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Item № 15929
CAS № 403811-55-2
Purity ≥95%
product image
                (CAS 403811-55-2)
     5 mg $49.00 0.00
     10 mg $83.00 0.00
     25 mg $147.00 0.00
     50 mg $270.00 0.00

Pricing updated 2019-04-23. Prices are subject to change without notice.


The Myc proto-oncogenes interact with Max to form a dimer that regulates gene transcription. The protein c-Myc, in particular, promotes gene expression relevant to cell growth and thus drives cancer. 10058-F4 is a cell-permeable thiazolidinone that inhibits the dimerization of c-Myc and Max at 64 µM, preventing c-Myc-dependent gene expression and cell proliferation.1 It induces cell cycle arrest, apoptosis, and myeloid differentiation at 100 µM in human acute myeloid leukemia cells.2 10058-F4 is rapidly metabolized in mice when given intravenously, limiting its effects on tumors in vivo.3 In addition to c-Myc, 10058-F4 inhibits the nuclear Myc protein, N-Myc, at 50 µM, inducing arrest, apoptosis, and differentiation in neuroblastoma cells overexpressing the gene for N-Myc.4 This compound can be used to delineate novel actions of Myc proteins, especially those related to lipid and glucose metabolism.4,5

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Molecular Formula
Formula Weight
A crystalline solid
233, 277, 379 nm
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Room temperature in continental US; may vary elsewhere
≥ 2 years
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References & Product Citations
Product Description References

1. Yin, X., Giap, C., Lazo, J.S., et al. Low molecular weight inhibitors of Myc-Max interaction and function Oncogene 22(40), 6151-6159 (2003).

2. Huang, M.J., Cheng, Y.C., Liu, C.R., et al. A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia Experimental Hematology 34(11), 1480-1489 (2006).

3. Guo, J., Parise, R.A., Joseph, E., et al. Efficacy, pharmacokinetics, tissue distribution, and metabolism of the Myc-Max disruptor, 10058-F4 [Z,E]-5-[4-ethylbenzylidine]-2-thioxothiazolidin-4-one, in mice Cancer Chemotherapy and Pharmacology 63(4), 615-625 (2009).

4. Zirath, H., Frenzel, A., Oliynyk, G., et al. MYC inhibition induces metabolic changes leading to accumulation of lipid droplets in tumor cells Proceedings of the National Academy of Sciences of the United States of America 110(25), 10258-10263 (2013).

5. Zhang, P., Metukuri, M.R., Bindom, S.M., et al. c-Myc is required for the ChREBP-dependent activation of glucose-responsive genes Molecular Endocrinology 24(6), 1274-1286 (2010).

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