Cabozantinib (XL184, BMS-907351)

Catalog No.S1119

Cabozantinib (XL184, BMS-907351) Chemical Structure

Molecular Weight(MW): 501.51

Cabozantinib (XL184, BMS-907351) is a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret, Kit, Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively.

Size Price Stock Quantity  
In DMSO USD 220 In stock
USD 110 In stock
USD 170 In stock
USD 470 In stock
USD 997 In stock
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6 Customer Reviews

  • 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.

Purity & Quality Control

Choose Selective VEGFR Inhibitors

Biological Activity

Description Cabozantinib (XL184, BMS-907351) is a potent VEGFR2 inhibitor with IC50 of 0.035 nM and also inhibits c-Met, Ret, Kit, Flt-1/3/4, Tie2, and AXL with IC50 of 1.3 nM, 4 nM, 4.6 nM, 12 nM/11.3 nM/6 nM, 14.3 nM and 7 nM in cell-free assays, respectively.
(Cell-free assay)
c-Met [1]
(Cell-free assay)
0.035 nM 1.3 nM
In vitro

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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
SNU-5  M13BXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFnLWHRKSzVyPTCxPUBvVQ>? NWKxeGp{OjF7Mk[xPVE>
Hs746T  MnjsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M{DJUGlEPTB;OT65JI5O MVmyNVkzPjF7MR?=
SNU-16 M3PwNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NILBWnZKSzVyPUGxOFkhdk1? MXGyNVkzPjF7MR?=
MDA-MB-231 M3vTfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFjj[m5KSzVyPTC2OFIyKG6P NV7JNFRPOjF7Mk[xPVE>
U87MG NVe2fIMzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH3tcYNKSzVyPUG4OVEhdk1? MnvQNlE6OjZzOUG=
H441  NFHOTphIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NHG4PYxKSzVyPUKxO|AxKG6P MW[yNVkzPjF7MR?=
H69 NWPER|hnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mm\2TWM2OD1{MEKwNEBvVQ>? NWjEXJRiOjF7Mk[xPVE>
PC3 NIXrWWJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYnaVHE{UUN3ME2xNFgxOCCwTR?= M3\l[FIyQTJ4MUmx
MTC-TT NULJfoxST3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml3hTWM2OD1yLkC0JEshOC5yMzFOwG0> M2fWZVIyPDdyOUm1
MZ-CRC MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1;j[mlEPTB-IEWg{txO M4\CVFIyPDdyOUm1
TPC-1 NITqSY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmrITWM2OD1yLkC2JEshOC5yMjFOwG0> M4fBN|IyPDdyOUm1

... Click to View More Cell Line Experimental Data

In vivo 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]


Cell Research:


+ Expand
  • Cell lines: ST88-14, STS26T, and MPNST724
  • Concentrations: Dissolved in DMSO, final concentrations ~10 μM
  • Incubation Time: 48 hours
  • Method:

    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.

    (Only for Reference)
Animal Research:


+ Expand
  • Animal Models: RIP-Tag2 transgenic mice in a C57BL/6 background with spontaneous pancreatic islet tumors
  • Formulation: Suspended at a concentration of 5 mg/mL in sterile saline or water
  • Dosages: ~60 mg/kg
  • Administration: Oral gavage
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (199.39 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+5% Tween 80+ddH2O
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.

Chemical Information

Molecular Weight 501.51


CAS No. 849217-68-1
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03685448 Not yet recruiting Renal Cell Carcinoma|Papillary Renal Cell Carcinoma Type 1|Papillary Renal Cell Carcinoma Type 2|Chromophobe Renal Cell Carcinoma|Sarcomatoid Renal Cell Carcinoma|Xp11.2 Translocation-Related Renal Cell Carcinoma Australian and New Zealand Urogenital and Prostate Cancer Trials Group January 30 2019 Phase 2
NCT03729245 Not yet recruiting Renal Cell Carcinoma|Metastatic Renal Cell Carcinoma Nektar Therapeutics|Bristol-Myers Squibb December 2018 Phase 3
NCT03612232 Not yet recruiting Adrenocortical Carcinoma Wuerzburg University Hospital December 2018 Phase 2
NCT03690388 Recruiting Differentiated Thyroid Cancer Exelixis October 2018 Phase 3
NCT03729297 Recruiting Salivary Gland Cancer Radboud University|Ipsen September 5 2018 Phase 2
NCT03667482 Recruiting Head and Neck Squamous Cell Cancer|Recurrent Head and Neck Squamous Cell Cancer|Metastatic Head and Neck Squamous Cell Cancer Memorial Sloan Kettering Cancer Center September 7 2018 Phase 1

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID