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Submit ReviewMIM1 is an inhibitor of Mcl-1. Inhibits Mcl-1 indirectly by induction of the proapoptotic Mcl-1 ligand NOXA via the unfolded protein response (UPR) pathway. Sensitizes leukemia cells to the Bcl-2 inhibitor venetoclax (ABT-199). Induces caspase-3/7 activation and cell death in Mcl-1-dependent leukemia cells. Also blocks Mcl-1-mediated suppression of tBID-induced Bax activation in vitro.
M. Wt | 347.43 |
Formula | C17H21N3O3S |
Storage | Store at +4°C |
PubChem ID | 135875424 |
InChI Key | RGGFUBMUOVFZEF-DLHVAJNCSA-N |
Smiles | CC2=CS/C(N2/N=C/C3=CC=C(O)C(O)=C3O)=N\C1CCCCC1 |
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.
References are publications that support the biological activity of the product.
Cohen et al (2012) A competitive stapled peptide screen identifies a selective small molecule that overcomes MCL-1-dependent leukemia cell survival. Chem.Biol. 19 1175 PMID: 22999885
Mallick et al (2019) Confounding off-target effects of BH3 mimetics at commonly used concentrations: MIM1, UMI-77, and A-1210477. Cell Death Dis. 10 185 PMID: 30796196
Keywords: MIM1, MIM1 supplier, Mcl-1, inhibitors, inhibits, proapoptotic, induces, apoptosis, caspases, activation, NOXA, Bcl-2, Family, 4762, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for MIM1 include:
Li et al (2014) The androgen receptor mediates antiapoptotic function in myometrial cells. Autophagy 5 e1338 PMID: 25032861
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Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.
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.