| Field | Specification |
|---|---|
| Target | |
| Alternative names | XL184 S-malate; BMS-907351 S-malate |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C32H30FN3O10 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Cabozantinib S-malate, also known as XL184 S-malate and BMS-907351 S-malate, is a potent inhibitor of multiple receptor tyrosine kinases. It inhibits VEGFR2, c-Met, Kit, Axl, and Flt3 with IC50 values of 0.035 nM, 1.3 nM, 4.6 nM, 7 nM, and 11.3 nM, respectively. It is supplied as a white to off-white solid (C32H30FN3O10, MW 635.59) at 99.90% purity.
Physical & Chemical Properties
| CAS Number | 1140909-48-3 |
|---|---|
| Molecular Formula | C32H30FN3O10 |
| Molecular Weight | 635.59 g/mol |
| Purity | 99.90% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O=C([C@H](CC(O)=O)O)O.O=C(NC1=CC=C(C=C1)OC2=CC=NC3=CC(OC)=C(C=C23)OC)C4(CC4)C(NC5=CC=C(C=C5)F)=O |
| Target | VEGFR2 |
| Signaling Pathway | Protein Tyrosine Kinase/RTK; Apoptosis |
| Solubility | In Vitro: DMSO: 100 mg/mL (157.33 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) H2O: < 0.1 mg/mL (insoluble) |
| Storage | Powder: -20°C, 3 years; 4°C, 2 years. In solvent: -80°C, 1 year; -20°C, 6 months. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target
|
VEGFR2 0.035 nM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| DMSO | 100 mg/mL (157.33 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
| H2O | < 0.1 mg/mL | insoluble |
Aliquot the stock solution and store it at -80°C (up to 1 year) or -20°C (up to 6 months); avoid repeated freeze-thaw cycles.
Data provided by the manufacturer.
In Vitro
At 0.1-0.5μM, Cabozantinib inhibits constitutive and inducible MET phosphorylation, along with the downstream signaling that results from it, in all MPNST cells. At > 0.1μM, Cabozantinib significantly inhibits MPNST cell growth, while inhibiting NSC growth requires higher doses. HGF-induced MPNST motility and invasion are blocked by Cabozantinib treatment (a similar effect is found on NSC)[2]. In cellular assays, phosphorylation of MET and VEGFR2, and also of KIT, FLT3, and AXL, is inhibited by cabozantinib (IC50 values of 7.8, 1.9, 5.0, 7.5, and 42 μM, respectively). Tubule formation in response to conditioned media from MDA-MB-231 (IC50=5.1 nM), A431 (IC50=4.1 nM), HT1080 (IC50=7.7 nM) and B16F10 (IC50=4.7 nM) cell cultures is also inhibited by cabozantinib[3].
In Vivo
In animals, Cabozantinib (60 mg/kg, i.p.) decreases tumor vascularity, with reductions between 67% at 3 mg/kg and 83% at 30 mg/kg over 7 days. In RIP-Tag2 mice treated for 7 days starting at age 10 weeks, tumors are 40% smaller after XL880 and 35% smaller after Cabozantinib, relative to the corresponding vehicle values[1]. Microvessel density in mice is significantly decreased by Cabozantinib (30 mg/kg)[2]. Cabozantinib (100 mg/kg, p.o.) inhibits HGF stimulation of MET phosphorylation in liver hepatocytes in vivo, as well as VEGF-stimulated phosphorylation of FLK1, and both targets stay inhibited through 8 hours postdose. Cabozantinib (100 mg/kg, p.o.) also disrupts tumor vasculature and promotes tumor and endothelial cell death. In vivo, Cabozantinib (1-60 mg/kg, p.o.) inhibits tumor growth and promotes tumor regression[3].
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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TRK xDFG Mutations Trigger a Sensitivity Switch from Type I to II Kinase Inhibitors. Cancer Discov 2021 Jan;11(1):126-141. PMID: 33004339
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. Sci Transl Med 2018 Jul 18;10(450):eaaq1093.
Targeting Wnt/β-Catenin and circadian regulator restores PRC2/EZH2 controlled chromatin bivalency and suppresses cell state diversity. J Clin Invest 2026 Mar 17:e200260. PMID: 41842971
Integrated Multi-Omics Profiling to Characterize Molecular Subtypes and Reveal Potential Therapeutic Strategies for Colorectal Cancer. MedComm (2020) 2025 Dec 8;6(12):e70492. PMID: 41377767
CAN-Scan: A multi-omic phenotype-driven precision oncology platform identifies prognostic biomarkers of therapy response for colorectal cancer. Cell Rep Med 2025 Apr 15;6(4):102053. PMID: 40187357
Automated discovery of nanomaterials via drug aggregation induced emission. Biomaterials 2022 Oct:289:121800. PMID: 36166893
Repurposing cabozantinib to GISTs: Overcoming multiple imatinib-resistant cKIT mutations including gatekeeper and activation loop mutants in GISTs preclinical models. Cancer Lett 2019 Apr 10:447:105-114. PMID: 30684595
Synergistic effects of methyl 2-cyano-3,11-dioxo-18beta-olean-1,-12-dien-30-oate and erlotinib on erlotinib-resistant non-small cell lung cancer cells. J Pharm Anal 2021 Dec;11(6):799-807. PMID: 35028186
Dual-Targeting Nanoliposome Improves Pro-inflammatory Immunomodulation of the Tumor Microenvironment. Adv Healthc Mater 2023 Dec;12(31):e2302046. PMID: 37605325
CXCR4, CXCR7 and PBRM1 are responsible for everolimus and cabozantinib resistance in human renal cancer cells. Cell Death Discov 2026 Mar 28. PMID: 41896541
