BGJ398 (NVP-BGJ398)

Catalog No.S2183

BGJ398 (NVP-BGJ398) Chemical Structure

Molecular Weight(MW): 560.48

BGJ398 (NVP-BGJ398) is a potent and selective FGFR inhibitor for FGFR1/2/3 with IC50 of 0.9 nM/1.4 nM/1 nM in cell-free assays, >40-fold selective for FGFR versus FGFR4 and VEGFR2, and little activity to Abl, Fyn, Kit, Lck, Lyn and Yes. Phase 2.

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3 Customer Reviews

  • Activation of FGFR2 and MAPK by FGFR2-AHCYL1 and its suppression by FGFR inhibitors. Lysates from NIN3T3 cells expressing FGFR2-AHCYL1 or EZR-ROS1 (control) treated with vehicle (DMSO), 0.2 and 1 µM BGJ398, and 0.2 and 1 µM PD173074 were immunoblotted with the relevant antibodies. β-actin was used as a loading control.

    Hepatology 2014 59(4), 1427-34. BGJ398 (NVP-BGJ398) purchased from Selleck.

    Anchorage-independent growth of NIN3T3 cells expressing FGFR2 fusions and its suppression by FGFR inhibitors (BGJ: BGJ398 and PD: PD173074). The percentage (+/- s.d.) of colonies formed in the presence of FGFR2 inhibitors (0.2 礛) and by KD mutants with respect to those formed by DMSO-treated cells are plotted at the bottom. The NIH3T3 clone expressing EZR-ROS1 was used as a negative control for FGFR inhibitors. *P<0.05.

    Hepatology 2014 59(4), 1427-34. BGJ398 (NVP-BGJ398) purchased from Selleck.

  • BGJ39 distinctly inhibited the inductive effect of FGF2. Just as the results of western blot, BGJ39 not only reversed the down-expression of E-cadherin, but also weakened the expression of BSP and OPN. However, combination of both TGF- β1 and FGF2 containing BGJ39 distinctly improved the expression of fibronectin and periostin. β-actin was used as an internal control for equal protein loading. * P < 0.05, ** P < 0.01.

    J Cell Physiol 2014 229(11), 1647-59. BGJ398 (NVP-BGJ398) purchased from Selleck.

Purity & Quality Control

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description BGJ398 (NVP-BGJ398) is a potent and selective FGFR inhibitor for FGFR1/2/3 with IC50 of 0.9 nM/1.4 nM/1 nM in cell-free assays, >40-fold selective for FGFR versus FGFR4 and VEGFR2, and little activity to Abl, Fyn, Kit, Lck, Lyn and Yes. Phase 2.
Targets
FGFR1 [1]
(Cell-free assay)
FGFR3 [1]
(Cell-free assay)
FGFR2 [1]
(Cell-free assay)
FGFR3 (K650E) [1]
(Cell-free assay)
FGFR4 [1]
(Cell-free assay)
0.9 nM 1.0 nM 1.4 nM 4.9 nM 60 nM
In vitro

BGJ398 also prevents VEGFR2 with low potency. The IC50 of BGJ398 for inhibiting VEGFR2 is 0.18 μM. BGJ398 suppresses other kinases including ABL, FYN, KIT, LCK, LYN and YES with IC50 of 2.3 μM, 1.9 μM, 0.75 μM, 2.5 μM, 0.3 μM and 1.1 μM, respectively. At the cellular level, BGJ398 inhibits the proliferation of the FGFR1-, FGFR2-Q, and FGFR3-dependent BaF3 cells with IC50 of 2.9 μM, 2.0 μM and 2 μM, respectively. BGJ398 interferes with autophosphorylation on specific tyrosine residues including FGFR-WT, FGFR2-WT, FGFR3-K650E, FGFR3-S249C and FGFR4-WT with IC50 of 4.6 nM, 4.9 nM, 5 nM, 5 nM and 168 nM, respectively. BGJ398 suppresses proliferation of the cancer cells with wild-type (WT) FGFR3 overexpression such as RT112, RT4, SW780 and JMSU1 with IC50 of 5 nM, 30 nM, 32 nM and 15 nM, respectively. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCC NU\E[VROT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2jFdVEuOjVyMDDuUS=> NHnUe|M1QCCq M4T0beKhUUN3ME2gNlM2QeLCiX7t NXmyRY02OjV4OEi3OFM>
HCC NVnrZ3VQT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnfmNU0zPTByIH7N Mn;rOFghcA>? MYLJR|UxRTFzMkVihKlvdQ>? MlfrNlU3QDh5NEO=
HCT116 NGW1NpRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmfVOFghcA>? MYXJR|UxRTNizszN NG\wUJIzPDVyM{WzPC=>
HKH2 M{Pudmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFHjeGo1QCCq MmfITWM2OD12IN88US=> NVWxWlFSOjR3MEO1N|g>
RKO NXmwSnJUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MXO0PEBp NEKzVlRKSzVyPUGuNkDPxE1? MYOyOFUxOzV|OB?=
LS174T MoLvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NI\pW3A1QCCq MWHJR|UxRTRizszN NWDZWVNkOjR3MEO1N|g>
HCD9 M4XPSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{XEelAvPS13IN88US=> M3vtflQ5Nzd{IHi= MWXEUXNQ NYTLcZVW\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5 MV:yOFE{PThzNh?=
HCT116 MkGzS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXPMeWZVOC53LUWg{txO NWTZUm1XPDhxN{KgbC=> M4f3T2ROW09? MojH[IVkemWjc3XzJINmdGxidnnhZoltcXS7 MYeyOFE{PThzNh?=
SNU-C1 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mo[4NE42NTVizszN MmWxOFgwPzJiaB?= NYPoOZBTTE2VTx?= Mmnpco8h\W[oZXP0 NVrF[mdrOjRzM{W4NVY>
MFE280 NWLoOoVzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4WyS2lEPTB;Mj62N{DDuSByLkiyJO69VQ>? M4G4XVI{PDR|OEC1
AN3CA NI\OWWdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mn\wTWM2OD1zLkCwJOKyKDBwMkCg{txO NH;LbIozOzR2M{iwOS=>
HEC155 NVTiWo9yT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGX0XY1KSzVyPUSuO|QhyrFiMT6wPUDPxE1? MWmyN|Q1OzhyNR?=
MFE296 M4TQ[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHj3W45KSzVyPUKuPFYhyrFiMD6yNEDPxE1? NVT2U2VbOjN2NEO4NFU>
SPAC1S MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4XxOGlEPTB;Mz6xPUDDuSByLkmzJO69VQ>? NUjtN3BJOjN2NEO4NFU>
RL952 MoDSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HjXGlEPTB;Mz60NUDDuSByLkKzJO69VQ>? MWGyN|Q1OzhyNR?=
EN1 MYjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIq0O5FKSzVyPUSuO|UhyrFiMD62NkDPxE1? NGDzSXIzOzR2M{iwOS=>
SNGII MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV3JR|UxRTRwMkmgxtEhOC53ODFOwG0> NVr4VG5JOjN2NEO4NFU>
ISHIKAWA NF7WVJNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFX1[FRKSzVyPUWuOFghyrFiMD6wN{DPxE1? NEfJb|czOzR2M{iwOS=>
HEC1A MUXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGTn[IFKSzVyPUGwMlAxKMLzIEGuNFAh|ryP NH;qNYozOzR2M{iwOS=>
KLE M13Yb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlvkTWM2OD1|LkCzJOKyKDBwMUGg{txO MUKyN|Q1OzhyNR?=
SNGM NV3Pc5NOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4jacWlEPTB;NT6wNEDDuSByLkSxJO69VQ>? M{TnVlI{PDR|OEC1
USPC2 NFfvTG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{f4fmlEPTB;Nz6wNEDDuSByLkKxJO69VQ>? M3H0bFI{PDR|OEC1
EN NUPYZ5ZNT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFnIfpNKSzVyPU[uNFMhyrFiMD6zNUDPxE1? M3vDbVI{PDR|OEC1
MFE319 NXjLTVV4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXvob5JrUUN3ME21MlM4KMLzIECuNFMh|ryP MnPNNlM1PDN6MEW=
EFE184 M4D2Wmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVjJR|UxRThwMESgxtEhOC54OTFOwG0> NFLI[oczOzR2M{iwOS=>
ECC1 NELsXYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXf0NIFCUUN3ME22Mlc1KMLzIECuOVkh|ryP MlnhNlM1PDN6MEW=
HEC1B MnHkS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUjVcYZMUUN3ME22MlQ2KMLzIECuOlch|ryP NUfsU5pMOjN2NEO4NFU>
USPC1 M4TwOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXPJR|UxRTVwN{WgxtEhOC53MDFOwG0> MXyyN|Q1OzhyNR?=
SPAC1L M3PEVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYi4XoRmUUN3ME20MlkzKMLzIECuOVAh|ryP M3joZVI{PDR|OEC1

... Click to View More Cell Line Experimental Data

In vivo In this orthotopic xenograft bladder cancer model, BGJ398 induces tumor growth inhibition and stasis after oral administration for 12 consecutive days at the doses of 10 and 30 mg/kg, respectively. Interestingly, the animals that received BGJ398 exhibits either no body weight loss (10 mg/kg) or 10% body weight gain (30 mg/kg), a further indication of efficacy. RT112 tumor-bearing and female Rowett rats receive a single oral administration of the monophosphate salt of BGJ398 at the doses of 4.25 and 8.51 mg/kg. BGJ398 significantly decreases the levels of pFRS2 and pMAPK in a dose-dependent manner. BGJ398 inhibits significantly bFGF-stimulated angiogenesis in a dose-dependent manner. However, BGJ398 does not impair VEGF-induced blood vessel formation. [1]

Protocol

Kinase Assay: [1]
+ Expand

Radiometric kinase assay:

The enzymatic kinase activity is assessed by measuring the phosphorylation of a synthetic substrate by the purified GST-fusion FGFR3-K650E kinase domain, in the presence of radiolabeled ATP. Enzyme activities are measured by mixing 10 μL of a 3-fold concentrated BGJ398 solution or control with 10 μL of the corresponding substrate mixture (peptidic substrate, ATP and [γ33P]ATP). The reactions are initiated by addition of 10 μL of a 3-fold concentrated solution of the enzyme in assay buffer. The final concentrations of the assay components are as following: 10 ng of GST-FGFR3-K650E, 20 mM Tris-HCl, pH 7.5, 3 mM MnCl2, 3 mM MgCl2, 1 mM DTT, 250 μg/mL PEG 20000, 2 μg/mL poly(EY) 4:1, 1% DMSO and 0.5 μM ATP (γ-[33P]-ATP 0.1 μCi). The assay is carried out according to the filter binding (FB) method in 96-well plates at room temperature for 10 minutes in a final volume of 30 μL including BGJ398. The enzymatic reactions are stopped by the addition of 20 μL of 125 mM EDTA, and the incorporation of 33P into the polypeptidic substrates is quantified as following: 30 μL of the stopped reaction mixture are transferred onto Immobilon-PVDF membranes previously soaked for 5 minutes with methanol, rinsed with water, soaked for 5 min with 0.5% H3PO4, and mounted on vacuum manifold with disconnected vacuum source. After spotting, vacuum is connected, and each well rinsed with 0.5% H3PO4 (200 μL). Free membranes are removed and ished four times on a shaker with 1% H3PO4 and once with ethanol. Membranes are dried and overlaid with addition of 10 μL/well of a scintillation fluid. The plates are eventually sealed and counted in a microplate scintillation counter. IC50 values are calculated by linear regression analysis of the percentage inhibition of the BGJ398.
Cell Research:[1]
+ Expand
  • Cell lines: Murine BaF3 cell lines
  • Concentrations: 0 μM-0.1 μM
  • Incubation Time: 48 hours
  • Method: Murine BaF3 cell lines, whose proliferation and survival has been rendered IL-3-independent by stable transduction with tyrosine kinases activated either by mutation or fusion with a dimerizing partner, are cultured in RPMI-1640 media supplemented with 10% FBS, 4.5 g/L glucose, 1.5 g/L sodium bicarbonate, and Pen/Strep. Cells are passaged twice weekly. BGJ398-mediated inhibition of BaF3 cell proliferation and viability is assessed using a Luciferase bioluminescent assay. Exponentially growing BaF3 or BaF3 Tel-TK cells are seeded into 384-well plates (4250 cells/well) at 50 μL/well using a μFill liquid dispenser in fresh medium. BGJ398 is serially diluted in DMSO and arrayed in a polypropylene 384-well plate. Then 50 nL of BGJ398 are transferred into the plates containing the cells by using the pintool transfer device, and the plates incubated at 37 °C (5% CO2) for 48 hours. Then 25 μL of Bright-Glo are added, and luminescence is quantified using an Analyst-GT. Custom curve-fitting software is used to produce a logistic fit of percent cell viability as a function of the logarithm of inhibitor concentration. The IC50 value is determined as the concentration of BGJ398 needed to reduce cell viability to 50% of a DMSO control.
    (Only for Reference)
Animal Research:[1]
+ Expand
  • Animal Models: Athymic nude-nu mice bearing parental RT112 cell line
  • Formulation: PEG300/D5W (2:1, v/v)
  • Dosages: 10 mg/kg/qd and 30 mg/kg/qd
  • Administration: Oral administration
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 1 mg/mL (1.78 mM) warming
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 30% PEG400+0.5% Tween80+5% propylene glycol 30 mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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.

Chemical Information

Molecular Weight 560.48
Formula

C26H31Cl2N7O3

CAS No. 872511-34-7
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02706691 Not yet recruiting Head and Neck Squamous Cell Carcinoma University of Chicago October 2016 Phase 2
NCT02657486 Recruiting Bladder Cancer|Non-Muscle-Invasive Urothelial Carcinoma Memorial Sloan Kettering Cancer Center January 2016 --
NCT02312804 Withdrawn Cancer of Cervix|Tumors The University of Texas Health Science Center at San Antonio January 2015 Phase 1
NCT02257541 Recruiting Advanced Gastrointestinal Stromal Tumor (GIST) Memorial Sloan Kettering Cancer Center|Dana-Farber Cancer Institute|M.D. Anderson Cancer Center|University of Pittsburgh October 2014 Phase 1|Phase 2
NCT02160041 Recruiting Solid Tumor|Hematologic Malignancies Novartis Pharmaceuticals|Novartis July 2014 Phase 2
NCT02150967 Active, not recruiting Advanced Cholangiocarcinoma Novartis Pharmaceuticals|Novartis July 2014 Phase 2

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID