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1                                              ddC (300 nM) reduced mitochondrial DNA levels from appro
2                                              ddC also targeted leukemic stem cells in secondary AML x
3                                              ddC and saline eyes were treated four times daily for 7
4                                              ddC demonstrated potent antiadenovirus activity in vitro
5                                              ddC is a selective inhibitor of the mitochondrial DNA po
6                                              ddC treatment inhibited mtDNA replication, oxidative pho
7                                              ddC was more potent than cidofovir for seven of nine ser
8                                              ddC was preferentially activated in AML cells compared w
9                                The 3% and 2% ddC treatments were significantly more efficacious than
10                          In vivo, 3% ddC, 2% ddC, and 0.5% cidofovir significantly reduced the number
11 to four topical treatment groups: 3% ddC; 2% ddC; 0.5% cidofovir; and saline.
12 vided into four topical treatment groups: 3% ddC; 2% ddC; 0.5% cidofovir; and saline.
13                                  In vivo, 3% ddC, 2% ddC, and 0.5% cidofovir significantly reduced th
14 g 3'-azido-2',3'-ddA (AZddA), 3'-azido-2',3'-ddC (AZddC), 3'-azido-2',3'-ddG (AZddG), AZT, and 3'-azi
15 ntrast, the rate of exonuclease removal of a ddC chain-terminated DNA occurs at least 2 orders of mag
16 sine or affect the mtDNA recovery rate after ddC treatment.
17 ic treatment with the anti-retroviral agent, ddC (Zalcitabine) with or without the concomitant delive
18 and D-FMAU, and D-dideoxynucleoside analogs, ddC and d4T.
19                                   As AZT and ddC are known to cause mitochondrial dysfunction, we exa
20                         We find that AZT and ddC treatment leads to greater depletion of mitochondria
21                                Zdv, ddI, and ddC mutations were detected frequently at baseline but w
22 e 5'-triphosphate forms of 3TC, (-)-FTC, and ddC.
23 alog prodrugs such as AraC, gemcitabine, and ddC.
24 (5-fluoro-2',3'-dideoxy-3'-thiacytidine) and ddC (2',3'-dideoxycytidine) were added to the cultures b
25 of the lymphocytes from control thymuses and ddC-induced lymphomas were positive for Thy-1.2 (pan-T),
26 stance to AZT-triphosphate (TP), ddA-TP, and ddC-TP, indicating an MDNR phenotype.
27 eralgesia caused by HIV/AIDS antiretroviral [ddC (2',3'-dideoxycytidine)] and anticancer (oxaliplatin
28 ast to ineffective chain terminators such as ddC.
29 rrently approved for antiviral therapy: AZT, ddC, D4T, 3TC and carbovir.
30                                      Because ddC induced lymphomas in two different mouse models, the
31 prevents the development of neurotoxicity by ddC, as judged by amelioration of ddC-induced "neuritic
32      The high toxicity of dideoxy compounds, ddC and ddI (metabolized to ddA), may be a combination o
33       Notably, the higher toxicities of d4T, ddC, and ddA arose from their 13-36-fold tighter binding
34                             Dideoxycytidine (ddC), which is known to have a delayed effect on mitocho
35 vels by treating with 2',3'-dideoxycytidine (ddC) and subsequently allowed recovery to normal levels
36                       2',3'-dideoxycytidine (ddC) is a synthetic pyrimidine nucleoside analogue appro
37 analogs, Zalcitabine (2',3'-dideoxycytidine (ddC)) and Lamivudine (beta-d-(+)-2',3'-dideoxy-3'-thiacy
38 deoxythymidine (D4T), 2',3'-dideoxycytidine (ddC), (-)-beta-L-2',3'-dideoxy-3'-thiacytidine (3TC), (-
39 tion caused by beta-d-2',3'-dideoxycytidine (ddC), 2',3'-didehydro-2',3'-dideoxythymidine, and 2',3'-
40 nalogs such as beta-D-2',3'-dideoxycytidine (ddC), beta-2'-fluoro-5-methyl-arabinofuranosyluracil (FM
41 ed a nucleoside analog 2'3'-dideoxycytidine (ddC), which is phosphorylated to the activated antimetab
42 w-level resistance to 2',3'-dideoxycytidine (ddC).
43   We show that among the dideoxynucleosides, ddC appears to be the most neurotoxic, followed by ddI a
44 nsitivity to other nucleoside analogs (i.e., ddC, ddI, and d4T).
45 ocular administration are needed to evaluate ddC as a topical antiviral treatment for adenoviral ocul
46                      The in vitro IC(50) for ddC ranged from 0.18 to 1.85 microg/mL, whereas those fo
47                                 Furthermore, ddC preferentially inhibited mtDNA replication in a subs
48 ral sensitivity that is exacerbated in gp120+ddC as compared to either treatment alone.
49 of HIV-gp120 to the rat sciatic nerve (gp120+ddC).
50 nsitivity to mechanical stimuli in the gp120+ddC model and reversal of some measures of thigmotaxis.
51 A approximately equal to d4T >> ddA (ddI) >> ddC.
52 ion of L-OddC, L-SddC, L-Fd4C, L-FMAU, and L-ddC were compared with D-deoxynucleoside analogs, AraC,
53  Immunohistochemical studies revealed little ddC-associated alteration in DRG phenotype, as compared
54 within 24 hr, which is in contrast to 300 nM ddC, which had no effect on cell growth for the first 4
55 he 50% inhibitory concentrations (IC(50)) of ddC and cidofovir were determined using standard plaque-
56 oxicity by ddC, as judged by amelioration of ddC-induced "neuritic pruning," neuronal mitochondrial d
57 igh correlation between the internal dose of ddC and the incidence of thymic lymphoma in both mouse m
58 and evaluated for toxicity, plasma levels of ddC, and pathological changes.
59 , we evaluated the carcinogenic potential of ddC in two different mouse models.
60                                   Removal of ddC was too slow to measure (<0.00002 s(-1)).
61  phosphorylated metabolites, whereas that of ddC and the L-deoxycytidine analogs may not involve dCMP
62 ong antiviral efficacy of 3TC versus that of ddC.
63 ats treated with perineural HIV-gp120 and/or ddC and there is a reduction in intraepidermal nerve fib
64 tment regimens that included ddI plus AZT or ddC plus AZT in situations in which the T215Y and/or M41
65 eared during drug regimens containing ddI or ddC, with prior or concurrent AZT treatment.
66 hat the failure of the exonuclease to remove ddC may play a major role in its greater toxicity.
67 riptase-resistant, azidothymidine-resistant, ddC/ddI-resistant, nivirapine-resistant, and other clini
68               Each pair of enantiomers of Se-ddC and Se-FddC was separated by an amylose chiral colum
69 s vary more than 500,000-fold for the series ddC > ddA (ddI) > 2',3'-didehydro-2',3'-dideoxythymidine
70                                     Systemic ddC treatment alone is associated with a persistent mech
71 n, and both are considerably less toxic than ddC.
72              Previous studies indicated that ddC has the potential to cause thymic lymphoma in C57BL/
73 ein was detected in only 20% (23/115) of the ddC-induced lymphomas with mostly minimal expression in
74 d as NKT (e.g. adefovir and cidofovir), two (ddC and ddI) manifested significantly higher affinity fo
75 3) is the major transporter interacting with ddC and ddI.
76 he delayed increase in lactate observed with ddC exposure, CldAdo-treated cells exhibited a 2-2.4-fol
77                   The mice were treated with ddC by gavage at 500 and 1000 mg/kg/day for up to 6 mont
78 hildren and adolescent patients treated with ddC.
79 n animal models of human AML, treatment with ddC decreased mtDNA, electron transport chain proteins,
80                               Treatment with ddC for 36 days and with FTC for 12 days resulted in eff
81 e (Ara-C), zidovudine (AZT) and zalcitabine (ddC)-we show that TDP1 is capable of removing the covale
82 ine (Zdv), didanosine (ddI), or zalcitabine (ddC) was acceptable.
83 ated with zidovudine (AZT) plus zalcitabine (ddC) and didanosine (ddI) develop AZT resistance mediate
84 rs of magnitude in the sequence zalcitabine (ddC) > didanosine (ddI metabolized to ddA) > stavudine (
85          IC(50) values for Zdv, zalcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were de
86 he findings support the clinical use of Zdv, ddC, ddI, and d4T but not of 3TC for the antiretroviral
87 -type HIV-1 were equally susceptible to Zdv, ddC, ddI, and d4T.

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