c-Myc Inhibitor

10058-F4 (c-Myc Inhibitor) is a cell-permeable thiazolidinone that specifically inhibits the c-Myc-Max interaction and prevents transactivation of c-Myc target gene expression; induces cell-cycle arrest and apoptosis.

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 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-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 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].

Inobrodib (CBP-IN-1) is a potent inhibitor of p300/CBP bromodomain.

NNK is a nitrosated derivative of nicotine that activates the ERK1/2 and PKCα signaling pathways, induces Bcl2 phosphorylation at Ser70, and activates c-Myc at Thr58 and Ser62, thereby promoting the proliferation and survival of human lung cancer cells, and is commonly used to establish lung cancer mouse models.

DK419 is an orally active inhibitor of Wnt/β-catenin signaling, with an IC50 of 0.19 μM. DK419 decreases protein lelvels of Axin2, β-catenin, c-Myc, Cyclin D1 and Survivin.It also induces production of pAMPK.

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.

USP28-IN-3 is a highly selective USP28 inhibitor with an IC50 value of 0.1 μM against USP28.USP28-IN-3 exhibits anticancer activity and inhibits USP2, USP7, USP8, USP9x, UCHL3, and UCHL5.USP28-IN-3 is cytotoxic to human colorectal and lung squamous carcinoma cells, inhibiting c-cells and c-neutralizing c-neutralizing c-neutralizing c-neutralizing c-neutralizing c-neutralizing c-neutralizing c-cells through the ubiquitin-proteasome system. -proteasome system to dose-dependently downregulate cellular levels of c-Myc.

Saxagliptin hydrate (Onglyza hydrate) is a selective and reversible DPP4 inhibitor (IC50: 26 nM; Ki: 1.3 nM).

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.

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.

Ralimetinib is a selective inhibitor that blocks phosphorylation of MK2 at Thr334, without affecting the phosphorylation of p38α MAPK, JNK, ERK1/2, c-Jun, ATF2, or c-Myc. Ralimetinib functions as an ATP-competitive inhibitor of p38 MAPK α/β, demonstrating IC50 values of 5.3 and 3.2 nM, respectively, and is under investigation as an anti-inflammatory and anticancer therapeutic.

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.

Dicyclanil is an insect growth regulator with a chemical structure similar to that of cyclopromazine.

FIDAS-3, a stilbene derivative and potent Wnt inhibitor with an IC50 of 4.9 μM for methionine S-adenosyltransferase 2A (MAT2A), exhibits anticancer activities by effectively competing with S-adenosylmethionine (SAM) for MAT2A binding.