Vismodegib (GDC-0449)


Vismodegib (GDC-0449) Chemical Structure

Molecular Weight(MW): 421.3

Vismodegib (GDC-0449)是一种新型有效的,特异性hedgehog抑制剂,无细胞试验中IC50为3 nM,也会抑制P-gp,IC50为3.0μM。

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RMB 730.63 现货
RMB 1398.12 现货
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  • SMOΔC captured on cholesterol beads in the presence of increasing concentrations of free vismodegib or 20(S)-OHC (h). Results from one of two independent pull-down experiments are shown.

    Nature, 2016, 535(7613):517-22.. Vismodegib (GDC-0449) purchased from Selleck.

    (B) qRT-PCR analysis and immunostaining of murine HSCs treated with GDC-0449 on culture days 4 through 7 (to inhibit SMO) or culture day 7 SMO-LoxP HSCs treated with adenoviral Cre on day 4 (to disrupt the Smo gene).

    Gastroenterology 2012 143, 1319-29. Vismodegib (GDC-0449) purchased from Selleck.

  • Hh signaling controls metabolic reprogramming during liver injury in vivo. Immunohistochemistry identifies cells expressing the M2 isozyme of PKM2, a specific marker of glycolytic activity, ( C) inhibited in aged MDR2 -/- mice by GDC-0449.

    Gastroenterology 2012 143, 1319-29. Vismodegib (GDC-0449) purchased from Selleck.

    Inhibition of Hedgehog (Hh) pathway prevents liver sinusoidal endothelial cell (LSEC) capillarisation in vivo. (A) Liver sections from dimethyl sulphoxide (DMSO) and GDC-0449-treated Mdr2 -/- mice were double-stained for Gli2 (brown, Hh target gene) and CD31 (blue, capillarisation marker). Note that LSEC co-express Gli2 and CD31 (arrow). Scale bar: 10 μm. The number of Gli2/CD31 double-positive cells per field (B) was counted in five random fields per mouse, ***p < 0.001, n = 3. (C) Liver sections from vehicle and cyclopamine-treated partial hepatectomised (PHx) mice were stained for Gli2 and CD31, and the number of Gli2/CD31 double-positive cells was counted. **p< 0.01, n = 3. Cyc, cyclopamine

    Gut 2013 62, 299-309. Vismodegib (GDC-0449) purchased from Selleck.

  • GDC-0449, a preclinical Hh pathway inhibitor, inhibits replication of JFH1 HCV in a dose-response manner. (A) Huh7.5 cells were mock-infected (control), infected with JFH1 HCV alone, JFH1 HCV plus vehicle (JFHþ DMSO), and JFH1 HCV plus GDC-0449 5 μM concentration. After 72 hours, relative RNA expression was analyzed for HCV RNA, Shh, and Gli1. Results are expressed as relative fold expression with mock-infected expression indexed to 1, except for HCV RNA sample, in which case JFH1 HCV alone was indexed to 1. (B) Protein lysates were created from the above-described experiment. Antibodies to HCV Core, Shh, and a-tubulin were used for analysis. (C) The above experiment was repli-cated with var ying concentrations of GDC-0449 to assess dose-response of anti-HCV activity. Concentrations used were: 0 μM, 0.05 μM, 0.5 μM, 5 μM, and 25 μM. After 72 hours, relative RNA expression was analyzed for HCV RNA, Shh, and Gli1. Results are expressed as relative fold expression with mock-infected expression indexed to 1, except for HCV RNA sample, in which case JFH1 HCV alone was indexed to 1. *P < 0.05, **P < 0.01, † P < 0.005.

    Hepatology 2011 54, 1580-90. Vismodegib (GDC-0449) purchased from Selleck.

    Changes in markers of Hh signaling were determined in HBx positive (X) and negative (CAT) HepG2 and Huh7 cells treated with DMSO or GDC- 0449. A and B, qRT- PCR results are shown as the mean±SEM of triplicate experiments. P < 0.05; P < 0.01;†, P < 0.005. C, representative Western blot analysis of total extracts from the cells above. D, quantification o f protein levels (mean expression±SD of 3 assays for each marker). DMSO controls are the black bars and cells treated with 1 μmol/L GDC- 0449 are the white bars.

    Cancer Res 2012 72, 5912-20. Vismodegib (GDC-0449) purchased from Selleck.

  • Phenotypic changes associated with Hh signaling in HBx positive and negative cells with or without GDC-0449. A, rep resentative images of HBx expressing cells that migrated through Matrigel basement membrane (×200). B, quantifi cation of the results in A (mean expression±D of 3 assays ). Cells were treated with DMSO (dark bars) or with GDC-0449 (light bars). P < 0.01; P < 0.02. C, anchorage-independent growth of Huh7X and HepG2X with or without GDC-0449. D, quantification o f the results in C (mean expression±D of 3 assays). Cells were treated with DMSO (dark bars) or with GDC-0449 (light bars).

    Cancer Res 2013 72, 5912-20. Vismodegib (GDC-0449) purchased from Selleck.

    Relationship between Hh signaling and HCC in HBxTg. A, HCC nodules (circled) on the surface of the liver. B, the number of visible nodules observed on livers ( n = 6 HBxTg per group) after inject ions of vehicle (dark bars) or GDC- 0449 (light bars). Tumor numbers for individual mice are shown above each bar. The average tumor number is shown above each group. C, Western blot analysis for Gli2 in livers from transgenic mice treated with vehicle (-) or GDC- 0449 (+). D, staining for Gli2 and Shh on serial section s of tumors (T) and nontumor (NT) livers from HBxTg treated with vehicle (top) or GDC- 0449 (bottom). Magnification is ?00 for each panel and ?00 for each insert.

    Cancer Res 2014 72, 5912-20. Vismodegib (GDC-0449) purchased from Selleck.

  • (A) GDC0449 dose-dependent inhibition of Shh-stimulated Hh pathway activity in the presence or absence of 10 μM FA , or SmoM2 expressing cell lines. (B) Representative images of Smo::EGFP/Ivs: :tagRFPT cells treated with GDC0449 and Shh in the presence or absence of 10 μM FA. GDC0449 was coapplied at 111 and 1,111 nM respectively with Shh and Shh+FA . (C) Relative Smo::EGFP+ cilium count of GDC0 449’s dose-dependent inhibition of Shh ligand-stimulated accumulation of cilia ry Smo in the presence or absence of 10 μM FA. Measurements were performed in quadruplicate. Several hundred cells were analyzed in each sample to asses s the accumulation of Smo in the PC from data in (B). Data plotte d are mean (±SD). Scale bar: 5 μm.

    Chem Biol 2012 19, 972-82. Vismodegib (GDC-0449) purchased from Selleck.

    Quantification of Smo ciliary localization (A) and representative images (B) of Smo::EGFP/Iv s::tagRFPT cells treated with GDC0449 and Shh in the presence or absence of 10 μM Bud. In (B), GDC0449 was coapplied at 1.6 nM with Shh and Shh+Bud, respectively. (C) GDC0449 dose-dependent inhibition of Shh-stimulated Hh pathway activity in the presence or absen ce of 10 μM Bud. Data plotted are mean (± SD) from four biological replicates (A) analyzing over a thousand of cells or three biological replicates (C). Scale bar: 5 μm.

    Chem Biol 2012 19, 972-82. Vismodegib (GDC-0449) purchased from Selleck.

  • Hh inhibitor, GDC-0449, blocks hepatic Hh activity in the irradiated mice. (A) H&E staining shows less fat accumulation in hepatocytes in liver from representative irradiated mice with GDC-0449 (IR+GDC) (X40). (B) Relative liver weight/body weight of mice. (C) The values of AST and ALT are graphed. (D) QRT-PCR analysis of liver mRNA from DMSO (DMSO), radiation treated mice with (IR+GDC) or without GDC-0449 (IR+DMSO) for smo, and gli2 ((n≥4 mice/group). Mean±SD results are graphed. (E) and (F). Western blot analysis of Smo, and Gli2 (GAPDH was used as an internal control). Data shown represent one of three experiments with similar results (E: Immuoblot/F: Band density) (n≥4 mice/group). Data represent the mean±SD of three independent experiments (*p<0.05, **p<0.005).

    PLoS One 2013 8, e74141. Vismodegib (GDC-0449) purchased from Selleck.

    Hedgehog (Hh) inhibitor, GDC-0449, abrogates effects of Hh signaling within liver parenchyma and HCC nodules. A. Liver sections stained for Gli2 from representative DMSO- and GDC-0449- treated mice (40×). Quantitative Gli2 immunohistochemistry data in non-tumor livers of mice treated with DMSO or GDC-0449 (n = 9–10/group) are graphed as mean ±SEM (**p < 0.01 . The number of ductular cells with Gli2 positive staining were counted in each portal tract/section under 40×magnification. B. Tumor sections from the same mice were also stained to demonstrate Gli2. Results from representative DMSO- and GDC-0449-treated mice are displayed. Quantitative Gli2 immunohistochemistry data were generated by counting nuclear Gli2 positive ductular and hepatocytic cells in tumor sections under 40×magnification. Results are graphed as mean ± SEM Gli2-positive cells/40×high power field (**p < 0.01)C–D Quantitative reverse transcription-PCR (qRT-PCR) analysis of whole liver RNA from DMSO-(open bar) and GDC-0449 (black bar) treated mice. C. PPAR-c, a gene that is normally repressed by Hh signaling. D.Gli1, a gene that is induced by Hh signaling. Mean±SEM are graphed (**p < 0.01).

    PLoS One 2011 6, e23943. Vismodegib (GDC-0449) purchased from Selleck.

  • GDC-0449 treatment reduces fibrosis in Mdr2 -/- mice. A. Immunohistochemical staining for α-SMA (top panel) and Sirius red (bottom panel) in sections of non-tumor liver from representative age-matched Mdr2 -/- and wildtype mice (10×). B. Pooled Hepatic hydroxyproline content of 2-52 wk-old wildtype (WT) and age-matched Mdr2 -/- mice (n = 3–5/group). Results in Mdr2 -/- mice were normalized to that of age-matched WT mice and graphed as fold change. Data are displayed as mean +/- SD (*p < 0.05)C. Non-tumor liver sections stained fora-SMA (top panel, 20×) and Sirius red (bottom panel, 10×) in representative DMSO- and GDC- treated Mdr2 -/- mice. D.Heptic hydroxyproline content of DMSO- and GDC- treated mice (n = 9/group). Results in GDC-0449-treated mice were normalized to that of DMSO vehicle-treated mice and graphed as fold change. Data are displayed as Mean +/- SEM (*p < 0.05).

    PLoS One 2011 6, e23943. Vismodegib (GDC-0449) purchased from Selleck.

    Inhibition of Hh signaling decreases osteopontin and osteopontin-responsive (CD44) positive cells in tumors and peritumoral tissues of aged Mdr2 -/- mice. A. Tumor sections from representative DMSO- and GDC-0449 treated Mdr2 -/- mice were stained to demonstrate osteopontin (OPN) Representative sections are displayed ( Right panel ). OPN staining was quantified by morphometric analysis of at least 5 HPF per tumor section using 20譵agnification (n = 5 mice/group). Results in the GDC-0449-treated group were normalized to that of the group treated with DMSO vehicle and graphed as fold change. Data are displayed as Mean 盨EM (**p < 0.01). B. Immunohistochemical staining for the osteopontin receptor, CD44, in peri-tumoral tissues of representative DMSO- and GDC-0449- treated Mdr2 -/- mice. (Right panel ) CD44 staining was quantified by morphometric analysis as described in A. Results in GDC-0449-treated mice were normalized to those of vehicle-treated controls and graphed as Mean盨EM (**p < 0.01). C. QRT-PCR analysis of liver tumor RNA from DMSO- (open bar) and GDC-0449- (closed bar) treated Mdr2 -/- mice for OPN (left) and CD44 (right). After normalization to results in the DMSO-treated group, Mean盨EM were graphed (*p < 0.05).

    PLoS One 2011 6, e23943. Vismodegib (GDC-0449) purchased from Selleck.

  • Mouse medulloblastoma primary cells (U51669) showed inhibition of Gli1 by GDC-0499 in dose dependent manner. *P<0.01.



    J Neuroncol 2011 105, 475-483. Vismodegib (GDC-0449) purchased from Selleck.


    Flow cytometry of purpurin-18 accumulation in the presence of the following inhibitors in mouse and human ABCG2-expressing sublines demonstrated a similar pattern of inhibition. The fold value is defined as the accumulation of Pp-18 in the presence of an inhibitor divided by the accumulation of Pp-18 in the absense of any inhibitor. Data represent mean±S.D. of three observation.

    Vismodegib (GDC-0449) purchased from Selleck.




产品描述 Vismodegib (GDC-0449)是一种新型有效的,特异性hedgehog抑制剂,无细胞试验中IC50为3 nM,也会抑制P-gp,IC50为3.0μM。
Hedgehog [1]
(Cell-free assay)
3 nM

GDC-0449有效抑制hedgehog通路,是一种新型及特定合成的小分子抑制剂,IC50为3nM。[1] GDC-0449作用于Hedgehog信号通路,阻断Hedgehog配位体,即细胞表面受体PTCH 及SMO的活性,从而阻断Hedgehog信号通路。在组织生长和修复方面,Hedgehog信号通路意义重大。Hedgehog通路信号的异常激活,及不受控制的细胞增殖,可能与Hedgehog配位体,即细胞表面受体PTCH 及SMO的突变有关。在体外,GDC-0449在不抑制胰脏细胞增殖的前提下阻止原代胰脏移植物的生长,这项结果最近已经应用到临床。GDC-0449也抑制ABCG2, P-糖蛋白, 及和MDR有关联的重要MRP1 ABC载体。GDC-0449也阻断其他多种ABC载体。ABC载体属于一个膜蛋白家族,它的过量表达和耐药性有关,这也是治疗癌症的一个重大障碍。GDC-0449强抑制两种ABC载体,ABCG2/BCRP和ABCB1/P-糖蛋白,也温和抑制ABCC1/MRP1。在ABCG2过量表达的HEK293细胞中, GDC-0449可以提高荧光ABCG2底物BODIPY-哌唑嗪的保持力,也可用米托蒽醌再次处理这些细胞,产生抗肿瘤的ABCG2底物。实验使Madin-Darby犬的肾脏细胞中过量表达P糖蛋白或者MRP1,GDC-0449 提高了钙黄绿素-AM的保持力,然后载用秋水仙素处理这些细胞。另外,用米托蒽醌,托泊替康,SN-38处理的过量表达ABCG2的人类非小细胞肺癌细胞NCI-H460/par和NCI-H460/MX20,用GDC-0449再次处理。GDC-0449 作用于ABCG2 和 Pgp 的IC50值分别为1.4μM和 3.0 μM。[2]GDC-0449 改变细胞内Ca2+ 平衡,且作用于抗cisplatin的肺癌细胞, 抑制细胞生长。[3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
IGROV-1 MXPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX7JR|UxRTBwMEeyOFgh|ryP M4nhVHNCVkeHUh?=
HCE-T M33DZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmLlTWM2OD1zLkOyNlQ4KM7:TR?= M4G5T3NCVkeHUh?=
D-542MG NHPrdGhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2L2NmlEPTB;MT64Olc{PyEQvF2= NF\PWINUSU6JRWK=
23132-87 NGDO[45Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGLDOXRKSzVyPUSuOFAyPDdizszN NHnEd3FUSU6JRWK=
HDLM-2 M2rE[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3jQN2lEPTB;OD6wOFc3PiEQvF2= NFTxdFNUSU6JRWK=
ACN NF6xTXZIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Ml35TWM2OD16LkWwNVA6KM7:TR?= MW\TRW5ITVJ?
HuO-3N1 MYrHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NXXHdJlKUUN3ME25MlYxOTB6IN88US=> MX7TRW5ITVJ?
MC-IXC M4rub2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGrzUGdKSzVyPUGyMlIzQTJizszN NGPyZolUSU6JRWK=
D-423MG NF25eGNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{TMW2lEPTB;MUKuO|Y2PyEQvF2= NHPIdmtUSU6JRWK=
HOS M1nseGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVnJR|UxRTF3Lk[3NVkh|ryP NYHtdWlKW0GQR1XS
NB7 M4nx[Gdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NUnpblcxUUN3ME2xOU45QTFizszN NVHiN5dLW0GQR1XS
DMS-273 MV\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\YeZJWUUN3ME2xOk43PzF|IN88US=> NVTHU4lPW0GQR1XS
DU-145 M4POc2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH:0[FJKSzVyPUG4MlMzKM7:TR?= NYfGWoI{W0GQR1XS
NCI-H82 NXfLO4Z4T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWHKdnd4UUN3ME2xPU45Ozh4IN88US=> MWnTRW5ITVJ?
C2BBe1 MUTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{Oyd2lEPTB;MkGuNVA2QCEQvF2= NHn2boFUSU6JRWK=
LB2241-RCC MkjNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NXrnRod6UUN3ME2yNU45PDRzIN88US=> MomyV2FPT0WU
EW-11 NIexcppIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mof2TWM2OD1{Mj64NFIzKM7:TR?= NILYSlZUSU6JRWK=
NCI-H526 MVHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MXHJR|UxRTJ|LkS3NVch|ryP NHi0[VVUSU6JRWK=
SF295 NFPyZ49Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkPVTWM2OD1{ND6wNlUzKM7:TR?= Mk\FV2FPT0WU
D-566MG NHXDS3FIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MmrVTWM2OD1{NT6yPVQ{KM7:TR?= M{PNN3NCVkeHUh?=
8505C M2TZXmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1LRUmlEPTB;MkWuOlM{OSEQvF2= Mn7nV2FPT0WU
HT-29 M3LXU2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{X1SGlEPTB;Mk[uNFQ{OSEQvF2= NFLSU45USU6JRWK=
NBsusSR NFfKWJVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1;0U2lEPTB;Mk[uPFAxPiEQvF2= M3HIPXNCVkeHUh?=
BV-173 M4TBeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVLCSJJPUUN3ME2yPE4{OTh{IN88US=> M1TRfHNCVkeHUh?=
CTB-1 M2\1NGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHLFeVJKSzVyPUOwMlExOzFizszN MoX5V2FPT0WU
JAR NWDocJZHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Mkm5TWM2OD1|Mj61N|cyKM7:TR?= MnT6V2FPT0WU
CAL-51 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIXq[|NKSzVyPUO0MlcyPzZizszN NFSyU4FUSU6JRWK=
A172 NIjweZFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3PGZmlEPTB;M{euOFkzOSEQvF2= MYrTRW5ITVJ?
AsPC-1 NYfIb286T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NInRTZFKSzVyPUO4MlQ3PTFizszN M4LqNHNCVkeHUh?=
ONS-76 MlXVS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUi1V3BvUUN3ME20N{4{ODV5IN88US=> MmK3V2FPT0WU
RS4-11 NWqyPIdYT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFK3eZpKSzVyPUS0MlA4PTJizszN MlrWV2FPT0WU
NOS-1 M{K4b2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYrtS3o3UUN3ME20OE43ODNzIN88US=> MoLTV2FPT0WU
A101D NVLKfmhDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGrYN3hKSzVyPUS0MlgxOjNizszN MkHQV2FPT0WU
HCC1806 NV3mT3lzT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Ml60TWM2OD12Nj6xNVQ5KM7:TR?= NGnJUHpUSU6JRWK=
CAL-27 M4jNXWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGHm[pNKSzVyPUS3MlczPDZizszN MWDTRW5ITVJ?
BT-549 NETMVJFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MkP3TWM2OD12OD61N|E2KM7:TR?= MmqxV2FPT0WU
A4-Fuk Mm\yS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIXqTYxKSzVyPUS5Mlg1QSEQvF2= NWj2WVJFW0GQR1XS
HD-MY-Z NEfL[lRIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MW\JR|UxRTVyLke3OlQh|ryP MmT4V2FPT0WU
NCI-H292 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUTXWZVLUUN3ME21NE45PzV6IN88US=> M{DjWnNCVkeHUh?=
Sk-ChA-1  MWfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1P3cVAvOjYkgKO1NEDPxE1? NV\KTplVPzJiaB?= M{C5SGlEPTB;N{SuOVTDuTJwNUlOwG0> NYrueFI{OjV5NEK0PFI>
Mz-ChA-1 NGPMNIxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MlT6NE4zPeLCk{WwJO69VQ>? MX23NkBp NEPreVZKSzVyPUW0Mlk4yrF|LkS1{txO MnPGNlU4PDJ2OEK=
Smo-WT MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEHiPIVKSzVywrDv[kAyPMLibl2= MmPpNlQzQTFzMES=
Smo-D473H  MVjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NEjKUY1KSzVywrDv[kA4NjIEoN88US=> M2frR|I1OjlzMUC0
K562 M2TjSmZ2dmO2aX;uJGF{e2G7 MlXhNVAh|ryP NWjUNVQ4PzJiaB?= NUHvV|AyemWmdXPld{B1cGViZYjwdoV{e2mxbjDv[kBIdGlzwrC= MmfPNlM{OTl6MkS=
T315I BCR-ABL BaF3 NEnLepJHfW6ldHnvckBCe3OjeR?= M3q2XlExKM7:TR?= NWXF[I1LPzJiaB?= NUHiR3BsemWmdXPld{B1cGViZYjwdoV{e2mxbjDv[kBIdGlzwrC= MkWzNlM{OTl6MkS=
TF-1 BCR-ABL MVnGeY5kfGmxbjDBd5NigQ>? NH\zcpcyOCEQvF2= M1HXb|czKGh? M1SzWpJm\HWlZYOgeIhmKGW6cILld5Nqd25ib3[gS4xqOcLi M3XlOlI{OzF7OEK0

... Click to View More Cell Line Experimental Data

体内研究 GDC-0449已经用于治疗动物模型的成髓细胞瘤。[2] GDC-0449 抑制原代胰腺移植瘤生长,但是不抑制细胞增殖。GDC-0449按25 mg/kg 以上剂量口服给药髓母细胞瘤Ptch(+/-)异体移植物模型,引起细胞衰退,按92 mg/kg剂量处理两种配位体依赖的结肠直肠癌模型D5123和1040830,每天处理两次,抑制肿瘤生长。分析Hh通路活性和 PK/PD 模型显示GDC-0449抑制 Gli1,IC50值与GDC-0449作用于髓母细胞瘤和D5123模型的IC50值差不多(分别为0.165 μM ±11.5% 和0.267 μM ±4.83%)。[4]


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  • Cell lines: MDCKII细胞
  • Concentrations: 20 μM
  • Incubation Time: 2小时
  • Method: MDCKII细胞按每孔3x105密度接种在24孔板中。培养液包含不同药物,实验组为50 µM VP,50 µM吲哚美辛,或者20 µM GDC-0449溶解在DMSO中,对照组只含有DMSO。然后加入非荧光的钙黄绿素-AM,最终浓度达到1.0 µM。然后在37oC温育2小时。细胞用含Ca2+,Mg2+的Hank's平衡盐溶液buffer冲洗2次,然后震荡1小时溶解在含0.01% Triton X-100的磷酸缓冲液中,然后放在4oC下过夜。溶解的物质然后转移到96孔板上,钙黄绿素引起的荧光信号用分光光度法定量。所有的实验操作需在暗中进行,所有的读数用平均值±SEM表示。
    (Only for Reference)
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  • Animal Models: Ptch(+/-)异体移植物模型
  • Formulation: In 0.5% methyl-cellulose, 0.2% tween-80
  • Dosages: 25 mg/kg,92 mg/kg
  • Administration: 口服
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 84 mg/mL (199.38 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用:
2% DMSO+30% PEG 300+5% Tween 80+ddH2O

* 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。


分子量 421.3


CAS号 879085-55-9
稳定性 powder
别名 N/A





质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)


  • 质量

*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。




开始浓度 x 开始体积 = 最终浓度 x 最终体积


稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1

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):




注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2


质量 浓度 体积 分子量


NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03035188 Not yet recruiting Basal Cell Carcinoma SRH Wald-Klinikum Gera GmbH January 2017 Phase 2
NCT02956889 Recruiting Carcinoma, Basal Cell Istituto Clinico Humanitas October 2016 Phase 2
NCT02925234 Recruiting Cancer|Tumors|Neoplasm|Neoplasia The Netherlands Cancer Institute|Amgen|AstraZeneca|Bayer|Bristol-Myers Squibb|Novartis|Roche Pharma AG August 2016 Phase 2
NCT02366312 Active, not recruiting Keratocystic Odontogenic Tumor The Bluestone Center for Clinical Research|Genentech, Inc. June 2016 Phase 2
NCT02694224 Recruiting Breast Cancer Clinica Universidad de Navarra, Universidad de Navarra April 2016 Phase 2
NCT02693535 Recruiting Lymphoma, Non-Hodgkin|Multiple Myeloma|Advanced Solid Tumors American Society of Clinical Oncology|AstraZeneca|Bayer|Bristol-Myers Squibb|Eli Lilly and Company|Genentech, Inc.|Merck Sharp & Dohme Corp.|Pfizer March 2016 Phase 2





  • * 必填项

Hedgehog/Smoothened Signaling Pathway Map

Hedgehog/Smoothened Inhibitors with Unique Features


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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID