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Submit ReviewPMX 464 is a putative inhibitor of the thioredoxin-thioredoxin reductase (Trx-TrxR) system. Shown to inhibit Trx and induce a G1/S block in HT29 cells; inhibits cell proliferation in various colorectal cancer cell lines and MCF7 cells. Also elicits an anti-inflammatory response in A549 cells.
M. Wt | 243.28 |
Formula | C13H9NO2S |
Storage | Store at -20°C |
Purity | ≥98% (HPLC) |
CAS Number | 485842-97-5 |
PubChem ID | 482697 |
InChI Key | SDYBYKXWYDVVKP-UHFFFAOYSA-N |
Smiles | O=C(C=C3)C=CC3(O)C2=NC1=CC=CC=C1S2 |
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.
Mukherjee et al (2007) A cellular and molecular investigation of the action of PMX464, a putative thioredoxin inhibitor, in normal and colorectal cancer cell lines. Br.J.Pharmacol. 151 1167 PMID: 17572693
Callister et al (2008) PMX464, a thiol-reactive quinol and putative thioredoxin inhibitor, inhibits NF-κB-dependent proinflammatory activation of alveolar epithelial cells. Br.J.Pharmacol. 155 661 PMID: 18587424
Mukherjee et al (2005) Cytotoxic and antiangiogenic activity of AW464 (NSC 706704), a novel thioredoxin inhibitor: an in vitro study. Br.J.Cancer 92 350 PMID: 15655539
Keywords: PMX 464, PMX 464 supplier, PMX464, PMX_464, antiproliferative, thioredoxin, reductase, TrxR, Trx1, inhibitors, inhibits, cell, proliferation, Thioredoxin, Reductases, 4996, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for PMX 464 include:
Schroeder (2017) Targeting Thioredoxin-1 by dimethyl fumarate induces ripoptosome-mediated cell death Sci Rep 7 43168 PMID: 28233787
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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.