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CGI-1746

(CAS No:910232-84-7)
CGI1746 is a potent and highly selective small-molecule inhibitor of the Btk with IC50 of 1.9 nM.
CAS No:910232-84-7
Molecular Weight(MW):579.69
Purity:99.00%
Specification:500MG;1G;5G;10G;50G;100G
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QC Documents
 COA  MSDS  HPLC  NMR
ChemicalInfomation
CAS No: 910232-84-7
Molecular formula(MF) C34H37N5O4
Molecular Weight(MW): 579.69
Alias
Solubility
In vitro DMSO 100 mg/mL (172.5 mM)
Ethanol 33 mg/mL warmed (56.92 mM)
Water <1 mg/mL
In vivo
Biological Activity
Description CGI1746 is a potent and highly selective small-molecule inhibitor of the Btk with IC50 of 1.9 nM.
Targets
BTK [1]
1.9 nM
In vitro

CGI1746 is specific for Btk, with ∼1,000-fold selectivity over Tec and Src family kinases. In an ATP-free competition binding assay, the dissociation constant for Btk is 1.5 nM. CGI1746 inhibits Btk activity in a new binding mode that stabilizes an inactive nonphosphorylated enzyme conformation. CGI1746 inhibits both auto- and transphosphorylation steps necessary for enzyme activation. CGI1746 completely inhibits anti-IgM–induced murine and human B cell proliferation, with IC50s of 134 nM and 42 nM, respectively, but had no effect on anti-CD3- and anti-CD28–induced T cell proliferation. CGI1746 potently inhibits the proliferation of CD27+IgG+ B cells isolated from the tonsils of four human donors with an average IC50 of 112 nM. In macrophages, CGI1746 abolishes FcγRIII-induced TNFα, IL-1β and IL-6 production. CGI1746 potently inhibits TNFα, IL-1β and, to a lesser extent, IL-6 (three- to eight-fold higher IC50) production in human monocytes stimulated with immobilized or soluble immune complexes. [1]

In vivo CGI1746 abrogates B cell–dependent arthritis. CGI1746 treatment (100 mg/kg, s.c, twice-daily dosing) results in significant inhibition (97%) of overall clinical arthritis scores. CGI1746 treatment substantially reduces TNFα, IL-1β and IL-6, as well as MCP1 and MIP-1α on both the mRNA and protein level in the passive anti-collagen II antibody–induced arthritis (CAIA) model. CGI1746 shows comparable efficacy to TNFα blockade and significantly reduces clinical scores, as well as joint inflammation, in mice or rats with established arthritis. [1]