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AM 92016 hydrochloride
Discontinued ProductAM 92016 hydrochloride (Cat. No. 0876) has been withdrawn from sale for commercial reasons.
A specific blocker of the time dependent delayed rectifier potassium current, devoid of any β-adrenoceptor blocking activity. Exhibits proarrhythmic and prohypertensive activity in vivo.
|Storage||Desiccate at RT|
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.
References are publications that support the biological activity of the product.
Conners et al (1992) Actions and mechanisms of action of novel analogues of sot. on guinea-pig and rabbit ventricular cells. Br.J.Pharmacol. 106 958 PMID: 1393293
Hagerty et al (1996) The in vivo cardiovascular effects of a putative class III anti-arrhythmic drug, AM 92016. J.Pharm.Pharmacol. 48 417 PMID: 8794994
Lei and Brown (1998) Inhibition by compound II, a sot. analogue, of delayed rectifier current (iK) in rabbit sino-atrial node cells. Naunyn Schmiedebergs Arch.Pharmacol. 357 260 PMID: 9550297
Palen et al (2005) Role of SHP-1, Kv1.2 and cGMP in nitric oxide-induced ERK1/2 MAP kinase dephosphorylation in rat vascular smooth muscle cells. Cardiovasc.Res. 68 268 PMID: 15967421
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Citations for AM 92016 hydrochloride
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Reviews for AM 92016 hydrochloride
Average Rating: 5 (Based on 1 Review.)
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Have used the product for carrying out study on Kv channel regulation by accessory subunits expressed differently on mouse. Found that it works ideally and also is a great stable product on lab conditions. Great buy and would purchase again soon.
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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.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.