SEL120 (SEL120-34A) hydrochloride

Catalog No.S8840 Synonyms: SEL120-34

For research use only.

SEL120 (SEL120-34, SEL120-34A) is a novel inhibitor of Cyclin-dependent kinase 8 (CDK8) with IC50 values of 4.4 nM and 10.4 nM for CDK8/Cyclin C and CDK19/CyclinC respectively.

SEL120 (SEL120-34A) hydrochloride Chemical Structure

CAS No. 1609452-30-3

Selleck's SEL120 (SEL120-34A) hydrochloride has been cited by 1 Publication

Purity & Quality Control

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Biological Activity

Description SEL120 (SEL120-34, SEL120-34A) is a novel inhibitor of Cyclin-dependent kinase 8 (CDK8) with IC50 values of 4.4 nM and 10.4 nM for CDK8/Cyclin C and CDK19/CyclinC respectively.
CDK8 [1]
(Cell-free assay)
CDK19 [1]
(Cell-free assay)
4.4 nM 10.4 nM
In vitro

SEL120-34A inhibits kinase activities of CDK8/CycC and CDK19/CycC complexes with an IC50 of 4.4 nM and 10.4 nM, respectively. It does not significantly inhibit other members of the CDK family in a single point inhibition assay, namely CDK1, 2, 4, 6, 5, 7 in vitro, with the exception of CDK9, however a calculated IC50 1070 nM, indicated an over 200 fold selectivity against this kinase. SEL120-34A inhibits phosphorylation of STAT1 S727 and STAT5 S726 in cancer cells, inhibits mitogen- induced expression of immediate early response (IER) genes and IFN- responsive genes expression in vitro[1]. In a broad panel of cancer cell lines, the compound shows the strongest activity in hematological malignancies, especially in selected acute myeloid leukemia (AML) (GI50 12 nM), acute lymphoblastic leukemia (ALL) and mantle cell lymphoma (MCL) models. SEL120−34A could alter transcriptional programs linked to differentiation of leukemia cells[2].

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HL60 MXvHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? Mn3zS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gTGw3OCClZXzsd{BjgSCjbHHtZZIh[my3ZTDhd5NigSxiR1m1NFwy|ryP NHzDVHU9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUK2Olk{Pyd-MkmyOlY6Ozd:L3G+
SKNO1 Ml\VS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NYfkUlZNT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hW0uQT{GgZ4VtdHNiYomgZYxidWG{IHLseYUh[XO|YYmsJGdKPTB:Md88US=> M4DEfFxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7Mk[2PVM4Lz5{OUK2Olk{PzxxYU6=
KG1 MkjUS5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? NHyxOJdIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBMTzFiY3XscJMh[nliYXzhcYFzKGKudXWgZZN{[XluIFfJOVA9Oc7:TR?= M{nTfVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7Mk[2PVM4Lz5{OUK2Olk{PzxxYU6=
MOLM16 NIPW[3dIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NWnvfIJQT3Kxd4ToJIlvcGmkaYTpc44hd2ZiaIXtZY4hVU:OTUG2JINmdGy|IHL5JIFt[W2jcjDicJVmKGG|c3H5MEBIUTVyPEJOwG0> NUHYNY1kRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkmyOlY6OzdpPkK5NlY3QTN5PD;hQi=>
MV4-11 NHjL[2dIem:5dHigbY5pcWKrdHnvckBie3OjeR?= NIX3WXNIem:5dHigbY5pcWKrdHnvckBw\iCqdX3hckBOXjRvMUGgZ4VtdHNiYomgZYxidWG{IHLseYUh[XO|YYmsJGdKPTB:Md88US=> MWG8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTJ4NkmzO{c,Ojl{Nk[5N|c9N2F-
OCI-AML2 MXPHdo94fGhiaX7obYJqfGmxbjDhd5NigQ>? M4HaWmdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJG9EUS2DTVyyJINmdGy|IHL5JIFt[W2jcjDicJVmKGG|c3H5MEBIUTVyPEJOwG0> M4r0WVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ7Mk[2PVM4Lz5{OUK2Olk{PzxxYU6=
OCI-AML3 NEOyTXZIem:5dHigbY5pcWKrdHnvckBie3OjeR?= M37FUWdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJG9EUS2DTVyzJINmdGy|IHL5JIFt[W2jcjDicJVmKGG|c3H5MEBIUTVyPEJOwG0> NH\HTZo9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9{OUK2Olk{Pyd-MkmyOlY6Ozd:L3G+
MOLM6 MlH4S5Jwf3SqIHnubIljcXSrb36gZZN{[Xl? MoDjS5Jwf3SqIHnubIljcXSrb36gc4YhcHWvYX6gUW9NVTZiY3XscJMh[nliYXzhcYFzKGKudXWgZZN{[XluIFfJOVA9Oc7:TR?= MUC8ZUB1[XKpZYS9K39jdGGwazegbJJm\j1paIT0dJM7Ny:ydXLt[YQvdmOkaT7ucI0vdmmqLnfvek8zQTJ4NkmzO{c,Ojl{Nk[5N|c9N2F-
Methods Test Index PMID
Western blot CDK8 / ERK ; pSTAT1 pS727 / pSTAT1 pY701 / STAT1 / pSTAT5 pS726 / pSTAT5 pY694 / STAT5 28422713
In vivo

SEL120-34A has favorable pharmacodynamics to be sufficient to affect expression of CDK8 and CDK19- dependent genes in vivo. SEL120-34A treatment causes specific alterations in interferon- responsive genes and inhibits the proliferation of AML cell lines in vivo. SEL120-34A does not affect normal hematopoiesis[1]. SEL120−34A effectively inhibits tumor growth in subcutaneous responder AML and MCL models when administered orally[2].

Protocol (from reference)

Cell Research:


  • Cell lines: HCT-116 cells
  • Concentrations: 0.1, 0.25, 0.5, 1, 2.5, 5 μM
  • Incubation Time: 5 h
  • Method:

    HCT-116 are seeded onto 6-well plates at 2.5×105/well. On the following day, cells are synchronized for 24 h by 0.5% FBS starvation, pretreated with 0.1% DMSO or SEL120-34A at the indicated concentration for 1 h and then supplemented with either 10% FBS, IFNg or IFNa in the presence of the inhibitor (4h). Cells are centrifuged at 1300 rpm for 5 min at 4°C, washed once with 1 ml of ice-cold PBS and stored at -80°C.

Animal Research:


  • Animal Models: SCID/beige C.B17 female mice xenografted with Colo-205 tumors
  • Dosages: 5, 15, 30 and 60 mg/kg BID
  • Administration: oral

Solubility (25°C)

In vitro

Chemical Information

Molecular Weight


CAS No. 1609452-30-3
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles CC1=C2C3=C(CCCN3C(=N2)N4CCNCC4)C(=C1Br)Br

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Tech Support

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