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KU60019 (925701-49-1)

KU-60019 is an improved analogue of KU-55933, with IC50 of 6.3 nM for ATM in cell-free assays, 270- and 1600-fold more selective for ATM than DNA-PK and ATR,and is a highly effective radiosensitizer.

Not Intended for Therapeutic Use. For research use only.

CAS: 925701-49-1 Category

KU60019 (925701-49-1) Description:

KU-60019 is a potent and selective ATM inhibitor. KU-60019 is 10-fold more effective than KU-55933 at blocking radiation-induced phosphorylation of key ATM targets in human glioma cells. As expected, KU-60019 is a highly effective radiosensitizer of human glioma cells. KU-60019 inhibits the DNA damage response, reduces AKT phosphorylation and prosurvival signaling, inhibits migration and invasion, and effectively radiosensitizes human glioma cells.

KU60019 (925701-49-1) Specifications:

Product Name KU60019
Synonym KU60019; KU 60019; KU-60019.
Chemical Name 2-((2S,6R)-2,6-dimethylmorpholino)-N-(5-(6-morpholino-4-oxo-4H-pyran-2-yl)-9H-thioxanthen-2-yl)acetamide.
Drug Class Antineoplastics
Purity ≥98% (HPLC)
CAS Number 925701-49-1
Molecular Formula C30H33N3O5S
Molecular Weight 547.66512
Monoisotopic Mass 547.21409 g/mol
MDL number MFCD19690944
InChi Code InChI=1S/C30H33N3O5S/c1-19-16-32(17-20(2)37-19)18-28(35)31-23-6-7-27-22(13-23)12-21-4-3-5-25(30(21)39-27)26-14-24(34)15-29(38-26)33-8-10-36-11-9-33/h3-7,13-15,19-20H,8-12,16-18H2,1-2H3,(H,31,35)/t19-,20+
SMILES O=C(NC1=CC(CC2=C(C(C3=CC(C=C(N4CCOCC4)O3)=O)=CC=C2)S5)=C5C=C1)CN6C[[email protected]](C)O[[email protected]](C)C6
Form Powder
Color White
Solubility  Soluble in DMSO, not soluble in water
Storage Temp.  0 – 4 C for short term (days to weeks), or -20 C for long term (months)
Shelf life >2 years if stored properly
Handling Protect from air and moisture
Application KU-60019 is a potent and selective ATM inhibitor


RIDADR NONH for all modes of transport


[1]. Vecchio D, Daga A, Carra E, Marubbi D, Baio G, Neumaier CE, Vagge S, Corvò R, Pia Brisigotti M, Louis Ravetti J, Zunino A, Poggi A, Mascelli S, Raso A, Frosina G. Predictability, efficacy and safety of radiosensitization of glioblastoma-initiating cells by the ATM inhibitor KU-60019. Int J Cancer. 2013 Dec 19. doi: 10.1002/ijc.28680. [Epub ahead of print] PubMed PMID: 24443327.

[2]. Zirkin S, Davidovich A, Don J. The PIM-2 kinase is an essential component of the ultraviolet damage response that acts upstream to E2F-1 and ATM. J Biol Chem. 2013 Jul 26;288(30):21770-83. doi: 10.1074/jbc.M113.458851. Epub 2013 Jun 11. PubMed PMID: 23760264; PubMed Central PMCID: PMC3724634.

[3]. Biddlestone-Thorpe L, Sajjad M, Rosenberg E, Beckta JM, Valerie NC, Tokarz M, Adams BR, Wagner AF, Khalil A, Gilfor D, Golding SE, Deb S, Temesi DG, Lau A, O’Connor MJ, Choe KS, Parada LF, Lim SK, Mukhopadhyay ND, Valerie K. ATM kinase inhibition preferentially sensitizes p53-mutant glioma to ionizing radiation. Clin Cancer Res. 2013 Jun 15;19(12):3189-200. doi: 10.1158/1078-0432.CCR-12-3408. Epub 2013 Apr 25. PubMed PMID: 23620409; PubMed Central PMCID: PMC3687028.

[4]. Golding SE, Rosenberg E, Adams BR, Wignarajah S, Beckta JM, O’Connor MJ, Valerie K. Dynamic inhibition of ATM kinase provides a strategy for glioblastoma multiforme radiosensitization and growth control. Cell Cycle. 2012 Mar 15;11(6):1167-73. doi: 10.4161/cc.11.6.19576. Epub 2012 Mar 15. PubMed PMID: 22370485; PubMed Central PMCID: PMC3335919.

[5].Gamper AM, Choi S, Matsumoto Y, Banerjee D, Tomkinson AE, Bakkenist CJ. ATM protein physically and functionally interacts with proliferating cell nuclear antigen to regulate DNA synthesis. J Biol Chem. 2012 Apr 6;287(15):12445-54. doi: 10.1074/jbc.M112.352310. Epub 2012 Feb 23. PubMed PMID: 22362778; PubMed Central PMCID: PMC3320994.