c-myc transcription

IZCZ-3,antitumor activity. is a potent c-MYC transcription inhibitor.

Ceramides Mixture, an endogenous ceramide, consists of hydroxy and non-hydroxy fatty acid-containing ceramides. It is involved in the regulation of cell cycle arrest, growth inhibition, and modulation of telomerase activity.

Vitamin K2 (Menatetrenone) is a menaquinone compound and form of vitamin K2 with potential antineoplastic activity. Menatetrenone may act by modulating the signaling of certain tyrosine kinases, thereby affecting several transcription factors including c-myc and c-fos. This agent inhibits tumor cell growth by inducing apoptosis and cell cycle arrest.

C-MYC PEPTIDE EPITOPE TFA, the product of the c-myc proto-oncogene, is a helix-loop-helix leucine zipper phosphoprotein that regulates gene transcription in cell proliferation, cell differentiation and apoptosis. This peptide is a human c-myc epitope.

OAC1 (BAS 00287861) is a compound activating Octamer-binding transcription factor 4 (Oct4). It enhances the iPSC reprogramming efficiency and accelerates the reprogramming process.

PLK1-IN-13 is a selective, orally active PLK1 inhibitor with an IC50 of 0.27 nM. It also inhibits PLK2 (IC50: 12.72 nM) and PLK3 (IC50: 4.12 nM). PLK1-IN-13 induces cell cycle arrest at the G2 phase, promotes apoptosis, and downregulates the transcription of the cancer-associated oncogene c-MYC. This compound inhibits tumor growth and is applicable for research in acute myeloid leukemia (AML).

c-Myc inhibitor16 iodide (Compound W11) is a selective inhibitor of the c-MycG-quadruplex (c-MycG4). It suppresses the transcription and translation of the c-Myc gene, disrupts the tumor cell cycle by halting growth at the G0/G1 phase, and activates mitochondrial apoptotic pathways, leading to early apoptosis in cancer cells. This compound shows potential for research in breast cancer.

c-Myc inhibitor13 (compound A6) is an inhibitor of c-MYC transcription. It selectively stabilizes c-MYCG4 and inhibits G4-related c-MYC transcription.

c-MYC/BCL2 ligand 1 iodide is a dual-target ligand that specifically interacts with the G-quadruplex (G4) regions of the c-MYC and Bcl-2 promoters, exhibiting Kd values of 0.90 μM for c-MYCG4 and 0.56 μM for Bcl-2G4. It works by binding to these G4-forming sequences to inhibit transcription of the c-MYC and Bcl-2 genes, leading to reduced protein expression. This compound effectively suppresses MCF-7 cell proliferation and migration, induces G1 phase cell cycle arrest, and triggers apoptosis. Additionally, it significantly hampers tumor growth in the 4T1 homogenous model with negligible toxicity. c-MYC/BCL2 ligand 1 iodide is applicable in breast cancer research.

STAT3-IN-46 is a selective, orally active inhibitor of the signal transducer and activator of transcription 3 (STAT3), with a KD value of 323.3 nM. It binds directly to the SH2 domain of STAT3, inhibiting the IL-6/JAK/STAT3 signaling pathway with an IC50 value of 0.87 μM, and decreases levels of c-Myc and Bcl-2. STAT3-IN-46 is applicable in cancer research, including studies on triple-negative breast cancer.

CDK9-IN-44 (Compound 7) is a selective inhibitor of CDK9 with an IC50 of 7.6 μM. It effectively inhibits CDK9/cyclin T1 kinase activity, impedes transcription elongation, reduces the expression of oncogenic proteins such as MCL1 and c-MYC, and induces apoptosis in tumor cells. CDK9-IN-44 shows potential for research in glioblastoma (GBM) and central nervous system (CNS) diseases.

SY-5102 is a potent, selective, orally active cyclin-dependent kinase (CDK7) inhibitor with a Kd of 0.03 nM. It exhibits antiproliferative activity against HCC70 cells with an EC50 of 9 nM. SY-5102 inhibits CDK7-mediated CAK function [downregulating CDK2Thr160 phosphorylation] and TFIIH transcription function [downregulating RNA polymerase II Ser5 phosphorylation]. The compound induces G2/M cell cycle arrest, downregulates the expression of the oncogene c-Myc, and ultimately triggers apoptosis in cancer cells. SY-5102 is applicable for research in triple-negative breast cancer (TNBC).

PROTACBRD4 Degrader-41 (Compound A5) is a BRD4 PROTAC degrader with a DC50 of 0.97 nM. It exhibits potent antiproliferative activity against various cancer cells, including AML, lymphoma, breast cancer, ovarian cancer, and non-small cell lung cancer. The compound induces G0/G1 phase arrest and apoptosis in MV4-11 cells and downregulates c-Myc transcription levels.

hnRNPK-IN-1 is a specific ligand that binds to the heterogeneous nuclear ribonucleoprotein K (hnRNPK) with high affinity, as evidenced by dissociation constant (Kd) values of 4.6 μM and 2.6 μM determined using surface plasmon resonance (SPR) and microscale thermophoresis (MST), respectively. This binding disrupts the interaction between hnRNPK and the c-myc promoter, thereby inhibiting c-myc transcription. Furthermore, hnRNPK-IN-1 induces apoptosis in HeLa cells and exhibits significant anti-tumor activity.

Idarubicin, a potent anthracycline antileukemic agent, is orally active in its application. It functions by inhibiting topoisomerase II, thus interfering with DNA replication and RNA transcription. Furthermore, Idarubicin induces DNA damage, inhibits DNA synthesis, and suppresses c-myc expression. It also demonstrates inhibitory effects on the growth of bacteria and yeasts [1] [2] [3] [4] [5].

Anticancer Agent 84, a cancer research compound, inhibits c-MYC transcription by stabilizing the G-quadruplex (G4) structure, offering potential for cancer investigation [1].

m-Se3 is a potent, selective inhibitor of c-MYC transcription with demonstrated capability to inhibit tumor growth and exhibit anti-cancer activity [1].

c-Myc Peptide Trifluoroacetate is a synthetic peptide corresponding to the C-terminal amino acids (410-419) of human c-myc protein. c-Myc Peptide Trifluoroacetate participates in regulation of growth-related gene transcription.

c-Myc Peptide is a useful displacement of c-Myc-tagged fusion proteins bound to anti-c-Myc antibodies in immunoassays. The successful inhibition of antibody binding by c-Myc peptide demonstrates binding is specific. c-Myc peptide participates in the regul

Inosine-5'-diphosphoric acid disodium salt, as a decoy substrate for NM23-H2, exhibits excellent binding ability at the GDP-binding site of NM23-H2 with a dissociation constant (KD) of 5.0 μM. It can inhibit c-MYC transcription by disrupting the interaction between NM23-H2-Pu27-GQ, thereby inducing apoptosis and G2/M cell cycle arrest without affecting the kinase activity mediated by NM23-H2. Inosine-5'-diphosphoric acid disodium salt also possesses anti-hypoxic, antihypertensive, and antiarrhythmic activities, protects organisms from γ-radiation damage, and can be used in research on cancers such as Burkitt lymphoma and cardiovascular diseases.