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Catalog No.S7153

69 publications

10058-F4 Chemical Structure

CAS No. 403811-55-2

10058-F4 is a c-Myc inhibitor that specificallly inhibits the c-Myc-Max interaction and prevents transactivation of c-Myc target gene expression. 10058-F4 promotes a caspase-3-dependent apoptosis and modulates autophagy.

Selleck's 10058-F4 has been cited by 69 publications

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Choose Selective Myc Inhibitors

Biological Activity

Description 10058-F4 is a c-Myc inhibitor that specificallly inhibits the c-Myc-Max interaction and prevents transactivation of c-Myc target gene expression. 10058-F4 promotes a caspase-3-dependent apoptosis and modulates autophagy.
c-Myc [1]
(Cell-free assay)
In vitro

10058-F4 inhibits growth of leukemic cells and dimerization of Myc and Max. 10058-F4 induces cell-cycle arrest and apoptosis of AML cells. 10058-F4 arrests AML cells at G0/G1 phase, downregulates c-Myc expression and upregulated CDK inhibitors, p21 and p27. Meanwhile, 10058-F4 induces apoptosis through activation of mitochondrial pathway shown by downregulation of Bcl-2, upregulation of Bax, release of cytoplasmic cytochrome C, and cleavage of caspase 3, 7, and 9. Furthermore, 10058-F4 also induces myeloid differentiation, possibly through activation of multiple transcription factors. Similarly, 10058-F4-induced apoptosis and differentiation could also be observed in primary AML cells. [1] 10058-F4 decreases c-Myc protein levels, inhibites proliferation of HepG2 cells likely through upregulation of cyclin-dependent kinase (cdk) inhibitor, p21WAF1 and lowers intracellular levels of [alpha]-fetoprotein (AFP). Treatment with 10058-F4 also downregulates human telomerase reverse transcriptase (hTERT) at the transcriptional level. In addition to inhibiting the proliferation of HepG2 cells, 10058-F4 enhances sensitivity to conventional chemotherapeutic agents, doxorubicin, 5-fluorouracil (5-FU) and cisplatin. [2]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
REH NHq2UIVHfW6ldHnvckBie3OjeR?= MUKwMVQxOOLCidM1US=> MUi0PEBp NFn5SYVz\WS3Y3XkJJRp\SCvZYThZo9tcWNiYXP0bZZqfHluIFnDOVA:PDByIN88US=> MmXXQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOzB7NUeyO|MoRjNyOUW3Nlc{RC:jPh?=
Nalm-6 Ml3YSpVv[3Srb36gZZN{[Xl? NIDVdpgxNTRyMPMAjeK2VQ>? MYq0PEBp MoXGdoVlfWOnZDD0bIUhdWW2YXLvcIlkKGGldHn2bZR6NCCLQ{WwQVQ{OCEQvF2= M4fFSFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyOUW3Nlc{Lz5|MEm1O|I4OzxxYU6=
Jurkat MVjGeY5kfGmxbjDhd5NigQ>? MUS2NEDPxE1? MlnxNlQhcA>? M1[5eoMuVXmlIHX4dJJme3Orb36gcIV3\Wy|IITy[YF1\WRid3n0bEBXWEFiKECsJFAvQCCjbnSgNU43KG2PKTDjc41jcW6nZDD3bZRpKDZyIN88UUAyODB3OD3GOEBl\WO{ZXHz[YQh\nW{dHjldkBkd22yYYLl[EB4cXSqIITo[UBkd3K{ZYPwc45lcW6pIHPvcpRzd2y| MVW8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zPTF{MEeyN{c,OjVzMkC3NlM9N2F-
CCRF-CEM MonKSpVv[3Srb36gZZN{[Xl? M1;ZTlYxKM7:TR?= NXTXRZV5OjRiaB?= M1P2RYMuVXmlIHX4dJJme3Orb36gcIV3\Wy|IITy[YF1\WRid3n0bEBXWEFiKECsJFAvQCCjbnSgNU43KG2PKTDjc41jcW6nZDD3bZRpKDZyIN88UUAyODB3OD3GOEBl\WO{ZXHz[YQh\nW{dHjldkBkd22yYYLl[EB4cXSqIITo[UBkd3K{ZYPwc45lcW6pIHPvcpRzd2y| M3KxdlxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ3MUKwO|I{Lz5{NUGyNFczOzxxYU6=
HL-60 MljvSpVv[3Srb36gZZN{[Xl? M{nic|YxKGGwZDCxNFAh|ryP MoKwNlQhcG:3coO= MkLF[IVkemWjc3XkJIxmfmWuczDv[kBkNU27YzDwdo91\Wmwcx?= MmHzQIEhfGG{Z3X0QUdg[myjbnunJIhz\WZ;J3j0eJB{Qi9xcIXicYVlNm6lYnmucoxuNm6raD7nc5YwOTdyNE[1OlcoRjF5MES2OVY4RC:jPh?=
U937 NVeybmlGTnWwY4Tpc44h[XO|YYm= MUG2NEBidmRiMUCwJO69VQ>? M3PQc|I1KGixdYLz NX;JUYJX\GWlcnXhd4VlKGyndnXsd{Bw\iClLV35Z{Bxem:2ZXnudy=> NITBZpM9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9zN{C0OlU3Pyd-MUewOFY2Pjd:L3G+
NB4 MnjESpVv[3Srb36gZZN{[Xl? MkfWOlAh[W6mIEGwNEDPxE1? NIPIflAzPCCqb4Xydy=> NUK0cYtk\GWlcnXhd4VlKGyndnXsd{Bw\iClLV35Z{Bxem:2ZXnudy=> NWixOnRTRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMUewOFY2PjdpPkG3NFQ3PTZ5PD;hQi=>
NB1643 Mn7udWhVWyCjc4PhfS=> NWC4fII{eUiWUzDv[kBx\WSrYYTybYMh[2GwY3XyJINmdGxibHnu[ZMhfG9iaXTlcpRq\nlibYXseIlxdGVib4Dwc5J1fW6rdHnld{Bnd3JiZIL1[{Bz\XC3coDvd4lv\zpiUILpcYFzgSC|Y4Ll[Y4h\m:{IF7CNVY1OyClZXzsdy=> NHLUW|c9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUSzOVE{QSd-Mkm0N|UyOzl:L3G+

... Click to View More Cell Line Experimental Data

Methods Test Index PMID
Western blot
p-EGFR / HIF-1α / c-Myc / Glut-1 ; 

PubMed: 30967777     

H1975 cells were treated with 10058-F4 for 24 h and cell lysates were used to test protein expression using specific antibodies.

Cyclin D2 / Cyclin D3 / p-21 / c-Myc / p-AKT / AKT ; 

PubMed: 28861328     

C. Immunoblotting demonstrating that 10058-F4 reduces cyclin D2 and D3 levels and induces p21Waf1/Cip1 expression. No caspase-3 activity was found. 

PARP / Caspase-3 / Myc ; 

PubMed: 25793663     

10058-F4 at 20 µM potently promotes apoptosis in Lck-Dlx5 lymphoma cells as early as 12 h after initiating treatment, and 10058-F4 treatment results in cleavage of Parp and caspase 3 as well as decreased expression of Myc in a dose-dependent manner.

30967777 28861328 25793663
Growth inhibition assay
Cell viability; 

PubMed: 28861328     

MTS assay depicting viability of MM cells treated with MYC inhibitor 10058-F4 at the indicated concentrations for 30 h. 

In vivo Peak plasma 10058-F4 concentrations of approximately 300 μM are seen at 5 min and declined to below the detection limit at 360 min following a single iv dose. Plasma concentration versus time data are best approximated by a two-compartment, open, linear model. The highest tissue concentrations of 10058-F4 are found in fat, lung, liver, and kidney. Peak tumor concentrations of 10058-F4 are at least tenfold lower than peak plasma concentrations. Eight metabolites of 10058-F4 are identified in plasma, liver, and kidney. The terminal half-life of 10058-F4 is approximately 1 h, and the volume of distribution is >200 ml/kg. No significant inhibition of tumor growth is seen after i.v. treatment of mice with either 20 or 30 mg/kg 10058-F4.[3]


Cell Research:


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  • Cell lines: HL-60, U937, and NB-4 cells
  • Concentrations: 0, 30, 60, 90, 120, 150 μM
  • Incubation Time: 72 h
  • Method:

    Cells, plated in 96-well plates (105/mL for cell lines and 5 × 105/mL for primary leukemic cells), are treated in triplicate with indicated concentrations of 10058-F4. At various time points, 20 μL 5 mg/mL MTT is added to each well. After incubation at 37°C for 3 hours, the MTT medium is removed and 100 μL DMSO lysis buffer is added. The number of viable cells is assessed by the percentage of absorbance of treated cells relative to that of solvent controls, using 570-nm wavelength on a spectrophotometer.

    (Only for Reference)
Animal Research:


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  • Animal Models: PC-3 and DU145 xenografted SCID mice
  • Dosages: 20 or 30 mg/kg
  • Administration: i.v.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 49 mg/mL (196.51 mM)
Water Insoluble
Ethanol '4 mg/mL
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+corn oil
For best results, use promptly after mixing.

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 249.35


CAS No. 403811-55-2
Storage powder
in solvent
Synonyms N/A
Smiles CCC1=CC=C(C=C1)C=C2C(=O)NC(=S)S2

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Myc Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID