Inhibits Mcl1-BIM interaction. Inhibits viability of Mcl1-dependent tumor cell lines. Induces cell death and decreased spheroid formation in Her2 positive breast cancer 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.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 415.45. Batch specific molecular weights may vary from batch to batch due to solvent 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||2.41 mL||12.04 mL||24.07 mL|
|5 mM||0.48 mL||2.41 mL||4.81 mL|
|10 mM||0.24 mL||1.2 mL||2.41 mL|
|50 mM||0.05 mL||0.24 mL||0.48 mL|
References are publications that support the biological activity of the product.
Bashari et al (2016) Mcl-1 confers protection of Her2-positive breast cancer cells to hypoxia: therapeutic implications. Breast Cancer Res. 18 26 PMID: 26921175
Bannister et al (2012) ML311: A small molecule that potently and selectively disrupts the protein-protein interaction of Mcl-1 and Bim: a probe for studying lymphoid tumorigenesis. Probe Reports from the NIH Molecular Libraries Program PMID: 23762927
If you know of a relevant reference for ML 311, please let us know.
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Keywords: ML 311, ML 311 supplier, ML311, myeloid, cell, leukemia, 1, mcl1, BIM, inhibitors, inhibits, interaction, Bcl-2, Family, 5733, Tocris Bioscience
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Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.
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.