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Merck

PZ0327

Sigma-Aldrich

PF06650833

≥98% (HPLC)

Sinónimos:

1-[[(2S,3S,4S)-3-Ethyl-4-fluoro-5-oxo-2-pyrrolidinyl]methoxy]-7-methoxy-6-isoquinolinecarboxamide, PF-06650833

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About This Item

Fórmula empírica (notación de Hill):
C18H20FN3O4
Número de CAS:
Peso molecular:
361.37
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77

Quality Level

assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 20 mg/mL, clear

storage temp.

room temp

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

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.

pictograms

Exclamation mark

signalword

Warning

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2 - STOT SE 3

target_organs

Respiratory system

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable


Certificados de análisis (COA)

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Visite la Librería de documentos

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)
Future therapeutic options for patients with Waldenstrom macroglobulinemia.
Castillo J J, et al.
Best Practice & Research. Clinical Haematology, 29(2), 206-215 (2016)
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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