Catalog No.S1421 Synonyms: CGP 41251

Staurosporine Chemical Structure

Molecular Weight(MW): 466.53

Staurosporine is a potent PKC inhibitor for PKCα, PKCγ and PKCη with IC50 of 2 nM, 5 nM and 4 nM, less potent to PKCδ (20 nM), PKCε (73 nM) and little active to PKCζ (1086 nM) in cell-free assays. Also shows inhibitory activities on other kinases, such as PKA, PKG, S6K, CaMKII, etc. Phase 3.

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3 Customer Reviews

  • Intracellular concentration of HSF1-phosphoserine 326, total HSF1, S6 kinase-phosphothreonine-389, total S6 kinase and β-actin, without or with heat shock in HeLa cells pretreated with mTOR inhibitors rapamycin (30 nM) and KU0063794 (2 uM) and kinase inhibitor staurosporine (100 nM) for 2 hr. Relative levels of HSF1-phosphoserine 326 in cells after the various treatments were determined by densitometric analysis of X-ray films, normalized to untreated cells (lane 1), and are indicated below the representation of the immunoblots.

    PLoS One 2012 7(6), e39679. Staurosporine purchased from Selleck.

    J Biomol Screen 2013 18(4), 388-99. Staurosporine purchased from Selleck.

  • J Biomol Screen 2013 18(4), 388-99. Staurosporine purchased from Selleck.

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2. For more details, such as half maximal inhibitory concentrations (IC50s) and working concentrations of each inhibitor, please click on the link of the inhibitor of interest.
3. "+" indicates inhibitory effect. Increased inhibition is marked by a higher "+" designation.
4. Orange "√" refers to compounds which do inhibitory effects on the related isoform, but without specific value.

Biological Activity

Description Staurosporine is a potent PKC inhibitor for PKCα, PKCγ and PKCη with IC50 of 2 nM, 5 nM and 4 nM, less potent to PKCδ (20 nM), PKCε (73 nM) and little active to PKCζ (1086 nM) in cell-free assays. Also shows inhibitory activities on other kinases, such as PKA, PKG, S6K, CaMKII, etc. Phase 3.
PKCα [1]
(Cell-free assay)
c-Fgr [2] phosphorylase kinase [2] PKCη [1]
(Cell-free assay)
PKCγ [1]
(Cell-free assay)
2 nM 2 nM 3 nM 4 nM 5 nM
In vitro

Staurosporine, a microbial alkaloid, significantly inhibits protein kinase C from rat brain with IC50 of 2.7 nM. Staurosporine displays strong inhibitory effect against HeLa S3 cells with IC50 of 4 nM. [1] Staurosporine also inhibits a variety of other protein kinases, including PKA, PKG, phosphorylase kinase, S6 kinase, Myosin light chain kinase (MLCK), CAM PKII, cdc2, v-Src, Lyn, c-Fgr, and Syk with IC50 of 15 nM, 18 nM, 3 nM, 5 nM, 21 nM, 20 nM, 9 nM, 6 nM, 20 nM, 2 nM, and 16 nM, respectively. [2] Staurosporine (1 μM) induces >90% apoptosis in PC12 cells. Consistently, Staurosporine treatment induces a rapid and prolonged elevation of intracellular free calcium levels [Ca2+]i, accumulation of mitochondrial reactive oxygen species (ROS), and subsequent mitochondrial dysfunction. [3] The apoptosis of MCF7 cells induced by Staurosporine can be enhanced by the expression of functional caspase-3 via caspase-8 activation and Bid cleavage. [4] Staurosporine treatment at 1 μM only partially inhibits IL-3-stimulated Bcl2 phosphorylation but completely blocks PKC-mediated Bcl2 phosphorylation. [5] Staurosporine induces apoptosis of human foreskin fibroblasts AG-1518, depending on the lysosomal cathepsins D mediated cytochrome c release and caspase activation. [6] In addition to activating the classical mitochondrial apoptosis pathway, Staurosporine triggers a novel intrinsic apoptosis pathway, relying on the activation of caspase-9 in the absence of Apaf-1. [7]

In vivo In the gerbil and rat ischemia models, Staurosporine pretreatment (0.1-10 ng) before ischemia prevents neuronal damage in a dose-dependent manner, suggesting the involvement of PKC in CAl pyramidal cell death after ischemia. [8]


Kinase Assay:


+ Expand

Enzyme assay and binding assay:

Protein kinase C is assayed in a reaction mixture (0.25 mL) containing 5 μmol of Tris/HCl, pH 7.5, 2.5 μmol of magnesium acetate, 50 μg of histone II S, 20 μg of phosphatidylserine, 0.88 μg of diolein, 125 nmol of CaCl2, 1.25 nmol of [γ-32]ATP (5-10 × 104 cpm/nmol) and 5 μg of partially purified enzyme. The binding of [3H]PDBu to protein kinase C is determined: Reaction mixture (200 μL contained 4 μmo1 of Tris/malate, pH 6.8, 20 μmol of KCl, 30 nmol of CaC12, 20 μg of phosphatidylserine, 5 μg of partially purified protein kinase C, 0.5% (final concentration) of DMSO,10 pmol of [3H]PDBu (l-3 × 104 cpm/pmol) and 10 μL of various amounts of Staurosporine.
Cell Research:


+ Expand
  • Cell lines: PC12
  • Concentrations: Dissolved in DMSO, final concentration 1 μM
  • Incubation Time: ~32 hours
  • Method:

    Cells are exposed to Staurosporine for ~32 hours. Cells are fixed in 4% paraformaldehyde and stained with the DNA-binding dye Hoechst 33342. Cells are visualized under epifluorescence illumination, and the percentage of apoptotic cells (cells with condensed and fragmented DNA) is determined.

    (Only for Reference)
Animal Research:


+ Expand
  • Animal Models: Male Mongolian gerbils or male Wistar rats subjected to transient ischemia
  • Formulation: Dissolved in DMSO, and diluted in saline
  • Dosages: ~10 ng
  • Administration: Stereotaxically administered into the bilateral CAl subfield of the hippocampus
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 4 mg/mL (8.57 mM)
Water <1 mg/mL
Ethanol <1 mg/mL
In vivo

* 1 mg/ml means slightly soluble or insoluble.
* 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 466.53


CAS No. 62996-74-1
Storage powder
in solvent
Synonyms CGP 41251

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Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT00301938 Completed Accelerated Phase Chronic Myelogenous Leukemia|Adult Acute Megakaryoblastic Leukemia (M7)|Adult Acute Minimally Differentiated Myeloid Leukemia (M0)|Adult Acute Monoblastic Leukemia (M5a)|Adult Acute Monocytic Leukemia (M5b)|Adult Acute Myeloblastic Leukemia With Maturation (M2)|Adult Acute Myeloblastic Leukemia Without Maturation (M1)|Adult Acute Myeloid Leukemia With 11q23 (MLL) Abnormalities|Adult Acute Myeloid Leukemia With Inv(16)(p13;q22)|Adult Acute Myeloid Leukemia With t(15;17)(q22;q12)|Adult Acute Myeloid Leukemia With t(16;16)(p13;q22)|Adult Acute Myeloid Leukemia With t(8;21)(q22;q22)|Adult Acute Myelomonocytic Leukemia (M4)|Adult Acute Promyelocytic Leukemia (M3)|Adult Erythroleukemia (M6a)|Adult Pure Erythroid Leukemia (M6b)|Blastic Phase Chronic Myelogenous Leukemia|Myelodysplastic/Myeloproliferative Neoplasms|Previously Treated Myelodysplastic Syndromes|Recurrent Adult Acute Lymphoblastic Leukemia|Recurrent Adult Acute Myeloid Leukemia|Relapsing Chronic Myelogenous Leukemia|Secondary Acute Myeloid Leukemia|T-cell Adult Acute Lymphoblastic Leukemia|Untreated Adult Acute Lymphoblastic Leukemia|Untreated Adult Acute Myeloid Leukemia National Cancer Institute (NCI) December 2005 Phase 1
NCT00098956 Completed Extensive Stage Small Cell Lung Cancer|Recurrent Small Cell Lung Cancer National Cancer Institute (NCI) January 2005 Phase 2
NCT00082017 Completed Lymphoma, Large-Cell, Ki-1|Lymphoma, T-Cell National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC) April 2004 Phase 2
NCT00072267 Completed Fallopian Tube Cancer|Ovarian Cancer|Primary Peritoneal Cavity Cancer University Health Network, Toronto|National Cancer Institute (NCI) January 2004 Phase 2
NCT00072189 Terminated Recurrent Melanoma|Stage IV Melanoma National Cancer Institute (NCI) November 2003 Phase 2
NCT00030888 Unknown status Kidney Cancer University of California, San Francisco|National Cancer Institute (NCI) December 2002 Phase 2

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PKC Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID