Cabozantinib malate (XL184)
Molecular Weight(MW): 635.59
Cabozantinib malate (XL184) is the malate of Cabozantinib, 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.
Cited by 13 Publications
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 malate (XL184) 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 mean盨.D. (*P<0.05; **P<0.01).
Cell Death Dis 2014 5, e1471. Cabozantinib malate (XL184) 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 malate (XL184) purchased from Selleck.
A summary of the postcabozantinib (Cabo.) changes in bone-seeking radionuclide uptake at sites of remodeling bone. C, A line graph of the SUV mean for 99m Tc-MDP uptake at the site of the fracture in the tibia shows the impact of cabozantinib therapy on radionuclide accumulation. Animals were treated once daily with cabozantinib at 30 mg/kg 1 day after the first SPECT scan. D, Representative maximum-intensity projection (MIP) images whose intensities were manually gated to provide a clear view of radionuclide uptake at the fracture site and the nearby anatomy. Quantification was not conducted using the MIP images; the MIP images are merely provided to show a global view of 99mTc-MDP distribution in the skeleton while underscoring the foci of high radionuclide uptake at the fracture. Unfortunately, centering the images on the slices with the fracture excluded the rest of the anatomy, resulting in images that are difficult to interpret visually. *p< .01. Rx 5 treatment.
Mol Imaging 2014 10.2310/7290.2014.00026. Cabozantinib malate (XL184) 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 malate (XL184) purchased from Selleck.
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|Description||Cabozantinib malate (XL184) is the malate of Cabozantinib, 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 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.  Cabozantinib 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. Cabozantinib also induces marked inhibition of Met and VEGFR2 phosphorylation in cytokine-stimulated human umbilical vein endothelial cells (HUVECs). Although Cabozantinib has no significant effect on MPNST cell growth at 0.1 μM, Cabozantinib at 5-10 μM significantly inhibits the MPNST cell growth. 
|In vivo||Cabozantinib 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. Cabozantinib also decreases invasiveness of primary tumors and reduces metastasis.  Cabozantinib at 30 mg/kg/day significantly abrogates human MPNST xenografts growth and metastasis in SCID mice.  Administration of Cabozantinib 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 Cabozantinib 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. |
|In vitro||DMSO||100 mg/mL (157.33 mM)|
|In vivo||30% propylene glycol, 5% Tween 80, 65% D5W||15 mg/mL|
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Clinical Trial Information
|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|
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