| Field | Specification |
|---|---|
| Alternative names | CFI-402257 hydrochloride |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C28H31ClN6O3 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
Luvixasertib hydrochloride, also known as CFI-402257 hydrochloride, is a highly selective and orally bioavailable TTK/Mps1 inhibitor, with an IC50 of 1.7 nM for TTK in vitro. It shows anti-cancer activity[1]. It is supplied as a light yellow to yellow solid (C28H31ClN6O3, MW 535.04) at 99.63% purity.
Physical & Chemical Properties
| CAS Number | 1610677-37-6 |
|---|---|
| Molecular Formula | C28H31ClN6O3 |
| Molecular Weight | 535.04 g/mol |
| Purity | 99.63% |
| Appearance | Solid |
| Color | Light yellow to yellow |
| SMILES | CC1=CC(C2=C3N=C(OC4=CN=CC=C4)C=C(NC[C@@H]5C[C@@](O)(C)C5)N3N=C2)=CC=C1C(NC6CC6)=O.Cl |
| Signaling Pathway | Cell Cycle/DNA Damage; Cytoskeleton |
| Solubility | In Vitro: DMSO: 100 mg/mL (186.90 mM; Requires sonication; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO) |
| Storage | 4°C, sealed storage, away from moisture and light. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target
IC50: 1.7 nM (TTK in vitro)[1].
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 (186.90 mM) | requires sonication; use freshly opened DMSO (absorbed moisture lowers solubility) |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture and light; 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 | ≥ 2.08 mg/mL (3.89 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 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 | ≥ 2.08 mg/mL (3.89 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 mg/mL (saturation not determined). For 1 mL of working solution: add 100 μL DMSO stock (20.8 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 | ≥ 2.08 mg/mL (3.89 mM); clear solution |
| How to prepare | Gives a clear solution at ≥ 2.08 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 (20.8 mg/mL) to 900 μL corn oil. |
Data provided by the manufacturer.
In Vitro
TTK is targeted by CFI-402257 with high selectivity. In a panel of human kinases tested at 1 μM, none of the 262 kinases is inhibited by CFI-402257. Cell growth is potently inhibited by CFI-402257[1]. A massive rise in chromosome missegregations results from CFI-402257 (200 nM, 6 h)[2]. Dose-dependent dysregulation of the cell cycle is induced by CFI-402257 (0, 50 or 100 nM), and more cells then show an aneuploid DNA content[2]. The effects seen with CFI-402257 fit Mps1 kinase inhibition, with SAC inactivation in particular, followed by chromosome missegregation, aneuploidy, and ultimately cell death[2].
Cell Cycle Analysis[2]
| Cell Line | HCT116 cells. |
|---|---|
| Concentration | 0 nM, 50 nM, 100 nM, 300 nM, 1000 nM, 3000 nM. |
| Incubation Time | 48 hours |
| Result | Resulted in an increase in the frequency of cells exhibiting an aneuploid DNA content. |
Western Blot Analysis[2]
| Cell Line | HCT116 cells. |
|---|---|
| Concentration | 0 nM, 50 nM or 100 nM. |
| Incubation Time | 8, 16, 24 and 48 hours. |
| Result | CFI-402257-induced aneuploidy was accompanied by a progressive accumulation of apoptotic cells that were detectable as early as 16 h following treatment. |
In Vivo
When given orally QD, CFI-402257 shows dose-dependent activity in mice with established tumors derived from xenografts of MDA-MB-231 human TNBC cells and MDA-MB-468 human TNBC cells. In a platinum-resistant PDX model of high-grade serous ovarian cancer, CFI-402257 demonstrates antitumor activity[2].
| Animal Model | Xenografted MDA-MB-231 human TNBC cells and MDA-MB-468 human TNBC cells in mice[2]. |
|---|---|
| Dosage | 5, 6 mg/kg. |
| Administration | Oral gavage, daily. |
| Result | Xenografted MDA-MB-231 human TNBC cells: 5 mg/kg, tumor growth inhibition (TGI) = 74%; 6 mg/kg, TGI = 89%. Xenografted MDA-MB-468 human TNBC cells: 5 mg/kg, tumor growth inhibition (TGI) = 75%; 6 mg/kg, TGI = 94%. |
| Animal Model | PDX model of high-grade serous ovarian cancer[2]. |
|---|---|
| Dosage | 6.5, 7.5 mg/kg. |
| Administration | Oral gavage, daily. |
| Result | 6.5 mg/kg, tumor growth inhibition (TGI) = 61%; 7.5 mg/kg, TGI = 97%. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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Cells Lacking the RB1 Tumor Suppressor Gene Are Hyperdependent on Aurora B Kinase for Survival. Cancer Discov 2019 Feb;9(2):230-247. PMID: 30373918
Integrated genomics and comprehensive validation reveal drivers of genomic evolution in esophageal adenocarcinoma. Commun Biol 2021 May 24;4(1):617. PMID: 34031527
Energy‑stress‑mediated activation of AMPK sensitizes MPS1 kinase inhibition in triple‑negative breast cancer. Oncol Rep 2024 Aug;52(2):101. PMID: 38904203
Barrier-to-autointegration factor protects against the cGAS-STING response to chromatin bridges. PLoS Genet 2026 Jun 3;22(6):e1012191. PMID: 42234713
Dual TTK/PLK1 inhibition has potent anticancer activity in TNBC as monotherapy and in combination. Front Oncol 2024 Aug 9:14:1447807. PMID: 39184047
bioRxiv. 2021 Feb 5.
