ライフサイエンスコーパス: ddI

1 s (indinavir, lamivudine, abacavir, AZT, and ddI) and the 3-plex significantly also impaired endothel

2 high toxicity of dideoxy compounds, ddC and ddI (metabolized to ddA), may be a combination of high r

3 (e.g. adefovir and cidofovir), two (ddC and ddI) manifested significantly higher affinity for mOat3,

4 e major transporter interacting with ddC and ddI.

5 of clinical toxicities than were d4T/ddI and ddI/3TC and with a higher rate of laboratory toxicities

6 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates and are appropriate

7 ine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

8 higher efficacy of the combination of HU and ddI compared with that of ddI monotherapy cannot be attr

9 ART drugs (3-plex; indinavir, stavudine, and ddI)] at their clinical plasma concentrations for 24 hou

10 FAAddP was also converted to 2'-F-ara-ddI at a slower rate in the brain than in the liver.

11 sult in increased brain delivery of 2'-F-ara-ddI in vivo, probably due to the slow conversion as obse

12 was an increase in the half-life of 2'-F-ara-ddI produced from FMAddA.

13 operties and tissue distribution of 2'-F-ara-ddI, two lipophilic prodrugs, 6-azido-2'-3'-dideoxy-2'-f

14 -ara-ddA followed by deamination to 2'-F-ara-ddI.

15 y followed by deamination, yielding 2'-F-ara-ddI.

16 e to AZT, or equimolar combinations of AZT + ddI, at exposure concentrations ranging from 3 to 30 tim

17 reverse transcriptase enzyme inhibitors AZT, ddI, 3TC, d4T, foscarnet, and nevirapine, as well as the

18 151-->M conferred partial resistance to AZT, ddI, zalcitibine, and stavudine, whereas a combination o

19 tions conferred increased resistance to AZT, ddI, zalcitibine, and stavudine.

20 pears to be the most neurotoxic, followed by ddI and then d4T.

21 ity of the Leu74Val mutant virus selected by ddI therapy provides a strong rationale for the lower vi

22 ins appeared during drug regimens containing ddI or ddC, with prior or concurrent AZT treatment.

23 [HR], 0.49; P = .02) ); regimens containing ddI were associated with a significantly lower rate of l

24 D4T/3TC, d4T/ddI, and ddI/3TC have similar toxicity rates and are app

25 V/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

26 er rate of clinical toxicities than were d4T/ddI and ddI/3TC and with a higher rate of laboratory tox

27 than 500,000-fold for the series ddC > ddA (ddI) > 2',3'-didehydro-2',3'-dideoxythymidine (d4T) >> (

28 ZT > PMPA approximately equal to d4T >> ddA (ddI) >> ddC.

29 vity to other nucleoside analogs (i.e., ddC, ddI, and d4T).

30 ndings support the clinical use of Zdv, ddC, ddI, and d4T but not of 3TC for the antiretroviral treat

31 HIV-1 were equally susceptible to Zdv, ddC, ddI, and d4T.

32 ase-resistant, azidothymidine-resistant, ddC/ddI-resistant, nivirapine-resistant, and other clinical

33 Didanosine (ddI) pharmacokinetics in antepartum and postpartum human

34 y virus type 1 who switched to a didanosine (ddI)-containing triple- or quadruple-drug regimen was co

35 (AZT) plus zalcitabine (ddC) and didanosine (ddI) develop AZT resistance mediated by mutations such a

36 herapy with zidovudine (AZT) and didanosine (ddI).

37 dovudine (AZT), stavudine (d4T), didanosine (ddI), and lamivudine (3TC), and the nucleotide RTI inhib

38 lues for Zdv, zalcitabine (ddC), didanosine (ddI), 3TC, and stavudine (d4T) were determined, using an

39 (D4T)] and 2'-3'-dideoxyinosine [didanosine (ddI)] likewise stimulated template-switch mutagenesis.

40 the sequence zalcitabine (ddC) > didanosine (ddI metabolized to ddA) > stavudine (d4T) >> lamivudine

41 ger efficacy trial of 2 doses of didanosine (ddI) monotherapy (Pediatric AIDS Clinical Trials Group 1

42 RT) develops as a consequence of didanosine (ddI) therapy and is associated with a decreased suscepti

43 either to add stavudine (d4T) or didanosine (ddI) to their current regimen or to switch to ddI or d4T

44 dine (AZT), abacavir, stavudine, didanosine (ddI), and lamivudine] individually or in combination [th

45 2 study, which demonstrated that didanosine (ddI) or zidovudine + ddI treatments were superior to zid

46 trains that confer resistance to didanosine (ddI) was analyzed in 2 groups of patients receiving eith

47 treatment with zidovudine (Zdv), didanosine (ddI), or zalcitabine (ddC) was acceptable.

48 dine (ZDV)/lamivudine (3TC), ZDV/didanosine (ddI), stavudine (d4T)/3TC, d4T/ddI, and ddI/3TC.

49 a trial (ACTG 241) of zidovudine/didanosine (ddI) versus zidovudine/ddI/nevirapine in nucleoside-expe

50 3'-azido-3'-deoxythymidine)] and didanosine [ddI (2',3'-dideoxyinosine)], in cultured human lymphobla

51 in arabinofuranyl-guanosine, dideoxyinosine (ddI), dideoxyadenosine (ddA), didehydrothymidine (d4T),

52 on from baseline between the dideoxyinosine (ddI) and zidovudine+ddI therapeutic arms, marginal super

53 ildren with HIV-1 disease progression during ddI therapy suggests that this mutation confers a fitnes

54 zed in 2 groups of patients receiving either ddI monotherapy or ddI plus hydroxyurea (HU) combination

55 -beta-D-threo-pentofuranosyl)hypoxanthine (F-ddI).

56 ca. 100 times more lipophilic than ddI or F-ddI.

57 failure of treatment regimens that included ddI plus AZT or ddC plus AZT in situations in which the

58 After iv ddI administration, only the maternal plasma clearance w

59 pregnant women received an intravenous (iv) ddI infusion (1.6 mg/kg/h) or an oral dose (200 mg bid o

60 Combinations of ddI plus HU did not prevent the onset of mutations, whic

61 Plasma concentrations of ddI were measured by radioimmunoassay.

62 The same oral dose of ddI (bid) was administered until labor began.

63 The pharmacokinetics of ddI in the neonates were highly variable.

64 bination of HU and ddI compared with that of ddI monotherapy cannot be attributed to a delayed or dec

65 Moreover, the extensive use of ddI and d4T has led to high frequencies of the K65R muta

66 4V/I mutation should not preclude the use of ddI in nucleoside-experienced patients.

67 ressors), were studied during 60-72 weeks of ddI therapy.

68 In subjects receiving ddI or ddI plus zidovudine, reductions were 0.39 and 0.56 log(1

69 patients receiving either ddI monotherapy or ddI plus hydroxyurea (HU) combination therapy.

70 We conclude that the oral ddI dose need not be adjusted during pregnancy.

71 al mutant in clinical isolates obtained post-ddI therapy.

72 In subjects receiving ddI or ddI plus zidovudine, reductions were 0.39 and 0.5

73 ounds are ca. 100 times more lipophilic than ddI or F-ddI.

74 ld not be prescribed in combination and that ddI provides greater antiviral activity than d4T in zido

75 These results show that ddI continues to provide activity against viruses with t

76 ients in this group compared with 25% of the ddI monotherapy group.

77 In this report, we provide evidence that the ddI-associated Leu74Val mutation confers a replication d

78 In addition, most patients for whom the ddI-containing regimen failed lost the M184V/I mutation.

79 Then, ddI was infused iv until delivery.

80 ene previously associated with resistance to ddI (L74V, K65R, or M184V).

81 to the virus that may include resistance to ddI.

82 delayed or decreased onset of resistance to ddI.

83 ssociated with a decreased susceptibility to ddI.

84 dI) to their current regimen or to switch to ddI or d4T monotherapy.

85 for the lower viral RNA levels observed with ddI therapy compared to zidovudine therapy in clinical t

86 c activity with AZT, but lacked synergy with ddI.

87 Zdv, ddI, and ddC mutations were detected frequently at basel

88 ZDV/ddI was associated with a lower rate of clinical toxicit

89 r rate of laboratory toxicities than was ZDV/ddI.

90 trated that didanosine (ddI) or zidovudine + ddI treatments were superior to zidovudine alone.

91 ween the dideoxyinosine (ddI) and zidovudine+ddI therapeutic arms, marginal superiority of the combin

92 idovudine/didanosine (ddI) versus zidovudine/ddI/nevirapine in nucleoside-experienced patients, basel