📚 Wiki Cognitive & Mood Ziconotide

Ziconotide

✓ Approved; research in pain mechanism and calcium channel biology
Ziconotide (Prialt; omega-Conotoxin MVIIA)
Also known as: SNX-111, Cone snail peptide, N-type calcium channel blocker, ω-conotoxin MVIIA
Brand names: Prialt
Page last reviewed

Quick Summary

Ziconotide is a synthetic version of omega-conotoxin MVIIA, a 25-amino acid peptide toxin from the venom of the marine cone snail Conus magus. It is the first non-opioid intrathecal analgesic approved by the FDA, indicated for severe chronic pain (2004) in patients who have failed or cannot tolerate oral analgesics, adjunctive therapies, or intrathecal morphine.

Pain Research Peptide FDA Approved (intrathecal)
Ziconotide is a synthetic version of omega-conotoxin MVIIA, a 25-amino acid peptide toxin from the venom of the marine cone snail Conus magus. It is the first non-opioid intrathecal analgesic approved by the FDA, indicated for severe chronic pain (2004) in patients who have failed or cannot tolerate oral analgesics, adjunctive therapies, or intrathecal morphine. Ziconotide selectively and reversibly blocks N-type voltage-gated calcium channels (Cav2.2) on primary afferent sensory neurons in the spinal cord dorsal horn, preventing calcium influx and neurotransmitter (substance P, cgrp/" class="wiki-internal-link">CGRP, glutamate) release triggered by nociceptive signals. Unlike opioids, ziconotide does not cause respiratory depression, physical dependence, or tolerance, making it an important option for refractory chronic pain states including cancer pain, failed back surgery syndrome, and neuropathic pain.
Storage Stability
Lyophilized
6–12 months (2–8°C)
Reconstituted
14 days (2–8°C)
Room temp
Avoid

Mechanism of Action

N-Type Calcium Channel Blockade

Ziconotide binds specifically and with high affinity (Kd ~0.1 nM) to the alpha1B subunit of N-type voltage-gated calcium channels (Cav2.2). N-type channels are concentrated at presynaptic terminals of C-fibers and A-delta fibers in the spinal dorsal horn. During nociceptive signaling, action potentials open N-type channels, allowing Ca2+ influx that triggers exocytosis of pain neurotransmitters (substance P, glutamate, cgrp/" class="wiki-internal-link">CGRP). Ziconotide blocks this Ca2+ influx, preventing transmitter release and interrupting pain signal transmission to ascending pathways.

Intrathecal Delivery Rationale

Systemic ziconotide is ineffective because it does not cross the blood-brain barrier, and systemic N-type channel blockade would cause cardiovascular and neural adverse effects. Intrathecal delivery concentrates the drug in CSF at the site of action (dorsal horn) while minimizing systemic exposure. The implanted pump allows continuous CSF infusion at nanogram-per-day doses that produce CSF concentrations sufficient for Cav2.2 blockade in the dorsal horn without systemic toxicity.

Opioid-Independent Analgesia

Ziconotide produces analgesia entirely independently of opioid receptors. It does not cross-react with mu, delta, or kappa opioid receptors and does not cause opioid-type side effects (respiratory depression, constipation, sedation in usual doses). This mechanism-independence means ziconotide remains effective in opioid-tolerant patients and does not exhibit tolerance with continued use, unlike opioids. It can be combined with intrathecal opioids for additive analgesia.


Research Summary

Severe Chronic Pain (Approved)

Standard of Care

Pivotal trials showed ziconotide produced clinically meaningful pain reduction in cancer pain, AIDS-related pain, and neuropathic pain. Visual Analog Scale of Pain Intensity (VASPI) scores improved 14-53% versus 7-18% for placebo. Efficacy is maintained long-term without tolerance. International Neuromodulation Society guidelines recommend ziconotide as a first-line intrathecal analgesic option for appropriate patients.

Cancer and Neuropathic Pain

Clinical

Ziconotide is particularly valuable in cancer pain with significant neuropathic component where high-dose opioids cause intolerable side effects or hyperalgesia. In failed back surgery syndrome with radiculopathy, ziconotide provides analgesia where spinal mechanisms are dysfunctional. Long-term follow-up (>1 year) studies confirm sustained efficacy without dose escalation, a major advantage over opioid pumps.

Pain Neurobiology Research

Research Tool

Omega-conotoxins including ziconotide are invaluable research tools for dissecting the role of Cav2.2 channels in pain processing, synaptic transmission, and neuronal excitability. They have revealed that N-type channels are the primary Ca2+ entry pathway for nociceptive neurotransmitter release, established target validation for Cav2.2 as a pain target, and inspired development of oral N-type channel blockers and state-dependent inhibitors.


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Research Protocols

GoalDoseFrequencyRoute
Chronic pain (IT pump)Start 0.1 mcg/h IT; titrate by no more than 2.4 mcg/day q2-7 daysContinuous IT infusion; titrate slowly over weeks to monthsIT via implanted programmable pump
Research (spinal cord preparation)0.1-100 nM in perfusion solutionContinuous perfusion during electrophysiology recordingSpinal superfusion (in vitro/in vivo)

Ziconotide requires very slow titration to minimize CNS adverse effects. Do not use IV, IM, or epidurally, intrathecal only. Psychiatric pre-screening required (contraindicated with psychosis or history of psychosis).


Interactions

Additive analgesia
Intrathecal opioids
Can be combined in intrathecal pump for additive pain relief; non-overlapping mechanisms
Additive sedation
CNS depressants
Ziconotide CNS side effects (dizziness, confusion, somnolence) additive with other CNS depressants
Inhibits release
Substance P
Ziconotide blocks substance P release from dorsal horn afferents, part of its analgesic mechanism
Inhibits release
CGRP
N-type channels mediate CGRP release from dorsal horn; ziconotide reduces this signaling

Safety Profile

Ziconotide's narrow therapeutic window and CNS side effects are its primary limitations. Common adverse effects: dizziness, nausea, confusion, abnormal gait, headache, memory impairment. Severe psychiatric adverse effects (psychosis, hallucinations, depression, suicidal ideation) occur in 3-5% of patients, psychiatric contraindications must be screened. Meningitis risk from intrathecal catheter. CK elevation (rhabdomyolysis-like) reported with high doses. Overdose causes cardiovascular and CNS toxicity requiring pump cessation. These risks require specialized pain management teams experienced with intrathecal therapy.


References

  • [1]Staats PS, et al. Intrathecal ziconotide in the treatment of refractory pain in patients with cancer or AIDS. JAMA. 2004;291:63-70.
  • [2]Atanassoff PG, et al. Ziconotide, a new N-type calcium channel blocker. Reg Anesth Pain Med. 2000.
  • [3]Rauck RL, et al. A randomized, double-blind, placebo-controlled study of intrathecal ziconotide in adults with severe chronic pain. J Pain Symptom Manage. 2006.
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Verified Scientific Data Last audited:
Data Sources & External References
Source: peer-reviewed literature  ·  Domain: ascendpeptide.org

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