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MRTX 849 is a mutant-selective inhibitor of KRASG12C (IC50 = 142 nM). MRTX 849 covalently binds to KRASG12C at the cysteine 12 residue and inhibits KRAS-dependent signal transduction by locking the protein in its inactive GDP-bound state. MRTX 849 induces pronounced tumor regression in 17 of 26 (65%) KRASG12C -positive cell lines and patient-derived xenograft models from multiple tumor types. It is orally bioavailable.
|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|
The following data is based on the product molecular weight 604.13. 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|
|1 mM||1.66 mL||8.28 mL||16.55 mL|
|5 mM||0.33 mL||1.66 mL||3.31 mL|
|10 mM||0.17 mL||0.83 mL||1.66 mL|
|50 mM||0.03 mL||0.17 mL||0.33 mL|
References are publications that support the biological activity of the product.
Hallin et al (2020) The KRAS G12C inhibitor MRTX849 provides insight toward therapeutic susceptibility of KRAS-mutant cancers in mouse models and patients. Cancer Discov. 10 54 PMID: 31658955
Fell et al (2020) Identification of the clinical development candidate MRTX849, a covalent KRASG12C inhibitor for the treatment of cancer. J.Med.Chem. 63 6679 PMID: 32250617
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Keywords: MRTX 849, MRTX 849 supplier, MRTX, 849, potent, mutation, selective, inhibitors, inhibits, KRASG12C, KRAS, G12C, Adagrasib, Ras, GTPases, 7488, Tocris Bioscience
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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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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.
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.
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.