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GLI antagonist that inhibits GLI1 and GLI2-induced transcription (IC50 ~ 5 μM). Inhibits the hedgehog (Hh) signaling pathway downstream of SMO and SUFU causing GLI1 nuclear accumulation. Displays antiproliferative and antitumor activity in vivo. Inhibits the pluripotency factors Oct4, Sox-2, Nanog and c-Myc in pancreatic cancer stem cells.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 429.61. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||2.33 mL||11.64 mL||23.28 mL|
|5 mM||0.47 mL||2.33 mL||4.66 mL|
|10 mM||0.23 mL||1.16 mL||2.33 mL|
|50 mM||0.05 mL||0.23 mL||0.47 mL|
References are publications that support the biological activity of the product.
Lauth et al (2007) Inhibition of GLI-mediated transcription and tumor cell growth by small molecule antagonists. Proc.Natl.Acad.Sci.USA 104 8455 PMID: 17494766
Fu et al (2012) GANT-61 inhibits pancreatic cancer stem cell growth in vitro and in NOD/SCID/IL2R gamma null mice xenograft. Cancer Lett. 330 22 PMID: 23200667
Mazumdar et al (2011) Blocking Hedgehog survival signaling at the level of the GLI genes induces DNA damage and extensive cell death in human colon carcinoma cells. Cancer Res. 71 5904 PMID: 21747117
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Keywords: GANT 61, GANT 61 supplier, GANT61, selective, GLI, Gli, antagonists, inhibitors, inhibits, hedgehog, Hh, signaling, signalling, pathways, Hedgehog, Signaling, Other, Transcription, Factors, Stem, Cell, 3191, Tocris Bioscience
5 Citations for GANT 61
Citations are publications that use Tocris products. Selected citations for GANT 61 include:
Todd and Fischer (2015) Hedgehog signaling stimulates the formation of proliferating Müller glia-derived progenitor cells in the chick retina. Development 142 2610 PMID: 26116667
Wellbrock et al (2015) Expression of Hedgehog Pathway Mediator GLI Represents a Negative Prognostic Marker in Human Acute Myeloid Leukemia and Its Inhibition Exerts Antileukemic Effects. Clin Cancer Res 21 2388 PMID: 25745035
Lim et al (2015) Mitochondria-derived reactive oxygen species drive GANT61-induced mesothelioma cell apoptosis. Oncotarget 6 1519 PMID: 25544756
Calcaterra et al (2018) Chemical, computational and functional insights into the chemical stability of the Hedgehog pathway inhibitor GANT61. J Enzyme Inhib Med Chem 33 349 PMID: 29338454
Oladapo (2017) Pharmacological targeting of GLI1 inhibits proliferation, tumor emboli formation and in vivo tumor growth of inflammatory breast cancer cells. Cancer Lett 411 136 PMID: 28965853
Do you know of a great paper that uses GANT 61 from Tocris? Please let us know.
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Stem Cells Scientific Review
Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. Compounds available from Tocris are listed.
Stem Cell Workflow Poster
Stem cells have potential as a source of cells and tissues for research and treatment of disease. This poster summarizes some key protocols demonstrating the use of small molecules across the stem cell workflow, from reprogramming, through self-renewal, storage and differentiation to verification. Advantages of using small molecules are also highlighted.