Our broad portfolio consists of multiplex panels that allow you to choose, within the panel, analytes that best meet your needs. On a separate tab you can choose the premixed cytokine format or a single plex kit.
Cell Signaling Kits & MAPmates™
Choose fixed kits that allow you to explore entire pathways or processes. Or design your own kits by choosing single plex MAPmates™, following the provided guidelines.
The following MAPmates™ should not be plexed together:
-MAPmates™ that require a different assay buffer
-Phospho-specific and total MAPmate™ pairs, e.g. total GSK3β and GSK3β (Ser 9)
-PanTyr and site-specific MAPmates™, e.g. Phospho-EGF Receptor and phospho-STAT1 (Tyr701)
-More than 1 phospho-MAPmate™ for a single target (Akt, STAT3)
-GAPDH and β-Tubulin cannot be plexed with kits or MAPmates™ containing panTyr
.
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Select A Species, Panel Type, Kit or Sample Type
To begin designing your MILLIPLEX® MAP kit select a species, a panel type or kit of interest.
Custom Premix Selecting "Custom Premix" option means that all of the beads you have chosen will be premixed in manufacturing before the kit is sent to you.
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Add Additional Reagents (Buffer and Detection Kit is required for use with MAPmates)
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48-602MAG
Buffer Detection Kit for Magnetic Beads
1 Kit
Space Saver Option Customers purchasing multiple kits may choose to save storage space by eliminating the kit packaging and receiving their multiplex assay components in plastic bags for more compact storage.
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The Aurora Kinase Inhibitor VI, ZM447439, also referenced under CAS 331771-20-1, controls the biological activity of Aurora Kinase. This small molecule/inhibitor is primarily used for Phosphorylation
More>>The Aurora Kinase Inhibitor VI, ZM447439, also referenced under CAS 331771-20-1, controls the biological activity of Aurora Kinase. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications. Less<<
MSDS (material safety data sheet) or SDS, CoA and CoQ, dossiers, brochures and other available documents.
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Description
Overview
A cell-permeable quinazoline compound that targets the ATP binding pocket and an adjacent cleft and acts as a potent and reversible inhibitor of Aurora A and Aurora B (IC50 = 110 and 130 nM, respectively) with moderate to excellent selectivity among closely related 16-kinase panel (IC50 = 0.88, 1.03 and 1.79 µM for Lck, Src and MEK1, respectively, and IC50 > 10 µM for Cdk1/2/4, Plk1, Chk1). Blocks phosphorylation of Histone H3-Ser10 in Xenopus cycling egg extracts at 20 µM, and reduces mitotic spindle assembly. Shown to repress kinetochore localization of BubR1, Cenp-E, and Mad2, and arrest the growth of proliferating tumor cells.
Note that this data sheet is not lot-specific and is representative of the current specifications for this product. Please consult the vial label and the certificate of analysis for information on specific lots. Also note that shipping conditions may differ from storage conditions.
A cell-permeable quinazoline compound that targets the ATP binding pocket and an adjacent cleft and acts as a potent and reversible inhibitor of Aurora A and Aurora B (IC50 = 110 and 130 nM, respectively) with moderate to excellent selectivity among closely related 16-kinase panel (IC50 = 0.88, 1.03 and 1.79 µM for Lck, Src and MEK1, respectively, and IC50 > 10 µM for Cdk1/2/4, Plk1, Chk1). Blocks phosphorylation of Histone H3-Ser10 in Xenopus cycling egg extracts at 20 µM, and reduces mitotic spindle assembly. Shown to repress kinetochore localization of BubR1, Cenp-E, and Mad2, and arrest the growth of proliferating tumor cells.
Form
White solid
Intert gas (Yes/No)
Packaged under inert gas
CAS number
331771-20-1
Chemical formula
C₂₉H₃₁N₅O₄
Structure formula
Purity
≥95% by HPLC
Solubility
DMSO (50 mg/ml)
Storage
Protect from light
+2°C to +8°C
Do Not Freeze
Ok to freeze
Special Instructions
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Toxicity
Regulatory Review
References
Gadea, B.B. and Ruderman, J.V., 2005. Mol. Biol. Cell16, 1305. Ditchfield, C., et al. 2003. J. Cell Biol.161, 267.
