- |
My Account- |
United States (Change Country)You can order by phone, email or fax Tel: +1-832-582-8158 Fax: +1-713-796-9816 Email: [email protected] |
| Formulation: | A collection of 785 FDA approved drugs supplied as lyophilized powder or pre-dissolved DMSO solutions. | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Container: | 96 Well Format Sample Storage Tube With Screw Cap and Optional 2D Barcode | ||||||||||||
| Stability: |
|
||||||||||||
| Shipping: | Blue ice | ||||||||||||
| Packaging: | Inert gas |
If you need to download the FDA Approved Drug Library Contents (.xlsx and .sdf), please contact us via [email protected]
| Vorinostat promotes C2C12 differentiation.In the image, the red is the myotube indicating differentiation ,the blue is the nuclei. |
Data independently produced by Dr Qi Long Lu of Carolinas Medical Center
Vorinostat (SAHA) purchased from Selleck
Vorinostat promotes C2C12 differentiation.In the image, the red is the myotube indicating differentiation ,the blue is the nuclei.
| Analysis of receptor mechanisms mediating the induction of MMP-9 expression in THP-1 cells by AFP. Maraviroc, an inhibitor of chemokine receptor CCR5, was added to the cells in the indicated concentrations 1 hour before addition of 50 μg/ml AFP (■) or 150 ng/ml RANTES (♦). After 24 hours of cell stimulation, conditioned media were collected and analyzed for MMP-9 activity by the method of zymography. |
Data independently produced by Dr Mikhail Menshikov of Cardiology Research Center
Maraviroc purchased from Selleck
Analysis of receptor mechanisms mediating the induction of MMP-9 expression in THP-1 cells by AFP. Maraviroc, an inhibitor of chemokine receptor CCR5, was added to the cells in the indicated concentrations 1 hour before addition of 50 μg/ml AFP (■) or 150 ng/ml RANTES (♦). After 24 hours of cell stimulation, conditioned media were collected and analyzed for MMP-9 activity by the method of zymography
| A,IC50 of Pazopanib 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 Pazopanib. |
Data from [Journal of Virology 2011.March;85:2296–2303]
Pazopanib HCL purchased from Selleck
A,IC50 of Pazopanib 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 Pazopanib.
| Cooperative Effects of AR and mTOR Inhibition In Vitro and In Vivo (A) In vitro response of Pten null;Ar+ murine (CaP8) and human (LNCaP) prostate cancer cells to AR knockdown (sh-AR) or pharmacological inhibition of AR (MDV3100, 10 mM) with and without rapamycin (R: 1 nM) treatment (Sc, control sh oligo). (B and D) In vivo response to treatments with castration, MDV3100, rapamycin, or their combinations as measured by cell proliferation (Ki67+cells) and (C and D) tumor burden in Pb-Cre+;-PtenL/L and Pb-Cre+;PtenL/L:ArL/Y mutants. Scale bars represent 2 mm (C), 200 mm (D), and 75 mm (D, inset). Error bars represent mean ± SD. |
Data from [Cancer Cell 2011.June;19:1–13]
Rapamycin(Sirolimus) purchased from Selleck
Cooperative Effects of AR and mTOR Inhibition In Vitro and In Vivo (A) In vitro response of Pten null;Ar+ murine (CaP8) and human (LNCaP) prostate cancer cells to AR knockdown (sh-AR) or pharmacological inhibition of AR (MDV3100, 10 mM) with and without rapamycin (R: 1 nM) treatment (Sc, control sh oligo). (B and D) In vivo response to treatments with castration, MDV3100, rapamycin, or their combinations as measured by cell proliferation (Ki67+cells) and (C and D) tumor burden in Pb-Cre+;-PtenL/L and Pb-Cre+;PtenL/L:ArL/Y mutants. Scale bars represent 2 mm (C), 200 mm (D), and 75 mm (D, inset). Error bars represent mean ± SD.
| Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of Temsirolimus for 24 hours. |
Data independently produced by Dr. Zhang of Tianjin Medical University
Temsirolimus(Torisel) purchased from Selleck
Breast cancer cells were pretreated with 100ng/ml EGF for 15 min and then treated with the indicated concentrations of Temsirolimus for 24 hours.
A collection of 715 inhibitors
A collection of 1463 bioactive compounds
A collection of 117 tyrosine kinase inhibitors
A collection of 271 kinase inhibitors
A collection of 144 natural products
A collection of 84 chemotherapeutic agents
