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.
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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 (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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