Crizotinib (PF-02341066)

Licensed by Pfizer 製品コードS1068

Crizotinib (PF-02341066)化学構造

分子量(MW):450.34

Crizotinib (PF-02341066)は一種の有効なc-MetとALK阻害剤で、細胞試験でIC50値が11 nMと24 nMです。

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文献中の引用(68)

カスタマーフィードバック(11)

  • (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) Immunoblots of MPM cells treated with the indicated concentrations of crizotinib alone for 24 h with HGF stimulation.

    Sci Rep, 2016, 6:32992. Crizotinib (PF-02341066) purchased from Selleck.

  • Combination of EGCG with c-MET inhibitor has enhanced inhibitory effects on the growth of OS cells. MG-63 and U-2OS cells were treated with crizotinib (0.05 mM) and/or EGCG (0.08 g/L) for 48 h, and the effects on cell apoptosis (b) were determined using flow cytometry. *P<0.05 versus the control; #P<0.05 versus crizotinib-treated groups or EGCG-treated groups

    Tumour Biol, 2016, 37(4):4373-82. 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.

    Crizotinib impaired tumor vascularization. a-e Representative photomicrographs (40×) of CD31 staining in negative control and indicated LFD, HFD, vehicle (veh) and crizotinib (criz) treated groups. b CD31 was quantified on 5–6 randomly selected regions of n = 2 sections each from each mouse. N = 9–10 mice (a vs b, Veh vs Criz, P = 0.0138)

    Springerplus, 2016, 5:348. 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.

製品安全説明書

c-Met阻害剤の選択性比較

生物活性

製品説明 Crizotinib (PF-02341066)は一種の有効なc-MetとALK阻害剤で、細胞試験でIC50値が11 nMと24 nMです。
ターゲット
c-Met [1]
(A549, MDA-MB-231, GTL-16, HT29, 786-O, Colo-205, A498 cells)
ALK [1]
(Karpas299 cells)
11 nM 24 nM
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
BAF3 NIXzXY5EgXSxdH;4bYMhSXO|YYm= NHrPW4Y1QCCq M1uyNmROW09? MlTOR5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgRmFHOyClZXzsd{BmgHC{ZYPzbY5oKEGOSzDGNVE4PExibYX0ZY51KGOxZYjwdoV{e2mwZzDFUWw1KHerdHigTWM2OCCxZjCwMlYzKM7:TR?= MnvYNlE2PzJ3OEm=
BAF3 NETqPIREgXSxdH;4bYMhSXO|YYm= M3Pj[VQ5KGh? Mn3vSG1UVw>? MkfIR5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgRmFHOyClZXzsd{BmgHC{ZYPzbY5oKEGOSzDMNVE6Pk1ibYX0ZY51KGOxZYjwdoV{e2mwZzDFUWw1KHerdHigTWM2OCCxZjCyMlIh|ryP MWGyNVU4OjV6OR?=
BAF3 MoHVR5l1d3SxeHnjJGF{e2G7 NWXrWpdnPDhiaB?= NFfifXZFVVOR NFLzPIJEgXSxdH;4bYNqfHliYXfhbY5{fCCvb4Xz[UBDSUZ|IHPlcIx{KGW6cILld5NqdmdiRV3MOE1CVEtid3n0bEBKSzVyIH;mJFAvOjhizszN NFr2XHczOTV5MkW4PS=>
Kelly NWrx[WVlS3m2b4TvfIlkKEG|c3H5 MXzEUXNQ M1\uOGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGtmdGy7IHPlcIx{KGW6cILld5NqdmdiQVzLJGYyOTd2TDDteZRidnRid3n0bEBKSzVyIH;mJFAvPDJizszN MXmyNVU4OjV6OR?=
SH-SY5Y MlHIR5l1d3SxeHnjJGF{e2G7 M1[1emROW09? Mn7NR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gV2guW1l3WTDj[YxteyCneIDy[ZN{cW6pIFHMT{BHOTF5NFygcZV1[W62IIfpeIghUUN3MDDv[kAxNjV|IN88US=> NHvjPHgzOTV5MkW4PS=>
SMS-KCN NYP6NpdMS3m2b4TvfIlkKEG|c3H5 NYLWRVBtTE2VTx?= NW\MbJk1S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW02VLVvDUkBk\WyuczDlfJBz\XO|aX7nJGFNUyCUMUK3OXEhdXW2YX70JJdqfGhiSVO1NEBw\iByLkmxJO69VQ>? MVKyNVU4OjV6OR?=
BAF3 M2\JOWN6fG:2b4jpZ{BCe3OjeR?= NGfN[mo1QCCq MV\EUXNQ NXj4V2JjS3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhSkGIMzDj[YxteyCneIDy[ZN{cW6pIGTlcE1CVEtid3n0bEBKSzVyIH;mJFAvOTlizszN NEH5W2YzOTV5MkW4PS=>
3T3 NFLCOnFHfW6ldHnvckBCe3OjeR?= MYixJIg> NHThNI9FVVOR NUjjNJpVUW6qaXLpeIlwdiCxZjDSU24h[XO|ZYPz[YQh[XNiZ4Lve5RpKG[jY4Tvdk1qdmS3Y3XkJIF2fG:yaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIECuNFgh|ryP NHjGeo8zOThzMkSxOC=>
3T3-E NWXxS4xrTnWwY4Tpc44hSXO|YYm= NWnlVlc1OSCq NX3lZoljTE2VTx?= MVjJcohq[mm2aX;uJI9nKFSLRUKgZZN{\XO|ZXSg[5Jwf3SqIH\hZ5Rwei2rbnT1Z4VlKGG3dH;wbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFAvPDR6IN88US=> MVqyNVgyOjRzNB?=
A549 MX7LbY5ie2ViQYPzZZk> M361V|EhcA>? NWfNTnZRTE2VTx?= NVHGRpY2UW6qaXLpeIlwdiCxZjDoeY1idiC{ZXPvcYJqdmGwdDDjMW1GXCCtaX7hd4Uh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IHnubIljcXSrb36gc4YhUEeILXnu[JVk\WRiYYX0c5Bpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOC5yMEig{txO M2XZ[lIyQDF{NEG0
BAF3-BCL MVjGeY5kfGmxbjDBd5NigQ>? NGnMcmoyKGh? NHjOZoVFVVOR Mlm5TY5pcWKrdHnvckBw\iCDQlygZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDFwMUW5JO69VQ>? MljmNlE5OTJ2MUS=
HEK293 NFnL[W5HfW6ldHnvckBCe3OjeR?= NWrDc3ZHOSCq NYG1cWVUTE2VTx?= MmfkTY5pcWKrdHnvckBw\iCDWFygZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMkm0JO69VQ>? M{\KT|IyQDF{NEG0
HEK293 NI\2OmxHfW6ldHnvckBCe3OjeR?= MlrLNUBp NVKzWFdwTE2VTx?= M3zRXmlvcGmkaYTpc44hd2ZiSWKgZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDJwOEi3JO69VQ>? M3v1d|IyQDF{NEG0
Jurkat NYDSdnFETnWwY4Tpc44hSXO|YYm= NXPnZXhEOSCq NFKx[5pFVVOR MVHJcohq[mm2aX;uJI9nKEyFSzDhd5Nme3OnZDDhd{Boem:5dHig[oFkfG:{LXnu[JVk\WRiYYX0c5Bpd3OyaH;yfYxifGmxbjD3bZRpKEmFNUCgc4YhOi55NEGg{txO MUSyNVgyOjRzNB?=
KARPAS299 MYDLbY5ie2ViQYPzZZk> NVe1RpdSOSCq M3[zb2ROW09? MmjuTY5pcWKrdHnvckBw\iCDTFugZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDBwMEKg{txO MYqyNVgyOjRzNB?=
PAE Ml7uSpVv[3Srb36gRZN{[Xl? MonkNUBp Mo\YSG1UVw>? Mn:4TY5pcWKrdHnvckBw\iCWUlvCJIF{e2W|c3XkJIF{KGe{b4f0bEBn[WO2b4KtbY5lfWOnZDDheZRweGixc4Doc5J6dGG2aX;uJJdqfGhiSVO1NEBw\iByLkO5PUDPxE1? M{mwVlIyQDF{NEG0
BAF3 NFrCNlNHfW6ldHnvckBCe3OjeR?= NXPO[|J{Oi1|IHS= NXKxS3NmTE2VTx?= NIK0bmpKdmirYnn0bY9vKG:oIGTFUE1nfXOnZDDpcpN2dGmwIILlZ4VxfG:{IHX4dJJme3OnZDD3bZRpKEmFNUCgc4YhOS54NEOg{txO MV[yN|c1OjJ3Mh?=
KARPAS299 MWjDfZRwfG:6aXOgRZN{[Xl? MojXNk0{KGR? MlzySG1UVw>? MojoTWM2OD1yLkC2OFIh|ryP Mmf3NlM4PDJ{NUK=
EBC1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUHlTJN1PzJiaB?= NFTzT3RFVVOR M1nkdGlEPTB;MD6wNlMh|ryP NETndmIzOzl7M{OyPC=>
HCT116 MmDXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Moi5O|IhcA>? NWSxWWJpTE2VTx?= MW\JR|UxRTF2LkiyJO69VQ>? MYSyN|k6OzN{OB?=
MCF7 MlfVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXi3NkBp MV3EUXNQ NF7lPVdKSzVyPUmuOVgh|ryP MoLuNlM6QTN|Mki=
MDA-MB-231 M362e2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3u2RVczKGh? NFTGSpFFVVOR NEnp[4VKSzVyPUGwMlgh|ryP M2OzWVI{QTl|M{K4
MKN45 M1\LeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MUO3NkBp M4HwU2ROW09? NUXSXYdCUUN3ME2wMlAyOyEQvF2= MWiyN|k6OzN{OB?=
NCI-H441 MnjSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWW3NkBp MkHBSG1UVw>? NULCeZBwUUN3ME2xO{4zPSEQvF2= MX6yN|k6OzN{OB?=
NCI-H661 M1T6cmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkLuO|IhcA>? NHj1bVRFVVOR M3u3V2lEPTB;MUGuOFch|ryP NIHI[ZAzOzl7M{OyPC=>
SK-MEL-28 NEDZWHZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NEX1XG84OiCq MorPSG1UVw>? MkD1TWM2OD1zMD65O{DPxE1? NUH6[pFTOjN7OUOzNlg>
SKOV3 MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? Mk\WO|IhcA>? M1TVWmROW09? MV7JR|UxRTF{Lki1JO69VQ>? NX;je4RtOjN7OUOzNlg>
SNU5 M17xSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHGO|IhcA>? NYnzeZFOTE2VTx?= MX3JR|UxRTBwMEG2JO69VQ>? M2rKfVI{QTl|M{K4
NCI-H2228 NXflb2c1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV3zeHZ6PzJiaB?= NXHqTFA4TE2VTx?= MUjJcohq[mm2aX;uJI9nKEGOSz3meZNqd25iZILpeoVvKGOnbHygdJJwdGmoZYLheIlwdiC5aYToJGlEPTBib3[gNE4yOThizszN NH;LO4czPDR|MkmwPS=>
NCI-H3122 MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUC3NkBp M1fWUmROW09? MmrhTY5pcWKrdHnvckBw\iCDTFut[pV{cW:wIHTybZZmdiClZXzsJJBzd2yrZnXyZZRqd25id3n0bEBKSzVyIH;mJFAvOTB6IN88US=> MkD0NlQ1OzJ7MEm=
NCI-H3122 MmjxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MUi3NkBp NUC0[WFUTE2VTx?= NV3mV41UUW6qaXLpeIlwdiCxZjDBUGsu\nW|aX;uJIRzcX[nbjDj[YxtKHC{b3zp[oVz[XSrb36gbY4hcHWvYX6gUmNKNUh|MUKyJINmdGy|IHjhdoJwemmwZzDBUGshTzF{NknBJI12fGGwdDD3bZRpKEmFNUCgc4YhOC54MkOg{txO NH\1UZEzPDR|MkmwPS=>
NCI-H3122 NHjGfJJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2e1RlczKGh? NHzpTZpFVVOR MVLJcohq[mm2aX;uJI9nKEGOSz3meZNqd25iZILpeoVvKGOnbHygdJJwdGmoZYLheIlwdiCrbjDoeY1idiCQQ1mtTFMyOjJiY3XscJMhcGG{Yn;ybY5oKEGOSzDMNVE6Pk1ibYX0ZY51KHerdHigTWM2OCCxZjCwMlg{QCEQvF2= M3P0bFI1PDN{OUC5
NIH-3T3 NEfU[WdMcW6jc3WgRZN{[Xl? MVWxJIg> NUXDem9DTE2VTx?= M{HqNmlvcGmkaYTpc44hd2ZiaIXtZY4hf2muZDD0fZBmKEWPTESt[pV{\WRiQVzLJIV5eHKnc4Pl[EBie3Onc4Pl[EBieyCyaH;zdIhwenmuYYTl[EBCVEtibHX2[Ywhf2m2aDDJR|UxKG:oIECuNFgh|ryP M4\YW|I1PDN{OUC5
NIH-3T3 MXzLbY5ie2ViQYPzZZk> MUSxJIg> M2nNOmROW09? MXzJcohq[mm2aX;uJI9nKGi3bXHuJGVOVDRvZoXz[YQhSUyNIFexNlY6SSCvdYThcpQh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IIDoc5NxcG9vQVzLJIxmfmWuIIfpeIghUUN3MDDv[kAxNjZyNTFOwG0> MnzNNlQ1OzJ7MEm=
NIH-3T3 MmXvT4lv[XOnIFHzd4F6 MXuxJIg> MojsSG1UVw>? NWH0[ZQ3UW6qaXLpeIlwdiCxZjDoeY1idiCHTVy0MYZ2e2WmIFHMT{BUOTJyNmmgcZV1[W62IHX4dJJme3OnZDDhd5Nme3OnZDDhd{BxcG:|cHjvMWFNUyCuZY\lcEB4cXSqIFnDOVAhd2ZiMD62NlYh|ryP NIjyeZczPDR|MkmwPS=>
NIH-3T3 NIjBZYhMcW6jc3WgRZN{[Xl? NFfJNoYyKGh? M3ixbmROW09? MVHJcohq[mm2aX;uJI9nKGi3bXHuJGVOVDRvZoXz[YQhSUyNIFyxNVk3VSCvdYThcpQh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IIDoc5NxcG9vQVzLJIxmfmWuIIfpeIghUUN3MDDv[kAxNjh2MzFOwG0> MoDrNlQ1OzJ7MEm=
NIH-3T3 M{TMbGtqdmG|ZTDBd5NigQ>? MlvmNUBp MX\EUXNQ Mk\MTY5pcWKrdHnvckBw\iCqdX3hckBGVUx2LX\1d4VlKEGOSzDMNVE2OlJibYX0ZY51KGW6cILld5Nm\CCjc4Pld5Nm\CCjczDwbI9{eGixLVHMT{Bt\X[nbDD3bZRpKEmFNUCgc4YhOS5yMk[g{txO M1LKNlI1PDN{OUC5
BAF3 MV\GeY5kfGmxbjDBd5NigQ>? NVu2OVhmPzJiaB?= MWjEUXNQ NVLRR5VVUW6qaXLpeIlwdiCxZjDOVG0wSUyNIITyZY5{\mWldHXkJIF{e2W|c3XkJIF{KGOnbHyg[5Jwf3SqIHnubIljcXSrb36ge4l1cCCLQ{WwJI9nKDBwMEWxJO69VQ>? NWf2bIZDOjR2Nki2N|I>
BAF3 MlLBR5l1d3SxeHnjJGF{e2G7 MX:3NkBp M2jjWWROW09? NVTjOFhWUUN3ME2wMlk5KM7:TR?= M{PSR|I1PDZ6NkOy
NIH-3T3 NH6wfnJMcW6jc3WgRZN{[Xl? NWDX[|BmOSCq MV3Jcohq[mm2aX;uJI9nKGi3bXHuJGVOVDRvZoXz[YQhSUyNIF[xNVc1VCCvdYThcpQh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IIDoc5NxcG9vQVzLJIxmfmWuIIfpeIghUUN3MDDv[kAxNjF4NTFOwG0> MkPWNlQ5OTlzMU[=
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GB-1 MkfXS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnzPTWM2OD1|NT6wOFY6KM7:TR?= NGnRbYFUSU6JRWK=
TE-15 NH32ZZZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MYfJR|UxRTN3LkKyN|gh|ryP NWXXTXVHW0GQR1XS
LC4-1 NYTWUYh3T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MUjJR|UxRTN3LkO4OFch|ryP NYS3PZgyW0GQR1XS
NCI-H747 M3SzcGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2TsbmlEPTB;M{[uNVM3QSEQvF2= NGP5R2hUSU6JRWK=
NTERA-S-cl-D1 M{DKbmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M364XWlEPTB;M{iuO|M1PyEQvF2= MmPyV2FPT0WU
SK-MM-2 Ml\QS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? Mn;oTWM2OD12MD6xNVQ3KM7:TR?= NWSyN2d2W0GQR1XS
TGW MkTWS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NG\NVnlKSzVyPUSxMlA2PjNizszN M2nreHNCVkeHUh?=
ONS-76 MnXIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGf6XWRKSzVyPUSyMlQ5QDNizszN NIXSPZpUSU6JRWK=
CPC-N M4W5eGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MlG1TWM2OD12Mj65PVcyKM7:TR?= NEnjTYNUSU6JRWK=
ES4 NFraT5dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3H5VmlEPTB;NESuOFE2OyEQvF2= M1LodHNCVkeHUh?=
Daudi M3jyT2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4nZRWlEPTB;NEWuNFgzPyEQvF2= MorLV2FPT0WU
MOLT-4 MnP2S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3fx[GlEPTB;NEWuNFg2OyEQvF2= NFWy[5hUSU6JRWK=
HT-144 M2L1PGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHjhPYtKSzVyPUS2MlczPiEQvF2= Mln3V2FPT0WU
SW872 MXXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{mwc2lEPTB;NEiuNVk{OyEQvF2= Mn;OV2FPT0WU
D-283MED M{nK[mdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NY\Hd|BJUUN3ME20PE4{PTR{IN88US=> NWrlN4p7W0GQR1XS
NCI-H2126 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVy0WmRtUUN3ME20PE45PDd4IN88US=> MnqyV2FPT0WU
NCI-SNU-16 MkfNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NX36XIM{UUN3ME20PU4zOTR|IN88US=> NFzBbJhUSU6JRWK=
CESS NYrHcm81T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHX2[4dKSzVyPUS5MlUxQDhizszN NGDxbGJUSU6JRWK=
A101D MV7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjGNGpKSzVyPUS5Mlk4OzZizszN M3;TdXNCVkeHUh?=

多くの細胞株試験データを見る場合、クリックしてください

体内試験 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]

お薦めの試験操作(参考用のみ)

キナーゼ試験:[1]
+ 展開

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.
細胞試験: [1]
+ 展開
  • 細胞株: GTL-16 gastric carcinoma cells and T47D breast carcinoma cells
  • 濃度: 0-256 nM
  • 反応時間: 1 hour
  • 実験の流れ: 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.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 9 mg/mL (19.98 mM)
Water Insoluble
Ethanol Insoluble
体内 順序で溶剤を入れること:
5% DMSO+30% PEG 300+dd H2O
5mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)で起きる正常な現象ですから、ご安心ください。

化学情報

分子量 450.34
化学式

C21H22Cl2FN5O

CAS No. 877399-52-5
保管
in solvent
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

臨床試験

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03052608 Not yet recruiting Carcinoma, Non-Small-Cell Lung Pfizer March 2017 Phase 3
NCT02838420 Recruiting Anaplastic Lymphoma Kinase-positive Non-small Cell Lung Cancer Hoffmann-La Roche August 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
NCT02946359 Recruiting Lung Adenocarcinoma Metastatic Chinese PLA General Hospital July 2016 Phase 2
NCT02679170 Recruiting Non-Small Cell Lung Cancer Pfizer June 2016 --
NCT02767804 Recruiting Non-small Cell Lung Cancer Xcovery Holding Company, LLC June 2016 Phase 3

技術サポート

ストックの作り方、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 必須

よくある質問(FAQ)

  • 問題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?

  • 回答:

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

c-Met信号経路図

c-Met Inhibitors with Unique Features

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Tags: Crizotinib (PF-02341066)を買う | Crizotinib (PF-02341066) ic50 | Crizotinib (PF-02341066)供給者 | Crizotinib (PF-02341066)を購入する | Crizotinib (PF-02341066)費用 | Crizotinib (PF-02341066)生産者 | オーダーCrizotinib (PF-02341066) | Crizotinib (PF-02341066)化学構造 | Crizotinib (PF-02341066)分子量 | Crizotinib (PF-02341066)代理店
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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID