c-Myc

Trachelogenin ((-)-Trachelogenin), isolated from Combretum fruticosum, is an HCV entry inhibitor with anti-proliferative effects. Its mechanism is related to affecting the phosphorylation of key proteins such as β-Catenin, c-Myc and GSK3 in the β-Catenin signaling pathway. chemical and concentration-dependent. Trachelogenin has antiviral, anti-inflammatory and analgesic activities with IC50 of 0.325 and 0.259 μg mL in HCVcc and HCVpp models, respectively.

Lusianthridin is a natural product from Dendrobium venustum. Lusianthridin exhibits anti-migratory property at nontoxic concentrations. Lusianthridin enhances c-Myc degradation through the inhibition of Src-STAT3 signaling.

NY2267 (Acetic acid, 2-[[6-[2-(cyclohexylamino)-1-[[(4-methoxyphenyl)methyl](2-pyridinylcarbonyl)amino]-2-oxoethyl]-2-naphthalenyl]oxy]-, 1,1-dimethylethyl ester) is a disruptor of Myc-Max interaction, with an IC50 of 36.5 μM.

10058-F4 (c-Myc Inhibitor) is a cell-permeable thiazolidinone that specifically inhibits the c-Myc-Max interaction and prevents transactivation of c-Myc target gene expression; induces cell-cycle arrest and apoptosis.

APTO-253 (LOR-253) inhibits c-Myc expression, stabilizes G-quadruplex DNA, and induces cell cycle arrest and apoptosis in acute myeloid leukemia cells. APTO-253 mediates anticancer activity through the induction of the KLF4 tumor suppressor.

10074-G5 is an inhibitor of c-Myc-Max dimerization.

BTYNB (MDK6620) is an inhibitor of the oncofetal mRNA-binding protein IMP1 (IC50 = 5 μM for IMP1 binding to c-Myc mRNA). MDK6620 downregulates β-TrCP1 mRNA and reduces activation of nuclear transcriptional factors-kappa B (NF-κB). It disrupts this enhancer function by impairing IGF2 mRNA-binding protein 1 (IGF2BP1)-RNA association

VPC-70063 (Thiourea, N-[3,5-bis(trifluoromethyl)phenyl]-N'-(phenylmethyl)-) is an inhibitor of c-Myc-MAX. VPC-70063 exhibits Myc-Max transcriptional activity inhibition of 106% with an IC50 of 8.9 μM and Myc-Max/UBE2C downstream pathway inhibition of 94%. VPC-70063 can be used for studies about anticancer.

IRES-C11 is a specific inhibitor of translation that targets the internal ribosome entry site (IRES) of the c-MYC gene. It functions by blocking the interaction between heterogeneous nuclear ribonucleoprotein A1, a trans-acting factor required for c-MYC IRES activity, and its corresponding IRES. Notably, IRES-C11 does not inhibit the IRES activity of BAG-1, XIAP, and p53.

KJ Pyr 9 is an MYC inhibitor (Kd: 6.5 nM in vitro assay).

CPI0610 (CPI-0610) is an effective, specific, and cell-active BET bromodomain inhibitor CPI-0610 inhibits BRD4-BD1 (IC50: nM).

Mycro 3 is potent and selective for c-Myc in whole cell assays.

Nicotinamide N-oxide (Nicotinamide 1-oxide) is recognized as an in vivo metabolite of nicotinamide which is a precurser of nicotinamide-adenine dinucleotide (NAD+) in animals. The enzyme that catalyzes the reduction of nicotinamide N-oxide to nicotinamide in the liver is xanthine oxidase.

ML327 is a MYC blocker. ML327 can also de-repress E-cadherin transcription and reverse Epithelial-to-Mesenchymal Transition (EMT).

sAJM589 is a Myc inhibitor that dose-dependently disrupts Myc-Max heterodimers, thereby decreasing Myc protein levels. Myc is a multifunctional nuclear phosphoprotein that plays a key role in cell cycle progression, apoptosis, and cellular transformation. sAJM589 inhibits the cellular proliferation of a variety of Myc-dependent cancer cell lines and the adherent, non-dependent growth of Raji cells’ Growth.

MYCi361 (NUCC-0196361) is an inhibitor of MYC (binding to MYC with Kd of 3.2 μM).

KL4-219A is a selective covalent degrader of the oncogenic transcription factor MYC, inhibiting MYC transcriptional activity and degrading MYC in a proteasome-dependent manner by targeting intrinsically disordered C203 and D205 residues.

JY-3-094 is a selective Myc inhibitor that targets the hydrophobic domain of Myc and inhibits the formation of the Myc-Max heterodimer, with an IC50 of 33 μM, and can be used for cancer research.

KSI-3716 is a c-Myc inhibitor used as a bladder chemotherapy agent. It blocks the formation of the c-MYC/MAX complex with the target gene promoter and induces cell cycle arrest and apoptosis. It can be used for bladder cancer research.

AZD-5991 Racemate is the racemate of AZD-5991. (Rac)-AZD-5991 is a novel Mcl-1 inhibitor with IC50 <3 nM in FRET assay and induces upregulation of BCL2,BCL-XL, CMYC and MCL1 in AML cell lines.

H122 is a TEADPROTAC degrader effective in degrading TEAD1 with a DC50 of 3 nM, and it shows strong affinity for TEAD2, TEAD3, and TEAD4 with Ki values of 2.0, 3.6, and 1.6 nM, respectively. H122 also downregulates Myc expression and inhibits the growth of MSTO-211H and NCI-H226 cells, with IC50 values of 21.3 nM and 0.6 nM, respectively, demonstrating antitumor activity in mouse models. (Pink: ligand for target protein; Black: linker; Blue: ligand for E3 ligaseCereblon)

Anticanceragent 263 (compound 7) is an effective anticancer agent. It binds with the G-quadruplex DNA (G4) sequence 22-mer Pu22 (a c-Myc DNA analog). As a structural modulator, Anticanceragent 263 significantly enhances the formation of protein α-helices and has the capacity to form a supramolecular network. Furthermore, Anticanceragent 263 exhibits no cytotoxicity.

Methylcarbamyl PAF C-8 is resistant to degradation by PAF-AH and has a half-life of over 100 minutes in platelet-poor plasma, exhibiting platelet aggregation activity. In NRK-49 cells overexpressing PAF receptor, it induces the expression of c-myc, c-fos, and activates mitogen-activated protein kinase (MAPK). Furthermore, Methylcarbamyl PAF C-8 can induce G1 phase cell cycle arrest. This compound shows potential for research in cardiovascular and anti-cancer applications.

SYHA1815, an orally active RET inhibitor (IC50=0.9 nmol L), demonstrates antitumor activity. It exhibits greater selectivity for RET over KDR (IC50=15.9 nmol L). SYHA1815 operates by downregulating c-Myc, arresting the G1 cell cycle, and inhibiting RET-driven cell proliferation.