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 26 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

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

PubMed: 27535980

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

PubMed: 27231203

Cancer Res, 2016, 76(22):6471-6482

PubMed: 27671675

Biomaterials, 2016, 78:115-28

PubMed: 26691234

Stem Cell Reports, 2018, 10(4):1308-1323

PubMed: 29526737

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

PubMed: 27098696
PLoS Genet, 2012, 8(2):e1002500

PubMed: 22383889

Osteoarthritis Cartilage, 2018, 26(12):1733-1743

PubMed: 30201491

Mol Oncol, 2018, 10.1002/1878-0261.12422

PubMed: 30537101

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

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	Ml;mS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NFjXWXVKSzVyPUCuNFEzOjVizszN	M4DNSHNCVkeHUh?=
KG-1	NVj3b3V1T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NFLQVFNKSzVyPUCuNFUyOjlizszN	NG[1d4NUSU6JRWK=
MFM-223	MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NHHhNmxKSzVyPUCuNlE2PzZizszN	NV\MN4lwW0GQR1XS
EoL-1-cell	MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{nGV2lEPTB;MD6zNlk5PCEQvF2=	MV\TRW5ITVJ?
ECC10	NUn2bVlTT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M3PqSWlEPTB;MD6zN\|g6QCEQvF2=	MnTlV2FPT0WU
H-EMC-SS	NULoT4Q1T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MnHnTWM2OD1yLkO0O\|E2KM7:TR?=	NVTJUY5sW0GQR1XS
AN3-CA	M4DV[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MoX6TWM2OD1yLkSwNVM{KM7:TR?=	M3LLWXNCVkeHUh?=
HuO-3N1	MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NFfUSlZKSzVyPUCuOVQ3PTNizszN	M1XIc3NCVkeHUh?=
RT-112	NWTWNHNjT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1fnTGlEPTB;MD61OFcxOSEQvF2=	NV3hU4Z{W0GQR1XS
NEC8	NHm4RWhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M{TpfWlEPTB;MD61OlI5QSEQvF2=	NXfTU29NW0GQR1XS
D-263MG	NUC5SZo3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1jQbmlEPTB;MD63NVE2QSEQvF2=	NV7CN5hsW0GQR1XS
SW962	MnPGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NIHkdnlKSzVyPUCuO\|g6QDhizszN	MY\TRW5ITVJ?
BV-173	M4qzSmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NF\4cFdKSzVyPUCuPFQ3OjNizszN	NVP1dYdrW0GQR1XS
MFE-280	M{\v[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M{TpcGlEPTB;MD64OVg4OiEQvF2=	M3[xPHNCVkeHUh?=
HuH-7	NVzmPFFnT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NWjsSlYxUUN3ME2xMlI1PDZ2IN88US=>	NGjhPXdUSU6JRWK=
RS4-11	MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MlyyTWM2OD1zLkOzPFg3KM7:TR?=	MXjTRW5ITVJ?
DMS-114	MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M1jpN2lEPTB;MT6zOlc{PyEQvF2=	NYrQboI1W0GQR1XS
MSTO-211H	MnL0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MWHJR\|UxRTFwNEezO\|gh\|ryP	NYjE[2M5W0GQR1XS
DU-145	M2fqVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M1rST2lEPTB;MT61PFIyPyEQvF2=	M3j1eXNCVkeHUh?=
A172	MmPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NVTjfWJVUUN3ME2xMlcxOzV3IN88US=>	NYf1bJdIW0GQR1XS
SBC-1	MoHxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MXrJR\|UxRTJwMEm0JO69VQ>?	MX;TRW5ITVJ?
H9	MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVfJR\|UxRTJwMUSzNFYh\|ryP	Mo\2V2FPT0WU
NCI-SNU-1	NHHHb3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M3Hje2lEPTB;Mj6xPFM6PCEQvF2=	NHfSOm5USU6JRWK=
NCI-H720	NUH1TnZMT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NHL5V\|hKSzVyPUKuNlEzQDNizszN	NXLqU41PW0GQR1XS
HCC2218	M1r2PGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MYXJR\|UxRTJwM{e5N\|kh\|ryP	M3m4NHNCVkeHUh?=
G-401	MXfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M4jrbWlEPTB;Mj60O\|E5QSEQvF2=	MUHTRW5ITVJ?
MPP-89	NHq4dZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MWnJR\|UxRTJwNEizOlQh\|ryP	NITKSJlUSU6JRWK=
697	NHLIbIlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NIT3d2VKSzVyPUKuOlU{OzFizszN	Mme4V2FPT0WU
KARPAS-45	M4TVWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M4C5c2lEPTB;Mj63NFc1PyEQvF2=	NXnMZoVzW0GQR1XS
MG-63	Ml7sS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NFPIeFJKSzVyPUKuPVQzPjJizszN	NV3mTmJlW0GQR1XS
NTERA-S-cl-D1	NF36NZlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M4fFPWlEPTB;Mz6wN\|Q4OiEQvF2=	NFe5T4NUSU6JRWK=
G-402	NIixVHdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M{mxS2lEPTB;Mz6xNlczPyEQvF2=	NVf6OJZKW0GQR1XS
NKM-1	MmjnS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MW\JR\|UxRTNwMUO1OlQh\|ryP	MV;TRW5ITVJ?
RH-18	MkPmS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NUDWV\|JzUUN3ME2zMlE6PTl6IN88US=>	Mn3xV2FPT0WU
NCI-H1092	NV\5e5h1T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MoT6TWM2OD1\|LkG5Olkh\|ryP	MlfBV2FPT0WU
RPMI-8226	NXXqTHJDT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MojQTWM2OD1\|LkKzOFQ4KM7:TR?=	Mlj1V2FPT0WU
GAMG	NFS4OZpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NWXCWo9EUUN3ME2zMlQ3PTd4IN88US=>	M{S4SHNCVkeHUh?=
HH	Mn\ES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MoP4TWM2OD1\|LkS3Olc3KM7:TR?=	M2HUO3NCVkeHUh?=
RO82-W-1	MorvS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NWPVdpVuUUN3ME2zMlQ6QDV3IN88US=>	NV\aN49vW0GQR1XS
CCRF-CEM	MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NF:yd5FKSzVyPUOuOVA1QDhizszN	NEntNZBUSU6JRWK=
NBsusSR	MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{LRRWlEPTB;Mz62N\|k3QSEQvF2=	MorZV2FPT0WU
CHL-1	M4rXfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGWwVWdKSzVyPUOuOlU4QTlizszN	M2nPfnNCVkeHUh?=
LK-2	NYfZZnR3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M{n1XGlEPTB;Mz62O\|E{OyEQvF2=	M4HMcHNCVkeHUh?=
Hs-578-T	NYrscFdmT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MnqzTWM2OD1\|Lk[3PFc{KM7:TR?=	NVTvOHJsW0GQR1XS
CTB-1	MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{PoTWlEPTB;Mz64NFA2OSEQvF2=	NUL3eWlHW0GQR1XS
ES5	MYDHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MnT6TWM2OD1\|LkizOlM4KM7:TR?=	NELrOYNUSU6JRWK=
A204	NFrIUJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MVnJR\|UxRTNwOUKwO\|Uh\|ryP	NYe1XGZ5W0GQR1XS
SW780	NUPwSoxnT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MVfJR\|UxRTNwOUKyOFUh\|ryP	MUjTRW5ITVJ?
EW-3	NHnZR3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MV;JR\|UxRTNwOUi5NlMh\|ryP	Mn65V2FPT0WU
A704	M3u5Z2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGDoW2FKSzVyPUSuNlg4OjNizszN	M2rSOnNCVkeHUh?=
LU-139	NFnuW5BIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NI\i[mlKSzVyPUSuN\|E2OzRizszN	MYXTRW5ITVJ?
CAL-72	M16wfmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NY\XSGx{UUN3ME20MlQyPzR4IN88US=>	NWfXc2g2W0GQR1XS
D-336MG	NWLkZ2w5T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NYO5WJNPUUN3ME20MlQ3QDF5IN88US=>	M2XmZnNCVkeHUh?=
LAMA-84	M37EN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NVS3SWd4UUN3ME20MlU{OzFizszN	M1\jNXNCVkeHUh?=
GI-ME-N	MWHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MUnJR\|UxRTRwNUS4NUDPxE1?	MYjTRW5ITVJ?
KM-H2	NH75b3VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NXGwXY1rUUN3ME20MlU2OjJ{IN88US=>	NFKwfIdUSU6JRWK=
NCI-H209	M{nXeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MWHJR\|UxRTRwNUiyPFMh\|ryP	NIH0WZRUSU6JRWK=
IGROV-1	Mn65S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MkLVTWM2OD12Lki3NVY5KM7:TR?=	M1;qTHNCVkeHUh?=
L-363	NV30[4lPT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NIPu[3BKSzVyPUSuPVY3PjVizszN	M3HzS3NCVkeHUh?=
SK-MEL-3	NV\zVIRGT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MWHJR\|UxRTVwMkSwOkDPxE1?	NI\2OGlUSU6JRWK=
HuO9	M3;2Vmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MYTJR\|UxRTVwM{i4OFMh\|ryP	M{PNZnNCVkeHUh?=
NOS-1	M4TkNGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NX;rOoU{UUN3ME21MlczQTJ5IN88US=>	M1S3S3NCVkeHUh?=
NCI-H1770	NEW5O2VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M{nje2lEPTB;NT65OVA{OiEQvF2=	Ml;RV2FPT0WU
SF126	NV\p[nFlT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MlfuTWM2OD14LkKxOFA3KM7:TR?=	M{D6SnNCVkeHUh?=
ML-2	NF7MfItIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NUK3VYpvUUN3ME22MlI1QTd5IN88US=>	M3\UWHNCVkeHUh?=
CHP-134	MnTOS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MmfLTWM2OD14LkK1NVgzKM7:TR?=	MVHTRW5ITVJ?
NCI-H1355	NE\NOXVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MlOyTWM2OD14LkSxO\|M{KM7:TR?=	MnjVV2FPT0WU
TE-12	MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M{nkVWlEPTB;Nj63NlY4OSEQvF2=	M2\mXXNCVkeHUh?=
A4-Fuk	NVTDdmYxT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MmPiTWM2OD14LkezNVQzKM7:TR?=	MkH3V2FPT0WU
MV-4-11	MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	Mn;sTWM2OD14Lke2OlI3KM7:TR?=	NUj6TW8yW0GQR1XS
SK-UT-1	M3O0OGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MkHITWM2OD14LkmxO\|g1KM7:TR?=	M2\YbHNCVkeHUh?=
J-RT3-T3-5	MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M2rMOWlEPTB;Nz6wO\|c3PCEQvF2=	M1L3fHNCVkeHUh?=
ME-180	NU\RdGszT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MnPTTWM2OD15LkGwOFA1KM7:TR?=	MWLTRW5ITVJ?
SK-MEL-28	NFLBd21Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NFzpWHJKSzVyPUeuN\|c5OTlizszN	MUXTRW5ITVJ?
HAL-01	MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NVHOS3hQUUN3ME23MlQ5OzRzIN88US=>	NV;XXXNlW0GQR1XS
ES8	MoDsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	M2L0fGlEPTB;Nz62PVYzPiEQvF2=	NY\BZVlNW0GQR1XS
DB	MXzHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M13Uc2lEPTB;OD6xNVUxPCEQvF2=	M3GyenNCVkeHUh?=
SK-NEP-1	MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MlTxTWM2OD16LkS4NVQ6KM7:TR?=	NYPTTVliW0GQR1XS
COR-L88	M3TlVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NFX4UVBKSzVyPUiuOVA6QDFizszN	NGOyfYRUSU6JRWK=
LB1047-RCC	M{TWXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NI\qdXdKSzVyPUiuOVIzOTJizszN	MnLtV2FPT0WU
NCI-H520	NXjyfmY4T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M{\LRWlEPTB;OD62NlE2PyEQvF2=	Mm\RV2FPT0WU
SW954	NF7MOFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	M{m4V2lEPTB;OD62PVc5PiEQvF2=	MkXmV2FPT0WU
TE-6	M4\neWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NFTOUJFKSzVyPUiuO\|UyPDNizszN	MXzTRW5ITVJ?
D-283MED	MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVPJR\|UxRTlwME[1N\|Qh\|ryP	NY\5blJ1W0GQR1XS
DBTRG-05MG	NXv0Z5p3T3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MUXJR\|UxRTlwMEm2NFch\|ryP	MoC2V2FPT0WU
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MOLT-4	NGK3NWFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NEnaTHFKSzVyPUO2MlIzQTRizszN	MUjTRW5ITVJ?
CAPAN-1	MnvTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NUTVOnRDUUN3ME2zOk41Pjl7IN88US=>	M4fsUHNCVkeHUh?=
SCC-9	Mon3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NVi1N4dFUUN3ME2zO{41ODJ5IN88US=>	M2P0SHNCVkeHUh?=
SF268	M1XYW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NF;jWVdKSzVyPUO4MlM1OzNizszN	MkHzV2FPT0WU
HGC-27	MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NVHqOJBFUUN3ME2zPE4{PzFzIN88US=>	MV;TRW5ITVJ?
DOHH-2	M{GyOmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MVzJR\|UxRTN6LkexOVgh\|ryP	MknzV2FPT0WU
KE-37	MkL5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MX7JR\|UxRTN6Lkm4Nlgh\|ryP	MkS4V2FPT0WU
MOLT-13	NGTl[JBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MV3JR\|UxRTN7LkK1NFIh\|ryP	M{LvVnNCVkeHUh?=
ES1	MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M2PEeGlEPTB;M{muN\|g2KM7:TR?=	M3rmd3NCVkeHUh?=
SK-OV-3	NXXqZW1XT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	Ml65TWM2OD1\|OT65OlQ{KM7:TR?=	NIGzUFNUSU6JRWK=
SNU-449	NHS3ZWtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MUPJR\|UxRTRyLkC3OlQh\|ryP	M1PiSXNCVkeHUh?=
KYSE-510	M3jN[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	M2XmXGlEPTB;NECuNVI6PSEQvF2=	NFHO[YxUSU6JRWK=
HL-60	MkjUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NXixU\|NTUUN3ME20NE46Pzh\|IN88US=>	MonkV2FPT0WU
DJM-1	MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	M2PncWlEPTB;NECuPVc6QSEQvF2=	MmTIV2FPT0WU
TGBC11TKB	MkPpS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NIXrN\|ZKSzVyPUSxMlA6OjZizszN	NV;TPZB5W0GQR1XS
U-2-OS	NGHYV\|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MXfJR\|UxRTR{LkK2OFEh\|ryP	M3LEbXNCVkeHUh?=
NCI-H2030	NGD2SGRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MXjJR\|UxRTR{LkSzOlgh\|ryP	MWLTRW5ITVJ?
LU-135	M4TxPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MoPITWM2OD12Mj61OFQ4KM7:TR?=	NE\pVVFUSU6JRWK=
ZR-75-30	NIDI[pVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NIThbYFKSzVyPUSzMlA1QTNizszN	MULTRW5ITVJ?
GT3TKB	M3vX[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	NGH1OIlKSzVyPUSzMlI3PzlizszN	MVXTRW5ITVJ?
RPMI-2650	MkP5S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	MkTVTWM2OD12Mz63PFE3KM7:TR?=	MknQV2FPT0WU
SAS	MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MonzTWM2OD12Mz65OVM1KM7:TR?=	MVTTRW5ITVJ?
MDA-MB-231	NU\HWnFET3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NWG3XWJYUUN3ME20N{46PjB7IN88US=>	NXX1Z4drW0GQR1XS
JVM-3	MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MWPJR\|UxRTR2LkC1N\|Mh\|ryP	MXvTRW5ITVJ?
COLO-320-HSR	MXLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MljSTWM2OD12ND61OlM{KM7:TR?=	MV7TRW5ITVJ?
SNB75	NXHVU\|dNT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MX;JR\|UxRTR2Lk[xNFUh\|ryP	NVjZPFZUW0GQR1XS
NCI-H441	NHjTe4lIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NFK3b4VKSzVyPUS0Mlk{OjhizszN	MVLTRW5ITVJ?
HCT-116	MX3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVXJR\|UxRTR2Lkm4Olgh\|ryP	Ml\xV2FPT0WU
NCI-H226	MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	Mo[1TWM2OD12NT62N\|Y5KM7:TR?=	MorpV2FPT0WU
CAL-33	MoLGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	NVHudYloUUN3ME20OU46OjF5IN88US=>	NVS1bXY{W0GQR1XS
NCI-H1437	MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MVnJR\|UxRTR4LkOyNUDPxE1?	M1XMUHNCVkeHUh?=
HCC1187	NVi3[YZVT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	M1HoWGlEPTB;NE[uOFI2PSEQvF2=	NXzrSJN{W0GQR1XS
NUGC-3	NIn5fo1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	NGXNRY1KSzVyPUS2MlU4ODlizszN	MV;TRW5ITVJ?
T98G	M2HLTmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MWjJR\|UxRTR5LkW0O{DPxE1?	NUjPZYIxW0GQR1XS
OVCAR-8	NEPXc4dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?=	MnvqTWM2OD12Nz62PFMh\|ryP	Mm[zV2FPT0WU
LB2241-RCC	MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	NVO5UoZuUUN3ME20O{44OjdizszN	M3rsVHNCVkeHUh?=
NCI-H358	NUPieJZtT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	MmLiTWM2OD12OD6xNVUzKM7:TR?=	NFzyVJFUSU6JRWK=
PANC-08-13	NX\2WHRrT3Kxd4ToJGlvcGmkaYTpc44hSXO\|YYm=	NYTqU2w1UUN3ME20PE4yQDV\|IN88US=>	NIi5PVJUSU6JRWK=
KP-N-YN	MmS4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl?	Mlz3TWM2OD12OD6yNVAzKM7:TR?=	NGXZbotUSU6JRWK=
NCI-H1755	MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>?	MYDJR\|UxRTR6LkK3NlYh\|ryP	MXXTRW5ITVJ?
NCI-N87	M3fv[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7	MnntTWM2OD12OD6yPVkyKM7:TR?=	M4TyfnNCVkeHUh?=

... 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

Bio Calculators

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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 Products4

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 26 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

Serial Dilutions

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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 Products4

Choose Your Country or Region

By Signaling Pathways

By product type

PD173074

Cited by 26 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 Products4

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