Cabozantinib (XL184, BMS-907351)

製品コードS1119

Cabozantinib (XL184, BMS-907351)化学構造

分子量(MW):501.51

Cabozantinib (XL184, BMS-907351)は一種の有効なVEGFR2阻害剤で、無細胞試験でIC50値が0.035 nMです。Cabozantinib (XL184, BMS-907351)はc-Met、 Ret、 Kit、Flt-1/3/4、Tie2和AXLに有効に作用する時のIC50値が1.3 nM,4 nM,4.6 nM,12 nM/11.3 nM/6 nM,14.3 nM 和 7 nMにそれぞれ分かれます。

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JPY 36520.00 あり
JPY 18260.00 あり
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JPY 165502.00 あり

カスタマーフィードバック(6)

  • Effects of AXL inhibitors on induction of pAKT and rescue of pERK following AXL overexpression. R428, 500 nmol/L; XL184, 3 umol/L; XL880, 100 nmol/L; in the presence or absence of 2 umol/L PLX4720. shAXL is a positive control.

    Cancer Discov 2014 4(7), 816-27. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

    Imaging and quantification of cabozantinib (XL-184) effects on EMT in vitro. A-C, Western blot analysis of E-cadherin and c-Met expression in the XL-184-treated RFPþ tumor cells. D-F, GFP imaging merged with bright field view of the XL-184–treated RFPþ tumor cells.

    Cancer Res, 2016, 76(8):2094-104. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

  • Cabozantinib specifically inhibited the phosphorylation of FLT3 (A) and downstream signaling molecules such as STAT5, Akt and ERK1/2 in FLT3-ITD MV4-11 cells (B). By contrast, the phosphorylation of downstream FLT3 signaling molecules was unaffected by cabozantinib in FLT3 wild-type OCI-AML3 cells (C). Cells were treated with cabozantinib for 2 h, and the expression of pFLT3, FLT3, pSTAT5, STAT5, pAkt, Akt, pErk1/2, and Erk1/2 was measured by Western blotting.

    Cancer Lett, 2016, 376(2):218-25. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

    Cabozantinib reduces viability and spheroid and colony formation of GCTB stromal cells. (a) Adherent-growing GCTB stromal cells derived from three different patients were left untreated (CO) or were treated with cabozantinib (10 uM, XL184) or methotrexate (100 uM, MTX). Seventy-two hours later, the viability was measured by the MTT assay, and the control was set to 100%. (b) Spheroidal cultures were established as described in b. After spheroid formation, the cells were left untreated or were treated as described above. Seven days later, spheroids were photographed, and the number and volume of spheroids (spheroid surface) were determined. The data shown are the MD. (*P<0.05; **P<0.01).

    Cell Death Dis 2014 5, e1471. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

  • The effect of cabozantinib on the accumulation of Dox and Rho123. (A) Fluorescence microscopy observation of the accumulation of Dox and Rho123. The scale bars represent 100 uM. (B) The accumulation of Dox and Rho123 was measured by flow cytometric analysis. The data were analysed using Kaluza software and are presented as fold-change in fluorescence intensity relative to the control HepG2/adr cells. The results are shown as the mean ± SD of three independent trials. *P < 0.05 vs. the control group.

    Liver Int 2014 10.1111/liv.12524. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

    Inhibition of breast cancer cell growth using XL184. MCF-7 breast cancer cells were treated with increasing concentrations of XL-184 for 5 days. Cell number was measured  using a colorimetric growth assay (crystal violet stain) and expressed relative to DMSO treated control cells.

     

    Christina W Yde/CDM Danish Cancer Society Research Center Denmark. Cabozantinib (XL184, BMS-907351) purchased from Selleck.

製品安全説明書

VEGFR阻害剤の選択性比較

生物活性

製品説明 Cabozantinib (XL184, BMS-907351)は一種の有効なVEGFR2阻害剤で、無細胞試験でIC50値が0.035 nMです。Cabozantinib (XL184, BMS-907351)はc-Met、 Ret、 Kit、Flt-1/3/4、Tie2和AXLに有効に作用する時のIC50値が1.3 nM,4 nM,4.6 nM,12 nM/11.3 nM/6 nM,14.3 nM 和 7 nMにそれぞれ分かれます。
ターゲット
VEGFR2/KDR [1]
(Cell-free assay)
c-Met [1]
(Cell-free assay)
0.035 nM 1.3 nM
体外試験

XL184 has weak inhibitory activity against RON and PDGFRβ with IC50 of 124 nM and 234 nM, respectivey, and has low activity against FGFR1 with IC50 of 5.294 μM. [1] XL184 at low concentration (0.1-0.5 μM) is sufficient to induce marked inhibition of constitutive and inducible Met phosphorylation and its resultant downstream signaling in MPNST cells, and inhibit HGF-induced MPNST cell migration and invasion. XL184 also induces marked inhibition of Met and VEGFR2 phosphorylation in cytokine-stimulated human umbilical vein endothelial cells (HUVECs). Although XL-184 has no significant effect on MPNST cell growth at 0.1 μM, XL184 at 5-10 μM significantly inhibits the MPNST cell growth. [2]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
E98NT  MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NHzkblIxNjBzLUGwJO69VQ>? MX3EUXNQ NG[0T29KSzVyPUi5JI5O NEXuPG4zOzR6NECwOi=>
SNU-5  MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXvxXlNPUUN3ME2gNVkhdk1? NUXpbWhrOjF7Mk[xPVE>
Hs746T  NW\Id|hIT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3VTWM2OD17Lkmgcm0> Mm[5NlE6OjZzOUG=
SNU-1  MoTjS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3i1VWlEPTB;NUKyN{BvVQ>? NUHCcnRSOjF7Mk[xPVE>
SNU-16 MVvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH30fYRKSzVyPUGxOFkhdk1? M1v2RlIyQTJ4MUmx
MDA-MB-231 NY\UOFlOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGfPU4RKSzVyPTC2OFIyKG6P NIPUfYIzOTl{NkG5NS=>
U87MG MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnWzTWM2OD1zOEWxJI5O NGLkUGQzOTl{NkG5NS=>
H441  MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXTJR|UxRTJzN{CwJI5O MXyyNVkzPjF7MR?=
H69 M1v4W2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFz2W5ZKSzVyPUKwNlAxKG6P NUmyWJA2OjF7Mk[xPVE>
PC3 NV7zbYc4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NYfGNmRoUUN3ME2xNFgxOCCwTR?= MUCyNVkzPjF7MR?=
MTC-TT M2jsRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NICwbFZKSzVyPUCuNFQhMyByLkCzJO69VQ>? NInQV3YzOTR5MEm5OS=>
MZ-CRC NVn0cokyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NUPLZWNuUUN3ME6gOUDPxE1? MYWyNVQ4ODl7NR?=
TPC-1 MlLPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NH[0N|lKSzVyPUCuNFYhMyByLkCyJO69VQ>? NV\6UmFGOjF2N{C5PVU>

多くの細胞株試験データを見る場合、クリックしてください

体内試験 XL184 treatment at 30 mg/kg in RIP-Tag2 mice with spontaneous pancreatic islet tumors disrupts 83% of the tumor vasculature, reduces pericytes and empty basement membrane sleeves, causes widespread intratumoral hypoxia and extensive tumor cell apoptosis, and slows regrowth of the tumor vasculature after drug withdrawal, more significantly compared with XL999 that blocks VEGFR but not c-Met, leading to only 43% reduction in vascularity, suggesting that concurrent inhibition of VEGFR and other functionally relevant receptor tyrosine kinases (RTK) amplifies angiogenesis inhibition. XL184 also decreases invasiveness of primary tumors and reduces metastasis. [1] XL184 at 30 mg/kg/day significantly abrogates human MPNST xenografts growth and metastasis in SCID mice. [2] Administration of XL184 induces dose-dependent inhibition of tumor growth in breast, lung, and glioma tumor models, in association with decreased tumor and endothelial cell proliferation as well as increased apoptosis. A single oral dose of XL184 is sufficient to induce sustained tumor growth inhibition in MDA-MB-231 tumor-bearing mice and C6 tumor-bearing rats at 100 mg/kg and 10 mg/kg, respectively. [3]

お薦めの試験操作(参考用のみ)

細胞試験:

[2]

+ 展開
  • 細胞株: ST88-14, STS26T, and MPNST724
  • 濃度: Dissolved in DMSO, final concentrations ~10 μM
  • 反応時間: 48 hours
  • 実験の流れ:

    Cells are exposed to various concentrations of XL184 for 48 hours. Cell growth is determined by MTS assays using CellTiter96 Aqueous Non-Radioactive Cell Proliferation Assay kit. Absorbance is measured at a wavelength of 490 nm, and the absorbance values of treated cells are presented as a percentage of the absorbance of untreated cells.


    (参考用のみ)
動物試験:

[1]

+ 展開
  • 動物モデル: RIP-Tag2 transgenic mice in a C57BL/6 background with spontaneous pancreatic islet tumors
  • 製剤: Suspended at a concentration of 5 mg/mL in sterile saline or water
  • 投薬量: ~60 mg/kg
  • 投与方法: Oral gavage
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 100 mg/mL (199.39 mM)
Water Insoluble
Ethanol Insoluble
体内 順序で溶剤を入れること:
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
5mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。

化学情報

分子量 501.51
化学式

C28H24FN3O5

CAS No. 849217-68-1
保管
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • 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):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01630590 Active, not recruiting Prostate Cancer M.D. Anderson Cancer Center|Exelixis|High Impact Clinical Research Support Program January 8, 2014 Phase 2
NCT01755195 Recruiting Refractory Soft Tissue Sarcomas National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) December 7, 2012 Phase 2
NCT01688999 Active, not recruiting Urothelial Carcinoma|Urethral Neoplasms|Ureteral Neoplasms|Urinary Bladder Neoplasms|Kidney Neoplasms National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) September 7, 2012 Phase 2
NCT01683994 Recruiting Prostatic Neoplasms National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) September 6, 2012 Phase 1|Phase 2
NCT01866293 Completed Relapsed or Refractory Multiple Myeloma Memorial Sloan Kettering Cancer Center|Exelixis May 28, 2013 Phase 1|Phase 2
NCT02867592 Not yet recruiting Adrenal Cortex Carcinoma|Adult Alveolar Soft Part Sarcoma|Adult Clear Cell Sarcoma of Soft Parts|Adult Hepatocellular Carcinoma|Adult Rhabdomyosarcoma|Adult Soft Tissue Sarcoma|Childhood Alveolar Soft Part Sarcoma|Childhood Central Nervous System Neoplasm|Childhood Clear Cell Sarcoma of Soft Parts|Childhood Hepatocellular Carcinoma|Childhood Rhabdomyosarcoma|Childhood Soft Tissue Sarcoma|Childhood Solid Neoplasm|Ewing Sarcoma|Hepatoblastoma|Hepatocellular Carcinoma|Recurrent Adrenal Cortex Carcinoma|Recurrent Adult Hepatocellular Carcinoma|Recurrent Adult Soft Tissue Sarcoma|Recurrent Alveolar Soft Part Sarcoma|Recurrent Childhood Central Nervous System Neoplasm|Recurrent Childhood Hepatocellular Carcinoma|Recurrent Childhood Soft Tissue Sarcoma|Recurrent Ewing Sarcoma|Recurrent Hepatoblastoma|Recurrent Renal Cell Carcinoma|Recurrent Rhabdomyosarcoma|Recurrent Solid Neoplasm|Renal Cell Carcinoma|Thyroid Gland Medullary Carcinoma|Wilms Tumor National Cancer Institute (NCI) July 2017 Phase 2

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

VEGFR信号経路図

VEGFR Inhibitors with Unique Features

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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID