myc-max

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.

MYCMI-6 (NSC-354961) is a potent and selective inhibitor of endogenous MYC:MAX protein interactions,reduces proliferation and induces massive apoptosis in tumor tissue from a MYC-driven xenograft tumor model without severe side effects.

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.

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.

VPC-70619 is a potent, orally active, and selective N-Myc inhibitor that blocks the binding of N-Myc-Max compounds to the E-box of DNA, thereby inhibiting cancer cell growth. It can be efficiently absorbed and utilized by the body through oral or intraperitoneal routes.

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.

MYCi975 (NUCC-0200975) is an orally active MYC inhibitor.

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.

c-Myc inhibitor15 (Compound A5) is a selective c-Myc inhibitor that disrupts the interaction between c-Myc and Max, leading to c-Myc protein degradation and apoptosis (Apoptosis). It exhibits potent cytotoxic activity with IC50 values of 4.08 μM and 7.86 μM in A549 and NCI–H1299 lung cancer cell lines, respectively. In an allogeneic tumor model, c-Myc inhibitor15 demonstrated outstanding antitumor efficacy, achieving a tumor growth inhibition rate of 76.4% and significantly reducing c-Myc protein expression. This compound shows promise for research related to c-Myc-associated lung cancer.

MY05 selectively targets c-MYC within cells and disrupts the interaction between MYC and MAX. It binds to intracellular c-MYC, modulating its thermal stability, reducing the transcriptional targets of c-MYC, and exhibiting anticancer activity (TNBC, triple-negative breast cancer).

MYC-IN-4 is a MYC inhibitor that disrupts the interaction between MYC/MAX proteins with an IC50 of 3.06 μM. It inhibits MYC-aberrant PC-3 prostate cancer cells, exhibiting an IC50 of 0.440 μM. In FVB mice with Myc-CaP prostate tumor xenografts, MYC-IN-4 demonstrates significant antitumor efficacy. This compound is useful for prostate cancer research.

MYRA-A is an inducer of apoptosis in a Myc-dependent manner that acts by inhibiting Myc-driven transformation and disrupting MYC-Max interaction.

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

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

Mycro2 is an inhibitor of the protein-protein interactions between the bHLHZip proteins c-Myc and Max.

Mycro1 is an inhibitor of the protein-protein interactions between the bHLHZip proteins c-Myc and Max.

MDEG-541 is a potent MYC-MAX degrader that exhibits antiproliferative activity by downregulating the expression of GSPT1, MYC, GSPT2, and PLK1 proteins [1].

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.