PD173074

Licensed by Pfizer Catalog No.S1264

Molecular Weight(MW): 523.67

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.

Cited by 21 Publications

Science, 2011, 331(6019):912-6

PubMed: 21330545

Cancer Discov, 2013, 3(6):636-47

PubMed: 23558953

Gut, 2014, 63(12):1932-42

PubMed: 24658599

Blood, 2014, 123(10):1516-24

PubMed: 24408322

Hepatology, 2014, 59(4):1427-34

PubMed: 24122810

J Thorac Oncol, 2015, 10(12):1736-44

PubMed: 26473643

Cancer Res, 2016, 10.1158/0008-5472.CAN-16-0058

PubMed: 27231203

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

PubMed: 27098696

PLoS Genet, 2012, 8(2):e1002500

PubMed: 22383889

Mol Cell Proteomics, 2012, 11(9):745-57

PubMed: 22700489

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

PubMed: 25407459

Mol Cancer Res, 2013, 11(12):1585-96

PubMed: 24092775
J Cell Sci, 2014, 127(23):5079-92

PubMed:

Am J Physiol Endocrinol Metab, 2017, ajpendo.00328.2016

PubMed: 28174179

Breast Cancer Res Tr, 2014, 143(3):435-46

PubMed: 24398778

Clin Exp Metastasis, 2012, 30(4):507-20

PubMed: 23212305

Exp Cell Res, 2015, 332(2):223-35

PubMed: 25704758

Exp Cell Res, 2015, 332(2):223-35

PubMed:

PLoS One, 2014, 9(4):e95434

PubMed: 24752320

PLoS One, 2013, 8(2):e56735

PubMed: 23468877

Celon Pharma Inc, 2013, Paulina Grygielewicz

PubMed:

7 Customer Reviews

The inhibitor PD173074 (A) or PD184352 (B) was administered to one uterine horn of Hand2d/d mice on day 3 of pregnancy (n = 5). The other horn served as vehicle-treated control. Uterine horns were collected on the morning of day 4, and sections were subjected to IHC to detect p-FRS2, p-ERK1/2, and Ki-67. (C) IHC of pERa and Muc-1 in uterine sections of Hand2d/d mice treated with PD173074 or PD184352.

Science 2011 331(6019), 912-6. PD173074 purchased from Selleck.

Inhibition of FGFR signaling pathway by FGFR inhibitor PD173074 in mouse xenograft tumors. Bladder cancer SW780 cells were implanted in mice and treated with PD173074 after tumor formation as shown in B. Protein lysates of tumor tissues were prepared and immunoblotted with antibodies against phospho-ERK1/2, pan-ERK1/2, and γ-tubulin.

Cancer Discov 2013 3(6), 636-47. PD173074 purchased from Selleck.
FGFR inhibitors block signaling in FGFR2-fusion-expressing cells. Activation of FGFR2 and MAPK by FGFR2-AHCYL1 and its suppression by FGFR inhibitors. Lysates from NIH3T3 cells expressing FGFR2-AHCYL1 or EZR-ROS1 (control) treated with vehicle (DMSO), 0.2 and 1 uM BGJ398, and 0.2 and 1 uM PD173074 were immunoblotted with the relevant antibodies. β-Actin was used as a loading control.

Hepatology 2014 59(4) ,1427-34. PD173074 purchased from Selleck.

The level of p-FRS2 was examined in the uterine sections of Msx1f/fMsx2f/f (upper panel) and Msx1d/dMsx2d/d (lower panel) mice on day 4 of pregnancy by immunohistochemistry. Magnification: a and d: 10 x, b and e: 20 x, c and f: 40x. FGFR-specific inhibitor PD173074 was applied to one uterine horn of Msx1d/dMsx2d/d (n = 3) mice on day 3 of pregnancy. The other horn served as vehicle-treated control. Uterine horns were collected on day 4 morning and sections were subjected to immunohistochemistry to detect p-FRS2, Ki67, and Muc-1.

PLoS Genet 2012 8(2), e1002500. PD173074 purchased from Selleck.
Cells were incubated with DMSO control, 10 uM TGFBR inhibitor or 10 uM FGFR inhibitor PD173074 for 1 h. Cells were fixed, labeled with anti-GM130 (red) and analyzed by confocal microscopy. Images were analyzed using Image J (n = 3 experiments, >100 cells per condition). Scale bars, 10 uM.

J Cell Sci 2014 10.1242/jcs.159608. PD173074 purchased from Selleck.

Effects of antagonists for RAGE (FPS-ZM), TLR-4 (TAK-242) and FGFR1 (PD and BGJ) on the S100B-induced alterations in glucose metabolism in L6 cells treated for 6 h. (A) Effects of FPS-ZM, (B) TAK-242 and (C) PD and BGJ on the S100B inhibition of glucose consumption.

Am J Physiol Endocrinol Metab, 2017, 312(6):E471-E481. PD173074 purchased from Selleck.
Effect of select kinase inhibitors on DF508-CFTR maturation analyzed by immunoblotting. 293MSR-GT cells stably expressing DF508-CFTR were treated with 15 uM kinase inhibitors or 0.3% DMSO (vehicle control), as indicated, grown at 37 ℃ for 48 h, and the appearance of the mature protein, band C, monitored by immunoblotting with anti-CFTR antibodies. Band B represents the immature protein. DMSO represents vehicle- alone control, 27℃ represents temperature rescue of F508-CFTR at 27℃, 37℃ represents untreated DF508-CFTR control, and WT represents WT-CFTR. Top panels depict the anti-CFTR immunoblot and bottom panels depict actin (loading) control. ** represents cellular toxicity.

Biochem Bioph Res Co 2012 11(9), 745-57. PD173074 purchased from Selleck.

Purity & Quality Control

Choose Selective FGFR Inhibitors

Biological Activity

Description

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.

Targets

FGFR1 ^[1] (Cell-free assay)	VEGFR2 ^[1] (Cell-free assay)
~25 nM	100 nM-200 nM

In vitro

PD173074 is an ATP-competitive inhibitor of FGFR1 with K_i of ~40 nM. PD173074 is also an effective inhibitor of VEGFR2. Compared to FGFR1, PD173074 weakly inhibits the activities of Src, InsR, EGFR, PDGFR, MEK, and PKC with 1000-fold or greater IC50 values. PD173074 inhibits autophosphorylation of FGFR1 and VEGFR2 in a dose-dependent manner with IC50 of 1-5 nM and 100-200 nM, respectively. ^[1] PD173074 inhibits FGF-2 promotion of granule neuron survival in a dose-dependent manner with IC50 of 12 nM, exhibiting 1,000-fold greater potency than that of SU 5402. ^[2] PD173074 specifically inhibits FGF-2-mediated effects on proliferation, differentiation, and MAPK activation in oligodendrocyte (OL) lineage cells. ^[3] PD173074 is active against the WT receptor and FGFR3 mutations in multiple myeloma (MM) cell lines. PD173074 also potently inhibits autophosphorylation of FGFR3 in a dose-dependent manner with IC50 of ~5 nM. PD173074 treatment potently reduces viability of FGFR3-expressing KMS11 and KMS18 cells with IC50 of <20 nM. Inhibition of aFGF-stimulated MM cell growth by PD173074 is highly correlated with the expression of FGFR3. PD173074 treatment completely abolishes NIH 3T3 transformation mediated by Y373C FGFR3 but not by Ras V12, demonstrating that PD173074 specifically targets FGFR3-mediated cell transformation and lacks nonspecific cytotoxic effect. PD173074 also induces functional maturation of KMS11 and KMS18 cells. ^[4]

Cell Data

Cell Lines	Assay Type	Activity Description	PMID
NCI-H1581	M2HuOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MY\JR\|UxRTBwMEGyNlUh\|ryP	M1\obnNCVkeHUh?=
KG-1	NUH5c3NRT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHHIT2pKSzVyPUCuNFUyOjlizszN	MV\TRW5ITVJ?
MFM-223	NF;6PFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NE\VNI1KSzVyPUCuNlE2PzZizszN	MVTTRW5ITVJ?
EoL-1-cell	NULYfJZ3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1Ozd2lEPTB;MD6zNlk5PCEQvF2=	Ml2wV2FPT0WU
ECC10	MnW2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M1f4SmlEPTB;MD6zN\|g6QCEQvF2=	M1PkXHNCVkeHUh?=
H-EMC-SS	NXSxR21iT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlP2TWM2OD1yLkO0O\|E2KM7:TR?=	MkD5V2FPT0WU
AN3-CA	MlL5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M{\ucWlEPTB;MD60NFE{OyEQvF2=	NIO0[ndUSU6JRWK=
HuO-3N1	M4PW[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MmLRTWM2OD1yLkW0OlU{KM7:TR?=	NUPPbVlmW0GQR1XS
RT-112	MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M4PHTmlEPTB;MD61OFcxOSEQvF2=	MkLIV2FPT0WU
NEC8	MlvTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MnTFTWM2OD1yLkW2Nlg6KM7:TR?=	MYXTRW5ITVJ?
D-263MG	NVHMbFY1T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MX\JR\|UxRTBwN{GxOVkh\|ryP	MoXPV2FPT0WU
SW962	MnroS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Mk[2TWM2OD1yLke4PVg5KM7:TR?=	Mn7EV2FPT0WU
BV-173	NULtZ5RxT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MkKwTWM2OD1yLki0OlI{KM7:TR?=	M2XrV3NCVkeHUh?=
MFE-280	NUHxeGc6T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NWDmfo5VUUN3ME2wMlg2QDd{IN88US=>	MUHTRW5ITVJ?
HuH-7	MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NIm3UFNKSzVyPUGuNlQ1PjRizszN	NVjHXmhjW0GQR1XS
RS4-11	NVTFcZZNT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M2m4TGlEPTB;MT6zN\|g5PiEQvF2=	NH;4enJUSU6JRWK=
DMS-114	M3X2NWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M4LDRmlEPTB;MT6zOlc{PyEQvF2=	MXzTRW5ITVJ?
MSTO-211H	MkLmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MWPJR\|UxRTFwNEezO\|gh\|ryP	M2O5OHNCVkeHUh?=
DU-145	NILzN4FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NY\5[GNSUUN3ME2xMlU5OjF5IN88US=>	NUH0WmhLW0GQR1XS
A172	NFnKT4FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MV\JR\|UxRTFwN{CzOVUh\|ryP	M{HlNHNCVkeHUh?=
SBC-1	MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M4HVfmlEPTB;Mj6wPVQh\|ryP	NVzVcFk5W0GQR1XS
H9	M4\uZmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MV\JR\|UxRTJwMUSzNFYh\|ryP	M2rX[nNCVkeHUh?=
NCI-SNU-1	M1vsb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M4TjVmlEPTB;Mj6xPFM6PCEQvF2=	MoD5V2FPT0WU
NCI-H720	MkTnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NXi1R417UUN3ME2yMlIyOjh\|IN88US=>	M4HvR3NCVkeHUh?=
HCC2218	M{X5eGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M1XrSWlEPTB;Mj6zO\|k{QSEQvF2=	Mne0V2FPT0WU
G-401	MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWLJR\|UxRTJwNEexPFkh\|ryP	MUHTRW5ITVJ?
MPP-89	NYPvVVN5T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MojWTWM2OD1{LkS4N\|Y1KM7:TR?=	NHraVHFUSU6JRWK=
697	M4DPOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MmTKTWM2OD1{Lk[1N\|MyKM7:TR?=	MoD5V2FPT0WU
KARPAS-45	M{KyNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NYHJW2NYUUN3ME2yMlcxPzR5IN88US=>	MmfQV2FPT0WU
MG-63	NGK0fJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M2XaRmlEPTB;Mj65OFI3OiEQvF2=	NGnMSIVUSU6JRWK=
NTERA-S-cl-D1	NFvKd5FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M3;kbWlEPTB;Mz6wN\|Q4OiEQvF2=	M2\xWXNCVkeHUh?=
G-402	MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M1zyWGlEPTB;Mz6xNlczPyEQvF2=	M3LUZ3NCVkeHUh?=
NKM-1	NXe3[nJzT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M2HJT2lEPTB;Mz6xN\|U3PCEQvF2=	NGGxe5lUSU6JRWK=
RH-18	MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MlP4TWM2OD1\|LkG5OVk5KM7:TR?=	MUHTRW5ITVJ?
NCI-H1092	NUf1fW5UT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M13oRWlEPTB;Mz6xPVY6KM7:TR?=	MlfhV2FPT0WU
RPMI-8226	Moi1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Mn7OTWM2OD1\|LkKzOFQ4KM7:TR?=	NFjWPWhUSU6JRWK=
GAMG	Mlr6S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M2\wR2lEPTB;Mz60OlU4PiEQvF2=	MX7TRW5ITVJ?
HH	NFG4UIVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	Mk\ZTWM2OD1\|LkS3Olc3KM7:TR?=	NH;6[WNUSU6JRWK=
RO82-W-1	NX7hVWFDT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NFWzUJRKSzVyPUOuOFk5PTVizszN	NXvHdmU{W0GQR1XS
CCRF-CEM	NX\tZZZiT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	Ml3DTWM2OD1\|LkWwOFg5KM7:TR?=	MWnTRW5ITVJ?
NBsusSR	MnfaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M1vDfmlEPTB;Mz62N\|k3QSEQvF2=	M2q4T3NCVkeHUh?=
CHL-1	M2rKdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	Ml:2TWM2OD1\|Lk[1O\|k6KM7:TR?=	MlPDV2FPT0WU
LK-2	NVLDU\|Y6T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MoDnTWM2OD1\|Lk[3NVM{KM7:TR?=	M{nxb3NCVkeHUh?=
Hs-578-T	NYPzUphsT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M{XkTWlEPTB;Mz62O\|g4OyEQvF2=	MmfQV2FPT0WU
CTB-1	MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M4TjcWlEPTB;Mz64NFA2OSEQvF2=	MnezV2FPT0WU
ES5	MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NHPmSHRKSzVyPUOuPFM3OzdizszN	NIfFZ5ZUSU6JRWK=
A204	M3LJeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M3f4TWlEPTB;Mz65NlA4PSEQvF2=	MVHTRW5ITVJ?
SW780	NIWwOlNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MknVTWM2OD1\|LkmyNlQ2KM7:TR?=	M2fZUnNCVkeHUh?=
EW-3	NICxSHpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NVvEb4FPUUN3ME2zMlk5QTJ\|IN88US=>	MnLnV2FPT0WU
A704	NYntOI1iT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1zZb2lEPTB;ND6yPFczOyEQvF2=	Mn7KV2FPT0WU
LU-139	NEfLSVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M17vRWlEPTB;ND6zNVU{PCEQvF2=	MmC0V2FPT0WU
CAL-72	NGrUPGpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWLnTI05UUN3ME20MlQyPzR4IN88US=>	NV;odnRHW0GQR1XS
D-336MG	M1P2bWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NFu1ZVhKSzVyPUSuOFY5OTdizszN	NGXMU5BUSU6JRWK=
LAMA-84	NIjnfW5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MnTBTWM2OD12LkWzN\|Eh\|ryP	M3Kxb3NCVkeHUh?=
GI-ME-N	NHzVcolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MUnJR\|UxRTRwNUS4NUDPxE1?	MUfTRW5ITVJ?
KM-H2	NYPLO\|VxT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MVTJR\|UxRTRwNUWyNlIh\|ryP	NVnDTItxW0GQR1XS
NCI-H209	Mlq3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NX7CRlNYUUN3ME20MlU5Ojh\|IN88US=>	NVH6dGlOW0GQR1XS
IGROV-1	NVu3[G5ET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHzmfIJKSzVyPUSuPFcyPjhizszN	NIDaWW1USU6JRWK=
L-363	MmGxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M2r3b2lEPTB;ND65OlY3PSEQvF2=	MVXTRW5ITVJ?
SK-MEL-3	MljaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Mly0TWM2OD13LkK0NFYh\|ryP	NYL4O25WW0GQR1XS
HuO9	NV7YNXJXT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NFjnVIpKSzVyPUWuN\|g5PDNizszN	MnHOV2FPT0WU
NOS-1	MnXJS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Mn7xTWM2OD13LkeyPVI4KM7:TR?=	NWXaRYd7W0GQR1XS
NCI-H1770	MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NV\iWGpMUUN3ME21Mlk2ODN{IN88US=>	NETNNZVUSU6JRWK=
SF126	MmTXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NEO0OXNKSzVyPU[uNlE1ODZizszN	MV3TRW5ITVJ?
ML-2	MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NWXsXFJ{UUN3ME22MlI1QTd5IN88US=>	M4HJZ3NCVkeHUh?=
CHP-134	Mn\2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NYTPeZhIUUN3ME22MlI2OTh{IN88US=>	MkL1V2FPT0WU
NCI-H1355	MYHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M3HYVmlEPTB;Nj60NVc{OyEQvF2=	NV;HUmNYW0GQR1XS
TE-12	MWnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M2nIPWlEPTB;Nj63NlY4OSEQvF2=	MYLTRW5ITVJ?
A4-Fuk	M2fxb2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NHzqZWFKSzVyPU[uO\|MyPDJizszN	M2PPcXNCVkeHUh?=
MV-4-11	MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NFjWfW5KSzVyPU[uO\|Y3OjZizszN	M1HWPHNCVkeHUh?=
SK-UT-1	NIHmSohIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MkjxTWM2OD14LkmxO\|g1KM7:TR?=	NFP6fodUSU6JRWK=
J-RT3-T3-5	MmnZS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NX7zZYk5UUN3ME23MlA4PzZ2IN88US=>	MVrTRW5ITVJ?
ME-180	M2DIZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M1P2fWlEPTB;Nz6xNFQxPCEQvF2=	MX;TRW5ITVJ?
SK-MEL-28	NXy4VI1rT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlLHTWM2OD15LkO3PFE6KM7:TR?=	NWfvRoRjW0GQR1XS
HAL-01	M3Pnc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M3;uVWlEPTB;Nz60PFM1OSEQvF2=	M{TK[3NCVkeHUh?=
ES8	NV;TOIpvT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M2\Ne2lEPTB;Nz62PVYzPiEQvF2=	MnLGV2FPT0WU
DB	NV\DUIRET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MkjQTWM2OD16LkGxOVA1KM7:TR?=	M4[0W3NCVkeHUh?=
SK-NEP-1	MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NES3UG1KSzVyPUiuOFgyPDlizszN	NH\BRWRUSU6JRWK=
COR-L88	NFnOZlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M2juO2lEPTB;OD61NFk5OSEQvF2=	NVmyS4FHW0GQR1XS
LB1047-RCC	M2H2Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M{TkcWlEPTB;OD61NlIyOiEQvF2=	MmXhV2FPT0WU
NCI-H520	NV;4Z4dVT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M3jhPWlEPTB;OD62NlE2PyEQvF2=	NYOwR2syW0GQR1XS
SW954	M1HDU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NYXBRXNHUUN3ME24MlY6Pzh4IN88US=>	M{DZbHNCVkeHUh?=
TE-6	NEfQNWZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWHYOHVkUUN3ME24Mlc2OTR\|IN88US=>	MkLVV2FPT0WU
D-283MED	NVHvVZZET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M13YOmlEPTB;OT6wOlU{PCEQvF2=	NUDyTFM{W0GQR1XS
DBTRG-05MG	NYP3epNjT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlO3TWM2OD17LkC5OlA4KM7:TR?=	M2jFUXNCVkeHUh?=
NCI-H446	MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NVXXUIR3UUN3ME25MlI6PTJ4IN88US=>	NGPHN3VUSU6JRWK=
HOS	MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{\sO2lEPTB;OT6zOVE{PCEQvF2=	NU[xeHFkW0GQR1XS
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OVCAR-3	M1;6Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NXqyN2hYUUN3ME2zOk4zODR3IN88US=>	M3n0T3NCVkeHUh?=
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SCC-9	MmHoS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NV62coF3UUN3ME2zO{41ODJ5IN88US=>	NGD5XZVUSU6JRWK=
SF268	Mn7oS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NYH1TYYzUUN3ME2zPE4{PDN\|IN88US=>	NH;6ZYxUSU6JRWK=
HGC-27	NVPqeXdYT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MnTsTWM2OD1\|OD6zO\|EyKM7:TR?=	NF3lOJVUSU6JRWK=
DOHH-2	MmS0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NWizU41JUUN3ME2zPE44OTV6IN88US=>	NXTGd3lOW0GQR1XS
KE-37	NWTDVWY3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NF3De5pKSzVyPUO4Mlk5OjhizszN	NGeycoRUSU6JRWK=
MOLT-13	MoXXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MV7JR\|UxRTN7LkK1NFIh\|ryP	NWjCXoNFW0GQR1XS
ES1	Mn\BS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MWXJR\|UxRTN7LkO4OUDPxE1?	NV\uNGJjW0GQR1XS
SK-OV-3	MkT0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MoHjTWM2OD1\|OT65OlQ{KM7:TR?=	MonlV2FPT0WU
SNU-449	M4npbWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MYTJR\|UxRTRyLkC3OlQh\|ryP	MoTYV2FPT0WU
KYSE-510	NYrvOWdET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M17UbWlEPTB;NECuNVI6PSEQvF2=	NVyyUXRsW0GQR1XS
HL-60	M{DoTGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MnG2TWM2OD12MD65O\|g{KM7:TR?=	M3fsRXNCVkeHUh?=
DJM-1	M2jkdmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NFPuVFlKSzVyPUSwMlk4QTlizszN	MlfEV2FPT0WU
TGBC11TKB	NXi3bWtzT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1;HeWlEPTB;NEGuNFkzPiEQvF2=	M4DRR3NCVkeHUh?=
U-2-OS	M1mzNmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NYTEbGVpUUN3ME20Nk4zPjRzIN88US=>	NID3PIZUSU6JRWK=
NCI-H2030	NF64UFlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NGTyUFdKSzVyPUSyMlQ{PjhizszN	NYDZUpdJW0GQR1XS
LU-135	MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MUjJR\|UxRTR{LkW0OFch\|ryP	NVXS[o5wW0GQR1XS
ZR-75-30	MWDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NWX1ZVNmUUN3ME20N{4xPDl\|IN88US=>	M4rQZXNCVkeHUh?=
GT3TKB	NEPqSWVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M1W3PGlEPTB;NEOuNlY4QSEQvF2=	MX\TRW5ITVJ?
RPMI-2650	MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NULtXJJLUUN3ME20N{44QDF4IN88US=>	NFi1OppUSU6JRWK=
SAS	M3\RRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MYnJR\|UxRTR\|Lkm1N\|Qh\|ryP	M2LwcXNCVkeHUh?=
MDA-MB-231	MkfxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M4DmN2lEPTB;NEOuPVYxQSEQvF2=	NXvvelM2W0GQR1XS
JVM-3	M4T3Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M4XOe2lEPTB;NESuNFU{OyEQvF2=	NYPYXpFyW0GQR1XS
COLO-320-HSR	MorlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NUHLNGhYUUN3ME20OE42PjN\|IN88US=>	M{TsT3NCVkeHUh?=
SNB75	MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NXL5T5V[UUN3ME20OE43OTB3IN88US=>	NH:4TotUSU6JRWK=
NCI-H441	NUHwWGp6T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NU\UW5R5UUN3ME20OE46OzJ6IN88US=>	M2PjfXNCVkeHUh?=
HCT-116	NETw[FdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NVrib3dpUUN3ME20OE46QDZ6IN88US=>	MWDTRW5ITVJ?
NCI-H226	NFjnR5BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MlPLTWM2OD12NT62N\|Y5KM7:TR?=	NYOyZWptW0GQR1XS
CAL-33	NXP1WJlbT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NGnqOm9KSzVyPUS1MlkzOTdizszN	MmDrV2FPT0WU
NCI-H1437	MorqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MoTDTWM2OD12Nj6zNlEh\|ryP	MYTTRW5ITVJ?
HCC1187	M2PweWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MkDSTWM2OD12Nj60NlU2KM7:TR?=	Mn;SV2FPT0WU
NUGC-3	M{OxOWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGPqTIJKSzVyPUS2MlU4ODlizszN	NEDmN\|RUSU6JRWK=
T98G	M4jMXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NWr6b4VvUUN3ME20O{42PDdizszN	NEW4[pdUSU6JRWK=
OVCAR-8	Mn3mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M4rl[mlEPTB;NEeuOlg{KM7:TR?=	NEOyN2FUSU6JRWK=
LB2241-RCC	NH6yN29Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NGDVSldKSzVyPUS3MlczPyEQvF2=	MUPTRW5ITVJ?
NCI-H358	MXjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{\pfmlEPTB;NEiuNVE2OiEQvF2=	M2XVbHNCVkeHUh?=
PANC-08-13	M1\TOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MWjJR\|UxRTR6LkG4OVMh\|ryP	NFLlc3NUSU6JRWK=
KP-N-YN	NUixN5dOT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MXvJR\|UxRTR6LkKxNFIh\|ryP	Mk\LV2FPT0WU
NCI-H1755	NHfJWVhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NFzXWppKSzVyPUS4MlI4OjZizszN	NUf1[ZoyW0GQR1XS
NCI-N87	NXizSFl[T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MUHJR\|UxRTR6LkK5PVEh\|ryP	M4\VTXNCVkeHUh?=

... Click to View More Cell Line Experimental Data

In vivo

Administration of PD173074 at 1 mg/kg/day or 2 mg/ka/day in mice can effectively block angiogenesis induced by either FGF or VEGF in a dose-dependent manner with no apparent toxicity. ^[1] PD173074 inhibits in vivo growth of mutant FGFR3-transfected NIH 3T3 cells in nude mice. Inhibition of FGFR3 by PD173074 delays tumor growth and increases survival of mice in a KMS11 xenograft myeloma model. ^[4] In the H-510 xenograft, oral aministration of PD173074 blocks tumor growth similar to that seen with single-agent cisplatin administration, increasing median survival compared with control sham-treated animals. In H-69 xenografts, PD173074 induces complete responses lasting >6 months in 50% of mice. These effects are correlated with increased apoptosis in excised tumors, but not a consequence of disrupted tumor vasculature. ^[5]

Protocol

Kinase Assay:^[1]	+ Expand In vitro kinase inhibition assays: Assays using the full-length FGFR-1 kinase are performed in a total volume of 100 μL containing 25 mM HEPES buffer (pH 7.4), 150 mM NaCl, 10 mM MnCl₂, 0.2 mM sodium orthovanadate, 750 μg/mL concentration of a random copolymer of glutamic acid and tyrosine (4:1), various concentrations of PD173074 and 60 to 75 ng of enzyme. The reaction is initiated by the addition of [γ-³²P]ATP (5 μM ATP containing 0.4 μCi of [γ-³²P]ATP per incubation), and samples are incubated at 25°C for 10 minutes. The reaction is terminated by the addition of 30% trichloroacetic acid and the precipitation of material onto glass-fiber filter mats. Filters are washed three times with 15% trichloroacetic acid, and the incorporation of [³²P] into the glutamate tyrosine polymer substrate is determined by counting the radioactivity retained on the filters in a Wallac 1250 betaplate reader. Nonspecific activity is defined as radioactivity retained on the filters following incubation of samples without enzyme. Specific activity is determined as total activity (enzyme plus buffer) minus nonspecific activity. The concentration of PD173074 that inhibits FGFR-1 enzymatic activity by 50% (IC50) is determined graphically.
Cell Research:^[4]	+ Expand Cell lines: KMS11 and KMS18 Concentrations: Dissolved in DMSO, final concentrations ~100 nM Incubation Time: 48 hours Method: Cells are incubated with increasing concentrations of PD173074 in the presence of aFGF/heparin for 48 hours. The percentage of viable cells is determined by MTT. (Only for Reference)
Animal Research:^[1]	+ Expand Animal Models: Swiss Webster mice with induced corneal angiogenesis Formulation: Prepared in sterile fashion Dosages: ~2 mg/kg/day Administration: Administered intraperitoneally (Only for Reference)

References

+ Expand

Solubility (25°C)

In vitro	DMSO	100 mg/mL (190.95 mM)
	Ethanol	100 mg/mL (190.95 mM)
	Water	Insoluble
In vivo	Add solvents to the product individually and in order(Data is from Selleck tests instead of citations): 5% DMSO+corn oil For best results, use promptly after mixing.	15mg/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 PD173074 SDF

Molecular Weight	523.67
Formula	C₂₈H₄₁N₇O₃
CAS No.	219580-11-7
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	N/A

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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.

Frequently Asked Questions

Question 1:
What is the half-life of PD173074(S1264) in vivo?
Answer:
According to literature research, PD173074 is given twice daily because it has a short half-life in vivo, please refer to the following link for detailed pharmacokinetic information (Supplementary Figure 8B): http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3990281/#!po=50.0000.

FGFR Signaling Pathway Map

FGFR Inhibitors with Unique Features

Pan FGFR Inhibitor

BGJ398 (NVP-BGJ398) : FGFR1/2/3-selective, IC50=0.9 nM/1.4 nM/1 nM.
Most Potent FGFR Inhibitor

AZD4547 : FGFR1, IC50=0.2 nM; FGFR2, IC50=2.5 nM; FGFR3, IC50=1.8 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.

Related FGFR Products

CH5183284 (Debio-1347) ^New

CH5183284 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. Phase 1.
BGJ398 (NVP-BGJ398)

BGJ398 (NVP-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.
AZD4547

AZD4547 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.

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.
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.
Dasatinib

Dasatinib 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.
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). Phase 2/3.

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

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PD173074

Cited by 21 Publications

7 Customer Reviews

Purity & Quality Control

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Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download PD173074 SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

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

The Serial Dilution Calculator Equation

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Molecular Weight Calculator

Total Molecular Weight: g/mol

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

Molarity Calculator

Tech Support

Frequently Asked Questions

FGFR Signaling Pathway Map

FGFR Inhibitors with Unique Features

Related FGFR Products

Choose Your Country or Region

By Signaling Pathways

By product type

PD173074

Cited by 21 Publications

7 Customer Reviews

Purity & Quality Control

Choose Selective FGFR Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download PD173074 SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

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

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

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

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

Molarity Calculator

Tech Support

Frequently Asked Questions

FGFR Signaling Pathway Map

FGFR Inhibitors with Unique Features

Related FGFR Products

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