omega-conotoxin-(conus-magus) and ziconotide

omega-conotoxin-(conus-magus) has been researched along with ziconotide* in 2 studies

Reviews

1 review(s) available for omega-conotoxin-(conus-magus) and ziconotide

ArticleYear
Bioactive Mimetics of Conotoxins and other Venom Peptides.
    Toxins, 2015, Oct-16, Volume: 7, Issue:10

    Ziconotide (Prialt®), a synthetic version of the peptide ω-conotoxin MVIIA found in the venom of a fish-hunting marine cone snail Conus magnus, is one of very few drugs effective in the treatment of intractable chronic pain. However, its intrathecal mode of delivery and narrow therapeutic window cause complications for patients. This review will summarize progress in the development of small molecule, non-peptidic mimics of Conotoxins and a small number of other venom peptides. This will include a description of how some of the initially designed mimics have been modified to improve their drug-like properties.

    Topics: Amino Acid Sequence; Animals; Calcium Channel Blockers; Calcium Channels, N-Type; Cell Line, Tumor; Humans; Models, Molecular; Molecular Sequence Data; Molecular Structure; Mollusk Venoms; omega-Conotoxins; Patch-Clamp Techniques; Peptidomimetics

2015

Other Studies

1 other study(ies) available for omega-conotoxin-(conus-magus) and ziconotide

ArticleYear
Cardiovascular effects of omega-conopeptides in conscious rats: mechanisms of action.
    Journal of cardiovascular pharmacology, 1992, Volume: 20, Issue:5

    We examined the effects of omega-conopeptides, a novel class of neuronal voltage-gated calcium channel antagonists, on hemodynamic responses in rats. Intravenous (i.v.) injections of SNX-111 (omega-conopeptide MVIIA) dose-dependently decreased arterial blood pressure (BP) in conscious rats. Intracerebroventricular (i.c.v.) SNX-111 injections (580 pmol) tended to increase BP and, after an initial decrease, to increase heart rate (HR). The dose-response curve for SNX-111 administered i.v. in conscious rats was biphasic. Beginning at subdepressor doses, SNX-111 caused a long-lasting blockade of pressor responses elicited by sympathetic nerve stimulation in pithed animals but did not prevent increases in BP evoked by exogenously administered norepinephrine (NE). Pretreatment of rats with histamine antagonists partially blocked the hypotensive effects of the higher (870 and 2,900 nmol/kg) doses of SNX-111. Substitution of alanine for arginine at position 10 ([Ala10]-MVIIA) markedly attenuated the histamine-mediated component of the vasodepressor response. Together, these findings indicate that SNX-111 administered i.v. decreases systemic BP by a combination of blockade of sympathetic neurotransmission and mast cell degranulation; the latter function appears to be dependent on the arginine residue in position 10 of the amino acid sequence of SNX-111.

    Topics: Amino Acid Sequence; Animals; Blood Pressure; Calcium Channel Blockers; Chlorpheniramine; Cimetidine; Decerebrate State; Dose-Response Relationship, Drug; Heart Rate; Injections, Intraventricular; Male; Molecular Sequence Data; Norepinephrine; omega-Conotoxins; Peptides; Peptides, Cyclic; Rats; Rats, Sprague-Dawley

1992