Cabozantinib (BMS-907351)

For research use only.

Catalog No.S1119 Synonyms: XL184

72 publications

Cabozantinib (BMS-907351) Chemical Structure

CAS No. 849217-68-1

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. Cabozantinib induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signaling pathway.

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Selleck's Cabozantinib (BMS-907351) has been cited by 72 publications

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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. Cabozantinib induces PUMA-dependent apoptosis in colon cancer cells via AKT/GSK-3β/NF-κB signaling pathway.
(Cell-free assay)
c-Met [1]
(Cell-free assay)
Axl [1]
(Cell-free assay)
0.035 nM 1.3 nM 7 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  NF;kNJZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYLUeWtFUUN3ME2gNVkhdk1? MomyNlE6OjZzOUG=
Hs746T  MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MkPVTWM2OD17Lkmgcm0> MYiyNVkzPjF7MR?=
SNU-1  NG\MemVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jXbmlEPTB;NUKyN{BvVQ>? MXKyNVkzPjF7MR?=
MDA-MB-231 NGjL[GFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWSxTIZ4UUN3ME2gOlQzOSCwTR?= Mo\nNlE6OjZzOUG=
U87MG M{jFSWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3HkfmlEPTB;MUi1NUBvVQ>? MVKyNVkzPjF7MR?=
H441  NH;5d4FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmrBTWM2OD1{MUewNEBvVQ>? NV3Ob3N5OjF7Mk[xPVE>
PC3 NHnxT3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlTYTWM2OD1zMEiwNEBvVQ>? NULGSHpuOjF7Mk[xPVE>
MTC-TT M1vO[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmD3TWM2OD1yLkC0JEshOC5yMzFOwG0> NXTHPZZyOjF2N{C5PVU>
TPC-1 NE\UUFhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2K2PGlEPTB;MD6wOkAsKDBwMEKg{txO NH76R5QzOTR5MEm5OS=>

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-MET(Y1234/1235) / MET / p-EGFR(Y1068) / EGFR / p-Gab1(Y627) / Gab1 / p-AKT(S473) / p-ERK / p-EIF4E; 

PubMed: 29188469     

MET kinase inhibitors but not emibetuzumab inhibited MET signaling pathway in Hs746t cells in vitro by western blot analysis. Hs746t cells were treated for 24 h with 133 nM (20 μg/ml) or 667 nM (100 μg/ml) emibetuzumab or MET kinase inhibitors (merestinib, PF04217903, crizotinib, cabozantinib) at 15.6, 62.5, 250 or 1000 nM.

p-MET / p-ERK / p-AKT; 

PubMed: 29520051     

Western blot analysis of cellular pathways modifications after CBZ 5 μM treatment in HOS, MG-63, Saos-2 and U-2 OS cells; (A) CBZ 5 μM inhibits c-MET phosphorilation after 1 hour of treatment; downstream ERK activation kinetic adopts a sigmoidal shape in all OS cell lines, whereas AKT activation is strongly inhibited in HOS, Saos-2 and U-2OS, but not in MG-63 cells.

29188469 29520051

PubMed: 29520051     

Immunostaining of mitotic spindle in control and CBZ 5 μM treated HOS cells using a monoclonal antibody against α-tubulin (in green); white arrows indicate the mitotic spindle poles; control cells show normal bipolar spindles during metaphase formation, whereas treated cells show tripolar spindles during prometaphase (II), metaphase (III) and anaphase (IV); bar scale = 10 μm.

Growth inhibition assay
Cell viability; 

PubMed: 23661005     

Cells were left untreated or were treated with 5, 7.5 or 10 μM cabozantinib (XL184). Seventy-two hours later viability was detected by MTT-assay and apoptosis by staining with annexinV-FITC followed by FACS-analysis.

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:


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  • 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:


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  • Animal Models: RIP-Tag2 transgenic mice in a C57BL/6 background with spontaneous pancreatic islet tumors
  • 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 XL184
Smiles COC1=CC2=C(C=CN=C2C=C1OC)OC3=CC=C(C=C3)NC(=O)C4(CC4)C(=O)NC5=CC=C(C=C5)F

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% DMSO % % Tween 80 % ddH2O

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Clinical Trial Information

NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04524208 Not yet recruiting Drug: Cabozantinib Neuroendocrine Tumors|Neuroendocrine Carcinoma Karsten Gavenis|University Medical Center Goettingen December 1 2020 Phase 2
NCT04300140 Not yet recruiting Drug: AVB-S6-500|Drug: Cabozantinib (Cabo) Clear Cell Renal Cell Carcinoma Aravive Inc. October 2020 Phase 1|Phase 2
NCT04471428 Recruiting Drug: Cabozantinib|Drug: Atezolizumab|Drug: Docetaxel Carcinoma Non-Small-Cell Lung Hoffmann-La Roche|Exelixis August 29 2020 Phase 3
NCT04454762 Not yet recruiting Drug: Cabozantinib Hepatocellular Carcinoma Johannes Gutenberg University Mainz|Interdisciplinary Center Clinical Trials (IZKS) University Medical Center Mainz August 1 2020 Phase 2
NCT04338269 Recruiting Drug: Atezolizumab|Drug: Cabozantinib Carcinoma Renal Cell Hoffmann-La Roche|Exelixis|Chugai August 21 2020 Phase 3

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID