Crizotinib (PF-02341066)

Licensed by Pfizer Catalog No.S1068

Crizotinib (PF-02341066) Chemical Structure

Molecular Weight(MW): 450.34

Crizotinib (PF-02341066) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.

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In DMSO USD 220 In stock
USD 110 In stock
USD 170 In stock
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Cited by 65 Publications

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  • (c) Western blot analyses of p-Akt (Ser473) and p-S6RP (Ser235 and Ser236) in two RCT-E565 transplanted tumors treated with vehicle or PF02341066. Samples were isolated 4 h after the last dose from mice treated with PF02341066 for 3 d. (d) Responses of RCT-E565 transplanted tumors in athymic mice to PF02341066 or vehicle. Data are means ±s.e.m. (each group, n = 6). *P < 0.005, **P < 0.001 (Student,s t test).

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

    Ba/F3 cells grown in the presence of IL-3, or Ba/F3 cells expressing native EML4-ALK (clone #2, #10, #101, and #155) and EML4-ALK L1196M (clone #216, #302, #303, and #355), were treated with CH5424802 or PF-02341066 for 48 hr, and then the viable cells were measured by the Cell Titer-Glo Luminescent Cell Viability Assay. IC50 values were determined by plotting the drug concentration versus percentage of cell growth inhibition. Data are shown as mean ±SD (n = 3).

     

     

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

  • Mice bearing Ba/F3-EML4-ALK (clone #10) and EML4-ALK L1196M (clone #303) were administered vehicle, CH5424802 (60 mg/kg), or PF-02341066 (100 mg/kg) orally once daily for 8 days. Tumor volume for each dose group was measured. Data are shown as mean ± SD (n = 5). Parametric Dunnett’s test: ***p < 0.001; N.S., not significant, versus vehicle treatment at final day. For pharmacodynamic assay, mice bearing Ba/F3-EML4-ALK (clone #10) and -EML4-ALK L1196M (clone #303) were orally administered at single dose of vehicle, CH5424802 (60 mg/kg), or PF-02341066 (100 mg/kg), and the tumors were collected and lysed at 4 hr post-dosing. STAT3 and phosphorylated STAT3 (Tyr 705) were detected by immunoblot analysis using antibodies against each of them (n = 2 per group).

     

     

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

    (A) VimPro-Fluc activity in spheroids after 72-h treatment with control modulators of epithelial-mesenchymal transition (EMT) normalized to spheroid viability and compared to vimentin protein expression using Western blot analysis. (B) Dose-response curves for both U0126 and axitinib control modulators of EMT. RLU, relative luminescence units.

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

  • Secondary assay development. The invasive potential of MDA-MB-231 spheroids was measured using modified Boyden chambers coated with Matrigel™. Invading cells were fixed, stained with DAPI, and quantified by fluorescence microscopy using 5 random fields per filter insert in triplicate. U0126, PF2341066, axitinib, and PKC412 inhibited the invasive potential of MDA-MB-231 spheroids by ~90% as compared to untreated spheroids (UT). ***p ≤ 0.001. IGF1R and dasatinib displayed no statistical difference as compared to UT MDA-MB-231 spheroids.

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

    Inhibition of signaling pathway activation in lung tumor cell lines by kinase inhibitors. Lung tumor cells were cultured in 10% FBS until reaching ∼80% confluence and then the cells were starved in serum-free medium for overnight, followed by 4-hour treatment with the inhibitors. Cell lysates were then prepared and used for determination of the pathway activation signals by the CEER assay.

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

  • Inhibition of anchorage-independent growth of lung tumor cell lines by selected inhibitors. Each selected cell line was treated with the indicated inhibitor at 0.1 μM and 1 μM concentrations for two weeks and cell colony size formation was scored under the Nikon inverted-phase microscope.

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

    Western blot analysis of c-Met, MAPK and Akt. 0-100nM PF2341066 was added.

     

     

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

Purity & Quality Control

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Notes:

2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description Crizotinib (PF-02341066) is a potent inhibitor of c-Met and ALK with IC50 of 11 nM and 24 nM in cell-based assays, respectively.
Targets
c-Met [1]
(A549, MDA-MB-231, GTL-16, HT29, 786-O, Colo-205, A498 cells)
ALK [1]
(Karpas299 cells)
11 nM 24 nM
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]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BAF3 MUTDfZRwfG:6aXOgRZN{[Xl? NG\5TVk1QCCq NWrZRVc{TE2VTx?= NWiwZpVuS3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhSkGIMzDj[YxteyCneIDy[ZN{cW6pIFHMT{BHOTF5NFygcZV1[W62IHPv[ZhxemW|c3nu[{BGVUx2IIfpeIghUUN3MDDv[kAxNjZ{IN88US=> NHvVUXEzOTV5MkW4PS=>
BAF3 MmjmR5l1d3SxeHnjJGF{e2G7 NVL2dFBQPDhiaB?= MlGySG1UVw>? M3TLcWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJGJCTjNiY3XscJMh\XiycnXzd4lv\yCDTFugUFEyQT[PIH31eIFvfCClb3X4dJJme3OrbnegSW1NPCC5aYToJGlEPTBib3[gNk4zKM7:TR?= NYjFN41[OjF3N{K1PFk>
BAF3 MUTDfZRwfG:6aXOgRZN{[Xl? Mnr3OFghcA>? NUfue5RDTE2VTx?= M2PySGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJGJCTjNiY3XscJMh\XiycnXzd4lv\yCHTVy0MWFNUyC5aYToJGlEPTBib3[gNE4zQCEQvF2= M1;YOFIyPTd{NUi5
Kelly M1PpS2N6fG:2b4jpZ{BCe3OjeR?= NVruV4hFTE2VTx?= NV;0TVNNS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hU2WubImgZ4VtdHNiZYjwdoV{e2mwZzDBUGshTjFzN{TMJI12fGGwdDD3bZRpKEmFNUCgc4YhOC52MjFOwG0> NEC1b5QzOTV5MkW4PS=>
SH-SY5Y M4j1cWN6fG:2b4jpZ{BCe3OjeR?= MWfEUXNQ NETqfXFEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBUUC2VWUXZJINmdGy|IHX4dJJme3OrbnegRWxMKEZzMUe0UEBufXSjboSge4l1cCCLQ{WwJI9nKDBwNUOg{txO NYnzWGVqOjF3N{K1PFk>
SMS-KCN M4rzT2N6fG:2b4jpZ{BCe3OjeR?= NWD3NoZnTE2VTx?= NV7RdYE5S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW02VLVvDUkBk\WyuczDlfJBz\XO|aX7nJGFNUyCUMUK3OXEhdXW2YX70JJdqfGhiSVO1NEBw\iByLkmxJO69VQ>? Mm\wNlE2PzJ3OEm=
BAF3 NGnq[JFEgXSxdH;4bYMhSXO|YYm= MX:0PEBp Mn7qSG1UVw>? NXvEcoo6S3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhSkGIMzDj[YxteyCneIDy[ZN{cW6pIGTlcE1CVEtid3n0bEBKSzVyIH;mJFAvOTlizszN MUGyNVU4OjV6OR?=
3T3 MlfuSpVv[3Srb36gRZN{[Xl? MlLRNUBp NVTQU4s2TE2VTx?= M1WxcWlvcGmkaYTpc44hd2ZiUl;OJIF{e2W|c3XkJIF{KGe{b4f0bEBn[WO2b4KtbY5lfWOnZDDheZRweGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkC4JO69VQ>? MWSyNVgyOjRzNB?=
3T3-E MWLGeY5kfGmxbjDBd5NigQ>? NHPCcHcyKGh? M2WyOWROW09? MnfnTY5pcWKrdHnvckBw\iCWSVWyJIF{e2W|c3XkJIdzd3e2aDDmZYN1d3JvaX7keYNm\CCjdYTvdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjR2ODFOwG0> NX7DfYo4OjF6MUK0NVQ>
A549 MmTNT4lv[XOnIFHzd4F6 NX7kXW5QOSCq M4HGbGROW09? MVjJcohq[mm2aX;uJI9nKGi3bXHuJJJm[2:vYnnuZY51KGNvTVXUJItqdmG|ZTDlfJBz\XO|ZXSgZZN{\XO|ZXSgZZMhcW6qaXLpeIlwdiCxZjDIS2YucW6mdXPl[EBifXSxcHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlAxQCEQvF2= M1TIVVIyQDF{NEG0
BAF3-BCL MXTGeY5kfGmxbjDBd5NigQ>? MljwNUBp MX3EUXNQ NULNdItwUW6qaXLpeIlwdiCxZjDBRmwh[XO|ZYPz[YQh[XNiZ4Lve5RpKG[jY4Tvdk1qdmS3Y3XkJIF2fG:yaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIEGuNVU6KM7:TR?= M4TGdFIyQDF{NEG0
HEK293 NIm0N2JHfW6ldHnvckBCe3OjeR?= M{\MRlEhcA>? M{DzPGROW09? MoOyTY5pcWKrdHnvckBw\iCDWFygZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMkm0JO69VQ>? NWDpSW0xOjF6MUK0NVQ>
HEK293 M4DFUWZ2dmO2aX;uJGF{e2G7 MUOxJIg> NX;tU5FSTE2VTx?= MVHJcohq[mm2aX;uJI9nKEmUIHHzd4V{e2WmIHHzJIdzd3e2aDDmZYN1d3JvaX7keYNm\CCjdYTvdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAzNjh6NzFOwG0> NGjqZYYzOThzMkSxOC=>
Jurkat NInZb45HfW6ldHnvckBCe3OjeR?= NHniSmoyKGh? M3HUe2ROW09? NUXac2V2UW6qaXLpeIlwdiCxZjDMR2sh[XO|ZYPz[YQh[XNiZ4Lve5RpKG[jY4Tvdk1qdmS3Y3XkJIF2fG:yaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIEKuO|QyKM7:TR?= M4fDblIyQDF{NEG0
KARPAS299 M2nMWGtqdmG|ZTDBd5NigQ>? NFXRTYEyKGh? MkPwSG1UVw>? M3jXeGlvcGmkaYTpc44hd2ZiQVzLJIF{e2W|c3XkJIF{KGe{b4f0bEBn[WO2b4KtbY5lfWOnZDDheZRweGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkCyJO69VQ>? NYfsdItjOjF6MUK0NVQ>
PAE M1;0TmZ2dmO2aX;uJGF{e2G7 M3r2[VEhcA>? NIPi[HpFVVOR MoH5TY5pcWKrdHnvckBw\iCWUlvCJIF{e2W|c3XkJIF{KGe{b4f0bEBn[WO2b4KtbY5lfWOnZDDheZRweGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkO5PUDPxE1? M4\4RlIyQDF{NEG0
BAF3 NWfZPHNLTnWwY4Tpc44hSXO|YYm= Ml;NNk0{KGR? MW\EUXNQ NVfESZNFUW6qaXLpeIlwdiCxZjDUSWwu\nW|ZXSgbY5{fWyrbjDy[YNmeHSxcjDlfJBz\XO|ZXSge4l1cCCLQ{WwJI9nKDFwNkSzJO69VQ>? M{HhOVI{PzR{MkWy
KARPAS299 MVXDfZRwfG:6aXOgRZN{[Xl? MXeyMVMh\A>? M2L4fmROW09? MXrJR|UxRTBwME[0NkDPxE1? NEThW2ozOzd2MkK1Ni=>
EBC1 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MV23NkBp MVXEUXNQ NG\O[lJKSzVyPUCuNFI{KM7:TR?= NF3rXmYzOzl7M{OyPC=>
HCT116 NUjP[|E4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnzBO|IhcA>? Mlq5SG1UVw>? M2HNeWlEPTB;MUSuPFIh|ryP M1PScFI{QTl|M{K4
MCF7 NInXcpJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF7jW2s4OiCq NWDROnJTTE2VTx?= M3:2dmlEPTB;OT61PEDPxE1? NVjLeJhlOjN7OUOzNlg>
MDA-MB-231 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MnuwO|IhcA>? NUf1V45tTE2VTx?= M2DtdGlEPTB;MUCuPEDPxE1? NF3pdYEzOzl7M{OyPC=>
MKN45 MknGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mo\GO|IhcA>? Mn36SG1UVw>? M3OySGlEPTB;MD6wNVMh|ryP MkezNlM6QTN|Mki=
NCI-H441 NYPpXGNuT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MVi3NkBp NXvQdZlkTE2VTx?= MlXXTWM2OD1zNz6yOUDPxE1? M1:3dVI{QTl|M{K4
NCI-H661 NGTPNXNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NITD[3A4OiCq M4HmWGROW09? NGfXWXpKSzVyPUGxMlQ4KM7:TR?= NY[5PZE5OjN7OUOzNlg>
SK-MEL-28 NEXJfYVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYnlbW1nPzJiaB?= NGS5TmdFVVOR MlK5TWM2OD1zMD65O{DPxE1? MlvQNlM6QTN|Mki=
SKOV3 M33pdGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGDYU4Y4OiCq M{TEZWROW09? MnPXTWM2OD1zMj64OUDPxE1? MXGyN|k6OzN{OB?=
SNU5 NUnZXldZT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MX:3NkBp NHTkNGpFVVOR NEXsU3hKSzVyPUCuNFE3KM7:TR?= M4LDbFI{QTl|M{K4
NCI-H2228 NX;nXIRoT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M3nlUVczKGh? M4[xO2ROW09? NFXL[|JKdmirYnn0bY9vKG:oIFHMT{1nfXOrb36g[JJqfmWwIHPlcIwheHKxbHnm[ZJifGmxbjD3bZRpKEmFNUCgc4YhOC5zMUig{txO Ml3ONlQ1OzJ7MEm=
NCI-H3122 Mn24S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3K4XFczKGh? Mmf2SG1UVw>? NUHyd2lNUW6qaXLpeIlwdiCxZjDBUGsu\nW|aX;uJIRzcX[nbjDj[YxtKHC{b3zp[oVz[XSrb36ge4l1cCCLQ{WwJI9nKDBwMUC4JO69VQ>? NWfifplOOjR2M{K5NFk>
NCI-H3122 M{f4WGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEHRRVA4OiCq MXTEUXNQ NF;iVJdKdmirYnn0bY9vKG:oIFHMT{1nfXOrb36g[JJqfmWwIHPlcIwheHKxbHnm[ZJifGmxbjDpckBpfW2jbjDOR2kuUDNzMkKgZ4VtdHNiaHHyZo9zcW6pIFHMT{BIOTJ4OVGgcZV1[W62IIfpeIghUUN3MDDv[kAxNjZ{MzFOwG0> NH;YcZkzPDR|MkmwPS=>
NCI-H3122 NVrpOoFVT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmKwO|IhcA>? NUP0VId2TE2VTx?= NES3SplKdmirYnn0bY9vKG:oIFHMT{1nfXOrb36g[JJqfmWwIHPlcIwheHKxbHnm[ZJifGmxbjDpckBpfW2jbjDOR2kuUDNzMkKgZ4VtdHNiaHHyZo9zcW6pIFHMT{BNOTF7Nl2gcZV1[W62IIfpeIghUUN3MDDv[kAxNjh|ODFOwG0> NEjzeZgzPDR|MkmwPS=>
NIH-3T3 MlvOT4lv[XOnIFHzd4F6 MnHXNUBp M1LqVWROW09? MoG0TY5pcWKrdHnvckBw\iCqdX3hckB4cWymIIT5dIUhTU2OND3meZNm\CCDTFug[ZhxemW|c3XkJIF{e2W|c3XkJIF{KHCqb4PwbI9zgWyjdHXkJGFNUyCuZY\lcEB4cXSqIFnDOVAhd2ZiMD6wPEDPxE1? Mn;sNlQ1OzJ7MEm=
NIH-3T3 MlzrT4lv[XOnIFHzd4F6 NUXITmwxOSCq NUfwXGQxTE2VTx?= NUfF[WF4UW6qaXLpeIlwdiCxZjDoeY1idiCHTVy0MYZ2e2WmIFHMT{BIOTJ4OVGgcZV1[W62IHX4dJJme3OnZDDhd5Nme3OnZDDhd{BxcG:|cHjvMWFNUyCuZY\lcEB4cXSqIFnDOVAhd2ZiMD62NFUh|ryP MYWyOFQ{OjlyOR?=
NIH-3T3 NVXaZmN{U2mwYYPlJGF{e2G7 MYSxJIg> NUHHVppTTE2VTx?= MUfJcohq[mm2aX;uJI9nKGi3bXHuJGVOVDRvZoXz[YQhSUyNIGOxNlA3YSCvdYThcpQh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IIDoc5NxcG9vQVzLJIxmfmWuIIfpeIghUUN3MDDv[kAxNjZ{NjFOwG0> MViyOFQ{OjlyOR?=
NIH-3T3 MmrJT4lv[XOnIFHzd4F6 NXP1SYJSOSCq NHHKfWJFVVOR NETse4ZKdmirYnn0bY9vKG:oIHj1cYFvKEWPTESt[pV{\WRiQVzLJGwyOTl4TTDteZRidnRiZYjwdoV{e2WmIHHzd4V{e2WmIHHzJJBpd3OyaH:tRWxMKGyndnXsJJdqfGhiSVO1NEBw\iByLki0N{DPxE1? M3u1ZVI1PDN{OUC5
NIH-3T3 NIrJcJZMcW6jc3WgRZN{[Xl? NEPTPFAyKGh? M1LHVGROW09? NIH3WlNKdmirYnn0bY9vKG:oIHj1cYFvKEWPTESt[pV{\WRiQVzLJGwyOTV{UjDteZRidnRiZYjwdoV{e2WmIHHzd4V{e2WmIHHzJJBpd3OyaH:tRWxMKGyndnXsJJdqfGhiSVO1NEBw\iBzLkCyOkDPxE1? MXmyOFQ{OjlyOR?=
BAF3 MYPGeY5kfGmxbjDBd5NigQ>? NGLqdVU4OiCq MVjEUXNQ MVXJcohq[mm2aX;uJI9nKE6STT;BUGshfHKjboPm[YN1\WRiYYPz[ZN{\WRiYYOgZ4VtdCCpcn;3eIghcW6qaXLpeIlwdiC5aYToJGlEPTBib3[gNE4xPTFizszN Mle0NlQ1Pjh4M{K=
BAF3 MYnDfZRwfG:6aXOgRZN{[Xl? MVi3NkBp MWnEUXNQ NHPQRWxKSzVyPUCuPVgh|ryP M4LjPVI1PDZ6NkOy
NIH-3T3 M4[2cmtqdmG|ZTDBd5NigQ>? NGLnbmMyKGh? NW[wRZdsUW6qaXLpeIlwdiCxZjDoeY1idiCHTVy0MYZ2e2WmIFHMT{BHOTF5NFygcZV1[W62IHX4dJJme3OnZDDhd5Nme3OnZDDhd{BxcG:|cHjvMWFNUyCuZY\lcEB4cXSqIFnDOVAhd2ZiMD6xOlUh|ryP M2\C[|I1QDF7MUG2
NIH-3T3 M3zJSWtqdmG|ZTDBd5NigQ>? M1jJSFEhcA>? NInEe25KdmirYnn0bY9vKG:oIHj1cYFvKEWPTESt[pV{\WRiQVzLJGMyOTV4WTDteZRidnRiZYjwdoV{e2WmIHHzd4V{e2WmIHHzJJBpd3OyaH:tRWxMKGyndnXsJJdqfGhiSVO1NEBw\iByLkS3PEDPxE1? MlT0NlQ5OTlzMU[=
NIH-3T3 NWnR[2lTU2mwYYPlJGF{e2G7 NEjBSnMyKGh? NFPnZ4FKdmirYnn0bY9vKG:oIHj1cYFvKEWPTESt[pV{\WRiQVzLJGcyOjB{UjDteZRidnRiZYjwdoV{e2WmIHHzd4V{e2WmIHHzJJBpd3OyaH:tRWxMKGyndnXsJJdqfGhiSVO1NEBw\iBzLkG0PEDPxE1? M1HzSVI1QDF7MUG2
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NCI-H747 NX3IXIt[T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M1nUcWlEPTB;M{[uNVM3QSEQvF2= M3TVbnNCVkeHUh?=
NTERA-S-cl-D1 NIPqXFBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWjJR|UxRTN6LkezOFch|ryP MY\TRW5ITVJ?
SK-MM-2 MlvBS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYLPOoVVUUN3ME20NE4yOTR4IN88US=> MnTaV2FPT0WU
TGW NWHMRYVrT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MmLUTWM2OD12MT6wOVY{KM7:TR?= NVrqOm93W0GQR1XS
ONS-76 Mn;oS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX;JR|UxRTR{LkS4PFMh|ryP NIHafXhUSU6JRWK=
CPC-N NHHCdXJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVTnZ4FtUUN3ME20Nk46QTdzIN88US=> NXnFWGdtW0GQR1XS
ES4 M1zEcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWLJR|UxRTR2LkSxOVMh|ryP MXrTRW5ITVJ?
Daudi NFu4fHhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3rpXGlEPTB;NEWuNFgzPyEQvF2= NGjBXFRUSU6JRWK=
MOLT-4 NFqwSWNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIjBSoFKSzVyPUS1MlA5PTNizszN NX7kZ|NSW0GQR1XS
HT-144 MYTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVXHVJdEUUN3ME20Ok44OjZizszN Mmi0V2FPT0WU
SW872 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MW\JR|UxRTR6LkG5N|Mh|ryP MWTTRW5ITVJ?
D-283MED MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MljUTWM2OD12OD6zOVQzKM7:TR?= MWXTRW5ITVJ?
NCI-H2126 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXfEZYg6UUN3ME20PE45PDd4IN88US=> NGDGNphUSU6JRWK=
NCI-SNU-16 M2XlSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NFT2XGFKSzVyPUS5MlIyPDNizszN NGmxe|dUSU6JRWK=
CESS MX;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NH;WbVVKSzVyPUS5MlUxQDhizszN M3fnZnNCVkeHUh?=
A101D MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4fvS2lEPTB;NEmuPVc{PiEQvF2= NHO5W29USU6JRWK=

... Click to View More Cell Line Experimental Data

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]

Protocol

Kinase Assay
+ Expand

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 Research
+ Expand
  • 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.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 9 mg/mL (19.98 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 5% DMSO+30% PEG 300+dd H2O 5mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* 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

Molecular Weight 450.34
Formula

C21H22Cl2FN5O

CAS No. 877399-52-5
Storage powder
in solvent
Synonyms N/A

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02838420 Recruiting Anaplastic Lymphoma Kinase-positive Non-small Cell Lung Cancer Hoffmann-La Roche July 2016 Phase 3
NCT02836847 Recruiting Cholangiocarcinoma of the Extrahepatic Bile Duct|Gallbladder Cancer Shanghai Jiao Tong University School of Medicine|Xinhua Hospital, Shanghai Jiao Tong University School of Medicine|Ruijin Hospital|RenJi Hospital|Eastern Hepatobiliary Surgery Hospital|Huashan Hospital July 2016 Phase 2
NCT02767804 Recruiting Non-small Cell Lung Cancer Xcovery Holding Company, LLC June 2016 Phase 3
NCT02679170 Recruiting Non-Small Cell Lung Cancer Pfizer June 2016 --
NCT02761057 Recruiting Recurrent Renal Cell Carcinoma|Stage III Renal Cell Cancer|Stage IV Renal Cell Cancer|Type 1 Papillary Renal Cell Carcinoma|Type 2 Papillary Renal Cell Carcinoma National Cancer Institute (NCI) April 2016 Phase 2
NCT02737501 Recruiting Non-small Cell Lung Cancer|Lung Cancer|Advanced Malignancies|Carcinoma Ariad Pharmaceuticals April 2016 Phase 3

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

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Frequently Asked Questions

  • Question 1:

    Could you tell me whether this product represents the pure R-form of crizotinib, or is the the racemic Crizotinib, so a mixture of the S- and the R-form?

  • Answer:

    Our S1068 Crizotinib is R enantiomer(except batch 05 and 06, they are racemate), and S7505 is S enantiomer.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID