1. Protein Tyrosine Kinase/RTK
  2. FGFR

Dovitinib lactate (Synonyms: CHIR-258 lactate; TKI-258 lactate)

Cat. No.: HY-10207 Purity: 99.77%
Handling Instructions

Dovitinib(CHIR-258; TKI258) lactate is a potent inhibitor of fibroblast growth factor receptor 3 (FGFR3) with an IC50 of 5 nM.

For research use only. We do not sell to patients.
Dovitinib lactate Chemical Structure

Dovitinib lactate Chemical Structure

CAS No. : 692737-80-7

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10 mM * 1 mL in DMSO USD 66 In-stock
5 mg USD 60 In-stock
10 mg USD 96 In-stock
50 mg USD 288 In-stock
100 mg USD 480 In-stock
200 mg USD 840 In-stock
500 mg USD 1560 In-stock
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Other Forms of Dovitinib lactate:

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  • Biological Activity

  • Protocol

  • Technical Information

  • Purity & Documentation

  • References


Dovitinib(CHIR-258; TKI258) lactate is a potent inhibitor of fibroblast growth factor receptor 3 (FGFR3) with an IC50 of 5 nM.

IC50 & Target[1]


5 nM (IC50)

In Vitro

Dovitinib potently inhibits FGFR3 with an IC50 of 5 nM in in vitro kinase assays and selectively inhibits the growth of B9 cells and human myeloma cell lines expressing wild-type or activated mutant FGFR3. Addition of interleukin 6 (IL-6) or insulin growth factor 1 or coculture on stroma does not confer resistance to dovitinib. In primary myeloma cells dovitinib inhibits downstream extracellular signal-regulated kinase (ERK) 1/2 phosphorylation with an associated cytotoxic response[1]. Treatment of SK-HEP1 cells with dovitinib results in G2/M cell cycle arrest, inhibition of colony formation in soft agar and blockade of bFGF-induced cell migration. Dovitinib inhibits basal expression and FGF-induced phosphorylation of FGFR-1, FRS2-α and ERK1/2[2].

In Vivo

Dovitinib demonstrates significant antitumor and antimetastatic activities in HCC xenograft models. Dovitinib potently inhibits tumor growth of six HCC lines. Inhibition of angiogenesis correlates with inactivation of FGFR/PDGFR-β/VEGFR-2 signaling pathways. Dovitinib also causes dephosphorylation of retinoblastoma, upregulation of p-histone H2A-X and p27, and downregulation of p-cdk-2 and cyclin B1, which results in a reduction in cellular proliferation and the induction of tumor cell apoptosis[2].

Clinical Trial
Preparing Stock Solutions
Concentration Volume Mass 1 mg 5 mg 10 mg
1 mM 2.0725 mL 10.3625 mL 20.7250 mL
5 mM 0.4145 mL 2.0725 mL 4.1450 mL
10 mM 0.2072 mL 1.0362 mL 2.0725 mL
Please refer to the solubility information to select the appropriate solvent.
Cell Assay

To determine IC50 for SK-HEP1 cells, cells are plated at a density of 2×104 cells per dish. After 48 h, cells are treated with 0, 0.01, 0.1, 1, 5, 10, 50, 100 μM dovitinib in DMEM containing 1% FBS for 24 h. Cell viability is determined with Cell Proliferation Assay. IC50 is calculated by nonlinear regression analysis using GraphPad Prism software[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration

Mice: Six HCC lines (06-0606, 26-0808A, 26-1004, 25-0705A, 5-1318, 21-0208) are used to establish tumors in male SCID mice. or dose-esponse experiments, mice bearing the 06-0606 xenografts re orally given vehicle (5% dextrose) or two doses of dovitinib (50 and 75 mg/kg) daily for 14 days. For time-dependent inhibition of dovitinib targets, mice bearing 06-0606 tumors are given orally 200 μL of either vehicle (n=6) or 50 mg/kg/day of dovitinib (n=10)[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Molecular Weight








Powder -20°C 3 years
  4°C 2 years
In solvent -80°C 6 months
  -20°C 1 month

Room temperature in continental US; may vary elsewhere

Solvent & Solubility

DMSO: ≥ 30 mg/mL

* "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

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