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1 rmediary metabolism in patients treated with beta-lapachone.
2 dependent apoptosis with PARP inhibitors and beta-lapachone.
3 nyboquinone-induced lethality, as noted with beta-lapachone.
4 1-dependent manner with greater potency than beta-lapachone.
5 ion path and in a later transition state for beta-lapachone.
6 of action and optimal therapeutic window of beta-lapachone.
7 o ROS formation and all cytotoxic effects of beta-lapachone.
8 NQO1) substantially enhances the toxicity of beta-lapachone.
9 must be added either simultaneously or after beta-lapachone.
10 n of Ipe extract caused the incorporation of beta-lapachone (137 mg/L) into the beverage and promoted
13 he tumor-selective overexpression of the key beta-lapachone activating enzymes NQO1 and 5-LO, the TME
14 hydrocostus lactone (DHL), parthenolide, and beta-lapachone, all of which are innocuous individually
16 arity between menadione, a para-quinone, and beta-lapachone, an ortho-quinone, together with their si
17 RN) is constructed by the coencapsulation of beta-lapachone and a reactive-oxygen-species (ROS)-respo
20 ism of action of beta-lapachone, a series of beta-lapachone and related naphthoquinones were synthesi
22 ture after treatment with the combination of beta-lapachone and taxol, two low molecular mass compoun
23 KP372-1 is ~ 10- to 20-fold more potent than beta-lapachone, another NQO1 substrate, against pancreat
30 Application of quinone drugs, particularly beta-lapachone (beta-lap), under normoxic and hypoxic co
35 iochemical studies suggest that reduction of beta-lapachone by NQO1 leads to a futile cycling between
37 of an ortho-quinone prodrug, a propargylated beta-lapachone derivative, through a palladium-mediated
38 al studies of the reduction reactions in nor-beta-lapachone derivatives including a nitro redox cente
43 orrelated with sensitivity to a 4-h pulse of beta-lapachone in a panel of breast cancer cell lines, a
44 ate that the most efficacious strategy using beta-lapachone in chemotherapy was to deliver the drug i
46 e.g., the environmental toxins menadione and beta-lapachone (in vivo IC(50) = 0.45 muM) also cause in
50 2-dimethyl-2H-naphtho[1,2-b]pyran-5,6-dione (beta-lapachone) inhibits DNA topoisomerase I by a mechan
57 S dual-responsive nanomedicine consisting of beta-lapachone (Lap), a pH-responsive polymer, and a ROS
58 s were killed in an NQO1-dependent manner by beta-lapachone (LD50, approximately 4 microM) with a min
59 activation-mediated programmed necrosis with beta-lapachone monotherapy to synergistic tumor-selectiv
60 mparing equivalent points on both alpha- and beta-lapachone potential energy surfaces (PES), accordin
62 t TOP1 inhibition with camptothecin (CPT) or beta-Lapachone results in a significant reduction in vir
63 droxybenzyl (PHB) moiety alkylated to one of beta-lapachone's carbonyls via an indium-mediated Barbie
66 ork explores the development of an optimized beta-lapachone small molecule prodrug platform that util
72 markers useful for in vivo dose responses of beta-lapachone treatment in humans, avoiding toxic side
73 oxidative flux due to NAD(+) depletion after beta-lapachone treatment of NQO1+ human pancreatic cance
74 ent may have the potential to synergize with beta-lapachone treatment, creating unique NQO1-selective
77 , we demonstrate that NQO1-targeting prodrug beta-lapachone triggers tumor-selective innate sensing l
79 ation of the electrophilic quinone moiety of beta-lapachone via a C(sp(3))-C(sp(3)) bond to a coumari
80 The regioselective formation of alpha- and beta-lapachone via hetero-Diels-Alder reactions was inve
81 n assays in cells, the protected analogue of beta-lapachone was activated by nontoxic amounts of nano