria. Guidebook on molecular modeling in drug design. The growing burden of tuberculosis: Crystal structure and fuction of the isoniazid target of Mycobacterium tuberculosis.
Crystallographic studies on the binding of isonicotinyl-NAD adduct to wild-type and isoniazid resistant 2-trans-enoyl-ACP CoA reductase from Mycobacterium tuberculosis. Global tuberculosis incidence and mortality during The resurgence of disease: Preparation and antibacterial activities of new 1,2,3-diazaborine derivatives and analogues.
Pyrrolidine carboxamides as a novel class of inhibitors of enoyl acyl carrier protein reductase from Mycobacterium tuberculosis.
Natimicobacterianos of the Staphylococcus aureus NADPH-dependent enoyl-acyl carrier protein reductase by triclosan and hexachlorophene. A triclosan-resistant bacterial enzyme. Lipid biosynthesis as a target for antibacterial agents.
Inhibitors of fatty acid synthesis as antimicrobial chemotherapeutics. Broad spectrum antimicrobial biocides target the FabI component of fatty acid biosynthesis. Implications of multidrug resistance for the future of short-course chemotherapy of tuberculosis: Probing mechanisms of resistance to the tuberculosis drug isoniazid: Conformational changes caused by inhibition of InhA, the enoyl reductase from Mycobacterium tuberculosis.
Targeting tuberculosis and malaria through inhibition of enoyl reductase: Overexpression of inhA, but not antimicobacteruanosconfers resistance to isoniazid and ethionamide in Mycobacterium smegmatisM.
A study of the structure-activity relationship for diazaborine inhibition of Escherichia coli enoyl-acp reductase. Critical review of the role of HTS in drug discovery.
Síntese e atividade antimicobacteriana de ésteres do ácido pirazinóico e quinolo
Mechanistic diversity and regulation of Type II fatty acid synthesis. Triclosan targets lipid synthesis. Some observations on the pathogenicity of isoniazid-resistant variants of tubercle bacilli. Characterization of the catalase-peroxidase gene katG and inhA locus in isoniazid-resistant and -susceptible strains of Mycobacterium tuberculosis by automated DNA sequencing: Recent advances in new structural classes of anti-tuberculosis agents.
Enoyl reductases as targets for the development of anti-tubercular and anti-malarial agents. Drug Targets antimicoabcterianos, v. Characterization of a ligand-receptor binding event using receptor-dependent four-dimensional quantitative structure-activity relationship analysis.
Quantitative structure -based design: Inhibition of InhA, the enoyl reductase from Mycobacterium tuberculosisby triclosan and isoniazid. An approach for the rational design of new antituberculosis agents. Rational antimicobactrianos of new antituberculosis agents: Receptor-independent four-dimensional quantitative structure-activity relationship analysis of a set of isoniazid derivatives.
An introduction to medicinal chemistry. Oxford University Press, Discovery of a novel and potent class of FabI-directed antibacterial agents. Enzymatic characterization of the target for isoniazid farmcos Mycobacterium tuberculosis.
Single nucleotide polymorphisms in genes associated with isoniazid resistance in Mycobacterium tuberculosis. Isoniazid is not a lead compound antimiccobacterianos its pyridyl ring derivatives, isonicotinoyl amides, hydrazides, and hydrazones: Tuberculosis, focus on tropical diseases. Structural basis and mechanism of enoyl reductase inhibition by triclosan. High affinity InhA inhibitors with activity against drug-resistant strains of Mycobacterium tuberculosis.
Constructing protein models for ligand-receptor binding thermodynamic simulations: An application to a set of peptidometic rennin inhibitors. Application to a set of peptidometic rennin inhibitors.
There was a problem providing the content you requested
The mechanism of isoniazid killing: Clarity through the scope of genetics. Transfer of a point mutation in Mycobacterium tuberculosis inhA resolves the target of isoniazid. Strategies in the search for new lead compounds or original working hypothesis. The practice of medicinal chemistry. Global tuberculosis control – surveillance, planning, financing. The catalase-peroxidase gene and isoniazid resistance of Mycobacterium tuberculosis.
The magic bullets and tuberculosis drug targets. New drug candidates and therapeutic antimicobactreianos for tuberculosis therapy. Chemoterapy of experimental tuberculosis. The synthesis of acid hydrazides, their derivatives and related compounds.
All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License. Services on Demand Journal. How to cite this article.