Molecular Weight(MW): 650.6
BGT226 (NVP-BGT226) is a novel class I PI3K/mTOR inhibitor for PI3Kα/β/γ with IC50 of 4 nM/63 nM/38 nM. Phase 1/2.
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IGROV1-R10 cells were treated with BGT266(250nM) for 8 h.The effect of BGT226 on PI3K/Akt/mTOR pathway activation (A) and on expression of Mcl-1 and Bim (B).
Cancer Lett 2014 348(1-2), 38-49. BGT226 (NVP-BGT226) purchased from Selleck.
A. Western blot analysis of Mahlavu, SNU475 and Hep3B cell lines treated for 24 h with increasing concentrations of the drug, ranging from 0.1 to 0.5 μM. Twenty-five μg of protein were blotted to each lane. β-Actin served as a loading control. B. Analysis of Annexin-V positive cells after BGT226 treatment using the Muse™ Cell Analyzer in Mahlavu, SNU475 and Hep3B cells. The analysis was performed after 24 h of treatment with increasing concentrations of BGT226. Results are the mean of three different experiments ± SD. Asterisks indicate significant differences compared with CTRL (*p < 0.05). C. DNA staining of Mahlavu cells with the fluorescent dye DAPI is reported. In these cells, treated with increasing concentrations of the BGT226 ranging from 0.1 to 0.5 μM, aspects of nuclear chromatin condensation (arrows), representing the apoptotic mode of cell death, are observable. Bar: 10 μm.
Oncotarget, 2015, 6(19):17147-60.. BGT226 (NVP-BGT226) purchased from Selleck.
Western Blot analysis in the ALL-SIL cell line treated with single administration of Imatinib, Nilotinib, GZD824, Torin-2 and BGT226 for 24 h. An increase of expression of fast-migrating (lipidated) LC3A/B after drug treatments is shown. Twenty-five μg of protein were blotted on each lane. β-Actin documented equal lane loading.
Oncotarget, 2016, 7(48):79842-79853. BGT226 (NVP-BGT226) purchased from Selleck.
Representative images of the redox ratio (1st row), NADH α1 (2nd row), and FAD α1 (third row) for SCC61 cells treated with control (1st column), cetuximab (2nd column), BGT226 (3rd column), or cisplatin (4th column). α1 quantifies the short lifetime component (α1+α2 = 1). NADH α1 represents the contribution from free NADH, while FAD α1 conversely represents the contribution from protein-bound FAD. Scale bar represents 30 um.
PLoS One 2014 9(3), e90746. BGT226 (NVP-BGT226) purchased from Selleck.
Western blotting analysis verifies molecular targeting of cetuximab and BGT226. Western blot for SCC61 cells. Epidermal growth factor (EGF) and transforming growth factor alpha (TGFα) activate the epidermal growth factor receptor (EGFR) and AKT pathways. Treatment with cetuximab decreases phosphorylated EGFR (pEGFR), and treatment with BGT226 decreases phosphorylated AKT (pAKT).
PLoS One 2014 9(3), e90746. BGT226 (NVP-BGT226) purchased from Selleck.
Purity & Quality Control
Choose Selective PI3K Inhibitors
|Description||BGT226 (NVP-BGT226) is a novel class I PI3K/mTOR inhibitor for PI3Kα/β/γ with IC50 of 4 nM/63 nM/38 nM. Phase 1/2.|
The anti-proliferative and pro-apoptotic effects of NVP-BGT226 are independent of bcr-abl status. The activation of the AKT/mTOR signal cascade is suppressed by NVP-BGT226 in a concentration- and time-dependent manner. Flow cytometric analysis exhibits an accumulation of cells in the G(0)-G(1) phase with concomitant loss in the S-phase. NVP-BGT226 displays potent growth-inhibitory activity against all tested cell lines including SCC4, TU183 and KB cell lines with the IC50 ranging from 7.4 to 30.1 nM. Notably, both Detroit 562 and HONE-1 cells, which express PIK3CA mutation H1047R, are still sensitive to the growth-inhibitory effect of NVP-BGT226 treatment. In addition, the sensitivity to NVP-BGT226 between HONE-1 cells and its cisplatin-resistant variant is almost identical. Results of the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay and the analysis of caspase 3/7 and PARP indicates that NVP-BGT226 induces cancer cell death through an apoptosis-independent pathway. NVP-BGT226 induces autophagy as indicated by the aggregation and upregulation of the microtubule-associated protein light chain 3B-II, and p62 degradation. Gene silencing of Beclin1 or cotreatment of the autophagosome inhibitor, 3-methyladenine, inhibits the NVP-BGT226-induced autophagy and leads to the retrieval of colony survival. NVP-BGT226 inhibits growth in common myeloma cell lines and primary myeloma cells (such as NCI-H929, U266, RPMI-8226 and OPM2 MM cell lines) at nanomolar concentrations in a time-dependent and dose-dependent manner. NVP-BGT226 inhibits phosphorylation of protein kinase B (Akt), P70S6k and 4E-BP-1 in a time-dependent and dose-dependent manner. The stimulatory effect of insulin-like growth factor 1, interleukin-6 and conditioned medium of HS-5 stromal cells on myeloma cell growth is completely abrogated by NVP-BGT226. Inhibition of phosphoinositol-3-kinase/mammalian target of rapamycin by NVP-BGT226 is highly effective, and NVP-BGT226 represents a potential new candidate for targeted therapy in multiple myeloma. Combined inhibition of PI3K and mammalian target of rapamycin (mTOR) by NVP-BGT226 has been proven to be very effective in terms of induction of apoptosis and inhibition of proliferation.  In another study, after 24 hours, 86.9% MiaPaCa-2 100 nM NVP-BGT226 treated cells arrests at the G0/G1 phase compared to 55.6% of control cells. 
|In vivo||In a xenografted animal model, NVP-BGT226 significantly delays tumor growth in a dose-dependent manner, along with suppressed cytoplasmic expression of p-p70 S6 kinase and the presence of autophagosome formation. NVP-BGT226 inhibits tumor growth in a dose-dependent manner in a FaDu cell xenografted mouse model. Oral administration of NVP-BGT226 at 2.5 and 5 mg/kg for 3 weeks causes 34.7% and 76.1% reduction of the tumor growth on day 21, respectively (compared with control). NVP-BGT226 displays comparable inhibition against tumor growth to rapamycin. The final volume of both groups is significantly smaller than those treated with LY294002 (a PI3K inhibitor) or the control. |
|In vitro||DMSO||30 mg/mL (46.11 mM)|
|In vivo||Add solvents to the product individually and in order:
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00742105||Completed||Cancer|Solid Tumor|Advanced Solid Tumor||Novartis Pharmaceuticals|Novartis||November 2008||Phase 1|
|NCT00600275||Completed||Solid Tumors|Breast Cancer|Cowden Syndrome||Novartis Pharmaceuticals|Novartis||December 2007||Phase 1|Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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Frequently Asked Questions
In the case to dissolve NVP-BGT226 for in vivo study , this solvent - 30% PEG400+0.5% Tween80+5% Propylene glycol is used as suggested by Selleck Chem. May I know how to prepare this solvent? Do I need to mix the above three into water, saline or DMSO or other solutions?
S2749 BGT226 (NVP-BGT226) can be dissolved in 30% PEG400+0.5% Tween80+5% Propylene glycol at 30mg/ml as a suspension for oral gavage. When prepare the solution, please add PEG 400 and Propylene glycol to the drug first. Please sonicate and warm it at about 45-50 degree to dissolve the drug as much as possible. Then add Tween, and mix the them homogeneously. Then dilute with water.