Gilteritinib (4 (link)) (ASP2215; Active Biochem, Maplewood, NJ) and quizartinib (4 (link)) (AC220; Selleck Chemicals, Houston, TX), type I and II FLT3 inhibitors, respectively, clinically active in FLT3-ITD AML, were used at pharmacologically relevant concentrations (23 (link),24 (link)). The SET-sequestering PAD FTY720 (25 (link)) (Fingolimod; Cayman Chemical Company, Ann Arbor, MI) was also used at pharmacologically relevant concentrations. DT-061, an orally bioavailable small molecule activator of PP2A (SMAP) developed by reengineering tricyclic neuroleptics and proposed to directly bind the PP2A Aα subunit (26 (link)–29 (link)), was provided by Dr. Goutham Narla. The pan-Pim inhibitor AZD1208 and GSK-3β inhibitors TC-G 24 and TWS119 were from Tocris Bioscience, Minneapolis, MN, the c-Myc inhibitor 10058-F4 from Sigma-Aldrich, and the pan-AKT inhibitor MK-2206 from Selleck Chemicals, Houston, TX.
Protocol detail
Inhibitors of FLT3, PP2A, and Signaling Pathways in AML
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Asp2215
Azd1208
Cayman
Fingolimod
Flt3
Fty720
Gilteritinib
Inhibitors
Mk 2206
Neuroleptics
Pp2a
Quizartinib
Subunit
Tws119
Corresponding Organization :
Other organizations : University of Maryland, Baltimore, University of Michigan–Ann Arbor
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Variable analysis
independent variables
- Gilteritinib (4 (link))
- Quizartinib (4 (link))
- FTY720 (25 (link))
- DT-061
- AZD1208
- TC-G 24
- TWS119
- 10058-F4
- MK-2206
- Not explicitly mentioned
- Pharmacologically relevant concentrations of Gilteritinib (23 (link),24 (link))
- Pharmacologically relevant concentrations of Quizartinib (23 (link),24 (link))
- Pharmacologically relevant concentrations of FTY720 (25 (link))
- No positive or negative controls were explicitly mentioned.
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