| Field | Specification |
|---|---|
| Target | |
| Alternative names | CHIR-258; TKI258 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C21H21FN6O |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Dovitinib, also known as CHIR-258 and TKI258, is an orally active, potent multi-targeted tyrosine kinase (RTK) inhibitor, with IC50 values of 1 nM, 2 nM, 36 nM, 8/9 nM, 10/13/8 nM and 27/210 nM against FLT3, c-Kit, CSF-1R, FGFR1/FGFR3, VEGFR1/VEGFR2/VEGFR3 and PDGFRα/PDGFRβ, respectively. It exhibits potent antitumor activity[1][2]. It is supplied as a light yellow to green yellow solid (C21H21FN6O, MW 392.43) at 99.88% purity.
Physical & Chemical Properties
| CAS Number | 405169-16-6 |
|---|---|
| Molecular Formula | C21H21FN6O |
| Molecular Weight | 392.43 g/mol |
| Purity | 99.88% |
| Appearance | Solid |
| Color | Light yellow to green yellow |
| SMILES | O=C1NC(C=CC=C2F)=C2C(N)=C1C3=NC4=CC=C(N5CCN(C)CC5)C=C4N3 |
| Target | FLT3, c-Kit, FGFR1, FGFR3, VEGFR3, VEGFR1, VEGFR2, PDGFRβ, PDGFRα, CSF-1R |
| Signaling Pathway | Protein Tyrosine Kinase/RTK |
| Solubility | In Vitro: DMSO: 23.33 mg/mL (59.45 mM; Requires sonication and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| 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[1]
|
FLT3 1 nM (IC50) |
c-Kit 2 nM (IC50) |
FGFR1 8 nM (IC50) |
FGFR3 9 nM (IC50) |
VEGFR3 8 nM (IC50) |
VEGFR1 10 nM (IC50) |
VEGFR2 13 nM (IC50) |
PDGFRβ 27 nM (IC50) |
PDGFRα 210 nM (IC50) |
CSF-1R 36 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 | 23.33 mg/mL (59.45 mM) | requires sonication and warming and heat to 60°C; use freshly opened DMSO (absorbed moisture lowers solubility) |
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.
In Vivo
Choose the formulation that suits the animal model and route of administration; percentages are volume ratios of the final working solution. Start from a clear DMSO stock (see In Vitro above), add the co-solvents one at a time in the order listed, mixing after each addition, and prepare the working solution fresh on the day of dosing. If precipitation or phase separation occurs, gentle warming or sonication can help.
Protocol 1
| Composition | 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% saline |
|---|---|
| Result | ≥ 2.5 mg/mL (6.37 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 400 μL PEG300; then 50 μL Tween-80; then 450 μL saline to bring the volume to 1 mL. Saline: dissolve 0.9 g sodium chloride in ddH2O and make up to 100 mL. |
Protocol 2
| Composition | 10% DMSO + 90% (20% SBE-β-CD in saline) |
|---|---|
| Result | ≥ 2.5 mg/mL (6.37 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL 20% SBE-β-CD in saline. 20% SBE-β-CD in saline: dissolve 2 g SBE-β-CD powder in 10 mL saline until clear (4°C, store up to one week). |
Protocol 3
| Composition | 10% DMSO + 90% Corn Oil |
|---|---|
| Result | ≥ 2.5 mg/mL (6.37 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.5 mg/mL (saturation not determined). Use with caution if continuous dosing will exceed two weeks. For 1 mL of working solution: add 100 μL DMSO stock (25.0 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
Dovitinib (CHIR-258) exerts more than 10-fold inhibition of InsR (IC50=2 μM) and EGFR1 (IC50=2 μM), of c-Met (IC50>3 μM), of EphrinA2 (EphA2; IC50=4 μM) and Tie2 (IC50=4 μM), and of IGFR1 (IC50>10 μM) and HER2 (IC50>10 μM)[1]. FGF-stimulated growth of B9 cells expressing WT or F384L-FGFR3 is potently inhibited by Dovitinib (12.5-400 nM; 48 hours), with IC50 values of 25 nM[1]. In FGFR3-expressing human myeloma cell lines, FGF-mediated ERK1/2 phosphorylation is inhibited and apoptosis is induced by Dovitinib (100, 500 nM; 96 hours)[1]. Dovitinib (72 hours) suppresses proliferation of KMS11 (FGFR3-Y373C) cells, OPM2 (FGFR3-K650E) cells, and KMS18 (FGFR3-G384D) cells, with IC50 values of 90 nM in KMS11 and OPM2 cells and 550 nM, in that order[1]. In KMS11 cells, Dovitinib (100 nM) augments the cytotoxicity of Dexamethasone (0.5 μM)[1]. In both SK-HEP1 and 21-0208 cells, Dovitinib significantly lowers the basal levels of phosphorylation of FGFR-1, FGFR substrate 2α (FRS2-α), and ERK1/2, while Akt is not reduced[2]. BMP-2-induced alkaline phosphatase (ALP) induction, a representative marker of osteoblast differentiation, is enhanced by Dovitinib. Translocation of phosphorylated Smad1/5/8 into the nucleus is also stimulated by Dovitinib, as is phosphorylation of mitogen-activated protein kinases such as ERK1/2 and p38[3]. Dovitinib strongly blocks TNIK-ATP interaction (Ki, 13 nM) and also activation of Wnt signaling effectors, among them β-catenin and TCF4. In IM-9 cells, caspase-dependent apoptosis is also induced by Dovitinib, without significant cytotoxicity in PBMCs[4].
Cell Viability Assay[1]
| Cell Line | WT and F384L-FGFR3-expressing B9 cells |
|---|---|
| Concentration | 12.5, 25, 50, 100, 200, 300, 400 nM |
| Incubation Time | 48 hours |
| Result | Potently inhibited the FGF-stimulated growth of the cells. |
Apoptosis Analysis[1]
| Cell Line | KMS11, OPM2, and KMS18 cells |
|---|---|
| Concentration | 100 nM or 500 nM |
| Incubation Time | 96 hours |
| Result | Induced apoptosis of FGFR3-expressing human myeloma cell lines. |
In Vivo
Gavage dosing of Dovitinib (CHIR-258) at 10-60 mg/kg/day for 21 days produces a significant antitumor effect[1]. At 50 and 75 mg/kg, Dovitinib yields 97% and 98% tumor growth inhibition, respectively, with maximal efficacy reached at 50 mg/kg[2].
| Animal Model | 6- to 8-week-old female BNX mice with KMS11 cells[1] |
|---|---|
| Dosage | 10, 30, 60 mg/kg |
| Administration | Gavage; daily for 21 days |
| Result | Had a significant antitumor effect in all 3 dose groups with 48%, 78.5%, and 94% growth inhibition in the 10 mg/kg, 30 mg/kg, and 60 mg/kg treatment. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
Need this compound in a format that drops straight into your assay? We can tailor formulation, chemistry, and documentation so your results stay consistent across runs and re-orders.
- Format options: solid or pre-dissolved solution (choose solvent), target concentration, aliquots, light/moisture-protected packaging
- Chemistry options: free base/acid vs salt forms, hydrate/solvate preference, stereoisomer control (single enantiomer or racemate), close analogs
- Add-on labels & handles: D/¹³C/¹⁵N isotopes (LC-MS/internal standards), azide/alkyne or other functional handles for conjugation
- QC & documentation: standard COA or enhanced analytical pack (HPLC/LC-MS/NMR), chiral purity, residual solvents, water content (KF), method-specific specs
- Scale & continuity: mg to gram scale, bulk pricing, lot reservation, repeat-order continuity
To quote quickly, tell us: compound name + CAS/structure (SMILES or mol file), intended assay context, solvent preference, salt/stereochemistry requirements, purity/QC level, and the amount (mg–g).
Can’t find the compound you’re looking for?
Send the CAS or structure and your specs. We can help source it, suggest close equivalents, or discuss custom synthesis with the right QC documentation (RUO).
PEAK1 maintains tight junctions in intestinal epithelial cells and resists colitis by inhibiting autophagy-mediated ZO-1 degradation. Nat Commun 2025 Jul 24;16(1):6777. PMID: 40707483
PP2A inhibition is a druggable MEK inhibitor resistance mechanism in KRAS-mutant lung cancer cells. Sci Transl Med 2018 Jul 18;10(450):eaaq1093.
Jujuboside A promotes Aβ clearance and ameliorates cognitive deficiency in Alzheimer's disease through activating Axl/HSP90/PPARγ pathway. Theranostics 2018 Jul 30;8(15):4262-4278.
Acta Pharm Sin B. 2026 Feb 10.
Comprehensive functional evaluation of variants of fibroblast growth factor receptor genes in cancer. NPJ Precis Oncol 2021 Jul 16;5(1):66. PMID: 34272467
An FGFR/AKT/SOX2 Signaling Axis Controls Pancreatic Cancer Stemness. Front Cell Dev Biol 2020 May 7:8:287. PMID: 32457900
Activation of Gcn2 by small molecules designed to be inhibitors. J Biol Chem 2023 Apr;299(4):104595. PMID: 36898579
Impact of anticancer drugs on human Tenon's fibroblast proliferation: implications for glaucoma surgery. BMJ Open Ophthalmol 2026 Jan 12;11(1):e002307. PMID: 41526033
Preprints. 2026 Jun 19.
University of Düsseldorf. 2024.
