ライフサイエンスコーパス: irofulven

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1 utes to S phase cell cycle arrest induced by irofulven.

2 ed in ovarian cancer cell lines treated with irofulven.

3 5 to characterize the plasma disposition of irofulven.

4 six patients were treated with 92 courses of irofulven.

5 tal synthesis of (-)-acylfulvene (1) and (-)-irofulven (2), which features metathesis reactions for t

6 the formation of (-)-acylfulvene (1) and (-)-irofulven (2).

7 The lead acylfulvene (4), irofulven (5), in a randomized phase IIB clinical trial

8 Irofulven (6-hydroxymethylacylfulvene, HMAF, MGI 114) is

9 Irofulven (6-hydroxymethylacylfulvene, HMAF, MGI 114, NS

10 We demonstrated previously that irofulven activates ATM and its targets, NBS1, SMC1, CHK

11 summary, we found that the anticancer agent, irofulven, activates the ATM-CHK2 DNA damage-signaling p

12 t cells, we demonstrated that in response to irofulven, BRCA1 contributes to the control of S and G(2

13 e to the DNA-damaging agents mitomycin C and Irofulven, but not etoposide and camptothecin, suggestin

14 phase I trial, 46 patients were treated with irofulven doses ranging from 1.0 to 17.69 mg/m(2) as a 5

15 Stereoselective synthesis of (-)-irofulven has been achieved by cycloaddition of (R)-5-ch

16 Many analogues of the antitumor agent irofulven have been readily prepared by replacing the al

17 hat ATR kinase does not play a major role in irofulven-induced CHK2 activation.

18 S scavenger N-acetyl cysteine attenuated the Irofulven-induced cytotoxicity in ERCC6L2-knockdown cell

19 The exact nature of irofulven-induced DNA damage is not completely understoo

20 nstrated that CHK2 activation contributes to irofulven-induced S phase arrest.

21 Mechanisms of action studies indicate that irofulven induces DNA damage, MAPK activation, and apopt

22 In this study, we hypothesize that irofulven induces DNA double-strand breaks and that BRCA

23 We observed that irofulven induces the formation of chromosome breaks and

24 We also provided evidence that irofulven induces the generation of DNA double-strand br

25 sults of this study, the recommended dose of irofulven is 10.64 mg/m(2) as a 5-minute IV infusion dai

26 s and clinical trials have demonstrated that irofulven is effective against several tumor cell types.

27 s and clinical trials have demonstrated that irofulven is effective against several tumor types.

28 d GM05849) indicated that CHK2 activation by irofulven is mediated by the upstream ATM kinase.

29 Irofulven is unique, as the primary allylic hydroxyl gro

30 he striking preclinical antitumor effects of irofulven observed on intermittent dosing schedules supp

31 Pharmacokinetic studies of irofulven revealed dose-proportional increases in both m

32 ofulven was 5 to 6 times less toxic than (-)-irofulven to adenocarcinoma (MV 522) cells.

33 repair, and genomic stability in response to irofulven treatment.

34 chromosome damage and chemosensitivity after irofulven treatment.

35 tion on serine 20 is dependent on CHK2 after irofulven treatment.

36 (+)-Irofulven was 5 to 6 times less toxic than (-)-irofulven

37 The enantiomer, (+)-irofulven, was prepared in a similar way starting with (

38 Analogues of acylfulvene (the precursor to irofulven) were also prepared by Michael reaction with a

39 an cancer cells, CHK2 kinase is activated by irofulven while CHK1 kinase is not activated even when t

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