MVIIA

MVIIA, also known as ω-conotoxin MVIIA, is a peptide toxin produced in the venom of the marine cone snail Conus magus. It is one of several ω-conotoxins that target voltage-gated calcium channels. The peptide consists of roughly 25 amino acids and contains multiple cysteine residues that form disulfide bonds characteristic of conotoxins.

MVIIA binds with high affinity to N-type voltage-gated calcium channels (CaV2.2) on presynaptic terminals, blocking calcium entry that triggers neurotransmitter release. By reducing release of excitatory neurotransmitters such as glutamate and substance P in pain pathways, MVIIA yields potent analgesia in various models and contexts.

MVIIA is the active component of the drug ziconotide, marketed as Prialt. Ziconotide was approved by the U.S. Food and Drug Administration in 2004 for the treatment of severe chronic pain in adults who have inadequate response to other therapies. The drug is administered intrathecally, i.e., directly into the intrathecal space of the spinal cord, using an implanted pump.

Because MVIIA is a peptide, it is not orally active and does not cross the blood–brain barrier efficiently, requiring intrathecal delivery. The therapeutic window is narrow and adverse effects can be serious; common side effects include dizziness, confusion, cognitive impairment, mood changes, and hypotension. The drug requires careful dose titration and monitoring, and is generally reserved for patients who have failed other analgesics.

MVIIA and related conotoxins have contributed to the study of pain pathways and the development of other calcium-channel blockers, though MVIIA/ziconotide remains a specialized therapy rather than a broad analgesic.