Staurosporine - CAS 62996-74-1

Staurosporine - CAS 62996-74-1 Catalog number: BADC-00329

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Staurosporine, also known as antibiotic AM-2282 or STS, is a broad spectrum protein kinase inhibitor produced by Streptomyces sp. Enzymes inhibited include protein kinase C (IC50 = 3 nM), protein kinase A (IC50 = 7 nM), p60v-src tyrosine protein kinase (IC50 = 6 nM) and CaM kinase II (IC50 = 20 nM). Staurosporine was discovered to have biological activities ranging from anti-fungal to anti-hypertensive.

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BADC-00329 25 mg $298
Staurosporine, also known as antibiotic AM-2282 or STS, is a broad spectrum protein kinase inhibitor produced by Streptomyces sp. Enzymes inhibited include protein kinase C (IC50 = 3 nM), protein kinase A (IC50 = 7 nM), p60v-src tyrosine protein kinase (IC50 = 6 nM) and CaM kinase II (IC50 = 20 nM). Staurosporine was discovered to have biological activities ranging from anti-fungal to anti-hypertensive.
NSC 25485; 2,3,10,11,12,13-hexahydro-10R-methoxy-9S-methyl-11R-methylamino-9S,13R-epoxy-1H,9H-diindolo[1,2,3-gh; 3',2',1'-lm]pyrrolo[3,4-j][1,7]benzodiazonin-1-one; NSC-25485; NSC25485
Canonical SMILES
1.56 g/cm3
Soluble in ethanol, methanol, DMF, DMSO
Melting Point
In Vitro
Staurosporine increased the cytosolic Ca(2+) concentration ([Ca(2+)](c)) after the inositol 1,4,5-trisphosphate (IP(3))-sensitive Ca(2+) store was depleted. Ionomycin caused only small increases in [Ca(2+)](c) after the depletion of the IP(3)-sensitive Ca(2+) store, whereas ionomycin+monensin caused large increases. However, ionomycin+monensin did not increase [Ca(2+)](c) when added after [Ca(2+)](c) was increased by staurosporine, indicating that the acidic Ca(2+) store was the main source of Ca(2+). The acidic Ca(2+) store appeared to be associated with secretory granules, since ionomycin+monensin- and staurosporine-induced [Ca(2+)](c) increases were significantly reduced when the acinar cells were degranulated. The effect of staurosporine on [Ca(2+)](c) was mimicked by other protein kinase C inhibitors.
In Vivo
Normal human mammary epithelial and immortalized cells with intact pRb treated with low concentrations of staurosporine arrested in the G(1) phase of the cell cycle, whereas pRb-defective cells showed no response. The duration of G(1) and transition from G(1) to S phase entry were modulated by staurosporine in Rb-intact cells. In pRb(+) cells, but not in Rb(-) cells, low concentrations of staurosporine also resulted in a significant decrease in cyclin-dependent kinase 4 (CDK4) expression and activity. Although Rb(+/+) MEFs were particularly sensitive to G(1) arrest mediated by staurosporine, pRb(-/-) cells were refractory to such treatment. Additionally, CDK4 expression was also inhibited in response to staurosporine only in Rb(+/+) MEFs. These results were recapitulated in breast cancer cells treated with siRNA to pRb to down-regulate the pRb expression.
Streptomyces sp.
Off-white Powder
Room temperature
Store at -20°C
Health Hazard; Environmental Hazard; Irritant; Acute Toxic; Flammable
Signal Word
Boiling Point
677.5°C at 760 mmHg
1.TRIM29 Overexpression Promotes Proliferation and Survival of Bladder Cancer Cells Through NF-κB Signaling.
Tan ST, Liu SY, Wu B. Cancer Res Treat. 2016 Mar 11. doi: 10.4143/crt.2015.381. [Epub ahead of print]
Purpose: TRIM29 overexpression has been reported in several human malignancies and showed correlation with cancer cell malignancy. The aim of the current study is to examine its clinical significance and biological roles in human bladder cancer tissues and cell lines.
2.Staurosporine allows dystrophin expression by skipping of nonsense-encoding exon.
Nishida A1, Oda A2, Takeuchi A3, Lee T4, Awano H5, Hashimoto N6, Takeshima Y4, Matsuo M7. Brain Dev. 2016 Mar 25. pii: S0387-7604(16)30020-1. doi: 10.1016/j.braindev.2016.03.003. [Epub ahead of print]
BACKGROUND: Antisense oligonucleotides that induce exon skipping have been nominated as the most plausible treatment method for dystrophin expression in dystrophin-deficient Duchenne muscular dystrophy. Considering this therapeutic efficiency, small chemical compounds that can enable exon skipping have been highly awaited. In our previous report, a small chemical kinase inhibitor, TG003, was shown to enhance dystrophin expression by enhancing exon skipping.
3.Melatonin behavior in restoring chemical damaged C2C12 myoblasts.
Salucci S1, Baldassarri V1, Canonico B1, Burattini S1, Battistelli M1, Guescini M1, Papa S1, Stocchi V1, Falcieri E1. Microsc Res Tech. 2016 Apr 5. doi: 10.1002/jemt.22663. [Epub ahead of print]
It is known that, besides a wide range of functions, melatonin provides protection against oxidative stress, thanks to its ability to act, directly, as a free radical scavenger and, indirectly, by stimulating antioxidant enzymes production and mitochondrial electron transport chain efficiency. Oxidative stress is one of the major players in initiating apoptotic cell death in skeletal muscle, as well as in other tissues. Apoptosis is essential for skeletal muscle development and homeostasis; nevertheless, its misregulation has been frequently observed in several myopathies, in sarcopenia, as well as in denervation and disuse. Melatonin activity was investigated in undifferentiated C2C12 skeletal muscle cells, after exposure to various apoptotic chemical triggers, chosen for their different mechanisms of action. Cells were pretreated with melatonin and then exposed to hydrogen peroxide, etoposide and staurosporine. Morphofunctional and molecular analyses show that in myoblasts melatonin prevents oxidative stress and apoptosis induced by chemicals following, at least in part, the mitochondria pathway.
4.Temporal Analyses of the Response of Intervertebral Disc Cells and Mesenchymal Stem Cells to Nutrient Deprivation.
Turner SA1, Wright KT1, Jones PN1, Balain B2, Roberts S1. Stem Cells Int. 2016;2016:5415901. doi: 10.1155/2016/5415901. Epub 2016 Feb 10.
Much emphasis has been placed recently on the repair of degenerate discs using implanted cells, such as disc cells or bone marrow derived mesenchymal stem cells (MSCs). This study examines the temporal response of bovine and human nucleus pulposus (NP) cells and MSCs cultured in monolayer following exposure to altered levels of glucose (0, 3.15, and 4.5 g/L) and foetal bovine serum (0, 10, and 20%) using an automated time-lapse imaging system. NP cells were also exposed to the cell death inducers, hydrogen peroxide and staurosporine, in comparison to serum starvation. We have demonstrated that human NP cells show an initial "shock" response to reduced nutrition (glucose). However, as time progresses, NP cells supplemented with serum recover with minimal evidence of cell death. Human NP cells show no evidence of proliferation in response to nutrient supplementation, whereas MSCs showed greater response to increased nutrition. When specifically inducing NP cell death with hydrogen peroxide and staurosporine, as expected, the cell number declined.

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