c-Myc Inhibitor

RS47 is a selective RelB inhibitor with a Kd value of 1.1 μM. RS47 also acts as an inhibitor of HCV replication. RS47 can block the non-canonical NF-κB signaling pathway without affecting the canonical pathway. RS47 exerts anti-tumor effects of inhibiting proliferation and promoting apoptosis on colorectal cancer, B-cell lymphoma and other related tumors both in vitro and in vivo by disrupting the binding of RelB to target DNA. RS47 can be used for the research of tumors and infectious diseases.

H122 is a PROTAC degrader for TEAD that degrades TEAD1 with a DC₅₀ of 3 nM. H122 exhibits good affinity to TEAD2, TEAD3, and TEAD4 with K_i values of 2.0, 3.6 and 1.6 nM, respectively. H122 relies on binding to TEAD1 and CRBN, functional E3 ligase activity, and a functional proteasome for degradation.H122 induces degradation of TEAD3 and forms a ternary complex with TEAD4 and CRBN/DDB1 to mediate degradation.H122 downregulates expression of Myc target genes. H122 exhibits antitumor efficacy in MSTO-211H mouse xenograft models.H122 can be used for the research of malignant mesothelioma.

Ganoderma Lucidum/Reishi Extract is a Ganoderma lucidum extract. Ganoderma Lucidum/Reishi Extract reduces the expression of c-Myc, BCL-2, BCL-XL, TERT, PDGFB, eIF4G, Survivin, β-catenin, and eIF4E. Ganoderma Lucidum/Reishi Extract downregulates the gene expression of MMP-9. Ganoderma Lucidum/Reishi Extract upregulates the expression of IL8. Ganoderma Lucidum/Reishi Extract is applicable to the research of inflammatory breast cancer. Ganoderma Lucidum is used in the research of various diseases, such as allergy, arthritis, hypertension, neurasthenia, inflammation, and cancer.

Mycro 3 is an orally active, potent and selective inhibitor of Myc-associated factor X (MAX) dimerization. Mycro 3 also inhibit DNA binding of c-Myc. Mycro 3 could be used for the research of pancreatic cancer.

IGF2BP1-IN-1, a Cucurbitacin B (HY-N0416) derivative, is a potent IGF2BP1 inhibitor (K_D = 2.88 nM). IGF2BP1-IN-1 binds directly to IGF2BP1, thereby inducing tumor cell cycle arrest, increasing apoptosis, and reducing autophagy. IGF2BP1-IN-1 can be used in research on NSLSC, colon, breast, liver, ovarian, pancreatic, and cervical cancers.

Ertabresib (INCB-057643) is an orally active BET protein inhibitor. Ertabresib blocks gene transcription by targeting the BET protein family, induces cell cycle arrest and apoptosis by downregulating proto-oncogenes such as c-MYC, and additionally reduces the expression of FOXP3 and PD-L1 to improve the immune microenvironment. It also exerts synergistic effects and overcomes drug resistance when combined with chemotherapy and XPO1 inhibitors. Ertabresib can be used in research related to high-grade B-cell lymphoma with MYC and BCL2 rearrangements, pancreatic cancer, pancreatitis, and metastatic castration-resistant prostate cancer.

Mollugin is an orally active and potent NF-κB inhibitor. Mollugin induces S-phase arrest of HepG2 cells, and increased intracellular reactive oxygen species (ROS) levels. Mollugin induces DNA damage in HepG2 cells, as well as an increase in the expression of p-H2AX. Mollugin shows anti-cancer effect by inhibiting TNF-α-induced NF-κB activation. Mollugin enhances the osteogenic action of BMP-2 (bone morphogenetic protein 2) via the p38-Smad signaling pathway.

dBET57 is a potent and selective BRD4_BD1 PROTAC degrader with a DC₅₀ of approximately 500 nM. dBET57 forms a ternary complex with CRL4^CRBN and BRD4_BD1, induces the ubiquitination and degradation of BRD4, and indirectly inhibits the transcription of MYCN, c-Myc and PD-L1, ultimately leading to cell cycle arrest and apoptosis. dBET57 can be used in related research on neuroblastoma, non-small cell lung cancer and colorectal cancer.

KI-CDK9d-32 is a selective CDK9 PROTAC degrader (IC₅₀ = 3 nM; DC₅₀ = 0.89 nM). KI-CDK9d-32 induces CDK9 degradation via the ubiquitin-proteasome pathway to abrogates CDK9 enzymatic and scaffolding functions, downregulates MYC expression and MYC-dependent signaling, represses TNF-alpha signaling pathways activity and pre-rRNA levels. KI-CDK9d-32 disrupts nucleolar homeostasis, blocks cell cycle progression and cellular translation by reducing 4EBP1 phosphorylation, and elicits cancer cell cytotoxicity in a CRBN-dependent manner, while high ABCB1 activity attenuates the efficacy. KI-CDK9d-32 can be used for the research of acute lymphoblastic leukemia, rhabdomyosarcoma, pancreatic adenocarcinoma.

VPC-70619 is a potent N-Myc inhibitor. VPC-70619 blocks the binding of the N-Myc-Max heterocomplex to the DNA E-box and exhibits potent inhibitory activity against N-Myc-dependent cell lines. VPC-70619 can partially reverse paclitaxel (HY-B0015) resistance in cells by reducing MYCN expression. VPC-70619 can be used for cancer research (e.g., neuroblastoma and thyroid cancer).

KSI-3716 is a potent c-Myc inhibitor that blocks c-MYC/MAX binding to target gene promoters. KSI-3716 is an effective intravesical chemotherapy agent for bladder cancer.

hnRNPK-IN-1 is a heterogeneous nuclear ribonucleoprotein K (hnRNPK) binding ligand with K_d values of 4.6 μM and 2.6 μM measured with SPR and MST, respectively. hnRNPK-IN-1 inhibits c-myc transcription by disrupting the binding of hnRNPK and c-myc promoter. hnRNPK-IN-1 induces Hela cells apoptosis and has strongly anti-tumor activities.

Ravoxertinib hydrochloride (GDC-0994 hydrochloride) is an orally active ERK1/2 inhibitor. Ravoxertinib hydrochloride inhibits the ERK1/2 MAPK signaling pathway and reduces the expression levels of c-Myc, HK2 and LDHA. Ravoxertinib hydrochloride decreases mammosphere formation, and exerts additive and/or superadditive cytotoxicity when combined with Ipatasertib (HY-15186) in 3D tumor sphere models. Ravoxertinib hydrochloride can be used in research related to various cancers including breast cancer, melanoma, head and neck cancer, non-small cell lung cancer, ovarian cancer and Merkel cell carcinoma.

MC-1-F2 is a FOXC2 inhibitor. MC-1-F2 shows a binding affinity (K_d) of 26 μM for full-length FOXC2. MC-1-F2 reduces epithelial-mesenchymal transition (EMT) markers in breast cancer cells, suppresses cancer stem cell (CSC) properties and reduces invasiveness in castration-resistant prostate cancer (CRPC) cells. MC-1-F2 can be used for the study of CRPC and breast cancer.

TCIP3 is a bivalent molecular glue degrader that binds dually to p300/CBP and BCL6. TCIP3 redirects p300 and CBP, thereby activating programmed cell death genes that are normally repressed by the oncogenic driver gene BCL6. TCIP3 induces acetylation of BCL6 and histone tails, inhibits c-MYC transcription. TCIP3 can be used for the research of diffuse large B-cell lymphoma (DLBCL).

NSC12 is an orally active pan-FGF trap. NSC12 inhibits the interaction between FGF2/FGFR. NSC12 suppresses the phosphorylation of FGFR3. NSC12 reduces c-Myc levels, induces DNA damage, triggers the cleavage of Caspase 3, and promotes ROS production. NSC12 exhibits anticancer activity against lung cancer and multiple myeloma.

Bruceantin ((-)-Bruceantin) is a quassinoid found in B. javanica. Bruceantin activates caspase signaling pathway, causes the mitochondrial dysfunction, inhibits cell proliferation, induces cell differentiation and apoptosis. Bruceantin exhibits anti-leukemia and antiprotozoal activities.

Briciclib (ON 014185) is a eukaryotic translation initiation factor 4E (eIF4E) inhibitor. Briciclib exhibits broad-spectrum anti-cancer activity, including in mantle cell leukemia, breast cancer, gastric cancer, and esophageal cancer cells. Briciclib reduces the expression of cyclin D1 and c-Myc, and enhances the expression of P53 and Cleaved Caspase 3 pro-apoptotic proteins. Briciclib can be used for the study of hematological system tumors and solid tumors.

Ifupinostat (BEBT-908) is a blood-brain barrier-permeable PI3K/HDAC inhibitor. Ifupinostat exerts anticancer activity against hematologic malignancies, lung cancer, colon cancer, brain cancer and other cancers. Ifupinostat inhibits the PI3K/AKT/mTOR signaling pathway, suppresses c-Myc expression and induces ferroptosis. Ifupinostat can be used in tumor research.

Tocopherols are orally effective antioxidants and ferroptosis inhibitors. Tocopherols scavenge ROS/RNS, alleviate DNA damage, downregulate cyclin D1/c-Myc/TFF/pS2/PGR in an ER-dependent manner, and inhibit ferroptosis mediated by lipid peroxidation. Tocopherols block the occurrence of ferroptosis in Gpx4-knockout Pfa1 cells, with an EC₅₀ value of 1.0-2.3 μM. Tocopherols inhibit tumor growth. Tocopherols can be used in studies related to estrogen-mediated ER⁺ breast cancer, oxidative stress-induced carcinogenesis, and ferroptosis regulation.