ライフサイエンスコーパス: obatoclax

1 omarker (PYCARD) for an investigational drug obatoclax.

2 ocation to mitochondria after treatment with obatoclax.

3 was to examine the single-agent activity of obatoclax, a BH3 mimetic in cholangiocarcinoma cell line

4 This in vitro obatoclax activity and its multiple killing mechanisms a

5 ed expression in infant ALL, and evidence of obatoclax activity with a favorable toxicity profile in

6 atment of melanomas with BRAF inhibitors and obatoclax, an inhibitor of BCL2A1 and other BCL2 family

7 e) and identified two novel anti-IAV agents, obatoclax and gemcitabine.

8 targeted by two pan-Bcl-2 family inhibitors, obatoclax and gossypol.

9 Moreover, we showed that obatoclax and SaliPhe inhibited IAV uptake and gemcitabi

10 oapoptotic small molecules (e.g. oblimersen, obatoclax, and gossypol), antifols (e.g. pralatrexate),

11 ential role in cell killing by lapatinib and obatoclax, as well as radiosensitization by this drug co

12 The PYCARD and obatoclax association is validated in 30 AML patient sam

13 rgeted knockdown of Bax doubled the IC50 for obatoclax but did not abrogate its cytotoxicity, whereas

14 We show that obatoclax can promote the release of cytochrome c from i

15 Coadministration of lapatinib with obatoclax caused synergistic cell killing by eliciting a

16 2 and Bcl-xL, effects that were abolished by obatoclax coadministration.

17 ated lethality triggered by the flavopiridol/obatoclax combination in vitro and in vivo.

18 Coadministration of lapatinib with obatoclax elicited autophagic cell death that was attrib

19 Pretreatment of tumor cells with obatoclax enhanced the lethality of lapatinib to a great

20 nduction of apoptosis was related to overall obatoclax exposure, as monitored by the plasma concentra

21 r administered singly or in combination with obatoclax, flavopiridol also induced upregulation of mul

22 nase inhibitor sorafenib and the BH3-mimetic obatoclax (GX15-070) were examined in human acute myeloi

23 ated the mechanism of apoptosis induction of obatoclax (GX15-070), a novel Bcl-2 homology domain-3 (B

24 ell CLL/lymphoma-2 (BCL-2) family antagonist obatoclax (GX15-070).

25 oethyl)]-4H-chromene-3-carboxylate (HA14-1), obatoclax (GX15-070)].

26 e absence of Bak/Bax or Bim, suggesting that obatoclax has additional targets that contribute to its

27 the combination of THZ1 and the BH3 mimetic obatoclax improves lymphoma growth control in a primary

28 hibitor flavopiridol and the pan-BH3 mimetic obatoclax in multiple myeloma (MM) cells in which Mcl-1

29 In a cell-free system, obatoclax induced an activating conformational change of

30 not induce apoptosis or decrease viability, obatoclax induced an S-G(2) cell-cycle block.

31 Obatoclax induced apoptosis in AML CD34+ progenitor cell

32 sypol was effective only in resistant cells, obatoclax induced cell death in both parental and ABT-73

33 Treatment with sorafenib/obatoclax induced pronounced apoptosis in and reduced th

34 together, our data argue that lapatinib and obatoclax-induced toxic autophagy is due to impaired aut

35 Obatoclax inhibited cell growth of HL-60, U937, OCI-AML3

36 Lapatinib and obatoclax-initiated autophagy depended on NOXA-mediated

37 t cancer cells have shown that lapatinib and obatoclax interact in a greater than additive fashion to

38 Previous studies showed that lapatinib and obatoclax interact in a greater-than-additive fashion to

39 ltogether, our results suggest that phase II obatoclax, investigational SaliPhe, and FDA/EMEA-approve

40 Lapatinib and obatoclax killed multiple CNS tumor isolates.

41 Lapatinib and obatoclax killed multiple tumor cell types, and cells la

42 receptors were most important for enhancing obatoclax lethality rather than ERBB2.

43 ockdown, significantly potentiated sorafenib/obatoclax lethality, indicating a cytoprotective role fo

44 exposure of leukemia cells to sorafenib and obatoclax markedly induced autophagy, reflected by rapid

45 that inhibit Mcl-1 and Bcl-2/Bcl-xL such as obatoclax may represent a novel and potentially effectiv

46 Obatoclax mesylate has biologic activity and modest sing

47 the pan-antiapoptotic BCL-2 family inhibitor obatoclax mesylate in diagnostic leukemia cells from 54

48 Obatoclax mesylate is a small molecule pan-Bcl-2 antagon

49 3 mimetics that are broad acting (ABT263 and obatoclax) or selective (ABT199, WEHI-539, and A1210477)

50 In conclusion, we show that obatoclax potently induces apoptosis and decreases leuke

51 Obatoclax prevented Mcl-1 recovery and caused release of

52 topic CNS tumor isolates with lapatinib- and obatoclax-prolonged survival.

53 periments demonstrated that Mcl-1 (target of obatoclax) provides a novel host target for IAV treatmen

54 ase inhibitor sorafenib with the BH3 mimetic obatoclax results in enhanced antileukemic effects compa

55 Bax, but not Noxa, significantly attenuated obatoclax/sorafenib lethality, whereas ectopic expressio

56 Coadministration of flavopiridol and obatoclax synergistically triggered apoptosis in both dr

57 Obatoclax synergized with the novel BH3 mimetic ABT-737

58 Despite single-agent activity by obatoclax, the mitochondria from these cells did not rel

59 Altogether, our data show that lapatinib and obatoclax therapy could be of use in the treatment of tu

60 mouse model revealed that combined sorafenib/obatoclax treatment markedly reduced tumor growth and si

61 In conclusion, single-agent obatoclax treatment results in Bax activation, which con

62 ches including flow cytometry, Western blot, obatoclax treatment with death pathway inhibition, micro

63 cells were radiosensitized by lapatinib and obatoclax treatment.

64 hibition of colony formation was observed by obatoclax treatment.

65 Obatoclax was administered to patients with advanced CLL

66 x)) and area under the curve (AUC) values of obatoclax were dose proportional.

67 VP-BEZ235, which targets the cell cycle, and Obatoclax, which targets survival, demonstrated synergis

68 ning the pan-Bcl-2 inhibitor GX15-070 (GX15; obatoclax) with immunotherapeutic modalities.