c-myc

C-Myc Inhibitor 7, serving as both a c-Myc inhibitor and a multi-target protein degrader, effectively degrades proteins c-MYC, CK1α, GSPT1, and IKZF1/2/3 across various tumor cell types. It holds potential for research into diseases associated with high c-Myc expression, including cancer, cardiovascular and cerebrovascular conditions, and viral infections.

c-Myc inhibitor 4 is a potent, orally active compound that reduces c-Myc, an important proto-oncogene closely associated with the development of many tumors.

C-Myc Inhibitor 8 is an effective compound for cancer research, inhibiting cell viability across a range of cancer types and demonstrating growth suppression in human prostate and lung cancers within mouse models. This inhibitor specifically targets the c-Myc pathway, showcasing its potential utility in oncological studies.

c-Myc Inhibitor 9 (Compound 332) is an effective c-Myc inhibitor, exhibiting a logEC50 of ≥6, and demonstrating significant tumor growth inhibition in nude mouse models. This compound is utilized in cancer research.

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].

C-Myc Inhibitor 10 (compound 17), exhibiting enhanced cellular potency, benefits from increased permeability due to the methylation of the morpholine nitrogen [1].

c-Myc inhibitor 11 (Compound 67e), a c-MYC inhibitor (p EC 50: 6.4), demonstrates high clearance, moderate volume of distribution, and a short half-life in rat pharmacokinetic assays, making it suitable for cancer research [1].

Compound 67h, also known as c-Myc inhibitor 12, is a potent inhibitor of c-Myc, exhibiting a pEC50 value of 6.4 [1].

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.

c-Mycligand 1 is a c-Myc inhibitor and functions as a ligand for target proteins in PROTAC (Proteolysis Targeting Chimeras). It is utilized in the synthesis of PROTAC c-Myc inhibitor 7.

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.

RK-9123016 is a SIRT2 inhibitor. RK-9123016 increases the acetylation level of eukaryotic translation initiation factor 5A (eIF5A), a physiological substrate of SIRT2, and reduces cell viability of human breast cancer cells accompanied with a decrease in c-Myc expression.

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.

Nicotinamide N-oxide (Nicotinamide 1-oxide) is recognized as an in vivo metabolite of nicotinamide which is a precurser of nicotinamide-adenine dinucleotide (NAD+) in animals. The enzyme that catalyzes the reduction of nicotinamide N-oxide to nicotinamide in the liver is xanthine oxidase.

APTO-253 (LOR-253) inhibits c-Myc expression, stabilizes G-quadruplex DNA, and induces cell cycle arrest and apoptosis in acute myeloid leukemia cells. APTO-253 mediates anticancer activity through the induction of the KLF4 tumor suppressor.

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

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.

MYCi361 (NUCC-0196361) is an inhibitor of MYC (binding to MYC with Kd of 3.2 μM).

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

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.

KJ Pyr 9 is an MYC inhibitor (Kd: 6.5 nM in vitro assay).

Anticanceragent 263 (compound 7) is an effective anticancer agent. It binds with the G-quadruplex DNA (G4) sequence 22-mer Pu22 (a c-Myc DNA analog). As a structural modulator, Anticanceragent 263 significantly enhances the formation of protein α-helices and has the capacity to form a supramolecular network. Furthermore, Anticanceragent 263 exhibits no cytotoxicity.