Nefopam Hydrochloride - CAS 23327-57-3
Catalog number: 23327-57-3
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Nefopam HCl is a centrally-acting but non-opioid analgesic drug by blocking voltage-gated sodium channel and inhibition of serotonin, dopamine and noradrenaline reuptake.It is widely used, mainly in European countries, for the relief of moderate to severe pain as an alternative to opioid analgesic drugs.
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Nefopam Hydrochloride
1.Nefopam inhibits calcium influx, cGMP formation, and NMDA receptor-dependent neurotoxicity following activation of voltage sensitive calcium channels
A. Novelli ,R.Dıaz-Trelles , A. Groppetti, and M. T. Fernandez-Sanchez. Amino Acids (2005) 28: 183–191
Thus, nefopam may share functional and structural properties with other drugs that are used for pathologies other than neuropathic pain, and may be a potential new drug for mood disorders and epilepsy. In addition, although investigations of the application of calcium channel antagonists for the treatment of acute neurodegenerative disorders that are caused by an excessive release of glutamate, such as stroke, have not yet led to the discovery of compounds with efficient neuroprotective activity (Kobayashi and Mori, 1998), it is interesting to note that drugs exerting multiple actions appeared to block the cascades of neuronal death more efficiently than drugs with a single action site (Spedding et al., 1995). For example, an efficient neuroprotective action of flunarizine has been shown in animal models of ischemia (Deshpande and Wieloch, 1986). Flunarizine is a potent non-selective VSCC antagonist which also interacts with Naþ channels. The same effect has also been reported for other VSCC antagonists with little channel selectivity (Benham et al., 1993; Goldin et al., 1995; Varming et al., 1996). Furthermore, a diltiazem analog (T-477) with little selectivity among VSCC types, showed neuroprotective activity in a rat stroke model (Ishii et al., 1996) while the more selective mother compound diltiazem did not show neuroprotection (Wauquier et al., 1985). In conclusion, this study has demonstrated that the analgesic nefopam hydrochloride can reduce calcium influx and effectively prevent intracellular formation of cGMP and neuronal death following the activation of voltage-sensitive calcium channels in cultured cerebellar neurons. Our data are consistent with a presynaptic action of nefopam that may be of interest in reducing the excessive release of endogenous glutamate involved in neurological and neuropsychiatric disorders.
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CAS 23327-57-3 Nefopam Hydrochloride

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