Bisindolylmaleimide II
Chemical Name: 3-(1H-Indol-3-yl)-4-[1-[2-(1-methyl-2-pyrrolidinyl)ethyl]-1H-indol-3-yl]-1H-pyrrole-2,5-dione
Purity: ≥97%
Biological Activity
Bisindolylmaleimide II is a potent, ATP-competitive protein kinase C (PKC) inhibitor (IC50 = 0.01 μM). Displays selectivity for PKC over protein kinase A (PKA) and phosphorylase kinase (PK) (IC50 values are 0.75 and 2μM for PK and PKA respectively). Also displays potent, noncompetitive antagonism at nicotinic cholinergic receptors (IC50 ~ 0.03 μM for inhibition of catecholamine secretion in nicotine-stimulated PC-12 cells).Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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The bisindolylmaleimide GF 109203X is a potent and selective inhibitor of protein kinase C.
Toullec et al.
J.Biol.Chem., 1991;266:15771 -
Chromaffin cell catecholamine secretion: bisindolylmaleimide compounds exhibit novel and potent antagonist effects at the nicotinic cholinergic receptor in pheochromocytoma cells.
Mahata et al.
Mol.Pharmacol., 2002;61:1340
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Citations for Bisindolylmaleimide II
The citations listed below are publications that use Tocris products. Selected citations for Bisindolylmaleimide II include:
4 Citations: Showing 1 - 4
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Contributing mechanisms underlying desensitization of cholecystokinin-induced activation of primary nodose ganglia neurons.
Authors: James H Et al.
Am J Physiol Cell Physiol 2020;318:C787-C796
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Small Molecule Inhibitor Screen Reveals Calcium Channel Signaling as a Mechanistic Mediator of Clostridium difficile TcdB-Induced Necrosis.
Authors: John Et al.
ACS Chem Biol 2020;15:1212-1221
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Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C.
Authors: O'Neill & Sylantyev
Exp Biol Med (Maywood) 2018;243:1046
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Regulation of SHP-1 tyrosine phosphatase in human platelets by serine phosphorylation at its C terminus.
Authors: Jones Et al.
PLoS One 2004;279:40475
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