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Biological Activity for Apamin
Apamin is a prototypical potent and highly selective inhibitor of the small-conductance Ca2+-activated K+-channel (KCa2, SK). Blocks medium after-hyperpolarization in vitro and is brain penetrant and convulsive in vivo.
Technical Data for Apamin
(Modifications: Disulfide bridges: 1-11, 3-15, His-18 = C-terminal amide)
|Storage||Store at -20°C|
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.
Solubility Data for Apamin
|Solubility||Soluble to 1 mg/ml in water|
References for Apamin
References are publications that support the biological activity of the product.
Habermann (1984) Apamin. Pharmacol.Ther. 25 255 PMID: 6095335
Stocker et al (2004) Matching molecules to function: neuronal Ca2+-activated K+ channels and afterhyperpolarizations. Toxicon 43 933 PMID: 15208027
Strong (1990) Potassium channel toxins. Pharmacol.Ther. 46 137 PMID: 2181489
van der Staay et al (1999) Behavioral effects of apamin, a selective inhibitor of the SKCa-channel, in mice and rats. Neurosci.Biobehav.Rev. 23 1087 PMID: 10643819
If you know of a relevant reference for Apamin, please let us know.
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Keywords: Apamin, Apamin supplier, K+, channels, blockers, small, conductance, ca2+-activated, ca2+-dependent, Potassium, KCa, KCa2, SK, venoms, Ca2+-Activated, Channels, 1652, Tocris Bioscience
23 Citations for Apamin
Citations are publications that use Tocris products. Selected citations for Apamin include:
Sargin et al (2016) Chronic social isolation reduces 5-HT neuronal activity via upregulated SK3 calcium-activated potassium channels Elife 5 e21416 PMID: 27874831
Lee et al (2015) The role of K+ conductances in regulating membrane excitability in human gastric corpus smooth muscle. FASEB J 308 G625 PMID: 25591864
Few et al (2012) Asynchronous Ca2+ current conducted by voltage-gated Ca2+ (CaV)-2.1 and CaV2.2 channels and its implications for asynchronous neurotransmitter release. Proc Natl Acad Sci U S A 109 E452 PMID: 22308469
Villalobos and Andrade (2010) Visinin-like neuronal calcium sensor proteins regulate the slow calcium-activated afterhyperpolarizing current in the rat cerebral cortex. Am J Physiol Gastrointest Liver Physiol 30 14361 PMID: 20980592
Whitaker et al (2017) Bidirectional Modulation of Intrinsic Excitability in Rat Prelimbic Cortex Neuronal Ensembles and Non-Ensembles after Operant Learning. J Neurosci 37 8845 PMID: 28779019
Gamble-George et al (2016) Cyclooxygenase-2 inhibition reduces stress-induced affective pathology. Elife 5 PMID: 27162170
Turker et al (2013) Amiodarone inhibits apamin-sensitive potassium currents. PLoS One 8 e70450 PMID: 23922993
Alpert and Alford (2013) Synaptic NMDA receptor-dependent Ca2+ entry drives membrane potential and Ca2+ oscillations in spinal ventral horn neurons. PLoS One 8 e63154 PMID: 23646190
Yu et al (2014) Apamin does not inhibit human cardiac Na+ current, L-type Ca2+ current or other major K+ currents. J Neurosci 9 e96691 PMID: 24798465
Chan and Cipolla (2011) Relaxin causes selective outward remodeling of brain parenchymal arterioles via activation of peroxisome proliferator-activated receptor-γ. Sci Rep 25 3229 PMID: 21602449
O'Malley et al (2020) TRPM4 Conductances in Thalamic Reticular Nucleus Neurons Generate Persistent Firing during Slow Oscillations. J Neurosci 40 4813 PMID: 32414784
Zachary and Fuchs (2015) Re-Emergent Inhibition of Cochlear Inner Hair Cells in a Mouse Model of Hearing Loss. J Neurosci 35 9701 PMID: 26134652
Hsueh et al (2013) Proarrhythmic effect of blocking the small conductance calcium activated potassium channel in isolated canine left atrium. Elife 10 891 PMID: 23376397
Geier et al (2011) Dynamic interplay of excitatory and inhibitory coupling modes of neuronal L-type calcium channels. Am J Physiol Cell Physiol 300 C937 PMID: 21228322
Meredith et al (2011) Postnatal expression of an apamin-sensitive k(ca) current in vestibular calyx terminals. J Membr Biol 244 81 PMID: 22057903
Zemkova et al (2011) NE causes a biphasic change in mammalian pinealocye membrane potential: role of alpha1B-adrenoreceptors, phospholipase C, and Ca2+. Endocrinology 152 3842 PMID: 21828176
Fernandez-Fernandez et al (2018) Activation of TREK currents by riluzole in three subgroups of cultured mouse nodose ganglion neurons. PLoS One 13 e0199282 PMID: 29928032
Lamy et al (2010) Allosteric block of KCa2 channels by apamin. J Neurosci 285 27067 PMID: 20562108
Han et al (2007) DArgic modulation of spinal neuronal excitability. J Biol Chem 27 13192 PMID: 18045913
Rau et al (2015) Increased Basolateral Amygdala Pyramidal Cell Excitability May Contribute to the Anxiogenic Phenotype Induced by Chronic Early-Life Stress. Heart Rhythm 35 9730 PMID: 26134655
Henry et al (2015) Cell type-specific transcriptomics of hypothalamic energy-sensing neuron responses to weight-loss. Mol Pain 4 PMID: 26329458
Thompson et al (2015) Small-conductance calcium-activated potassium (SK) channels in the amygdala mediate pain-inhibiting effects of clinically available R.zole in a rat model of arthritis pain. J Neurosci 11 51 PMID: 26311432
Gutzmann et al (2019) Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus. Front Cell Neurosci 13 27 PMID: 30846929
Do you know of a great paper that uses Apamin from Tocris? Please let us know.
Reviews for Apamin
Average Rating: 5 (Based on 1 Review.)
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Apamin is a potent SK channel blocker which was studied on BK channels. At low concentrations, it shows minimal blocking effect on BK channels but at higher concentrations moderate effects are shown. Great product and would recommend.
Literature in this Area
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Epilepsy is a brain disease that affects 60 million people globally. More than 20 anti-seizure drugs are currently available, but these do not address the underlying causes of the condition. This poster summarizes current knowledge about the development of the condition and highlights some approaches that have disease-modifying effects in proof-of-concept studies.