Gap19
Purity: ≥95%
Biological Activity
Gap19 is a selective connexin 43 (Cx43) hemichannel blocker; has no effect on gap junction coupling or Panx-1 channels. Reduces mitochondrial potassium influx in cardiomyocytes and attenuates glutamate-triggered ATP release in primary astrocytes. Modestly reduces infarct size in a mouse ischemia model.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 connexin43 mimetic peptide Gap19 inhibits hemichannels without altering gap junctional communication in astrocytes.
Abudara et al.
Front.Cell.Neurosci., 2014;8:1 -
Connexin 43 impacts on mitochondrial potassium uptake.
Boengler et al.
Front Pharmacol., 2013;4 -
Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury.
Wang et al.
Basic Res.Cardiol., 2013;108:309 -
Inhibition of connexin 43 attenuates oxidative stress and apoptosis in human umbilical vein endothelial cells
JW Ma, DD Ji, QQ Li, T Zhang, L Luo
BMC Pulm Med, 2020;20(1):19.
Product Datasheets
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Citations for Gap19
The citations listed below are publications that use Tocris products. Selected citations for Gap19 include:
5 Citations: Showing 1 - 5
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The Involvement of Cx43 in JNK1/2-Mediated Endothelial Mechanotransduction and Human Plaque Progression.
Authors: Miyuki Et al.
Int J Mol Sci 2023;24
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Abacavir Increases Purinergic P2X7 Receptor Activation by ATP: Does a Pro-inflammatory Synergism Underlie Its Cardiovascular Toxicity?
Authors: Juan V Et al.
Front Pharmacol 2021;12:613449
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Distinct initiating events underpin the immune and metabolic heterogeneity of KRAS-mutant lung adenocarcinoma.
Authors: Best Et al.
Nat Commun 2019;10:4190
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Inhibition of Connexin 43 Hemichannels Alleviates Cerebral Ischemia/Reperfusion Injury via the TLR4 Signaling Pathway.
Authors: Chen Et al.
Front Cell Neurosci 2018;12:372
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Connexin 43 in astrocytes contributes to motor neuron toxicity in amyotrophic lateral sclerosis.
Authors: Almad Et al.
Glia 2016;64:1154
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