1 tion of Anion Relay Chemistry (ARC) with the
Takeda and Hiyama palladium-mediated cross-coupling proc
2 TAK-013 (sufugolix; developed previously by
Takeda Chemical Industries) as a tool to elucidate the m
3 , small-molecule inhibitor of GRK2 and GRK3,
Takeda compound 101 (Cmpd101; 3-[[[4-methyl-5-(4-pyridyl
4 Both balanol and the
Takeda compounds induce a slight closure of the kinase d
5 In this issue of Neuron,
Takeda et al. (2015) use a combination of modern recordi
6 In this issue of the JCI,
Takeda et al. describe a novel epigenetic link between M
7 Takeda G protein receptor 5 (TGR5), a G protein-coupled
8 s of the antiinflammatory bile acid receptor
Takeda G protein-coupled receptor 5 (TGR5) and were part
9 e nuclear farnesoid X receptor (FXR) and the
Takeda G protein-coupled receptor 5 (TGR5).
10 n colon and that bile salt receptors VDR and
Takeda G-protein coupled receptor5 (TGR5) were highly ex
11 ion of the G-protein coupled receptor (GPCR)
Takeda G-protein receptor 5 (TGR5), also known as G-prot
12 farnesoid X receptor (FXR) and the membrane
Takeda G-protein receptor 5 (TGR5), are known to improve
13 xr) and membrane G-protein-coupled receptor (
Takeda G-protein-coupled receptor 5; Tgr5).
14 Effects of DCA were mimicked by the
Takeda GPCR 5 agonist, INT-777 (50 muM), but not by the
15 and HbetaD2 release from wild-type, but not
Takeda GPCR 5(-/-), mice.
16 NIH, NCI, NCTN, Millennium Pharmaceuticals,
Takeda Oncology Company, and Celgene Corporation.
17 ceuticals, Inc, a wholly owned subsidiary of
Takeda Pharmaceutical Company Limited.
18 harmaceuticals, a wholly owned subsidiary of
Takeda Pharmaceutical International Company.
19 Seattle Genetics Inc and
Takeda Pharmaceuticals International Co.
20 Seattle Genetics and
Takeda Pharmaceuticals International.
21 Several lead compounds developed by
Takeda Pharmaceuticals show high selectivity for GRK2 an