Selective, high affinity Mcl-1 inhibitor (Ki = 454 pM). Disrupts Mcl-BIM complexes (IC50 in low μM range). Also inhibits Mcl-1NOXA interactions. Exhibits no effect on Bcl-XL-Bim or Bcl-X-BCL-Xs interactions. Induces apoptosis in multiple myeloma and non-small cell lung cancer cell lines and exhibits a synergistic effect with NavitoclaxTM to induce apoptosis in vitro. Cell permeable.
|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|
|DMSO||1.7||2mM with gentle warming|
Preparing Stock Solutions
The following data is based on the product molecular weight 850.04. 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||1.18 mL||5.88 mL||11.76 mL|
|5 mM||0.24 mL||1.18 mL||2.35 mL|
|10 mM||0.12 mL||0.59 mL||1.18 mL|
|50 mM||0.02 mL||0.12 mL||0.24 mL|
References are publications that support the products' biological activity.
Bruncko et al (2015) Structure-guided design of a series of MCL-1 inhibitors with high affinity and selectivity. J.Med.Chem. 58 2180 PMID: 25679114
Leverson et al (2015) Potent and selective small-molecule MCL-1 inhibitors demonstrate on-target cancer cell killing activity as single agents and in combination with ABT-263 (navitoclax). Cell Death Dis. 6 e1590 PMID: 25590800
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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.