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Tozasertib CAS 639089-54-6 Cyclopropane carboxylic acid VX-680 Tozasertib Free Base 

Payment Terms: T/T,L/C,WU 
Place of Origin: Sichuan, China (Mainland) 
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Product Detail

Model No.: C23H28N8OS
Production Capacity: 50KG/YEAR
Delivery Date: within 7 days
Molecular Formula: C23H28N8OS
Content: ≥99%
Appearance: White to off-white solid po...
Solubility: DMSO 90 mg/mL; Water <1 ...
Self life: At least 5 years if properl...
Means of Transport: Ocean,Land,Air
Packing: as per request of clients
Molecular Weight: 464.59
Specification: CP/USP/EP
Structure: 1 H-NMR and MS spectrum of...
Shipping condition: Ambient temperature

Tozasertib is a synthetic, small-molecule Aurora kinase inhibitor with potential antitumor activity.

Tozasertib ( CAS: 639089-54-6)




Molecular Formula


Molecular Weight






Tozasertib, also known as VX-680, MK0457 or VE465,  is a synthetic, small-molecule Aurora kinase inhibitor with potential antitumor activity. Tozasertib binds to and inhibits Aurora kinases (AKs), thereby inducing apoptosis in tumor cells in which AKs are overexpressed. AKs, a family of serine-threonine kinases, are essential for mitotic progression, spindle formation, centrosome maturation, chromosomal segregation, and cytokinesis.


Although its multi-kinase profile, VX-680 induces similar cytotoxicity with IC50 of approximately 300 nM and exhibits an AUR B-like inhibitory phenotype of G2/M arrest, endoreduplication and apoptosis in BaF3 cells transfected with ABL or FLT-3 (mutant and wild type) kinases. VX-680 prevents the CAL-62 proliferation in a time-dependent manner. VX-680 treatment for 14 days significantly decreases the number and size of colonies by approximately 70% in the 8305C and 90% in the CAL-62, 8505C and BHT-101. Treatment of the different ATC cells with VX-680 inhibits proliferation with the IC50 between 25 and 150 ?nM. The VX-680 significantly impairs the ability of the different cell lines to form colonies in soft agar. Analysis of caspase-3 activity indicates that VX-680 induces apoptosis in the different cell lines. CAL-62 cells exposed for 12? hours to VX-680 showed an accumulation of cells with ≥4N DNA content. Time-lapse analysis demonstrates that VX-680-treated CAL-62 cells exit metaphase without dividing. Moreover, histone H3 phosphorylation is abrogated following VX-680 treatment.VX-680 has significant inhibitory activity against BCR-Abl bearing the T315I mutation in patient-derived samples.

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