Myc Inhibitors
The chemical class known as Myc Inhibitors encompasses a diverse array of compounds that act as direct or indirect inhibitors of Myc, a transcription factor with crucial roles in cell cycle progression, proliferation, and survival. These inhibitors employ various mechanisms to disrupt Myc function, either by directly interfering with the Myc-Max interaction, inhibiting the BET proteins' interaction with acetylated histones, or indirectly modulating Myc expression through pathways such as Akt signaling, RNA polymerase I inhibition, and Wnt/β-catenin modulation.
Direct inhibitors like 10058-F4 and JQ1 disrupt the Myc-Max interaction, preventing the formation of active complexes and subsequently inhibiting Myc transcriptional activation. Omomyc competitively binds to the DNA-binding domain of Myc, inhibiting its interaction with target genes. Indirect inhibitors such as 10-DEBC, OICR-9429, and CX-5461 influence Myc expression through modulation of the Akt signaling pathway, MAX protein interaction, and RNA polymerase I inhibition, respectively. BETd-246, KJ-Pyr-9, and A485 disrupt BET protein binding to acetylated histones, affecting Myc transcriptional activity. Furthermore, DZNep and 9-ING-41 indirectly influence Myc expression by altering cellular methylation and modulating the Wnt/β-catenin pathway, respectively. TG02, a multi-kinase inhibitor, affects Myc expression by inhibiting CDKs and inducing cell cycle arrest.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
10058-F4 | 403811-55-2 | sc-213577 sc-213577B sc-213577A sc-213577C | 5 mg 10 mg 25 mg 50 mg | $81.00 $134.00 $241.00 $426.00 | 9 | |
10058-F4 is a small molecule inhibitor that disrupts the Myc-Max interaction, preventing Myc transcriptional activation. This inhibition hinders the formation of active Myc-Max complexes and subsequently modulates downstream signaling pathways, leading to the suppression of Myc-mediated cellular processes such as proliferation and apoptosis resistance. | ||||||
(±)-JQ1 | 1268524-69-1 | sc-472932 sc-472932A | 5 mg 25 mg | $231.00 $863.00 | 1 | |
JQ1 is a bromodomain and extraterminal (BET) protein inhibitor that affects the expression of Myc by disrupting BET protein binding to acetylated histones. This disruption leads to the inhibition of Myc transcriptional activity and downstream signaling, contributing to the suppression of Myc-dependent cellular functions, including proliferation and survival. | ||||||
CX-5461 | 1138549-36-6 | sc-507275 | 5 mg | $245.00 | ||
CX-5461 is a selective RNA polymerase I (Pol I) inhibitor that indirectly affects Myc expression by disrupting ribosomal RNA synthesis. Inhibition of Pol I by CX-5461 leads to nucleolar stress and activation of p53, which, in turn, influences Myc expression. This indirect modulation of Myc expression by CX-5461 results in the inhibition of Myc-driven cellular processes, including proliferation and survival. | ||||||
BETd-246 | 2140289-17-2 | sc-507288 | 5 mg | $1071.00 | ||
BETd-246 is a bromodomain inhibitor that, similar to JQ1, disrupts the binding of BET proteins to acetylated histones. By interfering with this interaction, BETd-246 inhibits Myc transcriptional activity and downstream signaling pathways, leading to the suppression of Myc-dependent cellular functions such as proliferation and apoptosis resistance. | ||||||
KJ Pyr 9 | 581073-80-5 | sc-507276 | 5 mg | $140.00 | ||
KJ-Pyr-9 is a small molecule inhibitor that targets the Myc-associated factor X (MAX) protein, preventing its interaction with Myc. By disrupting the formation of Myc-MAX heterodimers, KJ-Pyr-9 inhibits Myc-dependent transcriptional activation, leading to the modulation of Myc target gene expression and influencing cellular processes related to proliferation and survival. | ||||||
Zotiraciclib | 937270-47-8 | sc-507450 | 10 mg | $202.00 | ||
This compound, also called TG-02, is a multi-kinase inhibitor that targets CDKs and FLT3 among other kinases, indirectly affecting Myc expression. Inhibition of CDKs by TG02 leads to cell cycle arrest, influencing Myc expression and downstream signaling. | ||||||