c-Myc Inhibitor

ZD-1-186 is a non-degradative, covalent-dependent molecular glue that targets BCL6 and BRD9. ZD-1-186 inhibits the transcriptional output of MYC, relieves the repression of canonical BCL6 target loci (including CDKN1A (p21)), and mediates the selective recruitment of BRD9 to BCL6. ZD-1-186 can be used for research on diffuse large B-cell lymphoma.

METTL3-IN-11 is an excellent, selective METTL3 inhibitor (IC₅₀ = 45.31 nM). METTL3-IN-11 exhibits high selectivity towards METTL3 compared to DNMT1, EZH1, MLL1, and PRMT1. METTL3-IN-11 reduces the m6A level of total RNA in MOLM-13 and SKOV3 cells, induces cell apoptosis, and inhibits cell migration. METTL3-IN-11 can reduce the expression of m6A downstream target genes (c-MYC and BCL2). METTL3-IN-11 can be used for the study of ovarian cancer and acute myeloid leukemia.

SKLB-C05 is a novel selective, orally active TOPK inhibitor, with an IC₅₀ of 0.5 nM. SKLB-C05 selectively inhibit TOPK kinase. SKLB-C05 induces Apoptosis, downregulates c-Myc, γ-H2AX, activates p53, blocks FAK/Src medicated migration-related signaling. SKLB-C05 disturbs cell mitosis. SKLB-C05 shows anticancer activity only against TOPK-positive colorectal cancer.

STAT3-IN-32 is an orally active, selective STAT3 SH2 domain inhibitor with a K_d of 21.3 nM, showing selectivity over STAT1/5. STAT3-IN-32 binds to the STAT3 SH2 domain, blocks Tyr705 and Ser727 phosphorylation, abrogates nuclear transcription and mitochondrial oxidative phosphorylation functions. STAT3-IN-32 inhibits tumor growth in mouse pancreatic cancer xenograft models. STAT3-IN-32 can be used for the research of pancreatic cancer.

PM54 is an antitumor agent with activity across multiple cancer types. PM54 acts as a transcription and WNT/β-catenin signaling pathway inhibitor. PM54 suppresses oncogenic transcriptional programs, and key malignant pathways, while inducing DNA double-strand breaks, S-phase cell cycle arrest and apoptosis. PM54 enhances innate immune recognition, remodels the tumor microenvironment. PM54 exhibits antitumor activity as monotherapy or in combination in xenograft models. PM54 is applicable to research on various cancers and advanced solid tumors.

SY-5102 is a potent, selective, and orally active cyclin-dependent kinase (CDK7) inhibitor with a K_d value of 0.03 nM. SY-5102 occupies the ATP-binding pocket of CDK7 via non-covalent binding to inhibit CDK7 activity, and downregulates its phosphorylation of cyclin CDK and RNA polymerase II. SY-5102 inhibits cancer cell proliferation, and induces tumor growth inhibition and regression. SY-5102 can be used in research related to triple-negative breast cancer.

PROTAC BRD4 Degrader-15 is a BRD4 PROTAC degrader with a DC₅₀ of 2.1 nM. PROTAC BRD4 Degrader-15 forms a ternary complex with BRD4 and VHL ubiquitin ligase to induce degradation. PROTAC BRD4 Degrader-15 inhibits the transcription level of the MYC gene. PROTAC BRD4 Degrader-15 suppresses human megakaryocytopoiesis and exhibits antigen-dependent tumor growth inhibition in xenograft models of prostate cancer and acute myeloid leukemia. PROTAC BRD4 Degrader-15 can be used in studies related to prostate cancer and acute myeloid leukemia.

c-Myc inhibitor 8 (compound 56) is a c-Myc inhibitor. c-Myc inhibitor 8 effectively inhibits cell viability of a variety of cancer cells. c-Myc inhibitor 8 inhibits human prostate and lung cancer growth in mouse models. c-Myc inhibitor 8 can be used for cancer research.

TNIK-IN-10 (Compound N15) is a TNIK inhibitor with an IC₅₀ of 0.49 nM against human TNIK. TNIK-IN-10 inhibits the enzymatic activity of TNIK, downregulates the expression of Wnt pathway target genes c-Myc and AXIN2, and reduces the protein expression of LRP5 and LRP6. TNIK-IN-10 induces apoptosis. TNIK-IN-10 exhibits anticancer activity against colorectal cancer. TNIK-IN-10 can be used in the research of colorectal cancer.

(S)-GNE-987 is an isomer of GNE-987 (HY-129937A), which loses VHL binding capacity and BRD4 protein degradation activity, but retains BRD4 inhibitory activity. (S)-GNE-987 is a BRD4/BET inhibitor that potently binds to the BD1 and BD2 bromodomains of BRD4, with a BRD4 BD1 IC₅₀ of 4.0 nM and a BRD4 BD2 IC₅₀ of 3.9 nM. (S)-GNE-987 inhibits MYC expression and exhibits inhibitory activity against acute myeloid leukemia cells, whereas its CLL1‑6 antibody-drug conjugate shows almost no in vivo antitumor efficacy in the HL‑60 xenograft tumor model. (S)-GNE-987 can be used in related research on acute myeloid leukemia.

SVC112 is a translation elongation inhibitor that prevents the cyclic dissociation of EF2 from the ribosome, thereby inhibiting the elongation step of translation. SVC112 shows activity in growth inhibition among cancer cell lines of various origins (acute myeloid leukemia (AML), multiple myeloma (Myeloma), colorectal cancer (CRC), and head and neck squamous cell carcinoma (HNSCC)). SVC112 preferentially impedes ribosomal processing of mRNAs, and decreaseds CSC-related proteins including Myc and Sox2. SVC112 induces apoptosis in hematologic cancer cell lines, while phosphorylation of c-Myc correlates with sensitivity to SVC112 in colorectal cancer cell lines. SVC112 inactivates HNSCC stem cells in vitro and prevents the regrowth of HNSCC tumor xenografts in mice. SVC112 can be used for the study of HNSCC.

c-Myc inhibitor 12 (compound 67h) is an inhibitor of c-Myc with a pEC₅₀ of 6.4.

Antitumor agent-174 (Compound 10) directly engages the N-terminal site of Hsp90 and promotes the degradation of β-catenin, thereby suppressing the Wnt/β-catenin signaling. Antitumor agent-174 effectively inhibits proliferation, induce S and G2/M phases arrest and block the clonogenic ability in CRC cells. Antitumor agent-174 down-regulates CDK1, Cyclin D1, c-Myc, Cyclin B1, and Cyclin A2, and upregulaties P21 proteins. Antitumor agent-174 has significant anti-tumor efficacy against colorectal cancer (CRC) with excellent pharmacokinetics and low toxicity.

WH23 is a dehydrogenase/reductase SDR family member 11 (DHRS11) inhibitor with IC₅₀ values of 0.037 μM. WH23 binds to DHRS11, forming a hydrogen bond with the enzyme’s His210 residue. WH23 suppresses androgen receptor mRNA and protein expression, reduces c-Myc expression, and inhibits cancer cell proliferation. WH23 inhibits PI3K/AKT signaling by reducing phosphorylation of PDK1, AKT, mTOR, and ERK. WH23 enhances Capivasertib (HY-15431)-induced cytotoxicity and apoptosis. WH23 can be used for the research of luminal androgen receptor-positive triple-negative breast cancer.

P300-IN-6 is an orally active histone acetyltransferase p300 HAT domain inhibitor with human IC₅₀ values of 7 nM. P300-IN-6 suppresses c-Myc expression, decreases H3K18ac and H3K27ac levels, and inhibits cancer cell proliferation.P300-IN-6 suppresses tumor growth in xenograft mouse models.P300-IN-6 can be used for the research of multiple myeloma.

BT-PROTAC is a bioorthogonally activatable BRD4/BRD3 PROTAC degrader prodrug. BT-PROTAC is inactive when present alone, but upon activation by tetrazine compounds, it promotes the degradation of BRD4 and BRD3 via the ubiquitin-proteasome system, inhibits c-Myc expression, activates caspase-3, and induces apoptosis in breast cancer cells. BT-PROTAC can be used for breast cancer research.

Y-99 is a PORCN inhibitor with an IC₅₀ of 155.4 nM against the Wnt/β-catenin signaling pathway. Y-99 inhibits the expression of p-LRP6, β-catenin, and c-Myc.

CDK9-IN-44 (Compound 7) is a selective CDK9 inhibitor (IC₅₀=7.6 μM). CDK9-IN-44 inhibits CDK9/cyclin T1 kinase activity, blocking transcriptional elongation, reducing the expression of pro-cancer proteins (such as MCL1, c-MYC), and inducing tumor cell apoptosis. CDK9-IN-44 is promising for research of glioblastoma (GBM) and central nervous system (CNS) disorders.

Y502-3888 is a c-Myc inhibitor. Y502-3888 binds to the c-Myc G4 structure, inhibits c-Myc transcription, and downregulates c-Myc expression at both mRNA and protein levels. Y502-3888 inhibits the viability of myeloma cells and induces cell apoptosis. Y502-3888 can be used for the research of multiple myeloma.

LQFM030 is a novel small molecule MDM2 inhibitor. LQFM030 exhibits concentration dependent cytotoxicity in K562 cells (IC₅₀ = 0.28 mM). LQFM030 induces cell apoptosis through G0/G1 phase cell cycle arrest and increased Caspase activity. LQFM030 downregulates the mRNA expression of MDM2, MDMX, p73, MYC, and NF-κB. LQFM030 is commonly used in research on cancers such as leukemia.