AZD4547

Name: AZD4547
Brand: Selleck Chemicals
SKU: S2801
Rating: 5 (85 reviews)

For research use only.

Catalog No.S2801 Synonyms: ABSK 091

85 publications

CAS No. 1035270-39-3

AZD4547 (ABSK 091) is a novel selective FGFR inhibitor targeting FGFR1/2/3 with IC50 of 0.2 nM/2.5 nM/1.8 nM in cell-free assays, weaker activity against FGFR4, VEGFR2(KDR), and little activity observed against IGFR, CDK2, and p38. Phase 2/3.

Selleck's AZD4547 has been cited by 85 publications

Cancer Cell, 2019, 35(3):504-518

PubMed: 30827889 ( click the link to review the publication )

Nature, 2018, 553(7686):101-105

PubMed: 29258295 ( click the link to review the publication )

Science, 2017, 10.1126/science.aan4368

PubMed: 29191878 ( click the link to review the publication )

Nature, 2016, 30;534(7609):647-51.

PubMed: 27338794 ( click the link to review the publication )

Acta Neuropathol, 2021, 10.1007/s00401-021-02327-x

PubMed: 34046693 ( click the link to review the publication )

Sci Adv, 2021, 7(7)eabd2645

PubMed: 33579708 ( click the link to review the publication )

Proc Natl Acad Sci U S A, 2021, 118(20)e2100342118

PubMed: 33975953 ( click the link to review the publication )

Cancer Res, 2021, canres.2276.2020

PubMed: 33685992 ( click the link to review the publication )

Cancer Res, 2021, canres.4048.2020

PubMed: 34083250 ( click the link to review the publication )

Cells, 2021, 10(6)1318

PubMed: 34070622 ( click the link to review the publication )

FASEB J, 2021, 35(2):e21286

PubMed: 33484478 ( click the link to review the publication )

Int J Oncol, 2021, 10.3892/ijo.2021.5167

PubMed: 33491755 ( click the link to review the publication )

Proc Natl Acad Sci U S A, 2020, 117(46):29025-29034

PubMed: 33144503 ( click the link to review the publication )

Genome Med, 2020, 18;12(1):17

PubMed: 32070411 ( click the link to review the publication )

EBioMedicine, 2020, 62:103131

PubMed: 33254023 ( click the link to review the publication )

Cancers (Basel), 2020, 12(9)E2697

PubMed: 32967224 ( click the link to review the publication )

Br J Cancer, 2020, 22

PubMed: 32439932 ( click the link to review the publication )

Br J Cancer, 2020, 10.1038/s41416-020-0952-1

PubMed: 32572172 ( click the link to review the publication )

Cell Oncol (Dordr), 2020, 10.1007/s13402-020-00562-0

PubMed: 33119860 ( click the link to review the publication )

Front Oncol, 2020, 10;10:331

PubMed: 32211337 ( click the link to review the publication )

Int J Mol Sci, 2020, 18;21(8):2825

PubMed: 32325639 ( click the link to review the publication )

Acta Pharmacol Sin, 2020, 10.1038/s41401-020-00567-3

PubMed: 33288861 ( click the link to review the publication )

Oncol Rep, 2020, 44(6):2581-2594

PubMed: 33125153 ( click the link to review the publication )

EMBO Mol Med, 2020, e11793

PubMed: 32720440 ( click the link to review the publication )
Biochem Genet, 2020, 10.1007/s10528-020-09982-x

PubMed: 32671511 ( click the link to review the publication )

BMC Pharmacol Toxicol, 2020, 21(1):61

PubMed: 32795383 ( click the link to review the publication )

Mol Cancer Res, 2020, 18(4):549-559

PubMed: 31941753 ( click the link to review the publication )

Stem Cell Res Ther, 2020, 11(1):67

PubMed: 32070424 ( click the link to review the publication )

Nat Commun, 2019, 10(1):2701

PubMed: 31221965 ( click the link to review the publication )

EMBO Mol Med, 2019, 11(2)

PubMed: 30610113 ( click the link to review the publication )

Cell Rep, 2019, 28(9):2331-2344

PubMed: 31461650 ( click the link to review the publication )

J Exp Clin Cancer Res, 2019, 38(1):372

PubMed: 31438996 ( click the link to review the publication )

Aging (Albany NY), 2019, 11(18):7780-7795

PubMed: 31545294 ( click the link to review the publication )

Mol Cancer Res, 2019,

PubMed: 30257990 ( click the link to review the publication )

J Cell Mol Med, 2019, 23(4):2933-2942

PubMed: 30761743 ( click the link to review the publication )

J Cell Mol Med, 2019, 101111/jcmm14793

PubMed: 31692229 ( click the link to review the publication )

Sci Rep, 2019, 9(1):8726

PubMed: 31217507 ( click the link to review the publication )

Sci Rep, 2019, 9(1):1875

PubMed: 30755670 ( click the link to review the publication )

Sci Rep, 2019, 9(1):6004

PubMed: 30979919 ( click the link to review the publication )

Front Pharmacol, 2019,

PubMed: 31998131 ( click the link to review the publication )

Transl Oncol, 2019, 12(3):432-440

PubMed: 30562682 ( click the link to review the publication )

Reprod Sci, 2019, 26(7):979-987

PubMed: 30270745 ( click the link to review the publication )

Ocul Immunol Inflamm, 2019, 10.1080/09273948.2019.1672196

PubMed: 31657648 ( click the link to review the publication )

Oncol Lett, 2019, 18(6):6249-6260

PubMed: 31788102 ( click the link to review the publication )

Oncol Lett, 2019, 17(2):2303-2307

PubMed: 30719110 ( click the link to review the publication )

Hepatology, 2018, 10.1002/hep.30127

PubMed: 30067876 ( click the link to review the publication )

Cancer Lett, 2018, 427:38-48

PubMed: 29679612 ( click the link to review the publication )

Mol Cell Proteomics, 2018, 17(5):850-870

PubMed: 29371290 ( click the link to review the publication )
Oncogenesis, 2018, 7(9):71

PubMed: 30237393 ( click the link to review the publication )

Sci Rep, 2018, 8(1):12087

PubMed: 30108259 ( click the link to review the publication )

J Biol Chem, 2018, 293(38):14839-14849

PubMed: 30093411 ( click the link to review the publication )

J Proteomics, 2018, 170:130-140

PubMed: 28842319 ( click the link to review the publication )

Oncotarget, 2018, 9(100):37352-37366

PubMed: 30647837 ( click the link to review the publication )

Clin Cancer Res, 2017, 23(4):962-973

PubMed: 27535980 ( click the link to review the publication )

Clin Cancer Res, 2017, 15;23(18):5527-5536

PubMed: 28630215 ( click the link to review the publication )

Theranostics, 2017, 7(4):974-986

PubMed: 28382169 ( click the link to review the publication )

Oncogene, 2017, 10.1038/onc.2016.512

PubMed: 28263980 ( click the link to review the publication )

BMC Cancer, 2017, 17(1):191

PubMed: 28292264 ( click the link to review the publication )

PLoS One, 2017, 12(8):e0183181

PubMed: 28806774 ( click the link to review the publication )

J Med Invest, 2017, 64(3.4):262-265

PubMed: 28954993 ( click the link to review the publication )

Oncotarget, 2017,

PubMed: 29050315 ( click the link to review the publication )

Oncotarget, 2017, 8(6):10007-10024

PubMed: 28052020 ( click the link to review the publication )

Oncotarget, 2017, 8(70):115596-115608

PubMed: 29383184 ( click the link to review the publication )

Clin Cancer Res, 2016, 22(15):3884-93

PubMed: 26936917 ( click the link to review the publication )

Cancer Res, 2016, 76(11):3285-94

PubMed: 27197170 ( click the link to review the publication )

Int J Cancer, 2016,

PubMed: 26481559 ( click the link to review the publication )

Oncogene, 2016, 10.1038/onc.2016.216

PubMed: 27345413 ( click the link to review the publication )

J Neurosci, 2016, 36(16):4534-48

PubMed: 27098696 ( click the link to review the publication )

J Proteome Res, 2016, 15(12):4490-4504

PubMed: 27794612 ( click the link to review the publication )

Hum Mol Genet, 2016, 25(1):9-23

PubMed: 26494904 ( click the link to review the publication )

Oncotarget, 2016, 7(31-:50161-50179

PubMed: 27367030 ( click the link to review the publication )

Oncotarget, 2016, 7(18-:25983-6002

PubMed: 27036020 ( click the link to review the publication )
Nat Commun, 2015, 6:7002

PubMed: 25926053 ( click the link to review the publication )

Mol Cancer Ther, 2015, 14(10):2292-302

PubMed: 26294741 ( click the link to review the publication )

J Biol Chem, 2015, 290(44):26752-64

PubMed: 26370090 ( click the link to review the publication )

Scand J Rheumatol, 2015, 6:1-10

PubMed: 25743336 ( click the link to review the publication )

PLoS One, 2015, 10(6):e0123967

PubMed: 26053020 ( click the link to review the publication )

PLoS One, 2015, 10(4):e0124562

PubMed: 25893435 ( click the link to review the publication )

Pathol Oncol Res, 2015, 10.1007/s12253-015-9916-9

PubMed: 25749811 ( click the link to review the publication )

Tumour Biol, 2015, 10.1007/s13277-015-3237-1

PubMed: 25691251 ( click the link to review the publication )

Oncotarget, 2015,

PubMed: 25576915 ( click the link to review the publication )

Cell Physiol Biochem, 2014, 33(3):633-45

PubMed: 24642893 ( click the link to review the publication )

Gastric Cancer, 2014, 10.1007/s10120-014-0444-1

PubMed: 25407459 ( click the link to review the publication )

Mol Cell Biol, 2014, 34(18):3535-45

PubMed: 25022753 ( click the link to review the publication )

Celon Pharma Inc, 2013, Paulina Grygielewicz

PubMed: ( click the link to review the publication )

Purity & Quality Control

Choose Selective FGFR Inhibitors

Biological Activity

Description

Features

Greater selectivity for FGFR1-3 over FGFR4. AZD4547 is active against the tyrosine kinase activity of both the wild-type and mutant forms of FGFR.

Targets

FGFR1 ^[1] (Cell-free assay)	FGFR3 ^[1] (Cell-free assay)	FGFR2 ^[1] (Cell-free assay)	KDR ^[1] (Cell-free assay)
0.2 nM	1.8 nM	2.5 nM	24 nM

In vitro

Compared to FGFR1-3, AZD4547 displays weaker activity against FGFR4 with IC50 of 165 nM. AZD4547 only inhibits recombinant VEGFR2 (KDR) kinase activity with IC50 of 24 nM, in the in vitro selectivity test against a diverse panel of representative human kinases. AZD4547 at 0.1 μM exhibits no activity against a range of recombinant kinases including ALK, CHK1, EGFR, MAPK1, MEK1, p70S6K, PDGFR, PKB, Src, Tie2, and PI3-kinase. Consistently, the potent selectivity of AZD4547 for FGFR1-3 over FGFR4, IGFR, and KDR is also observed in cellular phosphorylation assays. AZD4547 has potent in vitro antiproliferative activity only against tumor cell lines expressing deregulated FGFRs such as KG1a, Sum52-PE, and KMS11 with IC50 of 18-281 nM, and is inactive against MCF7 as well as more than 100 additional tumor cell lines. AZD4547 treatment potently inhibits FGFR and MAPK phosphorylation in human tumor cell lines in a dose-dependent manner. AZD4547 also potently inhibits the phosphorylation of FRS2 and PLCγ, downstream markers of FGFR signaling. Notably, AZD4547 affects the AKT phosphorylation in the breast cell lines, MCF7 and Sum52-PE but not in KG1a and KMS11 lines. AZD4547 treatment significantly induces apoptosis in Sum52-PE and KMS11 cells, dramatically increases G1 arrest but not apoptosis in KG1a cells, and has no effect on cell cycle distribution or apoptosis in MCF7 cells. ^[1]

Cell Data

Cell Lines	Assay Type	Concentration	Incubation Time	Activity Description	PMID
SNU449	NVvwdphOT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		MUm3NkBp	MV\JR\|UxRTBwMEiyJO69VQ>?	MVi8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjN3MUOyNEc,OjZ\|NUGzNlA9N2F-
SK-HEP-1	M3TSWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7		NGL1NG44OiCq	MV3JR\|UxRTBwMEi0JO69VQ>?	M4\KelxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4M{WxN\|IxLz5{NkO1NVMzODxxYU6=
SNU475	MoKwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?		MonkO\|IhcA>?	MkTGTWM2OD13LkSg{txO	MVG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjN3MUOyNEc,OjZ\|NUGzNlA9N2F-
Hep3B	NVnwbJh4T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		NFvKT3g4OiCq	M1j5[mlEPTB;Nj60N{DPxE1?	MUK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjN3MUOyNEc,OjZ\|NUGzNlA9N2F-
PLC/PRF5	MWLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		NVv0W2Q6PzJiaB?=	M{PtOGlEPTB;Nj61OUDPxE1?	NHHOfYg9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkO1NVMzOCd-Mk[zOVE{OjB:L3G+
Hur7	MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?		NF7BNYU4OiCq	NXHnZZBTUUN3ME23MlI2KM7:TR?=	M1nQdFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4M{WxN\|IxLz5{NkO1NVMzODxxYU6=
HepG2	NU\NeJZRT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=		M1PBdlczKGh?	NHLRW\|VKSzVyPUiuO\|Mh\|ryP	NFLzNlg9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkO1NVMzOCd-Mk[zOVE{OjB:L3G+
SNU449	MnTOR4xwdm:pZX7pZ{Bie3OjeR?=	MYSxJOK2VQ>?	MUWyOEBp	Mlf5[IVkemWjc3XzJINwdG:weTDmc5Ju[XSrb36gd4lodmmoaXPhcpRtgQ>?	MU[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjN3MUOyNEc,OjZ\|NUGzNlA9N2F-
SK-HEP-1	M{HOTWNtd26xZ3XubYMh[XO\|YYm=	MWqxJOK2VQ>?	NFHDXZozPCCq	NVy3S5VZ\GWlcnXhd4V{KGOxbH;ufUBnd3KvYYTpc44he2mpbnnmbYNidnSueR?=	M2nxWlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4M{WxN\|IxLz5{NkO1NVMzODxxYU6=
SNU449	NEnWcXlHfW6ldHnvckBCe3OjeR?=	MmCxNE0zKM7:TR?=	NGrudFM1QCCq	M4LWPYNifXOnczDhJIRm[3KnYYPlJI9nKE[UU{NvwKxCU1RuIHHu[EBGWkticHjvd5Bpd3K7bHH0bY9v	NUPCXnZDRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[zOVE{OjBpPkK2N\|UyOzJyPD;hQi=>
SK-HEP-1	MXvGeY5kfGmxbjDBd5NigQ>?	NVj6XlNlOC1{IN88US=>	NGDte201QCCq	MnXzZ4F2e2W\|IHGg[IVkemWjc3Wgc4YhTlKVMv-8kGFMXCxiYX7kJGVTUyCyaH;zdIhwenmuYYTpc44>	MYW8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjN3MUOyNEc,OjZ\|NUGzNlA9N2F-
BaF3 FLT3-TEL	MXvHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?			NI\ETGRIUTVyPUSuOkDDuSByLkW3O{DPxE1?	MkjWQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ{OUS3OFEoRjJ4Mkm0O\|QyRC:jPh?=
BaF3 RET-TEL	MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?			M{DCVGdKPTB;MD6zPUDDuSByLkC0PEDPxE1?	MkfHQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ{OUS3OFEoRjJ4Mkm0O\|QyRC:jPh?=
BaF3 Parental	NWH1R5NWT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=			NGrFZ5pIUTVy78olNVAh\|ryP	MnXBQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjZ{OUS3OFEoRjJ4Mkm0O\|QyRC:jPh?=
MOLM14 FLT3/ITD	NFTkTlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=			NYXMZ\|VYT0l3ME2wMlQ5PCEEsTCwMlE2PyEQvF2=	MUK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPjJ7NEe0NUc,OjZ{OUS3OFE9N2F-
MV4-11 FLT3/ITD	M3TMNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7			NX\ZO3lrT0l3ME2wMlQ2QSEEsTCwMlA1PiEQvF2=	NUjKS\|lMRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[yPVQ4PDFpPkK2Nlk1PzRzPD;hQi=>
TT RET C634W	NFfYWmVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=			NHfoTopIUTVyPUKuPUDDuSByLkmwOEDPxE1?	NULWcVQ2RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[yPVQ4PDFpPkK2Nlk1PzRzPD;hQi=>
AN3-CA FGFR2 N550K, K310R	MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?			MXjHTVUxRTBwMEOxJOKyKDBwMEKzJO69VQ>?	NUew[FVqRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[yPVQ4PDFpPkK2Nlk1PzRzPD;hQi=>
MFE296 FGFR2 N550K	MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?			NH:2N2lIUTVyPUCuO\|MxKMLzIECuNFU4KM7:TR?=	NWOzRm04RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMk[yPVQ4PDFpPkK2Nlk1PzRzPD;hQi=>
MFE280 FGFR2 S252W	MXTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?			MUDHTVUxRTBwMkG4JOKyKDBwMEezJO69VQ>?	M4j4e\|xiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4Mkm0O\|QyLz5{NkK5OFc1OTxxYU6=
Ishikawa FGFF2 over exp.	MmrsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?			NXTGWFhKT0l3ME20MlUhyrFiMT61NUDPxE1?	M1u5eFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4Mkm0O\|QyLz5{NkK5OFc1OTxxYU6=
HEC1A Normal FGFR2	NXXDNZRMT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=			NFTIW2NIUTVy78olNVAh\|ryP	NE[zb4Y9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkK5OFc1OSd-Mk[yPVQ4PDF:L3G+
A549	NX7BRnJxS2WubDD2bYFjcWyrdImgRZN{[Xl?	NV;HPZBkOC5zL{Gg{txO	MmqxOFghcA>?	M1\KdoVvcGGwY3XzJGVzdG:2aX7pZkBqdmS3Y3XkJJZq[WKrbHn0fUBtd3O\|	NEnrXI89[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NkC1N\|AzOCd-Mk[wOVMxOjB:L3G+
SGC-7901	MlTJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NYftfotzOSCwTT2xNEDPxE1?	NGPrSnQ4OiCq	MoLqTWM2OCCxZjC1MVExKM7:TTygbY5pcWKrdIOgZ4VtdCC4aXHibYxqfHliZH;z[UBl\XCnbnTlcpRtgQ>?	NInsOGs9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{NUW3OlkyPSd-MkW1O\|Y6OTV:L3G+
HGC-27	MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NX3hR5B3OSCwTT2xNEDPxE1?	NYLNU5RkPzJiaB?=	MYTJR\|UxKG:oIEWtNVAh\|ryPLDDpcohq[mm2czDj[YxtKH[rYXLpcIl1gSCmb4PlJIRmeGWwZHXueIx6	MnPMQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjV3N{[5NVUoRjJ3NUe2PVE2RC:jPh?=
MKN-28	MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NY\ySJoyOSCwTT2xNEDPxE1?	NF65Opc4OiCq	M{[5SGlEPTBib3[gOU0yOCEQvF2sJIlvcGmkaYTzJINmdGxidnnhZoltcXS7IHTvd4Uh\GWyZX7k[Y51dHl?	MYC8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPTV5NkmxOUc,OjV3N{[5NVU9N2F-
NCI-N87	MkfqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MmixNUBvVS1zMDFOwG0>	MYC3NkBp	MmfuTWM2OCCxZjC1MVExKM7:TTygbY5pcWKrdIOgZ4VtdCC4aXHibYxqfHliZH;z[UBl\XCnbnTlcpRtgQ>?	NVK0OYU4RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkW1O\|Y6OTVpPkK1OVc3QTF3PD;hQi=>
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NCI-H1581	NEjGZXpHfW6ldHnvckBie3OjeR?=		MnzKO\|IhcHK\|	MXrJcohq[mm2aX;uJI9nKE[JRmKxJIlvKGi3bXHuJG5EUS2KMUW4NUBk\WyuczDhd5Nme3OnZDDhd{BqdmirYnn0bY9vKG:oIHPlcIwheHKxbHnm[ZJifGmxbjDh[pRmeiB5MjDodpMh[nliY3XscEBkd3WwdHnu[{BscXRvODDhd5NigSxiSVO1NEA:KDBwME[yOkDPxE1w	M{XjSlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ6N{G0OlkzLz5{OEexOFY6OjxxYU6=
RT112	M1:wVWFvfGmycn;sbYZmemG2aY\lJIF{e2G7		MmfuO\|IhcHK\|	NIHQcVhCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIGLUNVEzKGOnbHzzJIV5eHKnc4PpcochTkeIUkOgZYZ1\XJiN{KgbJJ{NCCLQ{WwJF0hOC5yOEO4JO69VS5?	NVr5PIdXRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm3O\|U6OzdpPkK5O\|c2QTN5PD;hQi=>
RT112	MXfBcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>?		NWjiXVFxPzJiaILz	NUD2[mxMSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBHT0[UMz3hcZBtcW[rZXSgbJVu[W5iUmSxNVIh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IFPDT\|gwVVSWIHHzd4F6NCCLQ{WwJF0hOC5yOEi0JO69VS5?	MVu8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPzN2OEWzO{c,Ojd\|NEi1N\|c9N2F-
NCI-H1581	MV7BcpRqeHKxbHnm[ZJifGm4ZTDhd5NigQ>?		NVz2PGg3PzJiaILz	MYDBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IF\HSnIyNWGvcHzp[olm\CCqdX3hckBPS0lvSEG1PFEh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IFPDT\|gwVVSWIHHzd4F6NCCLQ{WwJF0hOC5yOUKxJO69VS5?	NYjieVNFRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkezOFg2OzdpPkK3N\|Q5PTN5PD;hQi=>
HeLa 229	NYPpUoFES3m2b4TvfIlkcXS7IHHzd4F6		NFjReJQ4OiCqcoO=	NFX5bIhEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJ\UyjIEKyPUBk\WyuczDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR\|UxKD1iMD6xOEDPxE1w	MXm8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPTd\|Nkm5N{c,OjV5M{[5PVM9N2F-
BAF3	M{T3d2FvfGmycn;sbYZmemG2aY\lJIF{e2G7		Mn7VO\|IhcHK\|	NUn6eGdxSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBud3W\|ZTDCRWY{KGOnbHzzJIV5eHKnc4PpcochXkWJRmKyJIFnfGW{IEeyJIhzeyxiSVO1NEA:KDBwMkKyJO69VS5?	NXv3ZolFRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm3O\|U6OzdpPkK5O\|c2QTN5PD;hQi=>
SGC7901	NHjUc3BCdnSrcILvcIln\XKjdHn2[UBie3OjeR?=		M33tdlczKGi{cx?=	MoiyRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCVR1O3PVAyKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDNWHQh[XO\|YYmsJGlEPTBiPTCyMlgh\|ryPLh?=	MnXYQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjd6Mkm1NVkoRjJ5OEK5OVE6RC:jPh?=
MGC803	NVPwPWhISW62aYDyc4xq\mW{YYTpeoUh[XO\|YYm=		NYC5TnlrPzJiaILz	MVzBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2JQ{iwN{Bk\WyuczDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR\|UxKD1iNj6yJO69VS5?	MnWzQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjd6Mkm1NVkoRjJ5OEK5OVE6RC:jPh?=
BGC823	NGrZRm9CdnSrcILvcIln\XKjdHn2[UBie3OjeR?=		NFH6RoQ4OiCqcoO=	MX3BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEKJQ{iyN{Bk\WyuczDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LDDJR\|UxKD1iNz65JO69VS5?	NFW0WIE9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{N{iyPVUyQSd-Mke4Nlk2OTl:L3G+
HL7702	MkKyR5l1d3SxeHnjbZR6KGG\|c3H5		MVe3NkBpenN?	MXnDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIUFc4ODJiY3XscJMh[W[2ZYKgO\|IhcHK\|IHL5JG1VXCCjc4PhfUwhUUN3MDC9JFE5NjJzIN88UU4>	MkL1QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjV5M{[5PVMoRjJ3N{O2PVk{RC:jPh?=
U-2 OS	M{\D[JFJXFNic4PhfS=>			NYXNVoJreUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IGWtNkBQWyClZXzsdy=>	NX7wT5oyRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
A673	MYLxTHRUKHO\|YYm=			M1zxNZFJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCDNkezJINmdGy\|	MVG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
Saos-2	M2D5eZFJXFNic4PhfS=>			MXHxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhW2Gxcz2yJINmdGy\|	NX7rfVd4RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
BT-37	MlO2dWhVWyC\|c3H5			NUjZSnNkeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IFLUMVM4KGOnbHzz	MVy8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
RD	NI\SWlRyUFSVIIPzZZk>			NETieZlyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiUlSgZ4VtdHN?	NHqzdJE9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N\|UyOzl:L3G+
SK-N-SH	NWnBeYNZeUiWUzDzd4F6			M1;vc5FJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCVSz3OMXNJKGOnbHzz	MXO8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
BT-12	NHHEWJhyUFSVIIPzZZk>			NEO0VlJyUFSVIH;mJJBm\GmjdILpZ{Bk[W6lZYKgZ4VtdCCuaX7ld{B1dyCrZHXueIlngSCvdXz0bZBt\SCxcIDvdpR2dmm2aXXzJIZweiCmcoXnJJJmeHW{cH;zbY5oQiCScnntZZJ6KHOlcnXlckBnd3JiQmStNVIh[2WubIO=	NUTze5BDRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
OHS-50	NHm2WGRyUFSVIIPzZZk>			NVjpXlFoeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IF;IV{02OCClZXzsdy=>	M3r3elxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7NEO1NVM6Lz5{OUSzOVE{QTxxYU6=
fibroblast cells	NELFZVFyUFSVIIPzZZk>			MmXidWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[\|ohWHKrbXHyfUB{[3KnZX6g[o9zKGOxboTyc4whUGhid3ns[EB1gXCnIH\pZpJw[myjc4SgZ4VtdHN?	NESzeo09[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N\|UyOzl:L3G+
Rh41	NHvUfIFyUFSVIIPzZZk>			MXPxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhWmh2MTDj[Yxtew>?	MV[8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
Rh30	NXy2VIV6eUiWUzDzd4F6			NVjqRZlReUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IGLoN\|Ah[2WubIO=	MV28ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
SJ-GBM2	NX;3[YgzeUiWUzDzd4F6			NXXYW4RUeUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC\|Y4Ll[Y4h\m:{IGPKMWdDVTJiY3XscJM>	MmX0QIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOjl2M{WxN\|koRjJ7NEO1NVM6RC:jPh?=
NB-EBc1	MnfYdWhVWyC\|c3H5			MVnxTHRUKG:oIIDl[IlifHKrYzDjZY5k\XJiY3XscEBtcW6nczD0c{Bq\GWwdHnmfUBufWy2aYDs[UBweHCxcoT1col1cWW\|IH\vdkBlenWpIILldJVzeG:\|aX7nPkBRemmvYYL5JJNkemWnbjDmc5IhVkJvRVLjNUBk\Wyucx?=	NWrKfphjRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC\|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm0N\|UyOzlpPkK5OFM2OTN7PD;hQi=>
LAN-5	MVPxTHRUKHO\|YYm=			M2nTUJFJXFNib3[gdIVlcWG2cnnjJINidmOncjDj[YxtKGyrbnXzJJRwKGmmZX70bYZ6KG23bITpdIxmKG:ycH;yeJVvcXSrZYOg[o9zKGS{dXegdoVxfXKyb4Ppcoc7KFC{aX3hdpkhe2O{ZXXuJIZweiCOQV6tOUBk\Wyucx?=	MYG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-
Rh18	MkjSdWhVWyC\|c3H5			MmfTdWhVWyCxZjDw[YRq[XS{aXOgZ4Fv[2W{IHPlcIwhdGmwZYOgeI8hcWSnboTp[pkhdXWudHnwcIUhd3Cyb4L0eY5qfGmnczDmc5Ih\HK3ZzDy[ZB2enCxc3nu[\|ohWHKrbXHyfUB{[3KnZX6g[o9zKFKqMUigZ4VtdHN?	MWK8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTR\|NUGzPUc,Ojl2M{WxN\|k9N2F-

... Click to View More Cell Line Experimental Data

Assay

Methods	Test Index	PMID
Western blot	p-FGFR / FGFR1 / p-AKT / AKT / p-ERK / ERK; PubMed: 28900173 Sci Rep Western blots (cropped) are shown for the indicated proteins in MDA-MB-361, BT474, and SKBR3 cells treated with AZD4547 (0, 1, 3, or 5 µM) for 72 hours. pFRS2; PubMed: 25576915 Oncotarget AZD4547 inhibits FGFR2 pathway activation in SNU16 and KATOIII cells. Cells were incubated with AZD4547 at the indicated doses. Cell lysates were immunoblotted for phospho-FGFR, phospho-FRS2, phospho- and total AKT, and phospho- and total ERK.	28900173 25576915
Growth inhibition assay	Cell viability; PubMed: 28900173 Sci Rep MDA-MB-361, BT474, and SKBR3 ErbB2-overexpressing breast cancer cells were treated with AZD4547 (0, 0.1, 0.3, 1, 3, or 5 µM) for 5 days. Then the viable fraction of each cell line was determined with an MTS assay. Cell viability; PubMed: 25576915 Oncotarget FGFR2-amplified GC cells are selectively sensitive to AZD4547. In vitro CCK-8 assay across a panel of 6 GC cells demonstrated that SNU16 and KATOIII cells were extremely sensitive to AZD4547 with IC50 values of 5-10 nM. Data (n = 6) are presented as mean ± SD.	28900173 25576915

In vivo

Oral administration of AZD4547 at 3 mg/kg twice daily in mice bearing KMS11 tumors results in significant tumor growth inhibition of 53% when compared with vehicle-treated controls, and AZD4547 at 12.5 mg/kg once daily or 6.25 mg/kg twice daily leads to complete tumor stasis, which is associated with dose proportional pharmacodynamic modulation of phospho-FGFR3 and reduced KMS11 tumor cell proliferation. Moreover, oral administration of AZD4547 at 12.5 mg/kg once daily results in 65% tumor growth inhibition in the FGFR1-fusion KG1a xenograft model. At efficacious dose levels, AZD4547 does not exhibit antiangiogenic effects. AZD4547 has no significant effect on blood pressure and therefore lacks in vivo anti-KDR activity. Consistently, dosing of 6.25 mg/kg orally twice daily AZD4547 is inactive in the cediranib-sensitive xenograft models including Calu-6, HCT-15 and LoVo. ^[1]

Protocol

Kinase Assay:^[1]	- Collapse AZD4547 kinase activity: The ability of AZD4547 to inhibit the human recombinant kinase activities of FGFR1-3 is tested using ATP concentrations at, or just below, the respective K_m.
Cell Research:^[1]	- Collapse Cell lines: KG1a, Sum52-PE, KMS11, and MCF7 Concentrations: Dissolved in DMSO, final concentrations ~1 μM Incubation Time: 72 hours Method: Cells are exposed to various concentrations of AZD4547 for 72 hours. The antiproliferative IC50 values are obtained by MTS proliferation assay. For fluorescence-activated cell sorting (FACS), cells are fixed with 70% ethanol and then incubated with propidium iodide/RNase A labeling solution. Cell cycle profiles are assessed with a FACSCalibur instrument and CellQuest analysis software. For apoptotic analysis, cells and media are gently harvested and centrifuged, followed by washing of cell pellets. Cells are then processed for Annexin V-fluorescein isothiocyanate (FITC) staining and propidium iodide uptake. The proportion of cells staining positive for Annexin V are then assessed with a FACSCalibur instrument and quadrant sorting is done by CellQuest analysis software. (Only for Reference)
Animal Research:^[1]	- Collapse Animal Models: Female swiss derived nude (nu/nu) and severe combined immunodeficient mice (SCID) injected s.c. with LoVo, HCT-15, Calu-6, KMS11 or KG1a Dosages: 1.5-50 mg/kg Administration: Oral gavage once daily or twice daily (Only for Reference)

References

[1] Gavine PR, et al. Cancer Res, 2012, 72(8), 2045-2056.

Solubility (25°C)

In vitro	DMSO	92 mg/mL (198.45 mM)
	Water	Insoluble
	Ethanol	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 4% DMSO+30% PEG 300+5% Tween 80+ddH2O For best results, use promptly after mixing.	5mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information Download AZD4547 SDF

Molecular Weight	463.57
Formula	C₂₆H₃₃N₅O₃
CAS No.	1035270-39-3
Storage	3 years-20°C powder 2 years-80°C in solvent
Synonyms	ABSK 091
Smiles	CC1CN(CC(N1)C)C2=CC=C(C=C2)C(=O)NC3=NNC(=C3)CCC4=CC(=CC(=C4)OC)OC

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Working concentration： mg/ml；

Method for preparing DMSO master liquid: ： mg drug pre-dissolved in μL DMSO (Master liquid concentration mg/mL， Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )

Method for preparing in vivo formulation：Take μL DMSO master liquid, next addμL PEG300， mix and clarify, next addμL Tween 80，mix and clarify, next add μL ddH₂O，mix and clarify.

Note：1.Please make sure the liquid is clear before adding the next solvent.
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Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration _(start) x Volume _(start) = Concentration _(final) x Volume _(final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

Serial Dilutions
Concertration (start):
Dilution-folds:

Computed Result

C1=C0/X	C1:	LOG(C1):
C2=C1/X	C2:	LOG(C2):
C3=C2/X	C3:	LOG(C3):
C4=C3/X	C4:	LOG(C4):
C5=C4/X	C5:	LOG(C5):
C6=C5/X	C6:	LOG(C6):
C7=C6/X	C7:	LOG(C7):
C8=C7/X	C8:	LOG(C8):

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2021-05-17)

NCT Number	Recruitment	interventions	Conditions	Sponsor/Collaborators	Start Date	Phases
NCT02824133	Completed	Drug: AZD4547	Recurrent IDHwt Gliomas With FGFR3-TACC3 Fusion\|Recurrent IDHwt Gliomas With FGFR1-TACC1 Fusion	Assistance Publique - Hôpitaux de Paris	September 2015	Phase 1\|Phase 2
NCT01824901	Completed	Drug: docetaxel\|Drug: AZD4547	Recurrent Non-small Cell Lung Cancer\|Squamous Cell Lung Cancer	ECOG-ACRIN Cancer Research Group\|National Cancer Institute (NCI)\|Eastern Cooperative Oncology Group	September 2013	Phase 1\|Phase 2
NCT01795768	Unknown status	Drug: AZD 4547	Gastric Cancer\|Oesophageal Cancer\|Breast Cancer\|Squamous Cell Carcinoma of the Lung	Royal Marsden NHS Foundation Trust\|AstraZeneca	September 2012	Phase 2
NCT01791985	Completed	Drug: AZD4547 / anastrozole or letrozole	Breast Cancer	Imperial College London\|Cancer Research UK\|AstraZeneca	July 2012	Phase 1\|Phase 2
NCT01213160	Completed	Drug: AZD4547	Cancer\|Advanced Solid Malignancies	AstraZeneca	November 2010	Phase 1

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

FGFR Signaling Pathway Map

FGFR Inhibitors with Unique Features

Selective FGFR Inhibitor

PD173074 : FGFR1-selective, IC50=~25 nM.
FDA-approved FGFR Inhibitor

Ponatinib (AP24534) : Approved by FDA for resistant or intolerant CML and Ph+ ALL.
Newest FGFR Inhibitor

SSR128129E ^New : Orally-active and allosteric FGFR1 inhibitor with IC50 of 1.9 μM, while not affecting other related RTKs.
Classic FGFR Inhibitor

Dovitinib (TKI-258, CHIR-258) : Multitargeted RTK inhibitor for class III (FLT3/c-Kit), class IV (FGFR1/3) and class V (VEGFR1-4) RTKs.

Related FGFR Products

CH5183284 (Debio-1347) ^New

CH5183284 (Debio-1347, FF284) is a selective and orally available FGFR inhibitor with IC50 of 9.3 nM, 7.6 nM, 22 nM, and 290 nM for FGFR1, FGFR2, FGFR3, and FGFR4, respectively. Phase 1.
BLU9931 ^New

BLU9931 is a potent, selective, and irreversible FGFR4 inhibitor with IC50 of 3 nM, about 297-, 184-, and 50-fold selectivity over FGFR1/2/3, respectively.
PX-478 2HCl ^New

PX-478 2HCl is an orally active, and selective hypoxia-inducible factor-1α (HIF-1α) inhibitor. PX-478 2HCl induces apoptosis and has anti-tumor activity. Phase 1.
PD173074

PD173074 is a potent FGFR1 inhibitor with IC50 of ~25 nM and also inhibits VEGFR2 with IC50 of 100-200 nM in cell-free assays, ~1000-fold selective for FGFR1 than PDGFR and c-Src. PD173074 reduces proliferation and promotes apoptosis in gastric cancer cells.
Infigratinib (BGJ398)

Infigratinib (BGJ398) is a potent and selective FGFR inhibitor for FGFR1/2/3 with IC50 of 0.9 nM/1.4 nM/1 nM in cell-free assays, >40-fold selective for FGFR versus FGFR4 and VEGFR2, and little activity to Abl, Fyn, Kit, Lck, Lyn and Yes. Phase 2.
SSR128129E

SSR128129E is an orally-active and allosteric FGFR1 inhibitor with IC50 of 1.9 μM, while not affecting other related RTKs.
LY2874455

LY2874455 is a pan-FGFR inhibitor with IC50 of 2.8 nM, 2.6 nM, 6.4 nM, and 6 nM for FGFR1, FGFR2, FGFR3, and FGFR4, respectively, and also inhibits VEGFR2 activity with IC50 of 7 nM. Phase 1.
Ibrutinib (PCI-32765)

Ibrutinib (PCI-32765) is a potent and highly selective Brutons tyrosine kinase (Btk) inhibitor with IC50 of 0.5 nM in cell-free assays, modestly potent to Bmx, CSK, FGR, BRK, HCK, less potent to EGFR, Yes, ErbB2, JAK3, etc. Ibrutinib is applicable as a Btk ligand in the synthesis of a series of PROTACs including P13I.
Dasatinib (BMS-354825)

Dasatinib (BMS-354825) is a novel, potent and multi-targeted inhibitor that targets Abl, Src and c-Kit, with IC50 of <1 nM, 0.8 nM and 79 nM in cell-free assays, respectively. Dasatinib induces autophagy and apoptosis with anti-tumor activity.
Saracatinib (AZD0530)

Saracatinib (AZD0530) is a potent Src inhibitor with IC50 of 2.7 nM in cell-free assays, and potent to c-Yes, Fyn, Lyn, Blk, Fgr and Lck; less active for Abl and EGFR (L858R and L861Q). Saracatinib induces autophagy. Phase 2/3.

Features:The 1st Src inhibitor to show inhibition of the Src pathway in human tumor tissue.

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AZD4547