You can now submit reviews for your favorite Tocris products. Your review will help other researchers decide on the best products for their research. Why not submit a review today?!Submit Review
ML 210 New
Glutathione peroxidase (GPX4) inhibitor. Kills mutant RAS-expressing cell lines (IC50 values are 71 and 272 nM for HRAS G12v mutant expressing cell lines BJeLR and BJeH-LT, respectively). Exhibits 4-fold selectivity for HRAS mutant-expressing cell lines. Induces ferroptosis in tumor initiation "persister" cells and drug-resistant tumor 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.
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 475.32. 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|
|0.5 mM||4.21 mL||21.04 mL||42.08 mL|
|2.5 mM||0.84 mL||4.21 mL||8.42 mL|
|5 mM||0.42 mL||2.1 mL||4.21 mL|
|25 mM||0.08 mL||0.42 mL||0.84 mL|
References are publications that support the biological activity of the product.
Weïwer et al (2012) Development of small-molecule probes that selectively kill cells induced to express mutant RAS. Bioorg.Med.Chem.Lett. 22 1822 PMID: 22297109
Yang et al (2014) Regulation of ferroptotic cancer cell death by GPX4. Cell 156 317 PMID: 24439385
Hangauer et al (2017) Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition. Nature 551 247 PMID: 29088702
If you know of a relevant reference for ML 210, please let us know.
View Related Products by Target
View Related Products by Product Action
Keywords: ML 210, ML 210 supplier, ML210, Glutathione, peroxidases, GPX4, inhibitors, inhibits, synthetically, lethal, compounds, mutant, RAS, HRAS, ferroptosis, tumor, initiation, cells, persister, drug, resistant, TICs, Ras, GTPases, Ferroptosis, Cancer, Stem, Cells, 6429, Tocris Bioscience
Citations for ML 210
Citations are publications that use Tocris products.
Currently there are no citations for ML 210. Do you know of a great paper that uses ML 210 from Tocris? Please let us know.
Reviews for ML 210
There are currently no reviews for this product. Be the first to review ML 210 and earn rewards!
Have you used ML 210?
Submit a review and receive an Amazon gift card.
$50/€35/£30/$50CAN/¥300 Yuan/¥5000 Yen for first to review with an image
$25/€18/£15/$25CAN/¥75 Yuan/¥1250 Yen for a review with an image
$10/€7/£6/$10 CAD/¥70 Yuan/¥1110 Yen for a review without an image
Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* or download your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
RAS Oncoproteins Scientific Review
Written by Kirsten L. Bryant, Adrienne D. Cox and Channing J. Der, this review provides a comprehensive overview of RAS protein function and RAS mutations in cancer. Key signaling pathways are highlighted and therapeutic vulnerabilities are explored. This review also includes a detailed section on RAS drug discovery and targeting synthetic lethal interactors of mutant RAS. Compounds available from Tocris are listed.
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. Adapted from the 2015 Cancer Product Guide, Edition 3, this poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.
Epigenetics in Cancer Poster
Adapted from the 2015 Cancer Product Guide Edition 3, this poster summarizes the main epigenetic targets in cancer. The dysregulation of epigenetic modifications has been shown to result in oncogenesis and cancer progression. Unlike genetic mutations, epigenetic alterations are considered to be reversible and thus make promising therapeutic targets.