BGJ398 (NVP-BGJ398)

目录号:S2183

BGJ398 (NVP-BGJ398) Chemical Structure

Molecular Weight(MW): 560.48

BGJ398 (NVP-BGJ398)是一种有效的,选择性FGFR抑制剂,作用于FGFR1/2/3,在无细胞试验中IC50为0.9 nM/1.4 nM/1 nM,作用于FGFR比作用于FGFR4和VEGFR2选择性高40倍以上,对Abl, Fyn, Kit, Lck, Lyn和Yes几乎没有抑制活性。Phase 2。

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RMB 902.78 现货
RMB 1411.94 现货
RMB 2215.49 现货
RMB 4650.25 现货
RMB 7960.75 现货
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客户使用该产品的5个实验数据:

  • 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.

  • we used a FGFR inhibitor (BGJ398) and a MEK inhibitor (PD98059) to confirm that the inhibition of FGF pathway was directly related to the fibroblast-like conversion, and same morphologic change and increased expression of Vim and COL I was observed

    Oncogene, 2017.. BGJ398 (NVP-BGJ398) purchased from Selleck.

    BGJ398 inhibits signaling in cell lines with activating FGFR alterations. Immunoblot demonstrates the expression of total/pFGFRs and total/pFRS2 in DMSO and BGJ398 in treated cell lines (A) DMS114. B, RT112. Lysates were prepared from cells exposed to BGJ398 (at the indicated concentrations) for 24 hours and immunoblots performed with the respective antibodies. Representative data are shown from three experimental replicates. Bar graphs display densitometric analysis of protein bands using GAPDH as a control. BGJ398 treatment results in decreased levels of pFGFR1/pFGFR3 and pFRS2/total FRS2, respectively.

    Mol Cancer Ther, 2017.. 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.

产品安全说明书

FGFR抑制剂选择性比较

生物活性

产品描述 BGJ398 (NVP-BGJ398)是一种有效的,选择性FGFR抑制剂,作用于FGFR1/2/3,在无细胞试验中IC50为0.9 nM/1.4 nM/1 nM,作用于FGFR比作用于FGFR4和VEGFR2选择性高40倍以上,对Abl, Fyn, Kit, Lck, Lyn和Yes几乎没有抑制活性。Phase 2。
靶点
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
体外研究

BGJ398抑制FGFR3-K650E,IC50 为4.9 nM。此外, BGJ398 也抑制VEGFR2。BGJ398 抑制其他激酶,包括ABL, FYN, KIT, LCK, LYN 和 YES,IC50分别为2.3 μM, 1.9 μM, 0.75 μM, 2.5 μM, 0.3 μM和1.1 μM。在细胞水平, BGJ398 抑制FGFR1-, FGFR2-Q, 和FGFR3-依赖的BaF3 细胞增殖,IC50分别为2.9 μM, 2.0μM和2 μM。BGJ398在特定酪氨酸残基,包括FGFR-WT, FGFR2-WT, FGFR3-K650E, FGFR3-S249C 和 FGFR4-WT处,干扰自磷酸化,IC50分别为4.6 nM, 4.9 nM, 5 nM, 5 nM 和168 nM。BGJ398 抑制过量表达野生型(WT)FGFR3的癌细胞,如RT112, RT4, SW780 和JMSU1 的增殖,IC50分别为5 nM, 30 nM, 32 nM 和15 nM。[1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HCC NXLEWoljT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVKxMVI2ODBibl2= Ml\0OFghcA>? MURCpGlEPTB;IEKzOVnjiImwbR?= M4LLZVI2Pjh6N{Sz
HCC NV;sc3BrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1P6elEuOjVyMDDuUS=> MYm0PEBp M{fobmlEPTB;MUGyOQKBkW6v NVL3d412OjV4OEi3OFM>
HCT116 NWfTXmJZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYLGc4tIPDhiaB?= NXroUZZbUUN3ME2zJO69VQ>? M4XD[|I1PTB|NUO4
HKH2 M3vqNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEfjWVQ1QCCq M3n5V2lEPTB;NDFOwG0> MUeyOFUxOzV|OB?=
RKO M2TpU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2ThdFQ5KGh? MW\JR|UxRTFwMjFOwG0> MXWyOFUxOzV|OB?=
LS174T MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NImxSVA1QCCq NIPiTYVKSzVyPUSg{txO NYXWRmoyOjR3MEO1N|g>
HCD9 M2DQN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NX7IeGY3OC53LUWg{txO MYq0PE84OiCq MkLaSG1UVw>? MkHF[IVkemWjc3XzJINmdGxidnnhZoltcXS7 NFLUW2MzPDF|NUixOi=>
HCT116 M1;OUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmHoNE42NTVizszN NInQNpU1QC95MjDo NVXMVolyTE2VTx?= NYfjS5l{\GWlcnXhd4V{KGOnbHygeoli[mmuaYT5 NXjDW4pSOjRzM{W4NVY>
SNU-C1 MmjtS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MoLJNE42NTVizszN NHPZPIY1QC95MjDo MVrEUXNQ NU\Mbldwdm9iZX\m[YN1 MmrYNlQyOzV6MU[=
MFE280 MkjNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnHFTWM2OD1{Lk[zJOKyKDBwOEKg{txO NGfVV4czOzR2M{iwOS=>
AN3CA MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWPrepJQUUN3ME2xMlAxKMLzIECuNlAh|ryP M{i5cFI{PDR|OEC1
HEC155 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHXYV5dKSzVyPUSuO|QhyrFiMT6wPUDPxE1? NWD6[Zk{OjN2NEO4NFU>
MFE296 MljOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIn3ZmtKSzVyPUKuPFYhyrFiMD6yNEDPxE1? NV7iTlJ4OjN2NEO4NFU>
SPAC1S NVzKflZST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVTiTpVNUUN3ME2zMlE6KMLzIECuPVMh|ryP MV[yN|Q1OzhyNR?=
RL952 MmP2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1m0NGlEPTB;Mz60NUDDuSByLkKzJO69VQ>? MnjmNlM1PDN6MEW=
EN1 MnW2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXHNppNUUN3ME20Mlc2KMLzIECuOlIh|ryP NFzZZ4MzOzR2M{iwOS=>
SNGII NGDxclBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NXPHcXU6UUN3ME20MlI6KMLzIECuOVgh|ryP MknhNlM1PDN6MEW=
ISHIKAWA MnzuS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NISyflRKSzVyPUWuOFghyrFiMD6wN{DPxE1? MoHnNlM1PDN6MEW=
HEC1A NV;LUIpPT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFjaeWNKSzVyPUGwMlAxKMLzIEGuNFAh|ryP M2LHRlI{PDR|OEC1
KLE MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljNTWM2OD1|LkCzJOKyKDBwMUGg{txO MmHKNlM1PDN6MEW=
SNGM NHv3WVRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2C1cWlEPTB;NT6wNEDDuSByLkSxJO69VQ>? NV3VRWl4OjN2NEO4NFU>
USPC2 NX7RUll5T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV3JR|UxRTdwMECgxtEhOC5{MTFOwG0> M2rYeVI{PDR|OEC1
EN NHzmeWRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYDkcIl6UUN3ME22MlA{KMLzIECuN|Eh|ryP NX\mTnVkOjN2NEO4NFU>
MFE319 MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NX\IRYVKUUN3ME21MlM4KMLzIECuNFMh|ryP Mn60NlM1PDN6MEW=
EFE184 M3n1T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFi2TlVKSzVyPUiuNFQhyrFiMD62PUDPxE1? NFrSSmwzOzR2M{iwOS=>
ECC1 NGDhR2FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MULJR|UxRTZwN{SgxtEhOC53OTFOwG0> MWOyN|Q1OzhyNR?=
HEC1B M4\PTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NG\vd4pKSzVyPU[uOFUhyrFiMD62O{DPxE1? M1[2b|I{PDR|OEC1
USPC1 MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mm\YTWM2OD13Lke1JOKyKDBwNUCg{txO NGTlWYIzOzR2M{iwOS=>
SPAC1L NHPGdZFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEL6RXhKSzVyPUSuPVIhyrFiMD61NEDPxE1? NUDrS3E2OjN2NEO4NFU>

... Click to View More Cell Line Experimental Data

体内研究 BGJ398按10和30 mg/kg剂量, 分别处理原位移植膀胱癌模型,持续12天,则抑制肿瘤生长,和引起淤血。BGJ398按10 mg/kg剂量处理实验动物,体重没有改变,按30 mg/kg剂量处理,则体重增加10%。BGJ398磷酸盐按 4.25和8.51 mg/kg剂量口服处理给药携带RT112肿瘤的雌性Rowett大鼠。BGJ398显著降低 pFRS2 和pMAPK水平,这种作用存在剂量依赖性。BGJ398显著抑制bFGF刺激的血管生成,这种作用存在剂量依赖性。然而, BGJ398不损害VEGF诱导的血管形成。[1]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:[1]
+ 展开

放射性激酶实验:

在有放射性标记ATP存在时,通过纯化的GST-融合FGFR3-K650E激酶域,测定合成底物的磷酸化,而测定激酶活性。通过混合10 μL 3倍浓度BGJ398 溶液和10 μL相应底物混合物 (肽底物, ATP 和 [γ33P]ATP)测定酶活性。在实验buffer中加入10 μL 3倍浓度酶溶液开始反应。实验组成的终浓度如下:10 ng 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 聚(EY) 4:1, 1% DMSO 及0.5 μM ATP (γ-[33P]-ATP 0.1 μCi)。包括BGJ398的终体积为30 μL的实验混合物根据过滤结合(FB)法在96孔板上室温下进行实验10分钟。加入20 μL 125 mM EDTA终止酶反应,按如下测定33P 渗透到肽底物的量: 30 μL 终止反应混合物转移到Immobilon-PVDF 膜上,之前用甲醇浸泡膜5分钟,用水冲洗,用0.5% H3PO4浸泡5分钟, 然后安装在真空歧管中。点样,连接真空,然后使用0.5% H3PO4 (200 μL)冲洗细胞。 移除膜,在摇床上使用1% H3PO4 处理四次,再使用乙醇处理一次。烘干膜,在膜上每孔覆盖 10 μL闪烁液。封闭实验板,在微板闪烁计数板上读数。通过线性回归分析 BGJ398抑制百分数,而计算IC50值。
细胞实验:[1]
+ 展开
  • Cell lines: 鼠BaF3细胞系
  • Concentrations: 0 μM-0.1 μM
  • Incubation Time: 48小时
  • Method: Murine 鼠BaF3细胞系接种在含10% FBS, 4.5 g/L葡萄糖, 1.5 g/L碳酸氢钠, 和Pen/Strep的 RPMI-1640培养基上。每周细胞传代两次。使用荧光素酶生物发光法检测测定BGJ398调节的抑制BaF3细胞增殖和活性。BaF3或 BaF3 Tel-TK细胞按每孔4250个细胞接种到384孔板上,在新鲜培养基中使用μFill液体分配器每孔加50 μL。BGJ398 在DMSO中连续稀释,然后排列在384孔板中。使用pintool传输设备使50 nL BGJ398 转移到含细胞的实验板上,然后实验板在37oC(5% CO2) 下温育48小时。然后加入25 μL Bright-Glo,使用 Analyst-GT测定荧光。测定IC50值。
    (Only for Reference)
动物实验:[1]
+ 展开
  • Animal Models: 携带亲本RT112细胞系的无胸腺裸鼠
  • Formulation: PEG300/D5W (2:1, v/v)
  • Dosages: 10 mg/kg/qd和30 mg/kg/qd
  • Administration: 口服处理
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 1 mg/mL warmed (1.78 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次加入纯溶剂:
30% PEG400+0.5% Tween80+5% propylene glycol
30 mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 560.48
化学式

C26H31Cl2N7O3

CAS号 872511-34-7
稳定性 powder
别名 N/A

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

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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操作手册

如果有其他问题,请给我们留言。

  • * 必填项

常见问题及建议解决方法

  • 问题 1:

    If you have any suggestions about the formulation of this compound for a direct oral gavage administration?

  • 回答:

    BGJ398 (S2183) can be dissolved in 30% PEG400/0.5% Tween80/5% Propylene glycol at 30 mg/ml as a suspension.

FGFR Signaling Pathway Map

FGFR Inhibitors with Unique Features

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID