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c-Myc is the master transcription factor for cell proliferation and is involved in numeroushematological and solidcancers.

Proto-oncogene c-Myc, encoding one of the most important transcription factors, plays a pivotal role in tumor initiation and progression. c-Myc regulates hundreds of disparate target genes that participate numerous biological effects, such as cell proliferation, apoptosis, differentiation, and stem cell self-renewal. c-Myc is one of the four factors used in reprogramming somatic cells to induce pluripotent stem (iPS) cells and is implicated in maintaining cancer stem-like cells (CSCs).

The transcription factor c-Myc is a key mediator of the Notch signaling–regulated T cell differentiation. In a well-established in vitro differentiation model of T lymphocytes from hematopoietic stem cells, Notch1 and 4 directly promotes c-Myc expression; dominant-negative (DN) c-Myc inhibits early T cell differentiation. Moreover, the c-Myc expression activated by Notch signaling increases the expression of survivin, an inhibitor of apoptosis (IAP) protein.

c-Myc gene, as a transcription factor of hTERT, is over expressed in a variety of tumors.c-Myc and hTERT expression in local recurrent gastric cancer tissues is much higher than in primary gastric cancer tissues at the protein and mRNA levels.

Cat. No. Product Name CAS No. Information



CMLD010509 is a rocaglate (flavagline) derivative that acts a highly specific inhibitor of the oncogenic translation program supporting MM, including key oncoproteins such as MYC, MDM2, CCND1, MAF, and MCL-1; induces apoptosis and inhibits the heat shock response in MM cells (IC50=10 nM), a potent and selective translation inhibitor through an eIF4E phosphorylation-independent mechanism and is highly effective in vivo in several mouse models.


MYC inhibitor DC-34


MYC inhibitor DC-34 is a potent small molecule that selectively inhibits MYC at the transcriptional level only when a G-quadruplex (G4) is present in the promoter, binds to MYC G4 with Kd of 9.4 uM; does not transcriptionally downregulate several other G4-dependent genes to the same extent; binds independently to the MYC G4 3'and 5' ends, demonstrates cytotoxicity in L363 MM cells with IC50 of 3.5 uM.


KJ Pyr 9


KJ-Pyr-9 is a novel small-molecule inhibitor of c-Myc (Kd=6.5 ± 1.0 nM); interferes with MYC-MAX complex formation and inhibits MYC-induced oncogenic transformation in cells; active in xenograft mice.




10074-G5 is a small molecules that disrupts c-Myc-Max heterodimerization; binds to and distorts the bHLH-ZIP domain of c-Myc; inhibits the growth of Daudi Burkitt's lymphoma cells and disrupts c-Myc/Max dimerization.




10058-F4 is a specific c-Myc inhibitor that disrupts the association between the c-Myc and Max, inhibits HL60 cell growth with IC50 of 51 uM; arrests AML cells at G0/G1 phase, downregulates c-Myc expression and upregulates CDK inhibitors p21 and p27; induces apoptosis through activation of mitochondrial pathway shown by downregulation of Bcl-2, upregulation of Bax, release of cytoplasmic cytochrome C, and cleavage of caspase 3, 7, and 9; also induces myeloid differentiation.




CBL0137 (Curaxin CBL0137) is a histone chaperone FACT (facilitates chromatin transcription) and MYC signal inhibitor that markedly reduced tumor initiation and progression in vivo; simultaneously activates p53 and inhibits NF-κB without causing detectable genotoxicity, causes phosphorylation of p53 Ser(392) by CK2 and inhibition of NF-κB-dependent transcription in neuroblastoma cells; eradicates drug resistant cancer stem cells and potentiates efficacy of gemcitabine in preclinical models of pancreatic cancer.




sAJM-589(sAJM589) is a novel, potent small molecule Myc inhibitor that disrupts the Myc-Max leucine-zipper heterodimer with IC50 of 1.8 uM; preferentially inhibits transcription of MYC target genes in P493-6 cell; suppresses cellular proliferation in diverse MYC-dependent cancer cell lines, including P493-6, Ramos, HL-60 and KG1a (IC50=0.8-2 uM); reduces Myc protein levels in these cells, possibly by promoting ubiquitination and degradation of Myc protein.




BTYNB is a potent and selective inhibitor of IMP1 binding to c-Myc mRNA with IC50 of 5 uM; has no effect on binding of PR to flPRE; destabilizes c-Myc mRNA, downregulates β-TrCP1 mRNA and reduces activation of NF-κB; also decreases oncogenic translation regulator eEF2 mRNA levels in cancer cells; potently inhibits proliferation of IMP1-containing ovarian cancer and melanoma cells with no effect in IMP1-negative cells.




MYCMI-6 (NSC354961) is a selective, high affinity inhibitor of MYC-MAX interaction, blocks MYC-driven transcription and binds selectively to the MYC bHLHZip domain with Kd of 1.6 uM in SPR assay; specifcally targets MYC:MAX interaction without interfering with other MYC activities, selectively suppresses MYC-driven tumor cell growth with high efficacy, efficiently inhibits anchorage-independent growth of MYCN-amplifed neuroblastoma cells with GI50 values of <0.4, 5 and 0.75 μM, respectively; reduces proliferation and induces massive apoptosis in tumor tissue from a MYC-driven xenograft tumor model without severe side effects.


APTO-253 hydrochloride


APTO-253 hydrochloride (APTO253;LOR253;LOR-253) is a small molecule inducer of KLF4, stabilizes G-quadruplex DNA and reduces MYC mRNA expression and protein levels; APTO-253 is converted intracellularly from a monomer to a ferrous complex [Fe(253)3]; selectively induces CDKN1A (p21), promotes G0-G1 cell-cycle arrest, and triggers apoptosis in acute myeloid leukemia (AML) cells without producing myelosuppression in various animal species and humans, induces DNA Damage in AML cells.

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