Ziconotide has been introduced as a new nonopioid treatment for chronic pain. 
Structurally, it is a peptide, the synthetic analog of the omega-conotoxin, 
derived from the marine snail, Conus magus. N-type voltage-sensitive calcium 
channels play a role in the transmission of nociceptive stimuli and also are 
involved in the release of neurotransmitters important in pain transmission. 
Ziconotide's therapeutic benefit derives from its potent and selective blockade 
of neuronal-type voltage-sensitive calcium channels. Blockade of the channels 
results in suppression of abnormal ectopic discharges from the injury site or 
the dorsal root ganglia, possibly resulting in decreased neuroplasticity, and 
decreased synaptic transmission that leads to the generation of chronic pain 
syndromes. The advantage of ziconotide is that tolerance does not occur, while 
disadvantages associated with ziconotide are the need for intrathecal 
administration and significant neurotoxicites associated with its use. When 
tested in clinical trials, ziconotide has been shown to have synergistic or 
additive value to the effect of morphine. Ziconotide, formerly known also as 
SNX- 111, represents a new class of agents, the N-type calcium channel blockers. 
These may represent another option for patients with refractory pain and 
refractory pain syndromes.