Vismodegib (GDC-0449)

Catalog No.S1082

Vismodegib (GDC-0449) Chemical Structure

Molecular Weight(MW): 421.3

Vismodegib (GDC-0449) is a potent, novel and specific hedgehog inhibitor with IC50 of 3 nM and also inhibits P-gp with IC50 of 3.0 μM in a cell-free assay.

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In DMSO USD 144 In stock
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Cited by 34 Publications

16 Customer Reviews

  • 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.

    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.

  • 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.

    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.

  • (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.

Purity & Quality Control

Choose Selective Hedgehog/Smoothened Inhibitors

Biological Activity

Description Vismodegib (GDC-0449) is a potent, novel and specific hedgehog inhibitor with IC50 of 3 nM and also inhibits P-gp with IC50 of 3.0 μM in a cell-free assay.
Hedgehog [1]
(Cell-free assay)
P-gp [1] P-gp [1]
3 nM 3 μM 5 μM
In vitro

GDC-0449 targets the Hedgehog signaling pathway, blocking the activities of the Hedgehog-ligand cell surface receptors PTCH and/or SMO and suppressing Hedgehog signaling. GDC-0449 prevents multiple ATP-binding cassette (ABC) transporters. GDC-0449 also blocks ABCG2, Pgp, and MRP1-important ABC transporters associated with MDR. GDC-0449 is a potent inhibitor of ABC transporters, ABCG2/BCRP and ABCB1/Pgp, and is a mild inhibitor of ABCC1/MRP1. In ABCG2-overexpressing HEK293 cells, GDC-0449 increases retention of the fluorescent ABCG2 substrate BODIPY-prazosin and resensitizes these cells to mitoxantrone. In Madin-Darby canine kidney II cells engineered to overexpress Pgp or MRP1, GDC-0449 increases the retention of calcein-AM and resensitizes them to colchicine. GDC-0449 also resensitizes human non-small cell lung carcinoma cells NCI-H460/par and NCI-H460/MX20, which overexpress ABCG2 in response to mitoxantrone, to mitoxantrone, and to topotecan or SN-38. The IC50 values of GDC-0449 for prevention of ABCG2 and Pgp are about 1.4 μM and 3.0 μM, respectively. [2] GDC-0449 alters intracellular Ca2+ homeostasis and inhibits cell growth in cisplatin-resistant lung cancer cells. [3]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
D-542MG M2ThZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MojITWM2OD1zLki2O|M4KM7:TR?= MUjTRW5ITVJ?
23132-87 MVTHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M4WzRmlEPTB;ND60NFE1PyEQvF2= NUewc4lNW0GQR1XS
HDLM-2 M4fQcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEjqSXFKSzVyPUiuNFQ4PjZizszN MoLFV2FPT0WU
ACN M2[zcWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NVXaco96UUN3ME24MlUxOTB7IN88US=> NX;ZPHhCW0GQR1XS
HuO-3N1 M3jkZWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NHfJ[VZKSzVyPUmuOlAyODhizszN M3PnUHNCVkeHUh?=
MC-IXC NEDtSolIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NVjhU4M{UUN3ME2xNk4zOjl{IN88US=> M3j6S3NCVkeHUh?=
D-423MG NW\kOmlDT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NF7PT3dKSzVyPUGyMlc3PTdizszN M37aRXNCVkeHUh?=
NY M3jB[2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 Mnj5TWM2OD1zND64PVA{KM7:TR?= MYjTRW5ITVJ?
NB7 NIW1V|JIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NX2xRoRTUUN3ME2xOU45QTFizszN Mke4V2FPT0WU
MDA-MB-361 NF\mTXFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MV3JR|UxRTF5LkK3NVEh|ryP M372WXNCVkeHUh?=
DU-145 NUnlUIc{T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= Moj2TWM2OD1zOD6zNkDPxE1? MYTTRW5ITVJ?
NCI-H82 M4HCPWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MXPJR|UxRTF7LkizPFYh|ryP MV3TRW5ITVJ?
NCI-SNU-1 M4HzRmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGP4TpBKSzVyPUKwMlAyQTZizszN NELZdlhUSU6JRWK=
C2BBe1 NGfyTHJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnniTWM2OD1{MT6xNFU5KM7:TR?= MYfTRW5ITVJ?
LB2241-RCC MkjPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVnJR|UxRTJzLki0OFEh|ryP M1HOb3NCVkeHUh?=
COLO-829 MX\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NE[0eHhKSzVyPUKyMlE5PzFizszN MXXTRW5ITVJ?
NCI-H526 M4\vWWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MWPJR|UxRTJ|LkS3NVch|ryP M3Prc3NCVkeHUh?=
SF295 NWLsc2NjT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NWnBblJUUUN3ME2yOE4xOjV{IN88US=> NWXI[Il1W0GQR1XS
D-566MG M17xTWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MY\JR|UxRTJ3LkK5OFMh|ryP Mn3yV2FPT0WU
8505C NVrZSHR2T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MWTJR|UxRTJ3Lk[zN|Eh|ryP NF7w[nZUSU6JRWK=
HT-29 NYfkT|NWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjsXXZKSzVyPUK2MlA1OzFizszN MkjYV2FPT0WU
NBsusSR MlfFS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NGHmdo9KSzVyPUK2MlgxODZizszN M1[xTnNCVkeHUh?=
BV-173 MU\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M{nnRmlEPTB;MkiuN|E5OiEQvF2= M4LGOHNCVkeHUh?=
CTB-1 Ml7vS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MVrJR|UxRTNyLkGwN|Eh|ryP NVfse4M1W0GQR1XS
CAMA-1 NG\ab2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3TLRmlEPTB;M{OuOFYyPSEQvF2= MVnTRW5ITVJ?
CAL-51 M3jDemdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MmOwTWM2OD1|ND63NVc3KM7:TR?= MWPTRW5ITVJ?
A172 MUPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIL1R|JKSzVyPUO3MlQ6OjFizszN MWPTRW5ITVJ?
AsPC-1 M2nkWmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NGnzbIdKSzVyPUO4MlQ3PTFizszN NIfKU2ZUSU6JRWK=
MKN7 NXe0ZnV6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NX\Sc49bUUN3ME2zPU4xODd7IN88US=> NVm3V4ZLW0GQR1XS
ONS-76 M3q2T2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4fGPWlEPTB;NEOuN|A2PyEQvF2= NVHDR5NZW0GQR1XS
A101D NUjqbm85T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXLCNZdMUUN3ME20OE45ODJ|IN88US=> NWC5VmtkW0GQR1XS
HCC1806 M2X3OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4K5OWlEPTB;NE[uNVE1QCEQvF2= Ml;GV2FPT0WU
CAL-27 MlzES5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3rvdWlEPTB;NEeuO|I1PiEQvF2= NEW4ZlhUSU6JRWK=
BT-549 M3n2OWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4fhVWlEPTB;NEiuOVMyPSEQvF2= M{GxfXNCVkeHUh?=
LCLC-97TM1 NGLNWG5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnjPTWM2OD12OT6yOFE{KM7:TR?= M3fHPHNCVkeHUh?=
A4-Fuk MkTNS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3jjbGlEPTB;NEmuPFQ6KM7:TR?= NVLZfpU1W0GQR1XS
OVCAR-4 M1rhfWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M{TMfmlEPTB;NUCuNFYxOSEQvF2= M{[2W3NCVkeHUh?=
HD-MY-Z M2DBVGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYfJR|UxRTVyLke3OlQh|ryP NUPB[nczW0GQR1XS
NCI-H292 Ml;SS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXKdlcyUUN3ME21NE45PzV6IN88US=> MWPTRW5ITVJ?
Sk-ChA-1  Mli1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXGwMlI26oDVNUCg{txO MWe3NkBp Mk\ITWM2OD15ND61OOKyOi53ON88US=> MUWyOVc1OjR6Mh?=
Mz-ChA-1 MXHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NWr5UY5KOC5{NfMAl|UxKM7:TR?= MXq3NkBp M1vYUmlEPTB;NUSuPVfDuTNwNEZOwG0> NWG1bY5[OjV5NEK0PFI>
Smo-WT MoK4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MX\JR|UxyqCxZjCxOOKhdk1? MXmyOFI6OTFyNB?=
Smo-D473H  NI[4bXlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M4jC[mlEPTEEoH;mJFcvOcLizszN NUT5NFlyOjR{OUGxNFQ>
K562 MojaSpVv[3Srb36gRZN{[Xl? NHfJR4gyOCEQvF2= NEDWT|k4OiCq MWjy[YR2[2W|IITo[UBmgHC{ZYPzbY9vKG:oIFfsbVHDqA>? Mn7LNlM{OTl6MkS=
T315I BCR-ABL BaF3 M4DMZ2Z2dmO2aX;uJGF{e2G7 NVrpcIM4OTBizszN M{DxV|czKGh? NYrK[FlsemWmdXPld{B1cGViZYjwdoV{e2mxbjDv[kBIdGlzwrC= MVeyN|MyQTh{NB?=

... Click to View More Cell Line Experimental Data

In vivo GDC-0449 has been used to treat medulloblastoma in animal models. [2] GDC-0449 prevents the growth of primary pancreatic xenografts without non-specifically inhibiting pancreatic cell proliferation. Oral dosing of GDC-0449 causes tumor regressions in the Ptch(+/-) allograft model of medulloblastoma at doses ≥25 mg/kg and tumor growth inhibition at doses up to 92 mg/kg dosed twice daily in two ligand-dependent colorectal cancer models, D5123, and 1040830. Analysis of Hh pathway activity and PK/PD modeling reveals that GDC-0449 inhibits Gli1 with a similar IC50 in both the medulloblastoma and D5123 models (0.165 μM and 0.267 μM, respectively). Pathway modulation is linked to efficacy using an integrated PK/PD model revealing a steep relationship where > 50% of the activity of GDC-0449 is associated with >80% repression of the Hh pathway. [4]


Cell Research:[2]
+ Expand
  • Cell lines: MDCKII cells
  • Concentrations: 20 μM
  • Incubation Time: 2 hours
  • Method: MDCKII cells are seeded into 24-well plates at a density of 3 × 105 cells per well and are allowed to attach. Medium is then changed to that containing different drugs (50 μM VP, 50 μM indomethacin, or 20 μM GDC-0449 in DMSO or DMSO alone as control, and nonfluorescent calcein-AM is added to a final concentration of 1.0 μM and incubated at 37 °C for 2 hours. Cells are then washed twice with Ca2+, Mg2+-containing Hank's balanced salt solution buffer and lysed by shaking in 0.01% Triton X-100 in PBS buffer for 1 hour at room temperature or overnight at 4 °C. The lysate is then transferred into 96-well plates, and the fluorescence signal caused by the cell-derived calcein is quantified spectrophotometrically with a SpectraMax M5 Multi-Detection Readerusing an excitation wavelength of 495 nm and an emission wavelength of 515 nm. All manipulations are performed in the dark. All readings are expressed as mean ?SEM normalized to the control.
    (Only for Reference)
Animal Research:[4]
+ Expand
  • Animal Models: Ptch(+/-) allograft model, D5123 and 1040830
  • Formulation: In 0.5% methyl-cellulose, 0.2% tween-80
  • Dosages: ~ 100 mg/kg
  • Administration: Orally
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 84 mg/mL (199.38 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo 2% DMSO+30% PEG 300+5% Tween 80+ddH2O 10mg/mL

* 1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 421.3


CAS No. 879085-55-9
Storage powder
in solvent
Synonyms N/A

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To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

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

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID