PI3K-Akt-mTOR Signaling Pathway Inhibitor Kit
Catalog No. K1020
A unique collection of 9 inhibitors for studying the PI3K/Akt/mTOR signaling pathway
Cited by 17 Publications
7 Customer Reviews
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.
A, ANOVA of IC50 values of the dual PI3K/mTOR inhibitor NVP-BEZ235 in 23 melanoma cell lines showing no significant difference in sensitivity to this compound in B-Raf mutant and Braf wild-type cells. B, decreases in pAkt and pP70S6K in a dose and time-dependent fashion in 2 melanoma cell lines treated with NVP-BEZ235. pP70S6K levels are undetectable at all concentrations and time points studied, whereas levels of pAkt start rising again after 4 hours of drug exposure in a dose-dependent fashion. C, clonogenic assays in 2 melanoma cell lines (YUVON and YUSIK) treated with NVP-BEZ235 at different concentrations. NVPBEZ235 was effective in inhibiting colony formation at low nanomolar concentrations.
Confocal microscopy images of NO formation. DAF 2 DA-loaded washed platelets (1.0109 platelets/mL) were preincubated at 378C with saline (A), and then stimulated for 1min with 0.1 (B), 1.0 (C) or 10 (D) mM AEA. In Panel (E–F–G) washed platelets were preincubated with 1 mM SR1 (E), 1 Mm MK2206 (F) or 20 mM LY294002 (G), and then stimulated for 1min with 1.0 mM AEA. In panel (H) is reported the effect of 5 mg/mL collagen, used as a positive control. All the experiments were carried out in the presence of 100 mM L-arginine. NO formation was visualized by confocal microscropy as detailed in Methods.
Mean IL-8 concentrations determined by ELISA of the supernatants of HeLa cells infected with wild-type Salmonella. Kinase inhibitors are indicated on the x axis, and the target families of the inhibitors are indicated above each column. CEC, chelerythrine; Pim Inh, Pim-1 inhibitor 2. Inhibitors that significantly affected IL-8 production relative to the control (P < 0.05, Bonferroni post hoc test from one-way ANOVA) are indicated with an asterisk. Relative cell viability is also shown, as determined by reduction of XTT by viable cells. A450, absorbance at 450 nm.
Three-dimensional responses of MCF7/IGF-1R cells to TAM (1 μM), E2 and IGF-1. Compared to parental MCF7 cells (a), MCF7/IGF-1R cells (b) in three-dimensional (3D) culture formed bigger acini in response to IGF-1 stimulation and displayed significant TAM resistance when treated with TAM (1 μM) + E2 + IGF-1, which was removable by kinase inhibitors BMS-536924, U0126 and BEZ235 (c). Cells (10,000/well) were seeded in 96-well plates. Acini were formed on 100% Matrigel and cultured for 14 days in starving medium containing 2% Matrigel and 5% charcoal/dextran-stripped fetal bovine serum with the treatments as indicated. Concentrations used: TAM (1 μM), E2 (1 nM) and IGF-1 (100 ng/mL). Confocal image original magnification, × 20. Red, rhodamine phalloidin (actin). Blue, Hoechst blue stain. Results are representative of two individual experiments.
Rapamycin (RPM) inhibits OA-induced lipogenesis. Male SD rats were divided into three groups, and then treated as follows for seven days: group I (control; Ctrl), normal diet + vehicle; group II (OA), 1% OA diet + vehicle; group III (OA + RPM), 1% OA diet + RPM. (A) Hepatic TG concentrations were determined using the serum triglyceride determination kit. (B) Fixed liver sections were subjected to HE and Oil Red O staining as well as immunohistochemistry assays with SREBP-1 antibody. Representative microphotographs of liver specimens from all groups of rats are shown. (C) The levels of mRNA of the indicated genes involved in lipogenesis were determined by real-time PCR. Each bar represents the mean ± SE of the results obtained from six rats. * P < 0.05, ** P < 0.01, *** P < 0.001.
|Cat.No.||Product Name||Targets and IC50s||Suggested Solvent||Amount Supplied|
|S2739||PKI-402||A selective, reversible and ATP-competitive Class I PI3K inhibitor. PI3Kα, IC50=1 nM; PI3Kβ, IC50=7 nM; PI3Kγ, IC50=16 nM; PI3Kδ, IC50=14 nM.||DMSO <1 mg/mL
Water <1 mg/mL
|S1039||Rapamycin (Sirolimus)||A specific mTOR inhibitor with an IC50 of 0.1 nM.||DMSO 183 mg/mL||5 mg|
|S1009||BEZ235 (NVP-BEZ235)||A dual ATP-competitive inhibitor of PI3K and mTOR. p110α, IC50=4 nM; p110β, IC50=75 nM; p110δ, IC50=7 nM; p110γ, IC50=5 nM.||DMSO 7 mg/mL||50 mg|
|S1078||MK-2206 dihydrochloride||A highly selective inhibitor of Akt. Akt1, IC50=8 nM; Akt2, IC50=12 nM; Akt3, IC50=65 nM.||DMSO 96 mg/mL
Water 96 mg/mL
|S2924||CHIR-99021 (CT99021) HCl||CHIR-99021 HCl (CT99021) is hydrochloride of CHIR-99021, which is a GSK-3α and GSK-3β inhibitor with IC50 of 10 nM and 6.7 nM, respectively.||DMSO 3 mg/mL||2 mg|
|S2638||NU7441 (KU-57788)||A potent and selective DNA-PK inhibitor with an IC50 of 14 nM.||DMSO 5 mg/mL||5 mg|
|S1092||KU-55933||A potent and specific ATM kinase inhibitor with an IC50 and a Ki of 13 nM and 2.2 nM, respectively.||DMSO 50 mg/mL||5 mg|
|S1275||BX-912||A selective potent PDK-1 inhibitor with an IC50 of 12 nM.||DMSO 94 mg/mL||2 mg|
|S1558||AT7867||A potent Akt inhibitor with an IC50 of 17 nM. AT7867 also inhibits structurally related AGC kinases p70S6K and PKA with IC50s of 20 nM and 85 nM, respectively.||DMSO 68 mg/mL||10 mg|
|Formulation||A unique collection of 9 inhibitors for studying the PI3K/Akt/mTOR signaling pathway supplied as lyophilized powder|
|Container||Screw Cap Micro Tubes of WATSON|