Nomenclature |
colony stimulating factor 1 receptor
|
fms related tyrosine kinase 3
|
HGNC, UniProt |
CSF1R, P07333
|
FLT3, P36888
|
EC number |
2.7.10.1
|
2.7.10.1
|
Common abreviation |
CSFR |
FLT3 |
Endogenous ligands |
G‐CSF (CSF3, P09919), GM‐CSF (CSF2, P04141), M‐CSF (CSF1, P09603) |
Fms‐related tyrosine kinase 3 ligand (FLT3LG, P49771) |
Inhibitors |
JNJ‐28312141 (pIC50 9.2) [116], Ki‐20227 (pK
d 9.1) [33], Ki‐20227 (pIC50 8.7) [143], GW‐2580 (pK
d 8.7) [33], JNJ‐28312141 (pK
d 8.5) [33] |
AC710 (pK
d 9.3) [108], linifanib (pK
d 9.2) [33], dovitinib (pK
d 9.2) [33], crenolanib (pK
d 9.1) [69], AST‐487 (pK
d 9.1) [33], ENMD‐2076 (pIC50 8.5) [149], tandutinib (pK
d 8.5) [33] |
Selective inhibitors |
GW‐2580 (pIC50 7.2) [27] |
G749 (pIC50 9.4) [97] |
Comments |
Upregulation of CSF1R expression is associated with migroglial activation and immune pathology in Alzhermer's disease (AD) [67, 61]. Pharmacological inhibition of CSF1R with GW‐2580 reduces microglial proliferation and prevents disease progression in a mouse model of AD, but this does not correlate with amyloid‐β plaque numbers [144]. |
5'‐fluoroindirubinoxime has been described as a selective FLT3 inhibitor [22]. |