Bay 65-1942 free base

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Bay 65-1942 free base is an ATP-competitive and selective IKKβ inhibitor.

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No. CAS : 600734-02-9

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Other In-stock Forms of Bay 65-1942 free base:

Bay 65-1942 hydrochloride

Other Forms of Bay 65-1942 free base:

Bay 65-1942 hydrochloride In-stock
Bay 65-1942 (R form) Obtener un presupuesto

4 Publications Citing Use of MCE Bay 65-1942 free base

RT-PCR

: Bay 65-1942 free base purchased from MedChemExpress. Usage Cited in: Oncogene. 2016 Aug 4;35(31):4036-47. [Abstract]; Effect of BEZ235 and Bay 65–1942 on CXCL1, CXCL2 and CXCL8 mRNAs in FUOV1, NIH:OVCAR3 and IGROV1 cells. Quantitative RT-PCR analysis is performed in cells treated with indicated inhibitors or DMSO control for 6 h.

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Pureza y Documentación
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Revisión del cliente

Descripciòn

Bay 65-1942 free base is an ATP-competitive and selective IKKβ inhibitor.

IC₅₀ & Target^[1]

IKKβ

In Vitro

Delivery of Bay 65-1942 prior to ischemia significantly decreases left ventricular infarct size compared with animals receiving vehicle. Compared with sham animals, animals receiving vehicle have a significant increase in the infarct-to-area at risk (AAR) ratio (70.7±3.4 vs. 5.8±3.4%, P<0.05). This ratio is significantly reduced by treatment with Bay 65-1942 at each time point (prior to ischemia 42.7±4.1%, at reperfusion 42.7±7.5%, 2 h of reperfusion 29.4±5.2%; each group P<0.05 vs. vehicle). Animals pretreated with Bay 65-1942 (n=3) have significantly attenuated CK-MB levels compared with those animals without treatment prior to IR (14,170 ±3,219 units, P<0.05 vs. vehicle)^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

Inhibitors of MEK (AZD6244) and IKK (BAY 65-1942) are used at their IC₅₀ concentrations, as determined by a 48 hour MTS assay, which achieve sufficient inhibition of kinase activity. MYL-R cells are treated for 24 hours with AZD6244 (5 µM), BAY 65-1942 (10 µM), or a combination of these inhibitors at the same concentrations. AZD6244 and BAY 65-1942 demonstrate synergistic inhibition of cell viability at the dose combination (5 µM AZD6244+10 µM BAY 65-1942), which correlates with IC₇₅ (CI = 0.48±0.01). Synergism is also indicated at the IC₅₀ (CI = 0.56±0.09) and IC₉₀ (CI = 0.46±0.02) dose combinations reported by the software (CI values are the mean of three independent experiments, ± standard deviation). AZD6244 and BAY 65-1942 treatment induces 2- and 1.3-fold caspase 3/7 activation, respectively, compared to the DMSO-treated cells. Treatment with a combination of AZD6244 plus BAY 65-1942 leads to a 3.2-fold increase in caspase 3/7 activity^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Peso molecular

395.45

Fòrmula

C₂₂H₂₅N₃O₄

No. CAS

600734-02-9

SMILES

O=C1OCC2=C([C@H]3CNCCC3)C=C(C4=C(O)C=CC=C4OCC5CC5)N=C2N1

Envío

Room temperature in continental US; may vary elsewhere.

Almacenamiento

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureza y Documentación

Instrucciones de manejo (2659 KB)

Referencias

[1]. Moss NC, et al. IKKbeta inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2248-53. [Content Brief]

[2]. Cooper MJ, et al. Application of multiplexed kinase inhibitor beads to study kinome adaptations in drug-resistant leukemia. PLoS One. 2013 Jun 24;8(6):e66755. [Content Brief]

Ensayo celular ^[2]	Cell viability is determined by seeding MYL-R cells on a 96-well plate at 4×10⁴ cells/well in 100 µL RPMI growth medium supplemented with kinase inhibitors. Growth media and kinase inhibitors are replenished at 24 hours, and at 48 hours. 20 µL of MTS assay reagent is added to each well. The plate is returned to the incubator for approximately 1 hour and the absorbance at 490 nm is recorded. For combination index (CI) experiments, cells are grown and assayed. To determine AZD6244 and BAY 65-1942 (10 µM) dose-effects, cells are treated with a series of three-fold dilutions of each drug singly, or in combination while maintaining a constant ratio of 1:2, respectively. Cell viability results are analyzed to derive CI values. The CI values from three independent experiments are averaged^[2]. MCE no ha confirmado la precisión de estos métodos independientemente. Son solo para referencia.
Administraciòn de animales ^[1]	Mice^[1] Male C57BL/6 mice, 8-10 wk of age are used. To investigate IKKβ inhibition in myocardial IR injury, mice are subjected to 30 min of cardiac ischemia followed by varying periods of reperfusion. An intraperitoneal injection of Bay 65-1942 (5 mg/kg) at appropriate dosing time points is administered. Nontreatment groups receive a vehicle of 10% cremaphor in water. In treatment groups, Bay 65-1942 is delivered either prior to ischemia, at the time of reperfusion, or 2 h after reperfusion injury. Infarct size is measured 24 h after reperfusion injury in sham, vehicle, and each treatment group. To confirm myocardial injury, serum creatine kinase-muscle-brain fraction (CK-MB) levels are measured 1 h after reperfusion in animals pretreated with Bay 65-1942. MCE no ha confirmado la precisión de estos métodos independientemente. Son solo para referencia.
Referencias	[1]. Moss NC, et al. IKKbeta inhibition attenuates myocardial injury and dysfunction following acute ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2248-53. [Content Brief] [2]. Cooper MJ, et al. Application of multiplexed kinase inhibitor beads to study kinome adaptations in drug-resistant leukemia. PLoS One. 2013 Jun 24;8(6):e66755. [Content Brief]