wx-554 Search Results


90
WILEX Inc wx-554
Wx 554, supplied by WILEX Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/wx-554/product/WILEX Inc
Average 90 stars, based on 1 article reviews
wx-554 - by Bioz Stars, 2026-04
90/100 stars
  Buy from Supplier

90
Celltech Inc wx-554
Growth inhibition induced by the PI3K inhibitor WX-037 and the MEK inhibitor <t>WX-554,</t> alone and in combination, in the HCT116 and HT29 cell lines. HCT116 ( a ) and HT29 ( b ) cells were treated with the indicated fractions of the GI 50 concentrations of the inhibitors, alone or in combination, derived from Supplementary Figure 1, for 72 h, and an SRB assay was subsequently performed. Growth is presented as a percentage of the control, in which cells were treated with 0.5% (v/v) DMSO. Points represent the mean of 3 independent experiments ± standard error. Lines were fitted using nonlinear regression analysis
Wx 554, supplied by Celltech Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/wx-554/product/Celltech Inc
Average 90 stars, based on 1 article reviews
wx-554 - by Bioz Stars, 2026-04
90/100 stars
  Buy from Supplier

Image Search Results


Growth inhibition induced by the PI3K inhibitor WX-037 and the MEK inhibitor WX-554, alone and in combination, in the HCT116 and HT29 cell lines. HCT116 ( a ) and HT29 ( b ) cells were treated with the indicated fractions of the GI 50 concentrations of the inhibitors, alone or in combination, derived from Supplementary Figure 1, for 72 h, and an SRB assay was subsequently performed. Growth is presented as a percentage of the control, in which cells were treated with 0.5% (v/v) DMSO. Points represent the mean of 3 independent experiments ± standard error. Lines were fitted using nonlinear regression analysis

Journal: Cancer Chemotherapy and Pharmacology

Article Title: Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037

doi: 10.1007/s00280-016-3186-4

Figure Lengend Snippet: Growth inhibition induced by the PI3K inhibitor WX-037 and the MEK inhibitor WX-554, alone and in combination, in the HCT116 and HT29 cell lines. HCT116 ( a ) and HT29 ( b ) cells were treated with the indicated fractions of the GI 50 concentrations of the inhibitors, alone or in combination, derived from Supplementary Figure 1, for 72 h, and an SRB assay was subsequently performed. Growth is presented as a percentage of the control, in which cells were treated with 0.5% (v/v) DMSO. Points represent the mean of 3 independent experiments ± standard error. Lines were fitted using nonlinear regression analysis

Article Snippet: This cytotoxicity is consistent with previous unpublished studies by UCB Celltech and Wilex where the observed growth inhibitory synergy with WX-037 and WX-554 in the SK-MEL-28 melanoma, HT29 colorectal, Mia PaCa-2 pancreatic and SKOV-3 ovarian carcinoma cell lines was found to correlate with the induction of apoptosis [ ].

Techniques: Inhibition, Derivative Assay, Sulforhodamine B Assay

Cell survival after 72-h exposure to 10 µM of the PI3K inhibitor WX-037 and 10 µM of the MEK inhibitor WX-554, alone and in combination, in the HCT116 cell line and HT29 cell lines. HCT116 ( a ) and HT29 ( b ) cells were treated with a fixed concentration of each inhibitor alone or in combination for 72 h, and cell survival was subsequently determined by clonogenic assay after 10–14 days of colony growth. Survival is presented as a percentage of the control, in which cells were treated with 0.5% (v/v) DMSO. Bars represent the mean of 3 independent replicates ± standard error. *Significantly different from either agent alone, p ≤ 0.05

Journal: Cancer Chemotherapy and Pharmacology

Article Title: Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037

doi: 10.1007/s00280-016-3186-4

Figure Lengend Snippet: Cell survival after 72-h exposure to 10 µM of the PI3K inhibitor WX-037 and 10 µM of the MEK inhibitor WX-554, alone and in combination, in the HCT116 cell line and HT29 cell lines. HCT116 ( a ) and HT29 ( b ) cells were treated with a fixed concentration of each inhibitor alone or in combination for 72 h, and cell survival was subsequently determined by clonogenic assay after 10–14 days of colony growth. Survival is presented as a percentage of the control, in which cells were treated with 0.5% (v/v) DMSO. Bars represent the mean of 3 independent replicates ± standard error. *Significantly different from either agent alone, p ≤ 0.05

Article Snippet: This cytotoxicity is consistent with previous unpublished studies by UCB Celltech and Wilex where the observed growth inhibitory synergy with WX-037 and WX-554 in the SK-MEL-28 melanoma, HT29 colorectal, Mia PaCa-2 pancreatic and SKOV-3 ovarian carcinoma cell lines was found to correlate with the induction of apoptosis [ ].

Techniques: Concentration Assay, Clonogenic Assay

Concentrations of the MEK inhibitor WX-554 alone and in combination with the PI3K inhibitor WX-037 in tumours from mice bearing HCT116 or HT29 human tumour xenografts. Tumour concentrations of WX-554 measured by LC–MS/MS from HCT116 ( a , c ) and HT29 ( b , d ) tumour xenograft-bearing mice at the indicated time points after a single p.o. dose of 1 mg/kg ( a , b ) or 5 mg/kg ( c , d ) WX-554 alone or combined with 20 or 100 mg/kg WX-037. Data are presented as the mean concentration from 3 mice in each group ± standard error. Horizontal dashed lines indicate the in vitro GI 50 concentration for the respective cell line, calculated from Supplementary Figure 1

Journal: Cancer Chemotherapy and Pharmacology

Article Title: Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037

doi: 10.1007/s00280-016-3186-4

Figure Lengend Snippet: Concentrations of the MEK inhibitor WX-554 alone and in combination with the PI3K inhibitor WX-037 in tumours from mice bearing HCT116 or HT29 human tumour xenografts. Tumour concentrations of WX-554 measured by LC–MS/MS from HCT116 ( a , c ) and HT29 ( b , d ) tumour xenograft-bearing mice at the indicated time points after a single p.o. dose of 1 mg/kg ( a , b ) or 5 mg/kg ( c , d ) WX-554 alone or combined with 20 or 100 mg/kg WX-037. Data are presented as the mean concentration from 3 mice in each group ± standard error. Horizontal dashed lines indicate the in vitro GI 50 concentration for the respective cell line, calculated from Supplementary Figure 1

Article Snippet: This cytotoxicity is consistent with previous unpublished studies by UCB Celltech and Wilex where the observed growth inhibitory synergy with WX-037 and WX-554 in the SK-MEL-28 melanoma, HT29 colorectal, Mia PaCa-2 pancreatic and SKOV-3 ovarian carcinoma cell lines was found to correlate with the induction of apoptosis [ ].

Techniques: Liquid Chromatography with Mass Spectroscopy, Concentration Assay, In Vitro

Concentrations of the PI3K inhibitor WX-037 alone and in combination with the MEK inhibitor WX-554 in tumours from mice bearing HCT116 or HT29 human tumour xenografts. Tumour concentrations of WX-037 measured by LC–MS/MS from HCT116 ( a , c ) and HT29 ( b , d ) tumour xenograft-bearing mice at the indicated time points after a single p.o. dose of 20 mg/kg ( a , b ) or 100 mg/kg ( c , d ) WX-037 alone or combined with 1 or 5 mg/kg WX-554. Data are presented as the mean concentration from 3 mice in each group ± standard error. Horizontal dashed lines indicate the in vitro GI 50 concentration for the respective cell line, calculated from Supplementary Figure 1

Journal: Cancer Chemotherapy and Pharmacology

Article Title: Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037

doi: 10.1007/s00280-016-3186-4

Figure Lengend Snippet: Concentrations of the PI3K inhibitor WX-037 alone and in combination with the MEK inhibitor WX-554 in tumours from mice bearing HCT116 or HT29 human tumour xenografts. Tumour concentrations of WX-037 measured by LC–MS/MS from HCT116 ( a , c ) and HT29 ( b , d ) tumour xenograft-bearing mice at the indicated time points after a single p.o. dose of 20 mg/kg ( a , b ) or 100 mg/kg ( c , d ) WX-037 alone or combined with 1 or 5 mg/kg WX-554. Data are presented as the mean concentration from 3 mice in each group ± standard error. Horizontal dashed lines indicate the in vitro GI 50 concentration for the respective cell line, calculated from Supplementary Figure 1

Article Snippet: This cytotoxicity is consistent with previous unpublished studies by UCB Celltech and Wilex where the observed growth inhibitory synergy with WX-037 and WX-554 in the SK-MEL-28 melanoma, HT29 colorectal, Mia PaCa-2 pancreatic and SKOV-3 ovarian carcinoma cell lines was found to correlate with the induction of apoptosis [ ].

Techniques: Liquid Chromatography with Mass Spectroscopy, Concentration Assay, In Vitro

Efficacy and tolerability of the PI3K inhibitor WX-037 and the MEK inhibitor WX-554 in mice bearing human HCT116 colorectal tumour xenografts. HCT116 tumour xenografts were treated with either vehicle control, 2 mg/kg of the MEK inhibitor WX-554 and 50 mg/kg of the PI3K inhibitor WX-037 alone, or 2 mg/kg of the MEK inhibitor WX-554 and 50 mg/kg of the PI3K inhibitor WX-037 in combination, p.o. once daily for 14 days. a Tumour growth curves: data are presented as the median relative tumour volume (RTV), where the growth is calculated for each tumour relative to its size on day 0. Points represent the median of the 10 mice in each group. The dashed line shows the point at which tumours reached four times the initial volume (RTV4). b Effects on body weight: data are presented as a percentage of starting body weight. Points represent the mean of the mice in each group ± standard error. c Time taken for xenografts to reach four times the initial volume (time to RTV4): data are presented as the time taken by each individual tumour in each group to quadruple in size, and lines to represent the mean of the mice in each group ± standard error. p values are given where the combination is significantly different from either agent alone ( p ≤ 0.05)

Journal: Cancer Chemotherapy and Pharmacology

Article Title: Enhanced anti-tumour activity of the combination of the novel MEK inhibitor WX-554 and the novel PI3K inhibitor WX-037

doi: 10.1007/s00280-016-3186-4

Figure Lengend Snippet: Efficacy and tolerability of the PI3K inhibitor WX-037 and the MEK inhibitor WX-554 in mice bearing human HCT116 colorectal tumour xenografts. HCT116 tumour xenografts were treated with either vehicle control, 2 mg/kg of the MEK inhibitor WX-554 and 50 mg/kg of the PI3K inhibitor WX-037 alone, or 2 mg/kg of the MEK inhibitor WX-554 and 50 mg/kg of the PI3K inhibitor WX-037 in combination, p.o. once daily for 14 days. a Tumour growth curves: data are presented as the median relative tumour volume (RTV), where the growth is calculated for each tumour relative to its size on day 0. Points represent the median of the 10 mice in each group. The dashed line shows the point at which tumours reached four times the initial volume (RTV4). b Effects on body weight: data are presented as a percentage of starting body weight. Points represent the mean of the mice in each group ± standard error. c Time taken for xenografts to reach four times the initial volume (time to RTV4): data are presented as the time taken by each individual tumour in each group to quadruple in size, and lines to represent the mean of the mice in each group ± standard error. p values are given where the combination is significantly different from either agent alone ( p ≤ 0.05)

Article Snippet: This cytotoxicity is consistent with previous unpublished studies by UCB Celltech and Wilex where the observed growth inhibitory synergy with WX-037 and WX-554 in the SK-MEL-28 melanoma, HT29 colorectal, Mia PaCa-2 pancreatic and SKOV-3 ovarian carcinoma cell lines was found to correlate with the induction of apoptosis [ ].

Techniques: