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About This Item
Empirical Formula (Hill Notation):
C18H20FN3O4
CAS Number:
Molecular Weight:
361.37
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
SMILES string
NC(C1=C(OC)C=C2C(C=CN=C2OC[C@@H]3[C@H](CC)[C@H](F)C(N3)=O)=C1)=O
InChI
1S/C18H20FN3O4/c1-3-10-13(22-17(24)15(10)19)8-26-18-11-7-14(25-2)12(16(20)23)6-9(11)4-5-21-18/h4-7,10,13,15H,3,8H2,1-2H3,(H2,20,23)(H,22,24)/t10-,13+,15-/m0/s1
InChI key
JKDGKIBAOAFRPJ-ZBINZKHDSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 20 mg/mL, clear
storage temp.
room temp
Quality Level
Biochem/physiol Actions
PF06650833 has been studied for its use in the treatment of Waldenstrom macroglobulinemia, indicated by overproduction of IgM (immunoglobulin M)-producing lymphoplasmacytic cells.
PF06650833 is an inhibitor of Interleukin-1 receptor associated kinase 4 (IRAK4). IRAK4 kinase is important in innate immunity, involved in initiating signaling from Toll-like receptors and members of th einterleukin-1 receptor family. IRAK4 kinase is an attractive target for the treatment of various diseases associated with deregulated inflammation, such as rheumatoid arthritis, osteoarthritis, inflammatory bowel disease, and systemic lupus erythematosus. PF06650833 has been investigated for treatment of lupus.
signalword
Warning
hcodes
Hazard Classifications
Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3
target_organs
Respiratory system
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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Future therapeutic options for patients with Waldenstrom macroglobulinemia.
Castillo J J, et al.
Best Practice & Research. Clinical Haematology, 29(2), 206-215 (2016)
Kinase inhibitors in clinical practice: An expanding world.
Pandey R and Reuben K
The Journal of Allergy and Clinical Immunology, 141(2), 522-524 (2018)
Sadiq Umar et al.
Cellular & molecular immunology (2020-05-18)
Flares of joint inflammation and resistance to currently available biologic therapeutics in rheumatoid arthritis (RA) patients could reflect activation of innate immune mechanisms. Herein, we show that a TLR7 GU-rich endogenous ligand, miR-Let7b, potentiates synovitis by amplifying RA monocyte and
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