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Crizotinib (PF-02341066) Licensed by Pfizer

PF-2341066 (Crizotinib) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nnM, respectivley.

Catalog No.S1068

8 Reviews 20 Product Citations

: Tel: +1-832-582-8158[email protected]

Crizotinib (PF-02341066) Chemical Structure
Molecular Weight: 450.34

Validation & Quality Control

Customer Reviews(8) in vivo invitation

Quality Control & MSDS

Related Compound Libraries

Crizotinib (PF-02341066) is available in the following compound libraries:

Cambridge Cancer Compound Library(96-well) Chemical Library (96-well) Inhibitor Library (96-well) Kinase Inhibitor Library (96-well) Pfizer Licensed Library Stem Cell Small Molecule Compound Library (96-well) Tyrosine Kinase Inhibitor Library (96-Well)

Product Information

Combination Therapy

Compare c-Met Inhibitors

Research Area
Research Area
Crizotinib (PF-02341066) Mechanism
Crizotinib (PF-02341066) Mechanism
c-Met is an α–β heterodimer with an extracellular α-chain disulfide linked to the membrane-spanning β-chain (1,390 residues) harboring the intracellular tyrosine kinase domain. On activation, Tyr1349 and Tyr1356 become auto-phosphorylated and serve as docking sites for a wide spectrum of transducers and adaptors. ^[1]
The co-crystal structure of PF-2341066 bound to the non-phosphorylated state of the c-MET kinase domain shows the compound binds to an auto-inhibitory kinase conformation in which a portion of the kinase activation loop makes direct interactions with the inhibitor. The potency of PF-2341066 in cells results from key interactions between the α-methylbenzyloxy unit and the unique c-MET A-loop conformation. The halogenated phenyl group of PF-2341066 takes a direct and favorable path to form a π–π interaction with Tyr1230, also achieving better distances and aligned geometry between the aryl groups for stacking. Another consequence of the more compact linker of PF-2341066 is noted when comparing co-crystal structures. The plane of the novel 2-aminopyridine core in PF-2341066 binds to the hinge in a position which is noted earlier to be tilted at approximately a 15° angle. Met-1211 has closer interactions with the phenyl group and 2-aminopyridine core via hydrophobic interactions. Both the 2-chloro and 3-fluoro elements on the 3-benzyloxy group in PF-2341066 point toward the N–H of Asp1222, indicating that there may be beneficial electrostatic interactions. According to the SAR, the α-methyl and 2,6-dichloro moieties on the 3-benzyloxy group in PF-2341066 are critical for establishing the low nanomolar cell potency against c-MET. The α-methyl group not only rigidifies the benzyl group but also makes favorable hydrophobic interactions in the pocket surrounded by side chains of residues Val1092, Leu1157, Lys1110, and Ala1108. The R-configuration of the α-methyl group provides the right fit in this lipophilic pocket. On the other side, the 5-pyrazol-4-yl group is bound through the narrow lipophilic tunnel surrounded by Ile1084 and Tyr1159. The terminal piperidine ring, attached to the N1 position of the pyrazol-4-yl, reaches out into the solvent. ^[1]
References
[1] Schiering N, et al. Proc Natl Acad Sci U S A. 2003, 100(22), 12654-12659.
[2] Padrique E, et al. J Med Chem. 2011, 54(18), 6342-6363.
Dr. Antonino Maria Sparta demonstrates a breakthrough in leukemia research by utilizing two inhibitors produced by Selleck Chemicals.

Cat.No.	Product Name	Solubility (25°C)
S1068	Crizotinib (PF-02341066)	<1 mg/mL	20 mg/mL	<1 mg/mL
S1119	XL-184 free base (Cabozantinib)	<1 mg/mL	100 mg/mL	<1 mg/mL
S1111	Foretinib (GSK1363089, XL880)	<1 mg/mL	127 mg/mL	<1 mg/mL
S1070	PHA-665752	<1 mg/mL	128 mg/mL	<1 mg/mL
S1080	SU11274	<1 mg/mL	92 mg/mL	2 mg/mL
S1094	PF-04217903	<1 mg/mL	5 mg/mL	<1 mg/mL
S1112	SGX-523	<1 mg/mL	2 mg/mL	<1 mg/mL
S1561	BMS 777607	<1 mg/mL	47 mg/mL	<1 mg/mL
S2753	ARQ 197 (Tivantinib)	<1 mg/mL	74 mg/mL	40 mg/mL
S1114	JNJ-38877605	<1 mg/mL	37 mg/mL	<1 mg/mL
S2788	INCB28060	<1 mg/mL	2 mg/mL	<1 mg/mL
S1361	MGCD-265	<1 mg/mL	104 mg/mL	<1 mg/mL
S2774	MK-2461	<1 mg/mL	99 mg/mL	<1 mg/mL
S1316	AMG-208	<1 mg/mL	0.25 mg/mL	<1 mg/mL
S2859	Golvatinib (E7050)	<1 mg/mL	20 mg/mL	<1 mg/mL
S2747	AMG458	<1 mg/mL	21 mg/mL	<1 mg/mL
S2201	BMS 794833	<1 mg/mL	94 mg/mL	<1 mg/mL
S2761	NVP-BVU972	<1 mg/mL	68 mg/mL	68 mg/mL

Product Description

Biological Activity Protocol Chemical Information Customer Reviews Product Citations Tech Support & FAQs

Biological Activity

Description	PF-2341066 (Crizotinib) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nnM, respectivley.
Targets	c-Met	ALK
IC50	11 nM	24 nM ^[1]
In vitro	PF-2341066 displays similar potency against c-Met phosphorylation in mIMCD3 mouse or MDCK canine epithelial cells with IC50 of 5 nM and 20 nM, respectivly. PF-2341066 shows improved or similar activity against NIH3T3 cells engineered to express c-Met ATP-binding site mutants V1092I or H1094R or the P-loop mutant M1250T with IC50 of 19 nM, 2 nM and 15 nM, respectively, compared with NIH3T3 cells expressing wild-type receptor with IC50 of 13 nM. In contrast, a marked shift in potency of PF-2341066 is observed against cells engineered to express c-Met activation loop mutants Y1230C and Y1235D with IC50 of 127 nM and 92 nM, respectively, compared with wild-type receptor. PF-2341066 also potently prevents the phosphorylation of c-Met in NCI-H69 and HOP92 cells, with IC50 of 13 nM and 16 nM, respectively, which express the endogenous c-Met variants R988C and T1010I, respectively. PF-2341066 is >1,000-fold selective for the VEGFR2 and PDGFRβ RTKs, >250-fold selective for IRK and Lck, and ∼40- to 60-fold selective for Tie2, TrkA, and TrkB, all compared with c-Met. PF-2341066 is 20- to 30-fold selective for RON and Axl RTKs. In contrast, PF-2341066 shows a near-equivalent IC50 of 24 nM against the nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK) oncogenic fusion variant of the ALK RTK expressed by the KARPAS299 human anaplastic large cell lymphoma (ALCL) cell line. PF-2341066 inhibits c-Met–dependent neoplastic phenotypes of cancer cells and angiogenic phenotypes of endothelial cells. PF-2341066 suppresses human GTL-16 gastric carcinoma cell growth with IC50 of 9.7 nM. PF-2341066 induces apoptosis in GTL-16 cells with IC50 of 8.4 nM. PF-2341066 inhibits HGF-stimulated human NCI-H441 lung carcinoma cell migration and invasion with IC50 of 11 nM and 6.1 nM, respectively. PF-2341066 inhibits MDCK cell scattering with IC50 of 16 nM. PF-2341066 prevents HGF-stimulated c-Met phosphorylation, cell survival, and Matrigel invasion with IC50 of 11 nM, 14 nM and 35 nM, respectively. In addition, PF-2341066 prevents serum-stimulated HMVEC branching tubulogenesis (formation of vascular tubes) in fibrin gels. ^[1] PF-2341066 also potently inhibits NPM-ALK phosphorylation in Karpas299 or SU-DHL-1 ALCL cells with an IC50 of 24 nM. PF-2341066 potently prevents cell proliferation, which is associated with G(1)-S-phase cell cycle arrest and induction of apoptosis in ALK-positive ALCL cells with IC50 of 30 nM, but not ALK-negative lymphoma cells. ^[2] Besides, PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth (i.e., proliferation and survival) as well as metastasis (eg, invasion and clonogenicity). ^[3]
In vivo	In the GTL-16 model, PF-2341066 reveals the ability to cause marked regression of large established tumors (>600 mm³) in both the 50 mg/kg/day and 75 mg/kg/day treatment cohorts, with a 60% decrease in mean tumor volume over the 43-day administration schedule. In an another study, PF-2341066 displays the ability to completely inhibits GTL-16 tumor growth for >3 months, with only 1 of 12 mice exhibiting a significant increase in tumor growth over the 3-month treatment schedule at 50 mg/kg/day. In the NCI-H441 NSCLC model, a 43% decrease in mean tumor volume is observed at 50 mg/kg/day during the 38-day PF-2341066 administration cycle. In the Caki-1 RCC model, a 53% decrease in mean tumor volume is observed to be associated with decreased volume of each tumor by at least 30% at 50 mg/kg/day during the 33-day PF-2341066 administration cycle. PF-2341066 also reveals near-complete prevention of the growth of established tumors at 50 mg/kg/day in the U87MG glioblastoma or PC-3 prostate carcinoma xenograft models, with 97% or 84% inhibition on the final study day, respectively. In contrast, PF-2341066 p.o. given at 50 mg/kg/day does not significantly inhibit tumor growth in the MDA-MB-231 breast carcinoma model, or the DLD-1 colon carcinoma model. A significant dose-dependent reduction of CD31–positive endothelial cells is observed at 12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day in GTL-16 tumors, indicating that inhibition of MVD shows a dose-dependent correlation to antitumor efficacy. PF-2341066 displays a significant dose-dependent reduction of human VEGFA and IL-8 plasma levels in both the GTL-16 and U87MG models. Marked inhibition of phosphorylated c-Met, Akt, Erk, PLCλ1, and STAT5 levels is observed in GTL-16 tumors following p.o. administration of PF-2341066.^[1] P.o. administration of PF-2341066 to severe combined immunodeficient-Beige mice bearing Karpas299 ALCL tumor xenografts leads to dose-dependent antitumor efficacy with complete regression of all tumors at the 100 mg/kg/d dose within 15 days of initial compound administration. In addition, inhibition of key NPM-ALK signaling mediators, including phospholipase C-gamma, signal transducers and activators of transcription 3, extracellular signal-regulated kinases, and Akt by PF-2341066 are observed at concentrations or dose levels, which correlated with inhibition of NPM-ALK phosphorylation and function.^[2] PF-2341066 prevents osteosarcoma behavior associated with primary tumor growth (eg, proliferation and survival) as well as metastasis (eg, invasion and clonogenicity). In nude mice treated with PF-2341066 via oral gavage, the growth and associated osteolysis and extracortical bone matrix formation of osteosarcoma xenografts are prevented by PF-2341066.^[3] Treatment of c-MET-amplified GTL-16 xenografts with 50 mg/kg PF-2341066 elicits tumor regression that is associated with a slow reduction in ¹⁸F-FDG uptake and decreases expression of the glucose transporter 1, GLUT-1.^[4]
Clinical Trials	PF-2341066 is currently in a Phase III clinical trial in the treatment of non squamous lung cancer.
Features

Protocol(Only for Reference)

Kinase Assay: ^[1]

Cellular kinase phosphorylation ELISA assays	Cells are seeded in 96-well plates in media supplemented with 10% fetal bovine serum (FBS) and transferred to serum-free media [with 0.04% bovine serum albumin (BSA)] after 24 h. In experiments investigating ligand-dependent RTK phosphorylation, corresponding growth factors are added for up to 20 min. After incubation of cells with PF-2341066 for 1 h and/or appropriate ligands for the designated times, cells are washed once with HBSS supplemented with 1 mM Na₃VO₄, and protein lysates are generated from cells. Subsequently, phosphorylation of selected protein kinases is assessed by a sandwich ELISA method using specific capture antibodies used to coat 96-well plates and a detection antibody specific for phosphorylated tyrosine residues. Antibody-coated plates are (a) incubated in the presence of protein lysates at 4°C overnight; (b) washed seven times in 1% Tween 20 in PBS; (c) incubated in a horseradish peroxidase–conjugated anti–total-phosphotyrosine (PY-20) antibody (1:500) for 30 min; (d) washed seven times again; (e) incubated in 3,3′,5,5′-tetramethyl benzidine peroxidase substrate to initiate a colorimetric reaction that is stopped by adding 0.09 N H₂SO₄; and (f) measured for absorbance in 450 nm using a spectrophotometer.

Cellular kinase phosphorylation ELISA assays

Cells are seeded in 96-well plates in media supplemented with 10% fetal bovine serum (FBS) and transferred to serum-free media [with 0.04% bovine serum albumin (BSA)] after 24 h. In experiments investigating ligand-dependent RTK phosphorylation, corresponding growth factors are added for up to 20 min. After incubation of cells with PF-2341066 for 1 h and/or appropriate ligands for the designated times, cells are washed once with HBSS supplemented with 1 mM Na₃VO₄, and protein lysates are generated from cells. Subsequently, phosphorylation of selected protein kinases is assessed by a sandwich ELISA method using specific capture antibodies used to coat 96-well plates and a detection antibody specific for phosphorylated tyrosine residues. Antibody-coated plates are (a) incubated in the presence of protein lysates at 4°C overnight; (b) washed seven times in 1% Tween 20 in PBS; (c) incubated in a horseradish peroxidase–conjugated anti–total-phosphotyrosine (PY-20) antibody (1:500) for 30 min; (d) washed seven times again; (e) incubated in 3,3′,5,5′-tetramethyl benzidine peroxidase substrate to initiate a colorimetric reaction that is stopped by adding 0.09 N H₂SO₄; and (f) measured for absorbance in 450 nm using a spectrophotometer.

Cell Assay: ^[1]

Cell lines	GTL-16 gastric carcinoma cells and T47D breast carcinoma cells
Concentrations	0-256 nM
Incubation Time	1 hour
Method	Cells including GTL-16 gastric carcinoma cells and T47D breast carcinoma cells are seeded in 96-well plates in media supplemented with 10% fetal bovine serum (FBS) and transferred to serum-free media [with 0.04% bovine serum albumin (BSA)] after 24 hours. In experiments investigating ligand-dependent RTK phosphorylation, corresponding growth factors are added for up to 20 minutes. After incubation of cells with PF-2341066 for 1 hour and/or appropriate ligands for the designated times, cells are washed once with HBSS supplemented with 1 mM Na₃VO₄, and protein lysates are generated from cells. Subsequently, phosphorylation of selected protein kinases is assessed by a sandwich ELISA method using specific capture antibodies used to coat 96-well plates and a detection antibody specific for phosphorylated tyrosine residues. Antibody-coated plates are (a) incubated in the presence of protein lysates at 4 °C overnight; (b) washed seven times in 1% Tween 20 in PBS; (c) incubated in a horseradish peroxidase–conjugated anti–total-phosphotyrosine (PY-20) antibody (1:500) for 30 min; (d) washed seven times again; (e) incubated in 3,3^′,5,5^′-tetramethyl benzidine peroxidase substrate to initiate a colorimetric reaction that is stopped by adding 0.09 N H₂SO₄; and (f) measured for absorbance in 450 nm using a spectrophotometer.

Animal Study: ^[1]

Animal Models	Female or male nu/nu mice bearing NCI-H441,or DLD-1, or MDA-MB-231
Formulation
Dosages	12.5 mg/kg/day, 25 mg/kg/day, and 50 mg/kg/day
Administration	Administered via p.o.

References

Chemical Information

Download Crizotinib (PF-02341066) SDF

Molecular Weight (MW)	450.34
Formula	C₂₁H₂₂Cl₂FN₅O
CAS No.	877399-52-5, 877399-53-6 (acetate)
Synonyms	N/A

Solubility (25°C) DMSO 20 mg/mL Water <1 mg/mL Ethanol <1 mg/mL
Storage	2 years -20°CPowder
	2 weeks4°Cin DMSO
	6 months-80°Cin DMSO

Chemical Name	3-((R)-1-(2,6-dichloro-3-fluorophenyl)ethoxy)-5-(1-(piperidin-4-yl)-1H-pyrazol-4-yl)pyridin-2-amine

Molarity Calculator Dilution Calculator Molecular Weight Calculator

Research Area

Customer Reviews (8)

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Rating

Source

Cancer Cell , 2011, 19, 679–690. Crizotinib (PF-02341066) purchased from Selleck

Method

Immunoblot analysis, Tumor growth inhibition Assay

Cell Lines

xenograft models

Concentrations

100 mg/kg

Incubation Time

8 days

Results

We showed that administration of CH5424802 led to signiﬁcant tumor regression against both native EML4-ALK- and L1196M-driven tumors. On the other hand, PF-02341066 (100 mg/kg) resulted in no signiﬁcant tumor growth inhibition against L1196M-driven tumors. Furthermore, we conﬁrmed that phospho-STAT3, one of the downstream targets of ALK, was abolished in both tumors that were treated with CH5424802.

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Rating

Source

Nat Med , 2011, 17, 1116-1120. Crizotinib (PF-02341066) purchased from Selleck

Method

Western blot

Cell Lines

RCT-E565 transplanted tumors

Concentrations

25 mg/kg/d, 50 mg/kg/d

Incubation Time

0-21 d

Results

We then treated mice bearing RCT-E565 tumor transplants with PF02341066, a c-Met inhibitor currently in clinical development. PF02341066 abrogated both p-Akt and p-S6RP signals as well as tumor growth.

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Rating

Source

Int J Proteomics , 2011, 2011, Article ID 215496. Crizotinib (PF-02341066) purchased from Selleck

Method

CEER assay

Cell Lines

H1993 cell line

Concentrations

0-10 μM

Incubation Time

4 h

Results

In the c-MET ampliﬁed cell line H1993, activation of this pathway was blocked by the treatment with PF-2341066, a c-MET kinase inhibitor.

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Rating

Source

Int J Proteomics , 2011, 2011, Article ID 215496. Crizotinib (PF-02341066) purchased from Selleck

Method

Nikon inverted-phase microscope

Cell Lines

lung tumor cell lines

Concentrations

0.1/1 µM

Incubation Time

two weeks

Results

Large colony formation of H1993 cells, whose proliferation in tissue culture was potently blocked by treatment with the c-MET kinase inhibitor PF-2341066, was also inhibited by treatment with the same inhibitor.

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Rating

Source

Dr. Zhang of Tianjin Medical University. Crizotinib (PF-02341066) purchased from Selleck

Method

Western blot

Cell Lines

MDA-MB-231 cell line

Concentrations

0-100 nM

Incubation Time

Results

Click to enlarge

Rating

Source

Cancer Cell , 2011, 19, 679–690. Crizotinib (PF-02341066) purchased from Selleck

Method

Cell Growth Inhibition Assay

Cell Lines

Ba/F3 cells

Concentrations

Incubation Time

48 h

Results

The sensitivities of L1196M-driven Ba/F3 cell clones to PF-02341066 were lower, closely resembling that of the Ba/F3 parental cells. The therapeutic indexes of CH5424802 and PF-02341066, the IC50 ratio of EML4-ALK L1196M-driven cell clones to the parental cells, were 7- to 12-fold and 1- to 2-fold.

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Rating

Source

J Biomol Screen , 2011, 16, 141-154. Crizotinib (PF-02341066) purchased from Selleck

Method

VimPro-Fluc-MDA-MB-231 spheroid viability, Western blot

Cell Lines

MDA-MB-231 spheroids

Concentrations

Incubation Time

Results

When Vimpro-Fluc downregulation reaches ≥70%, then downregulation of vimentin protein expression is more pronounced. of the modulators tested—U0126, dasatinib,axitinib, and pF2341066-all downregulated Vimpro-Fluc activity by ≥70%, which correlated with a significant down-reglation of vimentin protein expression. Finally, dose-response curves were generated with both U0126 (iC50 = 2.5 µM) and axitinib (iC50 = 0.25 µM), demonstrating that these small molecules modulate Vimpro-Fluc activity in a dose-dependent manner, indicating that their respective target(s) and signaling pathways play a significant role in maintaining vimentin expression and possibly mesenchymal homeostasis (Fig. B)

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Rating

Source

J Biomol Screen , 2011, 16, 141-154. Crizotinib (PF-02341066) purchased from Selleck

Method

Secondary assay

Cell Lines

MDA-MB-231 spheroids

Concentrations

10 µM

Incubation Time

Results

U0126, pF2341066, axitinib, and pKC412 caused significant inhibition of the invasive potential of Mda-Mb-231 spheroids. Conversely, dasatinib, a potent inhibitor of vimentin gene expression, did not significantly alter the invasive potential of Mda-Mb-231 spheroids.

Product Citations (20)

Widespread potential for growth-factor-driven resistance to anticancer kinase inhibitors. [Wilson TR, et al. Nature 2012;487(7408):505-9]
PubMed: 22763448
MED12 controls the response to multiple cancer drugs through regulation of TGF-β receptor signaling. [Huang S, et al. Cell 2012;151(5):937-50]
PubMed: 23178117
CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. [Sakamoto H, et al. Cancer Cell 2011;19(5), 679-690]
PubMed: 21575866

Oncogenic PIK3CA-driven mammary tumors frequently recur via PI3K pathway–dependent and PI3K pathway–independent mechanisms. [Liu P, et al. Nat Med 2011;17(9), 1116-1120]
PubMed: 21822287
Melanoma exosomes educate bone marrow progenitor cells toward a pro-metastatic phenotype through MET. [Peinado H, et al. Nat Med 2012;18(6):883-91]
PubMed: 22635005
A drug resistance screen using a selective MET inhibitor reveals a spectrum of mutations that partially overlap with activating mutations found in cancer patients. [Tiedt R, et al. Cancer Res 2011;71(15), 5255-5264]
PubMed: 21697284
ALK+ anaplastic large cell lymphoma exhibits phosphatidylinositol-3 kinase/Akt activity with retained but inactivated PTEN--a report from the Children's Oncology Group. [Heuckmann JM, et al. Clin Cancer Res 2011;17(23):7394-401]
PubMed: 21948233
Colloidal Aggregation Affects the Efficacy of Anticancer Drugs in Cell Culture. [Owen SC, et al. ACS Chem Biol 2012;7(8):1429-35]
PubMed: 22625864
Identification of basophils as a major source of hepatocyte growth factor in chronic myeloid leukemia: a novel mechanism of BCR-ABL1-independent disease progression. [Cerny-Reiterer S, et al. Neoplasia 2012;14(7):572-84]
PubMed: 22904675
Expression and clinical relevance of MET and ALK in Ewing sarcomas. [Fleuren ED, et al. Int J Cancer 2013;ahead of print]
PubMed: 23335077
Overcoming erlotinib resistance with tailored treatment regimen in patient-derived xenografts from naïve Asian NSCLC patients. [Yang M, et al. Int J Cancer 2013;132(2):E74-84]
PubMed: 22948846
Signatures of drug sensitivity in nonsmall cell lung cancer. [Gong HC, et al. Int J Proteomics 2011;2011, 215496]
PubMed: 22091388
A Receptor Tyrosine Kinase Network Comprised of FGFRs, EGFR, ERBB2 and MET Drives Growth and Survival of Head and Neck Squamous Carcinoma Cell Lines. [Singleton KR, et al. Mol Pharmacol 2013;ahead of print]
PubMed: 23371912
Disturbance of Ca2+ homeostasis converts Pro-Met into non-canonical tyrosine kinase p190MetNC in response to endoplasmic reticulum stress in MHCC97 cells. [Dai R, et al. J Biol Chem 2012;287(18):14586-97]
PubMed: 22418436
The Tyrosine Kinase c-Met Contributes to the Pro-tumorigenic Function of the p38 Kinase in Human Bile Duct Cholangiocarcinoma Cells. [Dai R, et al. J Biol Chem 2012;287(47):39812-23]
PubMed: 23024367
Crizotinib (PF‐02341066) Reverses Multidrug Resistance in Cancer Cells by Inhibiting the function of P‐glycoprotein. [Zhou WJ, et al. Br J Pharmacol 2012;166(5):1669-83]
PubMed: 22233293
Mouse Model for ROS1-Rearranged Lung Cancer. [Arai Y, et al. PLoS One 2013;8(2), e56010]
PubMed: 23418494
STAT3 is activated by JAK2 independent of key oncogenic driver mutations in non-small cell lung carcinoma. [Looyenga BD, et al. PLoS One 2012;7(2):e30820]
PubMed: 22319590
3D models of epithelial-mesenchymal transition in breast cancer metastasis: high-throughput screening assay development, validation, and pilot screen. [Li Q, et al. J Biomol Screen 2011;16(2), 141-154]
PubMed: 21297102
ALK mutations conferring differential resistance to structurally diverse ALK inhibitors. [Thakral C, et al. Pediatr Blood Cancer 2012;59(3):440-7]
PubMed: 22488797

Tech Support & FAQs

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

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RTKs and Angiogenesis Related Products

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Crizotinib (PF-02341066) + BEZ235	Combination of PD-325901 or BEZ235 with PF-2341066 is more effective in blocking the proliferation of the H1993 cells, which reveals a potently activated c-MET pathway, than by treating this cell line with the c-MET inhibitor PF-2341066 alone. ^[5]
Crizotinib (PF-02341066) + PD-0325901	Combination of PD-325901 or BEZ235 with PF-2341066 is more effective in blocking the proliferation of the H1993 cells, which reveals a potently activated c-MET pathway, than by treating this cell line with the c-MET inhibitor PF-2341066 alone. ^[5]

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Crizotinib (PF-02341066) Licensed by Pfizer