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10058-F4C-Myc-Max dimerization inhibitor

10058-F4

Catalog No. BCC1050
Size Price Stock
10mM (in 1mL DMSO) $55.00 In stock
5mg $45.00 In stock
10mg $70.00 In stock
50mg $220.00 In stock
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Quality Control of 10058-F4

Chemical structure

10058-F4

Biological Activity of 10058-F4

Cell permeable c-Myc-Max dimerization inhibitor. Inhibits proliferation, induces apoptosis and arrests cells in G0/G1 in rat1a-c-Myc cells.Downregulates c-Myc expression and upregulates CDK inhibitors, p21 and p27. Inhibits proliferation. Induces apoptosis and cell cycle arrest in G0/G1 phase. Also reduces tumor growth in vivo

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Chemical Properties of 10058-F4

Cas No. 403811-55-2 SDF Download SDF
Synonyms C-Myc Inhibitor; (5E)-5-(4-ethylbenzylidene)-2-mercapto-1,3-thiazol-4(5H)-one; 5-[(4-Ethylphenyl)methylene]-2-thioxo-4-thiazolidinone
Chemical Name 5-[(4-Ethylphenyl)methylene]-2-thioxo-4-thiazolidinone
SMILES CCC1=CC=C(C=C1)C=C2C(=O)NC(=S)S2
Standard InChIKey SVXDHPADAXBMFB-JXMROGBWSA-N
Standard InChI InChI=1S/C12H11NOS2/c1-2-8-3-5-9(6-4-8)7-10-11(14)13-12(15)16-10/h3-7H,2H2,1H3,(H,13,14,15)/b10-7+
Formula C12H11NOS2 M.Wt 249.35
Solubility Soluble to 100 mM in DMSO and to 20 mM in ethanol
Storage Store at +4°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 10058-F4

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.0104 mL 20.0521 mL 40.1043 mL 80.2085 mL 100.2607 mL
5 mM 0.8021 mL 4.0104 mL 8.0209 mL 16.0417 mL 20.0521 mL
10 mM 0.401 mL 2.0052 mL 4.0104 mL 8.0209 mL 10.0261 mL
50 mM 0.0802 mL 0.401 mL 0.8021 mL 1.6042 mL 2.0052 mL
100 mM 0.0401 mL 0.2005 mL 0.401 mL 0.8021 mL 1.0026 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Background on 10058-F4

10058-F4 is a novel small-molecule inhibitor of c-Myc. 10058-F4 prevented the binding of c-Myc/Max dimers to its DNA targets, inhibited leukemic proliferation, and induced apoptosis through mitochondrial pathway, such as downregulation of Bcl-2, upregulation of Bax and release of cytoplasmic cytochrome C. [1]

10058-F4 blocks the C-MYC/Max heterodimerization which is required for c-Myc activity as a transcription factor. 10058-F4 efficiently inhibits the induction of PGC-1β mRNA by both HRG and IGF-1 and also abolishes the induction of PGC-1β protein levels by HRG and IGF-1, confirming that the induction of PGC-1b protein by these growth factors is a transcriptional event requiring C-MYC activity.[2] 10058-F4 acts not only to block c-Myc function through the mechanism of c-Myc/Max heterodimer dissociation, but it also resulted in decreased c-Myc mRNA levels (65%, n = 3) in lymphoma cells.[3]

References:
[1] Huang MJ, Cheng YC, Liu CR, Lin SF, Liu H. E. A small-molecule c-Myc inhibitor, 10058-F4, induces cell-cycle arrest, apoptosis, and myeloid differentiation of human acute myeloid leukemia. Experimental Hematology. 2006; 34: 1480–1489.
[2] Ching-yi Chang, Dmitri Kazmin, Jeff S. Jasper, Rebecca Kunder, William J. Zuercher, Donald P. McDonnell. The Metabolic Regulator ERRα, a Downstream Target of HER2/IGF-1R, as a Therapeutic Target in Breast Cancer. Cancer Cell. 18 October 2011. 20(4): 500-510.
[3] Ilsa Gomez-Curet, R. Serene Perkins, Ryan Bennett, Katherine L. Feidler, Stephen P. Dunn, Leslie J. Krueger. c-Myc inhibition negatively impacts lymphoma growth. Journal of Pediatric Surgery. January 2006. 41(1): 207-211.

References on 10058-F4

Inhibition of c-Myc by 10058-F4 induces growth arrest and chemosensitivity in pancreatic ductal adenocarcinoma.[Pubmed: 26211592]


Pancreatic ductal adenocarcinoma (PDAC) is a formidable medical challenge due to its malignancies and the absence of effective treatment. c-Myc, as an important transcription factor, plays crucial roles in cell cycle progression, apoptosis and cellular transformation. The c-Myc inhibitor, 10058-F4, has been reported act as a tumor suppressor in several different tumors. In current study, the tumor-suppressive roles of 10058-F4 was observed in human pancreatic cancer cells in vitro as demonstrated by decreased cell viability, cell cycle arrest at the G1/S transition and increased caspase3/7 activity. And tumor responses to gemcitabine were also significantly enhanced by 10058-F4 in PANC-1 and SW1990 cells. In a subcutaneous xenograft model, however, 10058-F4 showed no significant influence on pancreatic tumorigenesis. When combined with gemcitabine, tumorigenesis was drastically attenuated compared with gemcitabine group or 10058-F4 group; this synergistic effect was accompanied with decreased PCNA-positive cells and reduced TUNEL-positive cells in the combined treated group. Subsequent studies revealed that decreased glycolysis may be involved in the inhibitory effect of 10058-F4 on PDAC. Taken together, this study demonstrates the roles of 10058-F4 in PDAC and provides evidence that 10058-F4 in combination with gemcitabine showed significant clinical benefit over the usage of gemcitabine alone.

10058-F4, a c-Myc inhibitor, markedly increases valproic acid-induced cell death in Jurkat and CCRF-CEM T-lymphoblastic leukemia cells.[Pubmed: 25120723]


Adult T-cell acute lymphoblastic leukemia (T-ALL) has a poor prognosis. Although it has been found that activation of Notch1 signaling occurs in >50% T-ALL patients, γ-secretase inhibitors that target Notch1 signaling are of limited efficacy. However, c-Myc is an important direct target of Notch1 and, thus, c-Myc is another potential therapeutic target for T-ALL. Valproic acid (VPA), a histone deacetylase inhibitor, has been reported to treat various hematological malignancies. In the present study, we showed that c-Myc expression, at a transcriptional level, was dose-dependently downregulated in VPA-induced growth inhibition in T-ALL cell lines, Jurkat and CCRF-CEM cells. 10058-F4, a small molecule c-Myc inhibitor, could increase the downregulation of c-Myc and markedly increase the growth inhibition and cell death induced by VPA in Jurkat and CCRF-CEM cells, which was accompanied by obvious cleavage of capase-3. Z-VAD-FMK, a caspase inhibitor, partially prevented the anti-leukemic effect. The results of the present study suggest that c-Myc inhibitors increase cell death induced by VPA in a caspase-dependent and -independent manner, and their combination could be a potent therapeutic strategy for adult T-ALL patients.

Efficacy, pharmacokinetics, tisssue distribution, and metabolism of the Myc-Max disruptor, 10058-F4 [Z,E]-5-[4-ethylbenzylidine]-2-thioxothiazolidin-4-one, in mice.[Pubmed: 18509642]


c-Myc is commonly activated in many human tumors and is functionally important in cellular proliferation, differentiation, apoptosis and cell cycle progression. The activity of c-Myc requires noncovalent interaction with its client protein Max. In vitro studies indicate the thioxothiazolidinone, 10058-F4, inhibits c-Myc/Max dimerization. In this study, we report the efficacy, pharmacokinetics and metabolism of this novel protein-protein disruptor in mice.

Small-molecule c-Myc inhibitor, 10058-F4, inhibits proliferation, downregulates human telomerase reverse transcriptase and enhances chemosensitivity in human hepatocellular carcinoma cells.[Pubmed: 17159602]


c-Myc oncogene is critical for the development of hepatocellular carcinoma. Given the successful use of small-molecule inhibitors on cancers, targeting c-Myc with small-molecule inhibitors represents a promising approach. The potential of using small-molecule c-Myc inhibitor, 10058-F4, was evaluated on hepatocellular carcinoma cell lines, HepG2 and Hep3B cells. HepG2 cells were more sensitive to 10058-F4 than Hep3B cells, as demonstrated by reduced cell viability, marked morphological changes and decreased c-Myc levels. 10058-F4 arrested the cell cycle (at G0/G1 phase) and induced apoptosis upon extended treatment. These observations might be attributable to the increased cyclin-dependent kinase inhibitor, p21, and decreased cyclin D3 levels. Besides, 10058-F4 also significantly decreased the alpha-fetoprotein levels, an indicator for hepatocellular carcinoma differentiation. We further found that 10058-F4 inhibited the transactivation of human telomerase reverse transcriptase, downregulated human telomerase reverse transcriptase expression and abrogated telomerase activity. In addition, pretreatment with 10058-F4 increased the chemosensitivity of HepG2 cells to low-dose doxorubicin, 5-fluorouracil and cisplatin. Therefore, small-molecule c-Myc inhibitors might represent a novel agent, alone or in combination with conventional chemotherapeutic agents, for anti-hepatocellular carcinoma therapy.

Kewords:

10058-F4,403811-55-2,C-Myc Inhibitor; (5E)-5-(4-ethylbenzylidene)-2-mercapto-1,3-thiazol-4(5H)-one; 5-[(4-Ethylphenyl)methylene]-2-thioxo-4-thiazolidinone,Cell Cycle/Checkpoint,c-Myc, supplier, inhibitor,Antagonist,Blocker,Modulator,Agonist, activators, activates, potent, BioCrick

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