Vemurafenib (PLX4032, RG7204)

目录号:S1267 别名: RO5185426

Vemurafenib (PLX4032, RG7204) Chemical Structure

Molecular Weight(MW): 489.92

Vemurafenib (PLX4032, RG7204)是一种新型有效的B-RafV600E抑制剂,IC50为31 nM。Vemurafenib对B-RafV600E的选择性比对野生型B-Raf的选择性高10倍,在细胞实验中,选择性可高100倍以上。

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客户购买Selleck的此次产品后发表的文献71篇:

客户使用该产品的18个实验数据:

  • The regressing tumour microenvironment stimulates the outgrowth, infiltration and metastasis of drug-resistant clones. b, Bioluminescent signal of drug-resistant A375RTGL cells in vemurafenib-sensitive, A375 tumours, treated with vehicle or vemurafenib for 5 days (vehicle, n = 36; vemurafenib, n = 15 tumours). D, day. c, EdU incorporation in A375R-TGL cells in A375/A375R-TGL tumours treated with vehicle or vemurafenib for 4 days, as determined by FACS (vehicle, n = 8; vemurafenib, n = 6 tumours). d, Bioluminescent signal of A375R-TGL tumours alone, treated with vehicle or vemurafenib for 5 days (vehicle, n 5 38; vemurafenib, n = 15 tumours). e, Bioluminescent signal of TGLexpressing drug-resistant cancer cells (A375R, M249R4, PC9 and H2030) in drug-sensitive tumours (Colo800, LOX, UACC62, M249, H3122 and HCC827) treated with vehicle or drugs (vemurafenib, crizotinib and erlotinib) for 5 days (n (from left to right on the graph) = 6, 7, 12, 12, 9, 9, 25, 26, 9, 12, 12, 12, 16 and 11 tumours). f, Spontaneous lung metastasis by A375R cells in mice bearing A375/A375R-TGL tumours treated with vehicle or vemurafenib (10 days), visualized by BLI (n = 4).

    Nature 2015 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    FRA1 downregulation during RAFi treatment drives the reactive secretome. c, Relative mRNA levels of FRA1 during vemurafenib exposure [0.1-1 uM]. d, Representative immunofluorescence staining of A375/A375R tumours for GFP (A375R, green) and FRA1 (red) after vehicle or vemurafenib treatment (5 days). DAPI, 49,6-diamidino-2-phenylindole. Scale bars, 50 um.

    Nature 2015 520(7547), 368-72. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Acquired EGFR expression in BRAF(V600E) mutant melanoma after vemurafenib resistance. Immunohistochemical (IHC) analysis (ultraView DAB stain, brown) showing increased EGFR expression in formalin-fixed paraffin embedded (FFPE) (Patient number 1-5) and frozen (Patient number 6) melanoma tissue sections from BRAF(V600E) mutant melanoma patients who developed resistance to vemurafenib, dabrafenib or trametinib as indicated. For each patient, the first biopsy is from the pre-treatment tumour; the second biopsy was performed after the tumour had progressed under treatment. For patient number 4, the first biopsy was performed when the patient was in partial response, but rapidly developed secondary resistance. Then 4.5 months later, the second biopsy was taken.

    Nature 2014 508(7494), 118-22. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Long-term colony formation assay of thyroid cancer (8505C), CRC (OXCO-1, COLO741 and WiDr) and melanoma (A375) cells. Cells were grown in the absence or presence of PLX4032 at the indicated concentrations for 10-14 days. For each cell line, all dishes were fixed at the same time, stained and photographed.

    Nature 2012 483(7387):100-3. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Resistance to BRAF(V600E) inhibition in WiDr cells is mediated through feedback activation of EGFR. Biochemical responses of WiDr cells treated with PLX4032, cetuximab or gefitinib, or their combinations, were documented by western blot analysis. Cells were harvested at 6 h after drug treatment. BRAF(V600E) inhibition results in strong upregulation of Tyr1068 p-EGFR and Ser473 phosphorylated-AKT (p-AKT), which is abrogated by EGFR inhibitors. Furthermore, combination treatments result in complete inhibition of phosphorylated MEK (p-MEK) and phosphorylated ERK (p-ERK). Heat shock protein 90 (HSP90) served as a control.

    Nature 2012 483(7387):100-3. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Co-stain and sort for EGFR and NGFR into four populations: double-negative and double-positive, and EGFR-positive or NGFR-positive only, followed by 1 μM vemurafenib (2 weeks). Resistant colonies circled in the images (1 of n = 2 biological replicates).

    Nature, 2017, 546(7658):431-435. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Box plot showing sgRNA frequencies after vemurafenib or control treatment from n = 4 infection replicates.

    Nature, 2017, 548(7667):343-346. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    a-c, Inhibitors of BRAFV600E (PLX4032) and MEK1/2 (PD98059 or AZD6244) increase PGC1α and ID2 expression (a, b) and repress integrin expression and signalling (b, c). Cells were treated with indicated concentration of inhibitors for 6 h (a, b) or 24 h (c). d, e, PLX4032 increases the interaction between ID2 and TCF4 (d) and decreases the occupancy of TCF4 at the promoters of integrin genes (e). f–g, PGC1α and ID2 are partially required for PLX4032-mediated inhibition of invasion and metastasis. For in vitro assays (f), A375 cells were incubated with 1 μM PLX4032 for 10 h. Images represent one picture captured per membrane with the scale bar representing 200 μm. Values in a, b, e and f represent mean±s.d. of independent biological triplicates; *P<0.05 and **P<0.01 by Student's t-test in a, b, e, f.

    Nature, 2016, 537(7620):422-426.. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • (A) Concentration-dependent target occupancy of vemurafenib and its cognate target BRAF compared with the off-target FECH. ITDR profiling was performed at 55°C with vemurafenib-treated K562 cells and showed concentration-dependent thermal stabilization of FECH and BRAF. The data are normalized so that the quantity of soluble target at the highest compound concentration, which reflects maximum thermal stabilization, is set to 1 and fixed for curve-fitting. (B) ITDR performed at 55°C with K562 cells treated with vemurafenib, alectinib, or crizotinib over a range of concentrations. Alectinib displays a more potent effect on FECH as compared with that by vemurafenib, whereas crizotinib, a drug not known to cause photosensitivity, has no effect.

    Science, 2014, 346(6205):1255784.. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Impact of BRAF and SYK/MEK inhibition on ERK activation in primary CLL cells. Representative Western blot analysis for pERK and tERK of the protein lysate at the indicated concentrations of vemurafenib and dabrafenib for patients 1 and 2. The experiment was performed 2 times with similar results.

    J Clin Invest 2014 124(11), 5074-84. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • The B-Raf inhibitor PLX4032 decreases cell surface DR5 levels . BCPAP cells were treated with the indicated concentrations of PLX4032 for 12 h and then harvested for extraction of cellular total RNA and subsequent RT-PCR to detection of DR5.

    Oncogene 2015 10.1038/onc.2015.97. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Stat3 is activated in melanoma cells with acquired resistance to vemurafenib. Sensitive and resistant A375 melanoma cells were stimulated by different doses of vemurafenib as indicated. Total protein was collected 6 hours after stimulation. Protein expressions of phospho–ERK1/2, Stat3, phospho-Stat3, and paired box homeotic gene 3 (PAX3) were analyzed by western blot along with tubulin, which served as a loading control.

    J Invest Dermatol 2013 133, 2041. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Clonogenic assays of VM21 (b) and VM1 (c) cells treated with 1 μM PD166866 (PD) and 0.1 μM RG7204 (RG) for 14 days. For VM21 cells, the combination index (CI) value indicating synergism is shown. For VM1 cells, inefficacy of 1 μM PD166866 alone precluded calculation of a CI value and P-values for reduction of clonal growth are shown instead. a, P<0.05 versus RG; b, P<0.01 versus PD.

    J Invest Dermatol 2011 131, 2087-95. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    BRAF inhibition improves autologous tumor recognition by CD8+ tumor-infiltrating lymphocytes. (A and B) Tumor-infiltrating lymphocytes (TILs) were co-cultured with autologous BRAFV600E mutant melanoma target cell lines treated with vemurafenib (Vem) at low or high dose, or left untreated. (A) Frequency of tumor necrosis factor α (TNF α)-and interferon γ (IFN γ)-producing CD8+ TILs. (B) Frequency of CD8+ TILs producing TNF α and IFN γ and simultaneously mobilizing CD107a upon co-culture with autologous tumor cells. *p < 0.05; ** p < 0.01; ***p < 0.001.

    Oncoimmunology 2012 1, 1476-1483. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • Fig 1 represents the cell cytotoxicity assay to study the effect of Vemurafenib on ABCC10 (MRP7) overexpressing cells. Table 1 shows the data suggesting reversal of resistance ABCC10 overexpressing cells with Vemurafenib at 20 μM using Paclitaxel as a substrate. HEK293 is a human embryonic kidney cell line while HEK293/MRP7 is an MRP7 overexpressing cell line generated by MRP7 gene transfection. Cepharanthine is a positive control. Vemurafenib (20 μM) in combination with Paclitaxel can reverse MDR mediated by MRP7 over-expressing cells as it decreased the resistance fold from 24-fold to 1-fold.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

    Fig 2 represents the cell cytotoxicity assay to study the effect of vemurafenib on ABCG2 (BCRP) overexpressing cells. Table 2 shows the data suggesting reversal of resistance ABCG2 overexpressing cells with vemurafenib at 20 μM using mitoxantrone as a substrate. H460 is a hepatic carcinoma cell line while H460/MX20 is an ABCG2 overexpressing cell line made resistant by drug selection with mitoxantrone. FTC (Fumitremorgin C) is a positive control. Vemurafenib (20 μM) in combination with Mitoxantrone can reverse MDR mediated by ABCG2 over-expressing cells as it decreased the resistance fold from 133-fold to 93-fold.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

  • represents the effect of Vemurafenib on the accumulation of [3H]-Mitoxantrone. Vemurafenib increased the intra-cellular accumulation of Mitoxantrone in ABCG2 overexpressing H460/MX20 cells compared with parental H460 cells. From the figure, the accumulation in H460/MX20 control is decreased whereas in presence of Vemurafenib 20 μM, it is significantly increases the [3H]-Mitoxantrone accumulation.

    Dr. Zhe-Sheng Chen of St. John's University. Vemurafenib (PLX4032, RG7204) purchased from Selleck.

     

    Anti-ErbB3 mAbs differently counteract the increase of ErbB3-dependent AKT phosphorylation and potentiate growth inhibition induced by vemurafenib. LOX IMVI melanoma cells serum starved and treated with vemurafenib (0.3μ M) for 24 h were incubated or not with 20 μ g/ml of anti-ErbB3 mAbs A4 (a),A3orA2(d). Western blot analysis shows that A4 and A3, but not A2 mAbs abrogate receptor phosphorylation and ATK signaling. For densitometric analysis pErbB3/ErbB3, pERK/ERK and pAKT/ATK values are expressed as fold change with respect to the control unstimulated cells to which value = 1 was assigned. Results are expressed as mean values from three independent experiments. LOX IMVI cells were grown in the presence of different doses of vemurafenib alone or in combination with 20 μg/ml of A4 (b),A3 or A2(e) mAbs for 10 days. Cells were then fixed and stained with crystal violet(c). Cells were then dissolved in a Methanol/SDS solution and the adsorbance (595 nm) was read using a microplate ELISA reader (b, e). Quantitative analysis for curve fitting and for IC50 evaluation, performed by KaleidaGraph software, shows that the treatment with A4 and A3 but not with A2 enhances the inhibitory effect of vemurafenib on cell growth (IC50 vem = 155 nM; IC50 vem + A4 = 36 nM; IC50 vem + A3 = 62, IC50 vem + A2 = 146 nM). Results are reported as mean values±standard deviation (SD) from three independent experiments. p-values were calculated using Student ’s t test and significance level has been defined as p < 0,05. For IC50 vem + A4 and IC50 vem + A3 p < 0,001 vs IC50 vem; IC50 vem + A2 NS vs IC50 vem.

    Vemurafenib (PLX4032, RG7204) purchased from Selleck.

产品安全说明书

Raf抑制剂选择性比较

生物活性

产品描述 Vemurafenib (PLX4032, RG7204)是一种新型有效的B-RafV600E抑制剂,IC50为31 nM。Vemurafenib对B-RafV600E的选择性比对野生型B-Raf的选择性高10倍,在细胞实验中,选择性可高100倍以上。
特性 PLX4032是新型有效的B-RAFV600E 肿瘤蛋白抑制剂。
靶点
SRMS [1]
(Cell-free assay)
ACK1 [1]
(Cell-free assay)
B-Raf (V600E) [1]
(Cell-free assay)
C-Raf [1]
(Cell-free assay)
MAP4K5 (KHS1) [1]
(Cell-free assay)
18 nM 19 nM 31 nM 48 nM 51 nM
体外研究

PLX4032抑制B-RAFV600E, C-RAF, 和 野生型B-RAF, IC50分别为31 nM, 48 nM, 和100 nM。PLX4032 也抑制一些非-RAF激酶,包括ACK1, KHS1,和SRMS, IC50 为18 nM 到51 nM。[1] PLX4032作用于黑色素瘤细胞系,抑制效果依赖于B-RAF突变状态,因为PLX4032有效抑制含B-RAFV600突变的细胞, 包括V600E, V600D, V600K, 和V600R, 但是对野生型或其他突变没有作用效果。PLX4032作用于MALME-3M, Colo829, Colo38, A375, SK-MEL28, 和A2058细胞时,IC50为20 nM 到 1 μM。0.1 μM 到30 μM PLX4032 也抑制MEK1/2 和ERK1/2磷酸化作用。[2] PLX4032高效作用于黑色素瘤的治疗 ,因为PLX4032有效抑制B-RAFV600E。PLX4032作用于结肠癌细胞,抑制B-RAF V600E导致 EGFR激活的快速回应,可用于补偿PLX4032抑制的细胞增殖。[3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
A375 MorNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1:5WlExOCEQvF2= NXPYXHZXQTZiaB?= NELlPJRFVVOR NVHBO2JrUUN3ME20O{BvVQ>? M{DYVVE5PDV6MEWz
ARO NIfKWWpIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVPUUmpYOTByIN88US=> NYntNpF1QTZiaB?= NEHHRmtFVVOR M3j2fGlEPTB;MkC1JI5O MX6xPFQ2QDB3Mx?=
NPA MYLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUPNemZoOTByIN88US=> NILXbmU6PiCq M3fQXGROW09? MnrUTWM2OD1{NjDuUS=> M4rtbVE5PDV6MEWz
TPCI MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWSxNFAh|ryP NVPEeIZOQTZiaB?= MWDEUXNQ MknuTWM2OD1zMD63O{DPxE1? NF;tOGcyQDR3OEC1Ny=>
A375 Mn7TRZBweHSxc3nzJGF{e2G7 MnWwNVAh|ryP MkPiSG1UVw>? M4HiN3Bzd22xdHXzJIFxd3C2b4TpZ{Bl\WG2aB?= M2riblE5PDV6MEWz
ARO M1TyWGZ2dmO2aX;uJGF{e2G7 M3rvbFExKM7:TR?= MXK3NkBp M1\KfWROW09? NYfmbHZUUW6mdXPld{B1cGVicnXlfJBz\XO|aX;uJI9nKHSqZTDOTXMheHWvcB?= MnnENVg1PThyNUO=
8505C (BRAF V600E/V600E) M4PtO2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NW\kbmQ1QTZiaB?= M33nemlEPTB;NUegcm0h MYKyNFE1QTF|Nh?=
SW1736 (BRAF WT/V600E) M3HMcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGH1RXg6PiCq MnuxTWM2OD1{OTDuUS=> NHX6e5QzODF2OUGzOi=>
BHT101 (BRAF WT/V600E) NFPFWI1Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2HHPFk3KGh? NFnpdmRKSzVyPUm3JI5O NYPYdpVOOjBzNEmxN|Y>
BCPAP (BRAF WT/V600E) NEHXTVdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX[5OkBp M3vydmlEPTB;N{igcm0> MViyNFE1QTF|Nh?=
C643 (HRAS G13R)≥ 500 MX7Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX[5OkBp NV;IPHl[UUN3MDFijcUhPTByIH7N Ml2zNlAyPDlzM{[=
HTH7 (NRAS Q61R) NELMbYJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFPUd2g6PiCq NIXNOmFKSzVy4polJFExODBibl2= NIC2N|YzODF2OUGzOi=>
CAL62 (KRAS G12R) > 1000 > 1000 M3HMN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NF3FOpA6PiCq MVnJR|UxRiBzMECwJI5O MV[yNFE1QTF|Nh?=
TPC-1 (RET/PTC1) MoXKS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MmrZPVYhcA>? NELF[WtKSzVy4polNVAxOCCwTR?= M1jvOVIxOTR7MUO2
PC NH[2fWNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUO5OkBp M1jVfmlEPTB-IEGwNFAhdk1? MYeyNFE1QTF|Nh?=
Calu-6 MX\GeY5kfGmxbjDBd5NigQ>? NYLVeZp{OeLCid88US=> M1XsTlEhcA>? Mkf1SG1UVw>? M13XOWFkfGm4YYTld{BOTUtxRWLLJIlvKGOnbHzzJJdqfGhid3ns[E11gXCnIFLSRWY> MYCyNFE4QTdyNR?=
C4 NYDNb|E4TnWwY4Tpc44hSXO|YYm= NEixTIk{KM7:TR?= MlviOFghcA>? MUjEUXNQ M1S3Umlv[3KnYYPld{Bkd2yuYXflckB{gW62aHXzbZMh[W6mIHTlZ5Jm[XOnczDJUE05KGW6cILld5Nqd25? MlW5NlU6QDl3ME[=
VMM12 MlnKSpVv[3Srb36gRZN{[Xl? M{HQUVMh|ryP NXfZUmJHPDhiaB?= Mm\hSG1UVw>? MmDLTY5kemWjc3XzJINwdGyjZ3XuJJN6dnSqZYPpd{BidmRiZHXjdoVie2W|IFnMMVkh\XiycnXzd4lwdg>? NUfwZVJNOjV7OEm1NFY>
SKMEL19 NUTiV|V2TnWwY4Tpc44hSXO|YYm= M1XSS|Yh|ryP MoHWOFghcA>? MX3EUXNQ M1rxNXRzcWepZYLzJGVTKHO2cnXzdy=> NGG2dnYzOzN4MkK0NC=>
UKF-NB-3 (ABCB1) NEX1Wo1HfW6ldHnvckBCe3OjeR?= MknsNU4zPSEEtV2= NV:1UVMzOiCq MoTsSG1UVw>? NInVeXRGdmijbnPld{Bi[2O3bYXsZZRqd25ib3[geIhmKG[udX;y[ZNk\W62IFHCR2IyKHO3YoP0doF1\SC{aH;kZY1qdmViMUKz MXKyOFc{PTd4Nh?=
UKF-NB-3 MoDtSpVv[3Srb36gRZN{[Xl? MmPtNU4zPSEEtV2= MV6yJIg> MlXLSG1UVw>? M1jNbXNq\26rZnnjZY51dHliYX\m[YN1eyCxbjDhZ4N2dXWuYYTpc44hd2ZidHjlJIZtfW:{ZYPj[Y51KEGEQ1KxJJN2[nO2cnH0[UBzcG:mYX3pcoUhOTJ| NUfic3d3OjR5M{W3OlY>
A375 (BRAFV600E) NWPiSYt2TnWwY4Tpc44hSXO|YYm= NWK5VWVjQCCq NGfQS4ZFVVOR MnS1TY5kemWjc3XzJIlvfHKjY3XscJVt[XJiUl;TJIFv\CCQTzDs[ZZmdHNi MlruNlU{PjN4NES=

... Click to View More Cell Line Experimental Data

体内研究 PLX4032按6 mg/kg-20 mg/kg 剂量作用于B-RAFV600E-突变鼠移植瘤模型,抑制肿瘤生长。[1] PLX4032按12.5 mg/kg-100 mg/kg剂量作用于携带LOX, Colo829, 和A375移植瘤小鼠,抑制肿瘤生长,延长小鼠寿命。[2]

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

激酶实验:

[1]

+ 展开

RAF激酶活性测定:

通过测量生物素化的BAD蛋白磷酸化而测定野生型RAF和突变型的激酶活性。在20 mM Hepes (pH 7.0), 10 mM MgCl2, 1 mM DTT, 0.01% (v/v) Tween-20, 50 nM 生物素-BAD 蛋白,和 1 mM ATP 的混合物中室温下进行反应。加入5 μL 含20 mM Hepes (pH 7.0), 200 mM NaCl, 80 mM EDTA, 0.3% (w/v) 牛血清蛋白 (BSA)的溶液,5分钟后,反应终止。终止溶液也包含p-BAD (Ser112) 抗体,链霉亲和素包被的供体小珠,蛋白A 受体小珠。抗体和小珠在终止溶液中黑暗环境下室温预温育30分钟。 最终抗体被稀释2000倍,每个小珠的终浓度为10 μg/mL。重复做三次单独纯化蛋白实验,去不同两批的平均值作为突变活性。
细胞实验:

[2]

+ 展开
  • Cell lines: MALME-3M, Colo829, Colo38, A375, SK-MEL28, 和 A2058 细胞
  • Concentrations: 0–10 μM , 溶于 DMSO
  • Incubation Time: 5 天
  • Method:

    通过MTT 实验测评细胞增殖。细胞按每孔1000到5000个接种在96孔板上,体积为180 μL。PLX4032按最终实验浓度的10倍储备在含1% DMSO的培养基中。细胞接种24小时后, 加入20 μL适当稀释的PLX4032。接种6天后,进行增殖实验。计算抑制百分数,根据抑制百分数与浓度的对数的回归分析测定IC50值。


    (Only for Reference)
动物实验:

[2]

+ 展开
  • Animal Models: 携带LOX, Colo829, 和A375移植瘤细胞的无胸腺裸鼠
  • Formulation: 配制成微沉淀散粉 (MBP), 按指定浓度悬浮在含2% Klucel LF的水溶液中,然后使用HCl调节pH为4
  • Dosages: 12.5 mg/kg–100 mg/kg
  • Administration: 口服饲喂,每天两次
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 97 mg/mL (197.99 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品:
4% DMSO+30% PEG 300+5% Tween 80+ddH2O
5mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 489.92
化学式

C23H18ClF2N3O3S

CAS号 918504-65-1
稳定性 powder
别名 RO5185426

计算器

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摩尔浓度计算器

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    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

临床试验信息

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT01585415 Terminated Metastatic Cancer|Melanoma National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) April 9, 2012 Phase 1
NCT01843738 Not yet recruiting BRAFV600 Mutation|Stage IV Melanoma University of Utah January 2017 Phase 1
NCT02314481 Not yet recruiting Non-small Cell Lung Cancer University College, London|Hoffmann-La Roche January 2017 Phase 2
NCT03013491 Recruiting Solid Tumor|Lymphoma CytomX Therapeutics January 2017 Phase 1|Phase 2
NCT02908672 Recruiting Melanoma Hoffmann-La Roche January 2017 Phase 3
NCT03005639 Recruiting Stage IIIB-C Melanoma Inova Health Care Services|Genentech, Inc. December 2016 Phase 2

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操作手册

如果有其他问题,请给我们留言。

  • * 必填项

常见问题及建议解决方法

  • 问题 1:

    How about the half-life of Vemurafenib(S1267)?

  • 回答:

    It was reported that the half-life of the compound is 57 hours.

  • 问题 2:

    The vemurafenib power, when prepared in 4% DMSO/30% PEG 300/5% Tween 80/ddH2O solutions, form a pellet down the tube?

  • 回答:

    When prepare this kind of vehicle, please dissolve the drug in DMSO clearly first. If it dissolves not readily, please sonicate and warm in the water bath at about 45 degree. Then add PEG and Tween. After they mixed homogeneously, then dilute with water.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID