10074-G5 | c-Myc inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $55.00 | ||
| 25 mg | $170.00 |
10074-G5 (413611-93-5) inhibits c-Myc by disrupting c-Myc/Max heterodimer formation and inhibiting its transcriptional activity.1 10074-G5 binds to the c-Myc bHLHZip domain with Kd=2.8 mM.1 It was cytotoxic in C-Myc-overexpressing cell lines (IC50s = 13 to 15 mM) but was not active in vivo due to rapid metabolism.2 10074-G5 is a useful tool to probe for involvement of c-Myc involvement in cellular processes.3,4 Binds to and sequesters the intrinsically disordered amyloid-β (Aβ) in its monomeric soluble state and rescues a C. elegans model of Aβ-associated toxicity.5
References/Citations:
- Follis et al. (2008), Structural rationale for the coupled binding and unfolding of the c-Myc oncoprotein by small molecules; Chem. Biol. 15 1149
- Clausen et al. (2010), In vitro cytotoxicity and in vivo efficacy, pharmacokinetics, and metabolism of 10074-G5, a novel small-molecule inhibitor of c-Myc/Max dimerization; J. Pharmacol. Exp. Ther. 335 715
- Velpula et al. (2012), Transcriptional repression of Mad-Max complex by human umbilical cord blood stem cells downregulates extracellular signal-regulated kinase in glioblastoma; Stem Cells Dev. 21 1779
- Wu et al. (2018), Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma; BMC Cancer 18 361
- Heller et al. (2020), Small-molecule sequestration of amyloid-β as a drug discovery strategy for Alzheimer’s disease; Sci. Adv. 6 eabb5924
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
10074-G5 (413611-93-5) inhibits c-Myc by disrupting c-Myc/Max heterodimer formation and inhibiting its transcriptional activity.1 10074-G5 binds to the c-Myc bHLHZip domain with Kd=2.8 mM.1 It was cytotoxic in C-Myc-overexpressing cell lines (IC50s = 13 to 15 mM) but was not active in vivo due to rapid metabolism.2 10074-G5 is a useful tool to probe for involvement of c-Myc involvement in cellular processes.3,4 Binds to and sequesters the intrinsically disordered amyloid-β (Aβ) in its monomeric soluble state and rescues a C. elegans model of Aβ-associated toxicity.5
References/Citations:
- Follis et al. (2008), Structural rationale for the coupled binding and unfolding of the c-Myc oncoprotein by small molecules; Chem. Biol. 15 1149
- Clausen et al. (2010), In vitro cytotoxicity and in vivo efficacy, pharmacokinetics, and metabolism of 10074-G5, a novel small-molecule inhibitor of c-Myc/Max dimerization; J. Pharmacol. Exp. Ther. 335 715
- Velpula et al. (2012), Transcriptional repression of Mad-Max complex by human umbilical cord blood stem cells downregulates extracellular signal-regulated kinase in glioblastoma; Stem Cells Dev. 21 1779
- Wu et al. (2018), Oxidative stress enhances tumorigenicity and stem-like features via the activation of the Wnt/β-catenin/MYC/Sox2 axis in ALK-positive anaplastic large-cell lymphoma; BMC Cancer 18 361
- Heller et al. (2020), Small-molecule sequestration of amyloid-β as a drug discovery strategy for Alzheimer’s disease; Sci. Adv. 6 eabb5924
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