Staurosporine - CAS 62996-74-1

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

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Staurosporine is broad spectrum protein kinase inhibitor. 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).

General Information

ADCs Cytotoxin
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Catalog Number
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Chemical Structure

  • Staurosporine

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Catalog Number Size Price Stock Quantity
BADC-00329 25 mg $298 In stock
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Soild powder
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
Soluble in ethanol, methanol, DMF or DMSO. Poor water solubility.
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Streptomyces sp.
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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