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Reductive Activation (reductive + activation)
Selected AbstractsReductive Activation of tripod Metal Compounds: Identification of Intermediates and Preparative Application,EUROPEAN JOURNAL OF INORGANIC CHEMISTRY, Issue 9 2008Jürgen Mautz Abstract [tripodCoCl2] {tripod = CH3C(CH2PPh2)3} when treated with KC8 in THF solution under an argon atmosphere produces a reactive species ["tripodCo0"] (A) which undergoes oxidative additions with stannanes, [tripodCo(H)2(SnBu3)] (4), formed, for example, by addition of Bu3SnH. Silanes, R3SiH, undergo the same type of reaction producing [tripodCo(H)2(SiR3)] (R = Et: 5a; R = Ph: 5b). The solid-state structures of all the compounds [tripodCo(H)2(ER3)] (E = Si, R = Ph; E = Sn, R = Ph, Bu) are rather similar. While they contain six-coordinate cobalt with the formal oxidation state of cobalt being +III the coordination geometry is not octahedral: the heteroelement E deviates from the position which it would have in octahedral coordination by around 40° while the other five ligands, three phosphorus and two hydrogen, have the expected interligand angles of around 90° and 180°, respectively. The deviation of the heteroelement E is such that it approaches the metal bonded hydrogen atoms leading to short H···E contacts of only about 190 pm (E = Si) and 230 pm (E = Sn), respectively. The generation of a reactive species ["tripodCo0"] (A) was transferred to the synthesis of a reactive tripodnickel(0) species by treating a THF solution of [(DME)NiBr2] with KC8 in the presence of tripod. This species reacts with two electron donor ligands L to produce the pseudo tetrahedral compounds [tripodNi(L)] {L = PPh3 (6), AsPh3 (7), cHexNC (8), tBuNC (9), C2H4 (10)}. The identity of the reactive nickel(0) species as unequivocally deduced from NMR experiments is [tripod4Ni3] (12). All compounds were characterised by the usual analytic techniques including X-ray analysis where applicable.(© Wiley-VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008) [source] Reductive Activation of Arenes.CHEMINFORM, Issue 1 2005Part 17. No abstract is available for this article. [source] ChemInform Abstract: Reductive Activation of Arenes.CHEMINFORM, Issue 38 2001Part 13. Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a "Full Text" option. The original article is trackable via the "References" option. [source] Role of glutathione in the formation of the active form of the oxygen sensor FNR ([4Fe-4S]·FNR) and in the control of FNR functionFEBS JOURNAL, Issue 15 2000Quang Hon Tran The oxygen sensor regulator FNR (fumarate nitrate reductase regulator) of Escherichia coli is known to be inactivated by O2 as the result of conversion of a [4Fe-4S] cluster of the protein into a [2Fe-2S] cluster. Further incubation with O2 causes loss of the [2Fe-2S] cluster and production of apoFNR. The reactions involved in cluster assembly and reductive activation of apoFNR isolated under anaerobic or aerobic conditions were studied in vivo and in vitro. In a gshA mutant of E. coli that was completely devoid of glutathione, the O2 tension for the regulatory switch for FNR-dependent gene regulation was decreased by a factor of 4,5 compared with the wild-type, suggesting a role for glutathione in FNR function. In isolated apoFNR, glutathione could be used as the reducing agent for HS, formation required for [4Fe-4S] assembly by cysteine desulfurase (NifS), and for the reduction of cysteine ligands of the FeS cluster in FNR. Air-inactivated FNR (apoFNR without FeS) could be reconstituted to [4Fe-4S]·FNR by the same reaction as used for apoFNR isolated under anaerobic conditions. The in vivo effects of glutathione on FNR function and the role of glutathione in the formation of active [4Fe-4S]·FNR in vitro suggest an important role for glutathione in the de novo assembly of FNR and in the reductive activation of air-oxidized FNR under anaerobic conditions. [source] Design of anticancer prodrugs for reductive activationMEDICINAL RESEARCH REVIEWS, Issue 1 2009Yu Chen Abstract Anticancer prodrugs designed to target specifically tumor cells should increase therapeutic effectiveness and decrease systemic side effects in the treatment of cancer. Over the last 20 years, significant advances have been made in the development of anticancer prodrugs through the incorporation of triggers for reductive activation. Reductively activated prodrugs have been designed to target hypoxic tumor tissues, which are known to overexpress several endogenous reductive enzymes. In addition, exogenous reductive enzymes can be delivered to tumor cells through fusion with tumor-specific antibodies or overexpressed in tumor cells through gene delivery approaches. Many anticancer prodrugs have been designed to use both the endogenous and exogenous reductive enzymes for target-specific activation and these prodrugs often contain functional groups such as quinones, nitroaromatics, N-oxides, and metal complexes. Although no new agents have been approved for clinical use, several reductively activated prodrugs are in various stages of clinical trial. This review mainly focuses on the medicinal chemistry aspects of various classes of reductively activated prodrugs including design principles, structure-activity relationships, and mechanisms of activation and release of active drug molecules. © 2008 Wiley Periodicals, Inc. Med Res Rev, 29, No. 1, 29,64, 2009 [source] | ||||||||||