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Bosutinib (SKI-606) Chemical Structure
Saracatinib (AZD0530)
Saracatinib (AZD0530) is a Src inhibitor of c-Src with IC50 of 2.7 nM.
Dasatinib (BMS-354825)
Dasatinib also known as BMS-354825, Sprycel, BMS354825 is ATP-competitive, dual SRC/ABL inhibitor. BMS-354825 inhibits all members of the Src family, including c-Src, Lck, Fyn, and Yes (IC50 < 1.1nmol/L).
Danusertib (PHA-739358)
Danusertib (PHA-739358) is a pyrrolo-pyrazole and small molecule aurora kinases and Bcr-Abl kinase inhibitor for aurora A, B, and C with IC50 of 13 nM, 79 nM, and 61 nM, respectively.
NVP-BHG712
NVP-BHG712 is a small molecule specific EphB4, VEGFR2, c-raf, c-src and c-Abl kinase inhibitor with ED50 of 25 nM, 4.2, 0.4, 1.3 and 1.7μM, respectively.
Quercetin (Sophoretin)
Quercetin (Sophoretin) is a PI3K and PKC inhibitor with IC50 of 3.8 μM and 15µg/ml.
PCI-32765 (Ibrutinib)
PCI-32765 (Ibrutinib) is a high potent irreversible BTK inhibitor with an IC50 of 0.46 nM for the purified Btk.
KX2-391
KX2-391 is a synthetic, orally bioavailable small molecule and non-ATP competitive Src tyrosine kinase signaling inhibitor with an IC50 of average 72 nM.
Linifanib (ABT-869)
Linifanib (ABT869) is a structurally novel, potent RTK and VEGF and PDGF receptor families inhibitor for, PDGFR-β, KDR, and CSF-1R, with IC50 of 0.2 nM, 2 nM, 4 nM, and 7 nM, respectively.
Axitinib
Axitinib (AG-013736) is a multiple receptor kinase inhibitor of VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-β and c-KIT with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM, respectively.
Saracatinib (AZD0530)
Saracatinib (AZD0530) is a Src inhibitor of c-Src with IC50 of 2.7 nM.
Biological Activity
The cellular Src (c-Src) protein is a nonreceptor tyrosine kinase normally maintained in an inactive conformation via intramolecular interactions.[1] c-Src coordinates multiple signaling pathways known to be involved in tumor progression, such as proliferation, survival, motility, angiogenesis, cell-cell communication, adhesion, and invasion.[2,3] SKI-606 inhibited migration of breast cancer cell lines with IC50 values of 0.1 to 0.3 umol/L; After a 48 h treatment with 1 Amol/L SKI-606, all the invasioncompetent cell lines were unable to cross the porous membrane; cell proliferation and survival were unaffected by SKI-606 at concentrations sufficient to block cell migration and invasion.
References on Bosutinib (SKI-606)
- [1] Biochimica et Biophysica Acta 2002;1602:114– 130
- [2] Annu. Rev. Cell Dev. Biol. 1997;13:513–609
- [3] Journal of Cell Science 2004;117:989-998
Product Information
| Molecular Weight (WM): | 530.45 |
|---|---|
| Formula: | C26H29Cl2N5O3 |
| CAS No.: | 380843-75-4 |
| Synonyms: |
N/A
|
| Dissolve in (25°C): | DMSO ≥53mg/mL |
| Water <1mg/mL | |
| Ethanol ≥24mg/mL | |
| Storage: | 2 years-20°CPowder |
| 1 week-4°Cin DMSO | |
| 1 month-80°in DMSO |
Quality Control & MSDS
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Selleck's high quality products have been used in several published research findings, including the following:
Inhibition of Ser/Thr Phosphatases Induces Capacitation-associated Signaling in the Presence of Src Kinase Inhibitors.
VEGFR2 and Src Kinase Inhibitors Suppress Andes Virus-Induced Endothelial Cell Permeability
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SFK inhibitors abrogate tyrosine phosphorylation associated with sperm capacitation. Mouse sperm were incubated in the absence or in the presence of SKI606 for 60 min in capacitating (cap, with HCO3) or non-capacitating media (NC, without HCO3). Western blot analyses were performed withanti-pY antibodies.
SFK inhibitors abrogate tyrosine phosphorylation associated with sperm capacitation. Mouse sperm were incubated in the absence or in the presence of SKI606 for 60 min in capacitating (cap, with HCO3) or non-capacitating media (NC, without HCO3). Western blot analyses were performed withanti-pY antibodies.
Data from [Journal of Biological Chemistry 2010.March;285:7977–7985] Bosutinib (SKI-606) purchased from Selleck
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Click to enlarge
A,IC50 of Bosutinib that block ANDV-induced EC permeability. Endothelial cells were ANDV infected, and 3 days postinfection the permeability of cells in response to VEGF addition was determined in the presence or absence of increasing amounts of kinase inhibitor. The effect of inhibitors is presented as the percentage of ANDV-induced permeability of inhibitor-treated monolayers 3 days postinfection and 30 min post-VEGF and FITC-dextran addition. B, VEGFR2-Src inhibitors block ANDV-induced permeability. Endothelial cells were plated on vitronectin-coated Transwell inserts and infected at an MOI of 0.5 in triplicate with ANDV. Three days postinfection, the permeability of ANDV- and mock-infected endothelial cell monolayers was determined as described for Fig. 1 at indicated times in the presence or absence of Bosutinib .
A,IC50 of Bosutinib that block ANDV-induced EC permeability. Endothelial cells were ANDV infected, and 3 days postinfection the permeability of cells in response to VEGF addition was determined in the presence or absence of increasing amounts of kinase inhibitor. The effect of inhibitors is presented as the percentage of ANDV-induced permeability of inhibitor-treated monolayers 3 days postinfection and 30 min post-VEGF and FITC-dextran addition. B, VEGFR2-Src inhibitors block ANDV-induced permeability. Endothelial cells were plated on vitronectin-coated Transwell inserts and infected at an MOI of 0.5 in triplicate with ANDV. Three days postinfection, the permeability of ANDV- and mock-infected endothelial cell monolayers was determined as described for Fig. 1 at indicated times in the presence or absence of Bosutinib .
Data from [Journal of Virology 2011.March;85:2296–2303] Bosutinib (SKI-606) purchased from Selleck
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Click to enlarge
Rescue ofPKAand tyrosine phosphorylation by Ser/Thr phosphatase inhibitors. A and B, spermwere incubated in capacitating medium supplemented with SFK inhibitors and different concentrations of okadaic acid (OA) (A) or calyculin-A (B), before immunodetection of p-PKA substrates (clone 100G7E). C and D, PVDF membranes used in A and B were stripped as described and used for Western blot immunodetection with anti-PY antibodies (clone 4G10).
Rescue ofPKAand tyrosine phosphorylation by Ser/Thr phosphatase inhibitors. A and B, spermwere incubated in capacitating medium supplemented with SFK inhibitors and different concentrations of okadaic acid (OA) (A) or calyculin-A (B), before immunodetection of p-PKA substrates (clone 100G7E). C and D, PVDF membranes used in A and B were stripped as described and used for Western blot immunodetection with anti-PY antibodies (clone 4G10).
Data independently produced by Dr Pablo E.Visconti from University of Massachusetts Bosutinib (SKI-606) purchased from Selleck
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SFK inhibitors abrogate tyrosine phosphorylation associated with sperm capacitation. Mouse sperm were incubated in the absence or in the presence of SKI606 for 60 min in capacitating (cap, with HCO3) or non-capacitating media (NC, without HCO3). Western blot analyses were performed withanti-pY antibodies. |
Data from [Journal of Biological Chemistry 2010.March;285:7977–7985]
A,IC50 of Bosutinib that block ANDV-induced EC permeability. Endothelial cells were ANDV infected, and 3 days postinfection the permeability of cells in response to VEGF addition was determined in the presence or absence of increasing amounts of kinase inhibitor. The effect of inhibitors is presented as the percentage of ANDV-induced permeability of inhibitor-treated monolayers 3 days postinfection and 30 min post-VEGF and FITC-dextran addition. B, VEGFR2-Src inhibitors block ANDV-induced permeability. Endothelial cells were plated on vitronectin-coated Transwell inserts and infected at an MOI of 0.5 in triplicate with ANDV. Three days postinfection, the permeability of ANDV- and mock-infected endothelial cell monolayers was determined as described for Fig. 1 at indicated times in the presence or absence of Bosutinib . |
Data from [Journal of Virology 2011.March;85:2296–2303]
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