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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  • (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 Ml3XR5l1d3SxeHnjJGF{e2G7 NXrUOZdZPDhiaB?= MnT4SG1UVw>? NYS5V5RnS3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4UhSkGIMzDj[YxteyCneIDy[ZN{cW6pIFHMT{BHOTF5NFygcZV1[W62IHPv[ZhxemW|c3nu[{BGVUx2IIfpeIghUUN3MDDv[kAxNjZ{IN88US=> M4L4[lIyPTd{NUi5
BAF3 M{XIbmN6fG:2b4jpZ{BCe3OjeR?= MmnmOFghcA>? M4D5W2ROW09? M4PWRWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJGJCTjNiY3XscJMh\XiycnXzd4lv\yCDTFugUFEyQT[PIH31eIFvfCClb3X4dJJme3OrbnegSW1NPCC5aYToJGlEPTBib3[gNk4zKM7:TR?= M3fpT|IyPTd{NUi5
BAF3 NG\ifWpEgXSxdH;4bYMhSXO|YYm= M4DuNlQ5KGh? MYXEUXNQ M1XrUmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KG2xdYPlJGJCTjNiY3XscJMh\XiycnXzd4lv\yCHTVy0MWFNUyC5aYToJGlEPTBib3[gNE4zQCEQvF2= MnvoNlE2PzJ3OEm=
Kelly M1rqcGN6fG:2b4jpZ{BCe3OjeR?= M{\rcWROW09? M3fJcGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGtmdGy7IHPlcIx{KGW6cILld5NqdmdiQVzLJGYyOTd2TDDteZRidnRid3n0bEBKSzVyIH;mJFAvPDJizszN MknVNlE2PzJ3OEm=
SH-SY5Y NVHGUlBoS3m2b4TvfIlkKEG|c3H5 MonYSG1UVw>? MWXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDTTE1UYTW\IHPlcIx{KGW6cILld5NqdmdiQVzLJGYyOTd2TDDteZRidnRid3n0bEBKSzVyIH;mJFAvPTNizszN NVrleoRuOjF3N{K1PFk>
SMS-KCN M3XNWWN6fG:2b4jpZ{BCe3OjeR?= M{KxT2ROW09? M2LkOWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHNOWy2NQ16gZ4VtdHNiZYjwdoV{e2mwZzDBUGshWjF{N{XRJI12fGGwdDD3bZRpKEmFNUCgc4YhOC57MTFOwG0> NV;ndmNUOjF3N{K1PFk>
BAF3 NEe0[FVEgXSxdH;4bYMhSXO|YYm= NH7ld481QCCq NFznTpNFVVOR MmrzR5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgRmFHOyClZXzsd{BmgHC{ZYPzbY5oKFSnbD3BUGshf2m2aDDJR|UxKG:oIECuNVkh|ryP NHXtb4QzOTV5MkW4PS=>
3T3 MlzVSpVv[3Srb36gRZN{[Xl? NILLV2MyKGh? Mlj1SG1UVw>? NIXZfWlKdmirYnn0bY9vKG:oIGLPUkBie3Onc4Pl[EBieyCpcn;3eIgh\mGldH;yMYlv\HWlZXSgZZV1d3Cqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wPEDPxE1? M3[wXlIyQDF{NEG0
3T3-E MVHGeY5kfGmxbjDBd5NigQ>? MU[xJIg> MmTPSG1UVw>? MUTJcohq[mm2aX;uJI9nKFSLRUKgZZN{\XO|ZXSg[5Jwf3SqIH\hZ5Rwei2rbnT1Z4VlKGG3dH;wbI9{eGixconsZZRqd25id3n0bEBKSzVyIH;mJFAvPDR6IN88US=> MX:yNVgyOjRzNB?=
A549 NGW2NWpMcW6jc3WgRZN{[Xl? MkK3NUBp M4XIXWROW09? NH:yR5hKdmirYnn0bY9vKG:oIHj1cYFvKHKnY3;tZolv[W62IHOtUWVVKGurbnHz[UBmgHC{ZYPz[YQh[XO|ZYPz[YQh[XNiaX7obYJqfGmxbjDv[kBJT0ZvaX7keYNm\CCjdYTvdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAxNjByODFOwG0> NYfTTmtNOjF6MUK0NVQ>
BAF3-BCL NUPhS45{TnWwY4Tpc44hSXO|YYm= Ml7QNUBp NUfiTYpyTE2VTx?= NYCxRohSUW6qaXLpeIlwdiCxZjDBRmwh[XO|ZYPz[YQh[XNiZ4Lve5RpKG[jY4Tvdk1qdmS3Y3XkJIF2fG:yaH;zdIhwenmuYYTpc44hf2m2aDDJR|UxKG:oIEGuNVU6KM7:TR?= M4\LUVIyQDF{NEG0
HEK293 MX\GeY5kfGmxbjDBd5NigQ>? MlXaNUBp NIj6b3lFVVOR NEHWfmFKdmirYnn0bY9vKG:oIFHYUEBie3Onc4Pl[EBieyCpcn;3eIgh\mGldH;yMYlv\HWlZXSgZZV1d3Cqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6yPVQh|ryP NXzGfnhkOjF6MUK0NVQ>
HEK293 NWPOeZhyTnWwY4Tpc44hSXO|YYm= NH35bWkyKGh? NYj3NpVUTE2VTx?= MX7Jcohq[mm2aX;uJI9nKEmUIHHzd4V{e2WmIHHzJIdzd3e2aDDmZYN1d3JvaX7keYNm\CCjdYTvdIhwe3Cqb4L5cIF1cW:wIIfpeIghUUN3MDDv[kAzNjh6NzFOwG0> NEjpOVMzOThzMkSxOC=>
Jurkat NITGNoRHfW6ldHnvckBCe3OjeR?= NXyxVXd5OSCq NUPjT5lYTE2VTx?= MkexTY5pcWKrdHnvckBw\iCOQ1ugZZN{\XO|ZXSgZZMh\3Kxd4ToJIZi[3Sxcj3pcoR2[2WmIHH1eI9xcG:|cHjvdplt[XSrb36ge4l1cCCLQ{WwJI9nKDJwN{SxJO69VQ>? M3LRO|IyQDF{NEG0
KARPAS299 NHnDbIpMcW6jc3WgRZN{[Xl? M4XWTFEhcA>? NGTNe5pFVVOR NHuzcmVKdmirYnn0bY9vKG:oIFHMT{Bie3Onc4Pl[EBieyCpcn;3eIgh\mGldH;yMYlv\HWlZXSgZZV1d3Cqb4PwbI9zgWyjdHnvckB4cXSqIFnDOVAhd2ZiMD6wNkDPxE1? Ml7MNlE5OTJ2MUS=
PAE Mn\iSpVv[3Srb36gRZN{[Xl? M4joV|EhcA>? NHrBSVNFVVOR NVLMfHZRUW6qaXLpeIlwdiCxZjDUVmtDKGG|c3Xzd4VlKGG|IHfyc5d1cCCoYXP0c5IucW6mdXPl[EBifXSxcHjvd5Bpd3K7bHH0bY9vKHerdHigTWM2OCCxZjCwMlM6QSEQvF2= NFnnOXczOThzMkSxOC=>
BAF3 NHHJVmtHfW6ldHnvckBCe3OjeR?= NGrqTnczNTNiZB?= NH:xOGZFVVOR NVXTcWZFUW6qaXLpeIlwdiCxZjDUSWwu\nW|ZXSgbY5{fWyrbjDy[YNmeHSxcjDlfJBz\XO|ZXSge4l1cCCLQ{WwJI9nKDFwNkSzJO69VQ>? MlvFNlM4PDJ{NUK=
KARPAS299 NUG3VWUxS3m2b4TvfIlkKEG|c3H5 M3HnV|IuOyCm NUPXcoNpTE2VTx?= NUHI[pQ1UUN3ME2wMlA3PDJizszN NW\RSZduOjN5NEKyOVI>
EBC1 NIj4R2dIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGTxVpM4OiCq NFW0[YdFVVOR NGSwTnhKSzVyPUCuNFI{KM7:TR?= M1\HZlI{QTl|M{K4
HCT116 MnnqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MlLVO|IhcA>? NFP3[nBFVVOR NEHQNo1KSzVyPUG0MlgzKM7:TR?= MYiyN|k6OzN{OB?=
MCF7 M1L6Omdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NIPQN5k4OiCq M37yfGROW09? NWP2PFh{UUN3ME25MlU5KM7:TR?= M33YNFI{QTl|M{K4
MDA-MB-231 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2f6OVczKGh? NUD4dpR4TE2VTx?= MlTVTWM2OD1zMD64JO69VQ>? MlLMNlM6QTN|Mki=
MKN45 Mli0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUX1VlNKPzJiaB?= Ml;uSG1UVw>? NFz3bJhKSzVyPUCuNFE{KM7:TR?= NIDwPWkzOzl7M{OyPC=>
NCI-H441 Mn\VS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnTUO|IhcA>? MV;EUXNQ MYTJR|UxRTF5LkK1JO69VQ>? NEHwUVEzOzl7M{OyPC=>
NCI-H661 NVuxXG9RT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NHS4bYg4OiCq NFnUVIRFVVOR MWXJR|UxRTFzLkS3JO69VQ>? MWCyN|k6OzN{OB?=
SK-MEL-28 MYnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M33K[|czKGh? NGSxTG9FVVOR M1XLNGlEPTB;MUCuPVch|ryP MojINlM6QTN|Mki=
SKOV3 MnnlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2DsVFczKGh? NHL2[IJFVVOR M4\k[mlEPTB;MUKuPFUh|ryP M2L5dFI{QTl|M{K4
SNU5 NYK0S3lnT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnH6O|IhcA>? M{O1OWROW09? MWXJR|UxRTBwMEG2JO69VQ>? NGqySW4zOzl7M{OyPC=>
NCI-H2228 NHTObplIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYj6PY9IPzJiaB?= MWTEUXNQ MmHCTY5pcWKrdHnvckBw\iCDTFut[pV{cW:wIHTybZZmdiClZXzsJJBzd2yrZnXyZZRqd25id3n0bEBKSzVyIH;mJFAvOTF6IN88US=> Mn;1NlQ1OzJ7MEm=
NCI-H3122 NHf1RlFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NV3LcnR{PzJiaB?= M2PBdmROW09? NVrhcGs6UW6qaXLpeIlwdiCxZjDBUGsu\nW|aX;uJIRzcX[nbjDj[YxtKHC{b3zp[oVz[XSrb36ge4l1cCCLQ{WwJI9nKDBwMUC4JO69VQ>? NHy3RnYzPDR|MkmwPS=>
NCI-H3122 MlrlS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXm3NkBp NFnVR3NFVVOR NGftfpBKdmirYnn0bY9vKG:oIFHMT{1nfXOrb36g[JJqfmWwIHPlcIwheHKxbHnm[ZJifGmxbjDpckBpfW2jbjDOR2kuUDNzMkKgZ4VtdHNiaHHyZo9zcW6pIFHMT{BIOTJ4OVGgcZV1[W62IIfpeIghUUN3MDDv[kAxNjZ{MzFOwG0> NIiwO4szPDR|MkmwPS=>
NCI-H3122 M2DhVWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYG0bJdiPzJiaB?= M1Tsc2ROW09? MW\Jcohq[mm2aX;uJI9nKEGOSz3meZNqd25iZILpeoVvKGOnbHygdJJwdGmoZYLheIlwdiCrbjDoeY1idiCQQ1mtTFMyOjJiY3XscJMhcGG{Yn;ybY5oKEGOSzDMNVE6Pk1ibYX0ZY51KHerdHigTWM2OCCxZjCwMlg{QCEQvF2= M3jzWFI1PDN{OUC5
NIH-3T3 NI\ETG5McW6jc3WgRZN{[Xl? NVTzNGh6OSCq NGDofW9FVVOR NIDFXWZKdmirYnn0bY9vKG:oIHj1cYFvKHerbHSgeJlx\SCHTVy0MYZ2e2WmIFHMT{BmgHC{ZYPz[YQh[XO|ZYPz[YQh[XNicHjvd5Bpd3K7bHH0[YQhSUyNIHzleoVtKHerdHigTWM2OCCxZjCwMlA5KM7:TR?= Ml3NNlQ1OzJ7MEm=
NIH-3T3 NH3YNY1McW6jc3WgRZN{[Xl? M3;VVVEhcA>? MWTEUXNQ M4HZOGlvcGmkaYTpc44hd2ZiaIXtZY4hTU2OND3meZNm\CCDTFugS|EzPjmDIH31eIFvfCCneIDy[ZN{\WRiYYPz[ZN{\WRiYYOgdIhwe3Cqbz3BUGshdGW4ZXyge4l1cCCLQ{WwJI9nKDBwNkC1JO69VQ>? NHSxOZYzPDR|MkmwPS=>
NIH-3T3 MknJT4lv[XOnIFHzd4F6 MmW5NUBp M4TBfWROW09? MVjJcohq[mm2aX;uJI9nKGi3bXHuJGVOVDRvZoXz[YQhSUyNIGOxNlA3YSCvdYThcpQh\XiycnXzd4VlKGG|c3Xzd4VlKGG|IIDoc5NxcG9vQVzLJIxmfmWuIIfpeIghUUN3MDDv[kAxNjZ{NjFOwG0> NXL6NHJ1OjR2M{K5NFk>
NIH-3T3 NEHDfIxMcW6jc3WgRZN{[Xl? M17RXlEhcA>? M1jjOmROW09? NIDKPG9KdmirYnn0bY9vKG:oIHj1cYFvKEWPTESt[pV{\WRiQVzLJGwyOTl4TTDteZRidnRiZYjwdoV{e2WmIHHzd4V{e2WmIHHzJJBpd3OyaH:tRWxMKGyndnXsJJdqfGhiSVO1NEBw\iByLki0N{DPxE1? NXTqc4M6OjR2M{K5NFk>
NIH-3T3 M{DmZmtqdmG|ZTDBd5NigQ>? M1TyNlEhcA>? NGjldYJFVVOR MoPvTY5pcWKrdHnvckBw\iCqdX3hckBGVUx2LX\1d4VlKEGOSzDMNVE2OlJibYX0ZY51KGW6cILld5Nm\CCjc4Pld5Nm\CCjczDwbI9{eGixLVHMT{Bt\X[nbDD3bZRpKEmFNUCgc4YhOS5yMk[g{txO NYr0VVlIOjR2M{K5NFk>
BAF3 NVL1NYZOTnWwY4Tpc44hSXO|YYm= MVS3NkBp MknLSG1UVw>? M3;y[GlvcGmkaYTpc44hd2ZiTmDNM2FNUyC2cnHud4Zm[3SnZDDhd5Nme3OnZDDhd{Bk\WyuIHfyc5d1cCCrbnjpZol1cW:wIIfpeIghUUN3MDDv[kAxNjB3MTFOwG0> MljuNlQ1Pjh4M{K=
BAF3 M{WyVmN6fG:2b4jpZ{BCe3OjeR?= MmnnO|IhcA>? M{LlcGROW09? NHG4U2pKSzVyPUCuPVgh|ryP NX3QeGRTOjR2Nki2N|I>
NIH-3T3 NV;RPW1GU2mwYYPlJGF{e2G7 NYDpd3VTOSCq M4PwdmlvcGmkaYTpc44hd2ZiaIXtZY4hTU2OND3meZNm\CCDTFugSlEyPzSOIH31eIFvfCCneIDy[ZN{\WRiYYPz[ZN{\WRiYYOgdIhwe3Cqbz3BUGshdGW4ZXyge4l1cCCLQ{WwJI9nKDBwMU[1JO69VQ>? MWWyOFgyQTFzNh?=
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LB831-BLC NV\CN2tOT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M2XmUmlEPTB;M{SuOVE5PCEQvF2= NVfpcpkxW0GQR1XS
NB5 MVfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYjI[HpSUUN3ME2zOE45PTN3IN88US=> MlLsV2FPT0WU
GB-1 NVeyVFVjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NV73TZdmUUN3ME2zOU4xPDZ7IN88US=> NVm1[GFiW0GQR1XS
TE-15 MWPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUTJR|UxRTN3LkKyN|gh|ryP NY\uT|VtW0GQR1XS
LC4-1 NEnvXmZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NYO5OW9rUUN3ME2zOU4{QDR5IN88US=> M{PuO3NCVkeHUh?=
NCI-H747 NETpNoJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV\JR|UxRTN4LkGzOlkh|ryP MVLTRW5ITVJ?
NTERA-S-cl-D1 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGDXVndKSzVyPUO4Mlc{PDdizszN Mom1V2FPT0WU
SK-MM-2 NGHodGVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2PmbWlEPTB;NECuNVE1PiEQvF2= MXzTRW5ITVJ?
TGW MXrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVniT29qUUN3ME20NU4xPTZ|IN88US=> NH7sbVZUSU6JRWK=
ONS-76 NH7Rd3RIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1uzdWlEPTB;NEKuOFg5OyEQvF2= MnHQV2FPT0WU
CPC-N NIHSZopIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mlr2TWM2OD12Mj65PVcyKM7:TR?= Mmr1V2FPT0WU
ES4 NIW4[GNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFvtOVBKSzVyPUS0MlQyPTNizszN NHXtdFFUSU6JRWK=
Daudi MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MVLJR|UxRTR3LkC4Nlch|ryP MlTSV2FPT0WU
MOLT-4 MoDNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NFHhRW1KSzVyPUS1MlA5PTNizszN NEjtS4tUSU6JRWK=
HT-144 NUC1V4VbT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MoPtTWM2OD12Nj63NlYh|ryP MmnHV2FPT0WU
SW872 MlfHS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHLwOYZKSzVyPUS4MlE6OzNizszN NXzXdIdZW0GQR1XS
D-283MED Mkn1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2i5fmlEPTB;NEiuN|U1OiEQvF2= NI\C[nZUSU6JRWK=
NCI-H2126 M121[Wdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHz6e4ZKSzVyPUS4Mlg1PzZizszN NI\4O|NUSU6JRWK=
NCI-SNU-16 MVrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlezTWM2OD12OT6yNVQ{KM7:TR?= M4LiPHNCVkeHUh?=
CESS NWW5XJVMT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{LjR2lEPTB;NEmuOVA5QCEQvF2= NHyyXppUSU6JRWK=
A101D NULrWZdUT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mnz1TWM2OD12OT65O|M3KM7:TR?= NVjuVHVLW0GQR1XS

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 slightly soluble or insoluble
Ethanol slightly soluble or 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