Research Area
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GDC-0941 Chemical Structure
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Biological Activity
GDC-0941 against p110a IC50=0.003μM,U87MG IC50=0.95μM, A2780 IC50=0.14 μM, and in vitro metabolic stability in mouse and human is 91.96%. The inhibitions of U87MG , PC3, MDA-MB-361 cancer cell proliferation are (IC50) 0.95, 0.28, 0.72 μM, respectively.
References on GDC-0941
- [1] J. Med. Chem 2008;51:5522–5532
Chemical Information
| Molecular Weight (WM): | 513.64 |
|---|---|
| Formula: | C23H27N7O3S2 |
| CAS No.: | 957054-30-7 |
| Synonyms: |
N/A
|
| Dissolve in (25°C): | DMSO ≥103mg/mL |
| Water ≥103mg/mL | |
| Ethanol <1mg/mL | |
| Storage: | 2 years-20°CPowder |
| 1 week-4°Cin DMSO | |
| 1 month-80°in DMSO |
Quality Control & MSDS
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Selleck's high quality products have been used in several published research findings, including the following:
PTEN Loss Confers BRAF Inhibitor Resistance to Melanoma Cells through the Suppression of BIM Expression
Transient PI3K inhibition induces apoptosis and overcomes HGF-mediated resistance to EGFR-TKIs in EGFR mutant lung cancer.
Akt determines cell fate through inhibition of the PERK-eIF2α phosphorylation pathway.
PI3K-targeted therapy can be evaded by gene amplification along the MYC-eukaryotic translation initiation factor 4E (eIF4E) axis
Vertical Inhibition of the mTORC1/mTORC2/PI3K Pathway Shows Synergistic Effects against Melanoma In Vitro and In Vivo
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Dual PI3K/BRAF inhibition upregulates BIM and enhances apoptosis in PTEN cells. A, left, Western blot of 1205Lu cells treated with PLX4720 (3 mmol/L, 48 hours), the PI3K inhibitor GDC-0941 (3 mmol/L, 48 hours), or both drugs in combination (PtG); right, immunofluorescence staining of BIM (green) and DAPI (blue) in PTEN cells following PLX4720 treatment (3mmol/L, 48 hours), the PI3K inhibitor LY294002 (10 mmol/L, 48 hours), or both drugs in combination (PLXtLY). B, left, immunofluorescence staining of PTEN 1205Lu following combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48hours) increases nuclear localization of FOXO3a (green). DAPI is shown in blue. Magnification 40. Right, combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48 hours) increases PTEN WM793 BIM mRNA levels to those observed with single BRAF inhibition (3 mmol/L PLX4720, 48 hours) in the PTENt WM35. C, PTEN cells were treated with PLX4720 (3 mmol/L, 48 hours), GDC-0941 (3 mmol/L, 48hours), or a combination of the 2 drugs (3Pt3G) before Annexin-V staining was analyzed by flow cytometry (*, P < 0.05 between the drug combination and each inhibitor alone). D, combined BRAF/PI3K inhibitor treatment blocks the escape of 1205Lu cells (PTEN) from therapy. Spheroids of 1205Lu cells were treated with either PLX4720 alone (3 and 10 mmol/L: data shows 3 mmol/L), LY294002 (10 mmol/L) alone or a combination of the 2 drugs for 72 hours. In other studies, spheroids were treated with drugs for 72 hours and then allowed to recover for 120 hours. Micrograph shows viability staining (green ?live cells, red ?dead cells). Magnification 10.
Dual PI3K/BRAF inhibition upregulates BIM and enhances apoptosis in PTEN cells. A, left, Western blot of 1205Lu cells treated with PLX4720 (3 mmol/L, 48 hours), the PI3K inhibitor GDC-0941 (3 mmol/L, 48 hours), or both drugs in combination (PtG); right, immunofluorescence staining of BIM (green) and DAPI (blue) in PTEN cells following PLX4720 treatment (3mmol/L, 48 hours), the PI3K inhibitor LY294002 (10 mmol/L, 48 hours), or both drugs in combination (PLXtLY). B, left, immunofluorescence staining of PTEN 1205Lu following combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48hours) increases nuclear localization of FOXO3a (green). DAPI is shown in blue. Magnification 40. Right, combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48 hours) increases PTEN WM793 BIM mRNA levels to those observed with single BRAF inhibition (3 mmol/L PLX4720, 48 hours) in the PTENt WM35. C, PTEN cells were treated with PLX4720 (3 mmol/L, 48 hours), GDC-0941 (3 mmol/L, 48hours), or a combination of the 2 drugs (3Pt3G) before Annexin-V staining was analyzed by flow cytometry (*, P < 0.05 between the drug combination and each inhibitor alone). D, combined BRAF/PI3K inhibitor treatment blocks the escape of 1205Lu cells (PTEN) from therapy. Spheroids of 1205Lu cells were treated with either PLX4720 alone (3 and 10 mmol/L: data shows 3 mmol/L), LY294002 (10 mmol/L) alone or a combination of the 2 drugs for 72 hours. In other studies, spheroids were treated with drugs for 72 hours and then allowed to recover for 120 hours. Micrograph shows viability staining (green ?live cells, red ?dead cells). Magnification 10.
Data from [Cancer Res 2011.February;71:2750-2760] GDC-0941 purchased from Selleck
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Click to enlarge
Combination of rapamycin and PI-103 leads to the suppression of AKT phosphorylation (phospho-specific western blot). Mel-Juso and 518A2 cells were treated with GDC-0941 from 0.05–1 mmol l1 alone and in combination with rapamycin (50 nmol l1) for 24 hours. Control treatment was with DMSO.
Combination of rapamycin and PI-103 leads to the suppression of AKT phosphorylation (phospho-specific western blot). Mel-Juso and 518A2 cells were treated with GDC-0941 from 0.05–1 mmol l1 alone and in combination with rapamycin (50 nmol l1) for 24 hours. Control treatment was with DMSO.
Data from [Journal of Investigative Dermatology 2010.November;131:495-503] GDC-0941 purchased from Selleck
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Click to enlarge
After starved in serum-free medium for 24h, Breast cancer cells incubated with the indicated concentrations of GDC-0941 for 3h,followed by 15-minute stimolation of 100ng/ml EGF.
After starved in serum-free medium for 24h, Breast cancer cells incubated with the indicated concentrations of GDC-0941 for 3h,followed by 15-minute stimolation of 100ng/ml EGF.
Data independently produced by Dr Zhang of Tianjin Medical University GDC-0941 purchased from Selleck
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We treated all of drugs in T47D which has a PI3KCA H1044R mutation with the concentration shown below for 1 hour and performed western blot analysis using antibodies to phospho-AKT(SERINE 472), and total AKT.
We treated all of drugs in T47D which has a PI3KCA H1044R mutation with the concentration shown below for 1 hour and performed western blot analysis using antibodies to phospho-AKT(SERINE 472), and total AKT.
Data independently produced by Saraswati Sukumar of Johns Hopkins University School of Medicine---GDC-0941 purchased from Selleck GDC-0941 purchased from Selleck
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Dual PI3K/BRAF inhibition upregulates BIM and enhances apoptosis in PTEN cells. A, left, Western blot of 1205Lu cells treated with PLX4720 (3 mmol/L, 48 hours), the PI3K inhibitor GDC-0941 (3 mmol/L, 48 hours), or both drugs in combination (PtG); right, immunofluorescence staining of BIM (green) and DAPI (blue) in PTEN cells following PLX4720 treatment (3mmol/L, 48 hours), the PI3K inhibitor LY294002 (10 mmol/L, 48 hours), or both drugs in combination (PLXtLY). B, left, immunofluorescence staining of PTEN 1205Lu following combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48hours) increases nuclear localization of FOXO3a (green). DAPI is shown in blue. Magnification 40. Right, combined inhibition (3 mmol/L PLX4720 t 10 mmol/L LY294002, 48 hours) increases PTEN WM793 BIM mRNA levels to those observed with single BRAF inhibition (3 mmol/L PLX4720, 48 hours) in the PTENt WM35. C, PTEN cells were treated with PLX4720 (3 mmol/L, 48 hours), GDC-0941 (3 mmol/L, 48hours), or a combination of the 2 drugs (3Pt3G) before Annexin-V staining was analyzed by flow cytometry (*, P < 0.05 between the drug combination and each inhibitor alone). D, combined BRAF/PI3K inhibitor treatment blocks the escape of 1205Lu cells (PTEN) from therapy. Spheroids of 1205Lu cells were treated with either PLX4720 alone (3 and 10 mmol/L: data shows 3 mmol/L), LY294002 (10 mmol/L) alone or a combination of the 2 drugs for 72 hours. In other studies, spheroids were treated with drugs for 72 hours and then allowed to recover for 120 hours. Micrograph shows viability staining (green ?live cells, red ?dead cells). Magnification 10. |
Data from [Cancer Res 2011.February;71:2750-2760]
Combination of rapamycin and PI-103 leads to the suppression of AKT phosphorylation (phospho-specific western blot). Mel-Juso and 518A2 cells were treated with GDC-0941 from 0.05–1 mmol l1 alone and in combination with rapamycin (50 nmol l1) for 24 hours. Control treatment was with DMSO.
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Data from [Journal of Investigative Dermatology 2010.November;131:495-503]
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