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Autophagy inhibitor. Inhibits growth and induces apoptosis of renal cancer cells in vitro. Also inhibits TLR9. Additionally inhibits PRC2 by inhibiting the allosteric binding of PRC2 to EED (embryonic ectoderm development) within the H3K27me3-binding pocket, and reduces H3K27me3 levels in multiple myeloma cells in vitro.
|Storage||Store at +4°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 433.95. 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||2.3 mL||11.52 mL||23.04 mL|
|5 mM||0.46 mL||2.3 mL||4.61 mL|
|10 mM||0.23 mL||1.15 mL||2.3 mL|
|50 mM||0.05 mL||0.23 mL||0.46 mL|
References are publications that support the biological activity of the product.
Lee et al (2015) Hydroxychloroquine Destabilizes Phospho-S6 in Human Renal Carcinoma Cells. PLoS ONE 10 e0131464 PMID: 26134285
Lamphier et al (2014) Novel small molecule inhibitors of TLR7 and TLR9: mechanism of action and efficacy in vivo. Mol.Pharmacol. 85 429 PMID: 24342772
Catalano et al (2019) A drug repurposing screening reveals a novel epigenetic activity of hydroxychloroquine. Eur.J.Med.Chem. 183 PMID: 31550663
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Keywords: Hydroxychloroquine sulfate, Hydroxychloroquine sulfate supplier, TLR9, toll-like, receptors, inhibitors, autophagy, inhibits, cancer, Toll-like, Receptors, Autophagy, Other, Lysine, Methyltransferases, 5648, Tocris Bioscience
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Literature in this Area
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Programmed Cell Death Poster
There are two currently recognized forms of programmed cell death: apoptosis and necroptosis. This poster summarizes the signaling pathways involved in apoptosis, necroptosis and cell survival following death receptor activation, and highlights the influence of the molecular switch, cFLIP, on cell fate.