myc-driven

DT-061 is an orally bioavailable protein phosphatase 2A (PP2A) activator. It could be applied in the therapy of KRAS-mutant and MYC-driven tumorigenesis.

DC-034 is a potent downregulator of MYC transcription in cancer cells by a G4-dependent mechanism, thereby selectively inhibiting MYC significantly greater than other G4-driven genes.

LL-K8-22 is a potent, selective, and durable dual degrader of CDK8-cyclin C, demonstrating DC50 values of 2.52 and 2.64 μM, respectively. This compound effectively suppresses STAT1 Ser 727 phosphorylation and inhibits carcinogenic transcriptional programs driven by E2F and MYC. LL-K8-22 is specifically utilized in research for triple-negative breast cancer (TNBC) [1].

MRT-2359 is a potent and orally available GSPT1 reducer with antitumour activity.MRT-2359 inhibits the growth of drug-resistant non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC) cells.MRT-2359 exhibits preferential activity in MYC-driven cell lines.

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.

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

T025 is a pan CLK inhibitor with Kds of 4.8, 0.096, 6.5, 0.61, and 0.074 nM for CLK1-4, respectively. T025 displays anti-proliferative activities with IC50s of 30-300 nM in hematological and solid cancer cell lines. T025 can be used in studies about MYC-driven diseases.

Sulfopin is a highly selective covalent inhibitor of Pin1 with an apparent Ki of 17nM. Sulfopin blocks Myc-driven tumors in vivo.

c-Myc Inhibitor 5 (DA3) is a fluorescent bispurine compound with a long-chain bridge that selectively binds to the c-MYC G-quadruplex, exhibiting a dissociation constant (K D) of 16 μM. Unlike other G4-driven oncogenes, this inhibitor specifically suppresses c-MYC expression [1].