Molecular Formula | C12H11NOS2 |
Molar Mass | 249.35 |
Water Solubility | Soluble in DMSO. Soluble in water at concentrations less than 2mg/ml |
Solubility | Soluble in DMSO: >10 mg/mL and Water: <2 mg/mL |
Appearance | Yellow solid |
Color | yellow |
Storage Condition | 2-8°C |
Stability | Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 1 month. |
MDL | MFCD00758517 |
Use | A c-Myc inhibitor and apoptosis inducer. |
In vitro study | 10058-F4 inhibits leukemia cell growth and inhibits Myc and Max dimerization. 10058-F4 induces cell cycle arrest and apoptosis of AML cells. 10058-F4 arrested AML cells in G0/G1 phase, down regulated the expression of c-Myc, and up-regulated CDK inhibitors p21 and p27. At the same time, 10058-F4 induced apoptosis by activating the mitochondrial pathway, with Bcl-2 down-regulation, Bax upregulation, cytosolic cytochrome C release, and caspase 3,7, and 9 cleavage observed. In addition, 10058-F4 also induces bone marrow cell differentiation, possibly by activating a variety of transcription factors. Similarly, 10058-F4 acts on primary AML cells, inducing apoptosis and differentiation. 10058-F4 reduces c-Myc protein levels and inhibits HepG2 cell proliferation, possibly by up-regulating cyclin-dependent kinase (CDK) inhibitor, p21WAF1, and reducing intracellular [α]-alpha-fetoprotein (AFP) the level. 10058-F4 treatment also down-regulates human telomerase reverse transcriptase (hTERT) at the transcriptional level. In addition to inhibiting HepG2 cell proliferation, 10058-F4 also enhances its sensitivity to conventional chemotherapeutic drugs, Doxorubicin, 5-fluorouraci (5-FU), and Cisplatin. 10058-F4 inhibits leukemia cell growth and inhibits Myc and Max dimerization. 10058-F4 induces cell cycle arrest and apoptosis of AML cells. 10058-F4 arrested AML cells in G0/G1 phase, down regulated the expression of c-Myc, and up-regulated CDK inhibitors p21 and p27. At the same time, 10058-F4 induced apoptosis by activating the mitochondrial pathway, with Bcl-2 down-regulation, Bax upregulation, cytosolic cytochrome C release, and caspase 3,7, and 9 cleavage observed. In addition, 10058-F4 also induces bone marrow cell differentiation, possibly by activating a variety of transcription factors. Similarly, 10058-F4 acts on primary AML cells, inducing apoptosis and differentiation. 10058-F4 reduces c-Myc protein levels and inhibits HepG2 cell proliferation, possibly by up-regulating cyclin-dependent kinase (CDK) inhibitor, p21WAF1, and reducing intracellular [α]-alpha-fetoprotein (AFP) the level. 10058-F4 treatment also down-regulates human telomerase reverse transcriptase (hTERT) at the transcriptional level. In addition to inhibiting HepG2 cell proliferation, 10058-F4 also enhances its sensitivity to conventional chemotherapeutic drugs, Doxorubicin, 5-fluorouraci (5-FU), and Cisplatin. |
In vivo study | 10058-F4 alone, I. V., peaked at 5 minutes at a concentration of approximately 300 μm and dropped below the lower limit of detection at 360 minutes. Blood concentration-time data are best plotted in a two-compartment, open, linear model. The highest tissue concentration of 10058-F4 was found in fat, lung, liver, kidney. The peak tumor concentration of 10058-F4 was at least ten-fold lower than the peak plasma concentration. Eight metabolites of 10058-F4 were identified in plasma, liver and kidney. The terminal half-life of 10058-F4 is approximately 1 hour and the volume of distribution is> 200/kg. Mice treated with 10058-F4 at 20 or 30 mg/kg intravenously had no significant tumor growth inhibition. 10058-F4, injected intravenously alone, reached a peak plasma concentration of approximately 300 μm at 5 minutes and fell below the lower limit of detection at 360 minutes. Blood concentration-time data are best plotted in a two-compartment, open, linear model. The highest tissue concentration of 10058-F4 was found in fat, lung, liver, kidney. The peak tumor concentration of 10058-F4 was at least ten-fold lower than the peak plasma concentration. Eight metabolites of 10058-F4 were identified in plasma, liver and kidney. The terminal half-life of 10058-F4 is approximately 1 hour and the volume of distribution is> 200/kg. Mice treated with 10058-F4 at 20 or 30 mg/kg intravenously had no significant tumor growth inhibition. |
Hazard Symbols | Xi - Irritant |
Risk Codes | R36 - Irritating to the eyes R43 - May cause sensitization by skin contact |
Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S36/37 - Wear suitable protective clothing and gloves. |
WGK Germany | 3 |
Hazard Class | IRRITANT |
biological activity | 10058-F4 is a c-Myc inhibitor that specifically inhibits c-Myc-Max interaction and inhibits transcriptional activation of c-Myc target gene expression. 10058-F4 is a c-Myc inhibitor that specifically inhibits c-Myc-Max interaction and prevents transcriptional activation of c-Myc target gene expression. 10058-F4 can promote Caspase-3-dependent apoptosis and regulate autophagy. |
in vitro study | 10058-F4 inhibits the growth of leukemia cells and inhibits the dimerization of Myc and Max. 10058-F4 induces cell cycle arrest and apoptosis in AML cells. 10058-F4 arrested AML cells in G0/G1 phase, down-regulated c-Myc expression, up-regulated CDK inhibitors p21 and p27. At the same time, 10058-F4 induced apoptosis by activating mitochondrial pathway. Bcl-2 down-regulation, up-regulation of Bax, release of cytochrome C in cytoplasm, and cleavage of caspase3,7, and 9 were observed. In addition, 10058-F4 also induces bone marrow cell differentiation, possibly by activating a variety of transcription factors. Similarly, 10058-F4 acts on primary AML cells to induce apoptosis and differentiation. 10058-F4 reduces c-Myc protein levels and inhibits HepG2 cell proliferation, possibly by up-regulating cyclin-dependent kinase (CDK) inhibitors, p21WAF1, and reducing intracellular [α]-fetoprotein (AFP) levels. 10058-F4 treatment also down-regulated human telomerase reverse transcriptase (hTERT) at the transcriptional level. In addition to inhibiting HepG2 cell proliferation, 10058-F4 also enhances its sensitivity to conventional chemotherapy drugs, Doxorubicin, 5-fluorouracil (5-FU) and Cisplatin. 10058-F4 inhibits the growth of leukemia cells and inhibits the dimerization of Myc and Max. 10058-F4 induces cell cycle arrest and apoptosis in AML cells. 10058-F4 arrested AML cells in G0/G1 phase, down-regulated c-Myc expression, up-regulated CDK inhibitors p21 and p27. At the same time, 10058-F4 induced apoptosis by activating mitochondrial pathway. Bcl-2 down-regulation, up-regulation of Bax, release of cytochrome C in cytoplasm, and cleavage of caspase3,7, and 9 were observed. In addition, 10058-F4 also induces bone marrow cell differentiation, possibly by activating a variety of transcription factors. Similarly, 10058-F4 acts on primary AML cells to induce apoptosis and differentiation. 10058-F4 reduces c-Myc protein levels and inhibits HepG2 cell proliferation, possibly by up-regulating cyclin-dependent kinase (CDK) inhibitors, p21WAF1, and reducing intracellular [α]-fetoprotein (AFP) levels. 10058-F4 treatment also down-regulated human telomerase reverse transcriptase (hTERT) at the transcriptional level. In addition to inhibiting HepG2 cell proliferation, 10058-F4 also enhances its sensitivity to conventional chemotherapy drugs, Doxorubicin, 5-fluorouracil (5-FU) and Cisplatin. |
in vivo study | 10058-F4 was injected intravenously alone, reaching a plasma peak at 5 minutes, with a concentration of about 300 μM, and falling below the detection limit at 360 minutes. Blood concentration-time data is best plotted into a two-compartment, open, linear model. The highest tissue concentration of 10058-F4 was found in fat, lung, liver, kidney. The peak tumor concentration of 10058-F4 is at least ten times lower than the peak plasma concentration. Eight metabolites of 10058-F4 were determined in plasma, liver and kidney. The terminal half-life of 10058-F4 is about 1 hour, and the distribution volume is> 200 ml/kg. Mice treated with 10058-F4 intravenously at doses of 20 or 30 mg/kg had no significant tumor growth inhibition. 10058-F4 was injected intravenously alone, reaching a peak plasma concentration of about 300 μM at 5 minutes, and falling below the lower detection limit at 360 minutes. Blood concentration-time data is best plotted into a two-compartment, open, linear model. The highest tissue concentration of 10058-F4 was found in fat, lung, liver, kidney. The peak tumor concentration of 10058-F4 is at least ten times lower than the peak plasma concentration. Eight metabolites of 10058-F4 were determined in plasma, liver and kidney. The terminal half-life of 10058-F4 is about 1 hour, and the distribution volume is> 200 ml/kg. Mice treated with 10058-F4 intravenously at doses of 20 or 30 mg/kg had no significant tumor growth inhibition. |
target | TargetValue c-Myc |
Target | Value |