ライフサイエンスコーパス: 5-fluorocytosine

1 replaced with the mechanism-based inhibitor 5-fluorocytosine.

2 ible to AmB and resistant to fluconazole and 5-fluorocytosine.

3 nucleotides identical in sequence containing 5-fluorocytosine.

4 me manner as cytosine, 5-methylcytosine, and 5-fluorocytosine.

5 follows: amphotericin B, 1.0 micrograms/ml; 5-fluorocytosine, 0.25 micrograms/ml; fluconazole, 8.0 m

6 ar (PBM) cells, among which the cytosine 17, 5-fluorocytosine 18, and adenine 27 derivatives showed p

7 Cytosine 23, 5-fluorocytosine 25, and adenine 36 derivatives exhibite

8 ), guanine (18), 2,6-diaminopurine (20), and 5-fluorocytosine (30) derivatives were found to exhibit

9 (50) = 0.13 microM; EC(90) = 1.7 microM) and 5-fluorocytosine 35 (EC(50) = 0.031 microM; EC(90) = 0.3

10 we show that concurrent addition of prodrugs 5-fluorocytosine (5-FC) and ganciclovir (GCV) was less e

11 apy using bacterial cytosine deaminase (bCD)/5-fluorocytosine (5-FC) enzyme/prodrug strategy is limit

12 We used the cytosine deaminase (CD) 5-fluorocytosine (5-FC) enzyme/prodrug system and studie

13 (Ad) vector-mediated cytosine deaminase (CD)/5-fluorocytosine (5-FC) gene therapy has the potential t

14 y using the cytosine deaminase (CD) gene and 5-fluorocytosine (5-FC) has shown promising results for

15 the vv containing CD followed by the prodrug 5-fluorocytosine (5-FC) in a murine model of disseminate

16 sine deaminase, which converts the non-toxic 5-fluorocytosine (5-FC) into the toxic 5-fluorouracil (5

17 using bacterial cytosine deaminase (bCD) and 5-fluorocytosine (5-FC) is currently under investigation

18 observing the CD-catalyzed conversion of the 5-fluorocytosine (5-FC) prodrug to the chemotherapeutic

19 e, which efficiently metabolizes the prodrug 5-fluorocytosine (5-FC) to 5-fluorouracil (5-FU).

20 eaminase (CD) and is capable of metabolizing 5-fluorocytosine (5-FC) to 5-fluorouracil.

21 cytosine deaminase (CD) converts the prodrug 5-fluorocytosine (5-FC) to 5-FU.

22 no acid substitutions confers sensitivity to 5-fluorocytosine (5-FC) when expressed in the chloroplas

23 toconazole, amphotericin B, caspofungin, and 5-fluorocytosine (5-FC), respectively.

24 es the deamination of the nontoxic pro-drug, 5-fluorocytosine (5-FC), thus converting it to the cytot

25 ls followed by administration of the prodrug 5-fluorocytosine (5-FC).

26 imaging) to detect activation of the prodrug 5-fluorocytosine (5-FCyt) to the cytotoxic species 5-flu

27 ues with improved leaving ability, including 5-fluorocytosine, 5-bromocytosine, and 5-hydroxycytosine

28 terodimers of cytosine and 5-methylcytosine, 5-fluorocytosine, 5-bromocytosine, and 5-iodocytosine ar

29 (1, neplanocin A), cytosine (55, CPE-C), and 5-fluorocytosine (56) analogues exhibited moderate to po

30 Also, cytosine (55) and 5-fluorocytosine (56) analogues exhibited the most poten

31 h CD-expressing tumor cells are treated with 5 fluorocytosine (5FC), an inert prodrug that is convert

32 ion of amphotericin B deoxycholate (AmB) and 5-fluorocytosine (5FC) by use of the Greco model of drug

33 uconazole, itraconazole, amphotericin B, and 5-fluorocytosine (5FC) by using National Committee for C

34 D) gene, which converts the nontoxic prodrug 5-fluorocytosine (5FC) into the chemotoxin 5-fluorouraci

35 5-fluorocytosine (5FC) is metabolized in CD-expressing c

36 CD also converts 5-fluorocytosine (5FC) to 5-fluorouracil, an inhibitor o

37 lso catalyzes the deamination of the prodrug 5-fluorocytosine (5FC) to form the anticancer drug 5-flu

38 f two substrates of the enzyme, cytosine and 5-fluorocytosine (5FC), can be detected using saturation

39 and C. zeylanoides) against amphotericin B, 5-fluorocytosine (5FC), fluconazole, and itraconazole.

40 ctor were much more sensitive to the prodrug 5-fluorocytosine (5FC), which is converted from the 5FC

41 vements in the ability to sensitize cells to 5-fluorocytosine (5FC).

42 cil, thymine, N4-benzoylcytosine, N4-benzoyl-5-fluorocytosine, 6-chloropurine, and 6-chloro-2-fluorop

43 itional expression of Fcy::Fur combined with 5-fluorocytosine administration improves tumor shrinkage

44 ynthesized racemic nucleosides, cytosine and 5-fluorocytosine analogues exhibited potent anti-HIV and

45 improved with intravenous amphotericin B and 5-fluorocytosine and did not require surgical interventi

46 nt Ad5-CD/TKrep virus followed by 2 weeks of 5-fluorocytosine and ganciclovir prodrug therapy can be

47 Two days later, patients were given 5-fluorocytosine and ganciclovir prodrug therapy for 1 (

48 t killing by the normally innocuous prodrugs 5-fluorocytosine and ganciclovir.

49 rvival of PC-3 cells in the presence of both 5-fluorocytosine and ganciclovir.

50 ene concomitant with increasing durations of 5-fluorocytosine and valganciclovir prodrug therapy and

51 Two days later, patients were administered 5-fluorocytosine and valganciclovir prodrug therapy for

52 sponse of HT-29 xenografts to treatment with 5-fluorocytosine and yCD adenovirus driven by either the

53 ity is strain-dependent, and fluconazole and 5-fluorocytosine are not active.

54 tosine deaminase is used in combination with 5-fluorocytosine as an enzyme-prodrug combination for ta

55 Oligonucleotides containing 5-bromo- or 5-fluorocytosine can bind to proteins that selectively b

56 adenoviral (Ad5)-directed cytosine deaminase/5-fluorocytosine (CD/5-FC) enzyme/prodrug gene therapy t

57 Cytosine deaminase/5-fluorocytosine (CD/5-FC) is a promising strategy for l

58 a target oligodeoxyribonucleotide containing 5-fluorocytosine confirmed the existence of this dihydro

59 as active and formed a covalent complex with 5-fluorocytosine-containing RNA, whereas the mutant at t

60 Moreover, the efficiency of 5-fluorocytosine conversion into 5-fluorouracil in tumor

61 ir/herpes simplex virus thymidine kinase and 5-fluorocytosine/cytosine deaminase.

62 When 5-fluorocytosine (F) is placed at the targeted cytosine

63 The MICs of amphotericin B, 5-fluorocytosine, fluconazole, and itraconazole were det

64 UPRT that could catalyze the modification of 5-fluorocytosine into chemotherapeutic 5-fluorouracil (5

65 in converting systemically injected nontoxic 5-fluorocytosine into the toxic anticancer drug 5-fluoro

66 genetically modified cells are combined with 5-fluorocytosine, it creates a potent negative selection

67 They are rejected by normal mice without 5-fluorocytosine prodrug treatment.

68 nce of the systemically administered prodrug 5-fluorocytosine produced statistically significant redu

69 form abortive covalent complexes at targeted 5-fluorocytosine residues in DNA.

70 hecin glucuronide to 9-aminocamptothecin and 5-fluorocytosine to 5-fluorouracil (5-FU) and further to

71 ast cytosine deaminase (yCD), which converts 5-fluorocytosine to 5-fluorouracil, to increase targetin

72 same enzyme also catalyzes the conversion of 5-fluorocytosine to 5-fluorouracil; this activity allows

73 e, catalyzes the deamination of cytosine and 5-fluorocytosine to form uracil and 5-fluorouracil, resp

74 Resistance to the antifungal drug 5-fluorocytosine was not deleterious and appeared to be

75 be, MICs of amphotericin B, fluconazole, and 5-fluorocytosine were determined.

76 -fluorouracil (5-FU) from the benign prodrug 5-fluorocytosine within colorectal cancers.

77 nciclovir (TK/GCV), yeast cytosine deaminase/5-fluorocytosine (yCD/5-FC) and nitroreductase/CB1954 (N