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1 inhibitor olaparib and the pan-BCL inhibitor obatoclax.
2 omarker (PYCARD) for an investigational drug obatoclax.
3 ocation to mitochondria after treatment with obatoclax.
4  was to examine the single-agent activity of obatoclax, a BH3 mimetic in cholangiocarcinoma cell line
5                                This in vitro obatoclax activity and its multiple killing mechanisms a
6 ed expression in infant ALL, and evidence of obatoclax activity with a favorable toxicity profile in
7 atment of melanomas with BRAF inhibitors and obatoclax, an inhibitor of BCL2A1 and other BCL2 family
8 e) and identified two novel anti-IAV agents, obatoclax and gemcitabine.
9 targeted by two pan-Bcl-2 family inhibitors, obatoclax and gossypol.
10                     Moreover, we showed that obatoclax and SaliPhe inhibited IAV uptake and gemcitabi
11 oapoptotic small molecules (e.g. oblimersen, obatoclax, and gossypol), antifols (e.g. pralatrexate),
12 ential role in cell killing by lapatinib and obatoclax, as well as radiosensitization by this drug co
13                               The PYCARD and obatoclax association is validated in 30 AML patient sam
14 rgeted knockdown of Bax doubled the IC50 for obatoclax but did not abrogate its cytotoxicity, whereas
15                                 We show that obatoclax can promote the release of cytochrome c from i
16           Coadministration of lapatinib with obatoclax caused synergistic cell killing by eliciting a
17 2 and Bcl-xL, effects that were abolished by obatoclax coadministration.
18 ated lethality triggered by the flavopiridol/obatoclax combination in vitro and in vivo.
19           Coadministration of lapatinib with obatoclax elicited autophagic cell death that was attrib
20             Pretreatment of tumor cells with obatoclax enhanced the lethality of lapatinib to a great
21 nduction of apoptosis was related to overall obatoclax exposure, as monitored by the plasma concentra
22 r administered singly or in combination with obatoclax, flavopiridol also induced upregulation of mul
23 nase inhibitor sorafenib and the BH3-mimetic obatoclax (GX15-070) were examined in human acute myeloi
24 ated the mechanism of apoptosis induction of obatoclax (GX15-070), a novel Bcl-2 homology domain-3 (B
25 ell CLL/lymphoma-2 (BCL-2) family antagonist obatoclax (GX15-070).
26 oethyl)]-4H-chromene-3-carboxylate (HA14-1), obatoclax (GX15-070)].
27 e absence of Bak/Bax or Bim, suggesting that obatoclax has additional targets that contribute to its
28  the combination of THZ1 and the BH3 mimetic obatoclax improves lymphoma growth control in a primary
29 hibitor flavopiridol and the pan-BH3 mimetic obatoclax in multiple myeloma (MM) cells in which Mcl-1
30                       In a cell-free system, obatoclax induced an activating conformational change of
31  not induce apoptosis or decrease viability, obatoclax induced an S-G(2) cell-cycle block.
32                                              Obatoclax induced apoptosis in AML CD34+ progenitor cell
33 sypol was effective only in resistant cells, obatoclax induced cell death in both parental and ABT-73
34                     Treatment with sorafenib/obatoclax induced pronounced apoptosis in and reduced th
35  together, our data argue that lapatinib and obatoclax-induced toxic autophagy is due to impaired aut
36                                              Obatoclax inhibited cell growth of HL-60, U937, OCI-AML3
37                                Lapatinib and obatoclax-initiated autophagy depended on NOXA-mediated
38 t cancer cells have shown that lapatinib and obatoclax interact in a greater than additive fashion to
39   Previous studies showed that lapatinib and obatoclax interact in a greater-than-additive fashion to
40 ltogether, our results suggest that phase II obatoclax, investigational SaliPhe, and FDA/EMEA-approve
41                                Lapatinib and obatoclax killed multiple CNS tumor isolates.
42                                Lapatinib and obatoclax killed multiple tumor cell types, and cells la
43  receptors were most important for enhancing obatoclax lethality rather than ERBB2.
44 ockdown, significantly potentiated sorafenib/obatoclax lethality, indicating a cytoprotective role fo
45  exposure of leukemia cells to sorafenib and obatoclax markedly induced autophagy, reflected by rapid
46  that inhibit Mcl-1 and Bcl-2/Bcl-xL such as obatoclax may represent a novel and potentially effectiv
47                                              Obatoclax mesylate has biologic activity and modest sing
48 the pan-antiapoptotic BCL-2 family inhibitor obatoclax mesylate in diagnostic leukemia cells from 54
49                                              Obatoclax mesylate is a small molecule pan-Bcl-2 antagon
50 we have investigated the mechanisms by which obatoclax (OLX) and ABT-737 Bcl-2 inhibitors exhibited a
51 [MMF], and mycophenolic acid [MPA]), but not obatoclax or Osu-03012, showed potent anti-influenza vir
52 3 mimetics that are broad acting (ABT263 and obatoclax) or selective (ABT199, WEHI-539, and A1210477)
53                  In conclusion, we show that obatoclax potently induces apoptosis and decreases leuke
54                                              Obatoclax prevented Mcl-1 recovery and caused release of
55 topic CNS tumor isolates with lapatinib- and obatoclax-prolonged survival.
56 periments demonstrated that Mcl-1 (target of obatoclax) provides a novel host target for IAV treatmen
57 ase inhibitor sorafenib with the BH3 mimetic obatoclax results in enhanced antileukemic effects compa
58  Bax, but not Noxa, significantly attenuated obatoclax/sorafenib lethality, whereas ectopic expressio
59         Coadministration of flavopiridol and obatoclax synergistically triggered apoptosis in both dr
60                                              Obatoclax synergized with the novel BH3 mimetic ABT-737
61             Despite single-agent activity by obatoclax, the mitochondria from these cells did not rel
62 Altogether, our data show that lapatinib and obatoclax therapy could be of use in the treatment of tu
63 mouse model revealed that combined sorafenib/obatoclax treatment markedly reduced tumor growth and si
64                  In conclusion, single-agent obatoclax treatment results in Bax activation, which con
65 ches including flow cytometry, Western blot, obatoclax treatment with death pathway inhibition, micro
66  cells were radiosensitized by lapatinib and obatoclax treatment.
67 hibition of colony formation was observed by obatoclax treatment.
68                                              Obatoclax was administered to patients with advanced CLL
69 x)) and area under the curve (AUC) values of obatoclax were dose proportional.
70 VP-BEZ235, which targets the cell cycle, and Obatoclax, which targets survival, demonstrated synergis
71 ning the pan-Bcl-2 inhibitor GX15-070 (GX15; obatoclax) with immunotherapeutic modalities.