Ziconotide

Identification

Summary

Ziconotide is an N-type calcium channel antagonist used to manage patients with severe chronic pain who cannot tolerate, or who have not responded adequately to other treatments such as intrathecal morphine and systemic analgesics.

Brand Names

Prialt

Generic Name

Ziconotide

DrugBank Accession Number

DB06283

Background

Ziconotide (also known as SNX-111) is a neurotoxic peptide derived from the cone snail Conus magus comprising 25 amino acids with three disulphide bonds.^7,18 Other such peptides, collectively termed conotoxins, exist, and some have shown efficacy in binding specific subsets of calcium channels; ziconotide is used in part because it can be synthesized without loss of proper bond formation or structural elements.^5,6 Ziconotide is used to manage severe chronic pain refractory to other methods, through its ability to inhibit N-type calcium channels involved in nociceptive signalling.^{5,7,8,9,12,14,18}

Ziconotide was granted FDA approval on December 28, 2004 for marketing by TerSera therapeutics LLC. under the name Prialt.¹⁸ To date, ziconotide is the only calcium channel blocking peptide approved for use by the FDA.⁷

Type

Small Molecule

Groups

Approved

Structure

Similar Structures

Weight: Average: 2639.14
Monoisotopic: 2637.09833574
Chemical Formula: C₁₀₂H₁₇₂N₃₆O₃₂S₇

Synonyms

Ziconotida
Ziconotide

External IDs

SNX-111

Pharmacology

Indication

Ziconotide is indicated for the management of severe chronic pain in patients refractory to other treatments, and for whom intrathecal therapy is warranted.¹⁸

Reduce drug development failure rates

Build, train, & validate machine-learning models
with evidence-based and structured datasets.

See how

Build, train, & validate predictive machine-learning models with structured datasets.

See how

Associated Conditions

Severe, Chronic Pain

Contraindications & Blackbox Warnings

Avoid life-threatening adverse drug events

Improve clinical decision support with information on contraindications & blackbox warnings, population restrictions, harmful risks, & more.

Learn more

Avoid life-threatening adverse drug events & improve clinical decision support.

Learn more

Pharmacodynamics

Ziconotide inhibits N-type calcium channels involved in nociceptive signalling, primarily in the dorsal horn of the spinal cord.^{5,7,8,9,12,14,18} Although binding is reversible, careful dosing is required to ensure therapeutic effects while minimizing adverse effects, and ziconotide has been described as possessing a narrow therapeutic window.^13,18 Patients taking ziconontide may experience cognitive and neuropsychiatric symptoms, reduced levels of consciousness, and elevated serum creatine kinase levels. In addition, ziconotide may increase the risk of infection, including serious cases of meningitis. Patients who withdraw from opiates for ziconotide initiation are advised to taper off the dose.¹⁸

Mechanism of action

Nociceptive pain signalling is a complex processing pathway involving peripheral nociceptors, primary afferent nerve fibres, and downstream CNS neurons located in the spinal cord.^8,14 Voltage-gated calcium channels (VGCCs) are important regulatory components of neural signalling and include the N-type (Cav2.2) heteromultimeric high-voltage type calcium channels.¹⁰ Chronic pain conditions, including inflammatory and neuropathic pain, often involve the aberrant upregulation of VGCC activity through various cellular mechanisms, which can lead to allodynia and hyperalgesia.¹⁴

Specifically, N-type channel activation in lightly myelinated Aδ- and C-fibres is known to mediate the release of neurotransmitters substance P (SP), calcitonin gene-related peptide (CGRP), and glutamate, which influence downstream neural activation and pain perception.^{8,14,15,16,17} In addition, SP and CGRP induce inflammation, potentially exacerbating pre-existing inflammatory chronic pain.¹⁴

Ziconotide belongs to the ω-conotoxin class of neurotoxic peptides derived from the cone snail Conus magus which are capable of inhibiting N-type VGCCs.^4,5,7,9,18 Although the exact mechanism is yet to be elucidated, it is thought that ω-conotoxins function through direct occlusion of the ion pore to prevent calcium translocation across the membrane.⁹ Additional studies involving expression of chimeric subunits and molecular modelling suggest that insertion of the ziconotide Met¹² residue into a hydrophobic pocket formed by Ile³⁰⁰, Phe³⁰², and Leu³⁰⁵ of Cav2.2 increases binding and may be associated with toxic adverse effects.¹¹

Target	Actions	Organism
AVoltage-dependent N-type calcium channel subunit alpha-1B	inhibitor	Humans
NVoltage-dependent P/Q-type calcium channel subunit alpha-1A	inhibitor	Humans

Absorption

Ziconotide administered intrathecally over one hour in doses between 1 and 10 mcg produced calculated AUC values between 83.6-608 ng*h/mL and C_max between 16.4-132 ng/mL; these values are approximately dose-proportional. Given the intrathecal administration and low membrane permeability due to its size, ziconotide is expected to remain primarily in the CSF; plasma levels, where detected, remain constant up to nine months following administration.¹⁸

Volume of distribution

In patients administered 1-10 mcg intrathecal ziconotide over one hour, the apparent volume of distribution was calculated as 155 ± 263 mL; this value is roughly equivalent to the expected CSF volume.¹⁸ Although intravenous administration is not indicated, intravenous administration of between 0.3-10 mcg/kg/day ziconotide resulted in an apparent volume of distribution of 30,460 ± 6366 mL.¹⁸

Protein binding

Ziconotide is roughly 50% bound to human plasma proteins.¹⁸

Metabolism

Ziconotide is expected to be processed by various peptidases upon entering systemic circulation; no detailed information on ziconotide metabolism has been reported.¹⁸

Route of elimination

A small fraction of intravenous ziconotide (< 1%) is recovered in urine.¹⁸

Half-life

In patients administered 1-10 mcg intrathecal ziconotide over one hour, the elimination half-life was calculated as 4.6 ± 0.9 hr. Although intravenous administration is not indicated, intravenous administration of between 0.3-10 mcg/kg/day ziconotide resulted in an elimination half-life of 1.3 ± 0.3 hr.¹⁸

Clearance

Ziconotide CSF clearance is 0.38 ± 0.56 mL/min while plasma clearance is 270 ± 44 mL/min.¹⁸

Adverse Effects

Improve decision support & research outcomes

With structured adverse effects data, including: blackbox warnings, adverse reactions, warning & precautions, & incidence rates.

Learn more

Improve decision support & research outcomes with our structured adverse effects data.

Learn more

Toxicity

Symptoms of overdose include neurological effects such as ataxia, nystagmus, stupor, sedation, speech difficulties, dizziness, nausea, and vomiting, and may also cause other effects such as hypotension; overdose is not associated with respiratory depression. In case of overdose, symptom-related supportive care up to and including hospitalization is recommended. Ziconotide has no known antidote, but the withdrawal of ziconotide generally allows patients to clear the drug and recover within 24 hours. As ziconotide does not bind to opiate receptors, opioid antagonists are not effective at ameliorating overdose effects.¹⁸

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Not Available

Interactions

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

Drug	Interaction
Integrate drug-drug interactions in your software
1,2-Benzodiazepine	The risk or severity of CNS depression can be increased when Ziconotide is combined with 1,2-Benzodiazepine.
Acarbose	The risk or severity of hypoglycemia can be increased when Ziconotide is combined with Acarbose.
Acebutolol	Acebutolol may increase the arrhythmogenic activities of Ziconotide.
Acetazolamide	The risk or severity of CNS depression can be increased when Acetazolamide is combined with Ziconotide.
Acetohexamide	The risk or severity of hypoglycemia can be increased when Ziconotide is combined with Acetohexamide.
Acetophenazine	The risk or severity of CNS depression can be increased when Acetophenazine is combined with Ziconotide.
Acetyldigitoxin	Acetyldigitoxin may increase the arrhythmogenic activities of Ziconotide.
Adenosine	Adenosine may increase the arrhythmogenic activities of Ziconotide.
Agomelatine	The risk or severity of CNS depression can be increased when Ziconotide is combined with Agomelatine.
Ajmaline	Ajmaline may increase the arrhythmogenic activities of Ziconotide.

Identify potential medication risks

Easily compare up to 40 drugs with our drug interaction checker.

Get severity rating, description, and management advice.

Learn more

Food Interactions

Avoid excessive or chronic alcohol consumption. Ingesting alcohol may increase the CNS depressive effects of ziconotide.

Products

Drug product information from 10+ global regions

Our datasets provide approved product information including:
dosage, form, labeller, route of administration, and marketing period.

Access now

Access drug product information from over 10 global regions.

Access now

Product Ingredients

Ingredient	UNII	CAS	InChI Key
Ziconotide acetate	T2I226K69M	914454-03-8	Not applicable

Brand Name Prescription Products

Name	Dosage	Strength	Route	Labeller	Marketing Start	Marketing End
Prialt	Injection, solution	25 ug/1mL	Intrathecal	Elan Pharmaceuticals	2004-12-28	2012-01-01
Prialt	Injection, solution	100 ug/1mL	Intrathecal	Jazz Pharmaceuticals, Inc.	2004-12-28	2022-08-31
Prialt	Injection, solution	100 ug/1mL	Intrathecal	Jazz Pharmaceuticals, Inc.	2004-12-28	2022-09-30
Prialt	Injection, solution	100 μg/ml	Intrathecal	Esteve Pharmaceuticals Gmb H	2016-09-08	Not applicable
Prialt	Injection, solution	100 ug/1mL	Intrathecal	Elan Pharmaceuticals	2004-12-28	2013-04-01
Prialt	Injection, solution	100 ug/1mL	Intrathecal	Tersera Therapeutics Llc	2018-10-15	Not applicable
Prialt	Injection, solution	25 μg/ml	Intrathecal	Esteve Pharmaceuticals Gmb H	2016-09-08	Not applicable
Prialt	Injection, solution	25 ug/1mL	Intrathecal	Jazz Pharmaceuticals, Inc.	2004-12-28	2022-07-31
Prialt	Injection, solution	100 μg/ml	Intrathecal	Esteve Pharmaceuticals Gmb H	2016-09-08	Not applicable
Prialt	Injection, solution	100 ug/1mL	Intrathecal	Elan Pharmaceuticals	2004-12-28	2013-04-01

Chemical Identifiers

UNII: 7I64C51O16
CAS number: 107452-89-1
InChI Key: BPKIMPVREBSLAJ-QTBYCLKRSA-N
InChI: InChI=1S/C102H172N36O32S7/c1-50(2)34-63-91(161)127-62(26-33-171-5)90(160)129-64(35-53-22-24-54(143)25-23-53)92(162)130-65(36-78(148)149)93(163)135-72-48-175-173-45-69(80(108)150)133-86(156)58(18-8-12-29-105)121-76(146)39-117-85(155)66(41-139)131-88(158)61(21-15-32-114-102(111)112)126-96(166)70-46-176-177-47-71(97(167)132-68(43-141)95(165)125-60(87(157)128-63)20-14-31-113-101(109)110)134-89(159)59(19-9-13-30-106)123-81(151)51(3)119-74(144)37-115-83(153)56(16-6-10-27-103)120-75(145)38-116-84(154)57(17-7-11-28-104)124-82(152)55(107)44-172-174-49-73(137-98(72)168)99(169)138-79(52(4)142)100(170)118-40-77(147)122-67(42-140)94(164)136-70/h22-25,50-52,55-73,79,139-143H,6-21,26-49,103-107H2,1-5H3,(H2,108,150)(H,115,153)(H,116,154)(H,117,155)(H,118,170)(H,119,144)(H,120,145)(H,121,146)(H,122,147)(H,123,151)(H,124,152)(H,125,165)(H,126,166)(H,127,161)(H,128,157)(H,129,160)(H,130,162)(H,131,158)(H,132,167)(H,133,156)(H,134,159)(H,135,163)(H,136,164)(H,137,168)(H,138,169)(H,148,149)(H4,109,110,113)(H4,111,112,114)/t51-,52+,55-,56-,57-,58-,59-,60-,61-,62-,63-,64-,65-,66-,67-,68-,69-,70-,71-,72-,73-,79-/m0/s1
IUPAC Name: 2-[(1R,4S,7S,13S,16R,21R,24S,27S,30S,33S,36S,39S,42R,45S,48S,54S,60S,63R,68R,71S,77S)-63-amino-13,45,54,60-tetrakis(4-aminobutyl)-4,36-bis(3-carbamimidamidopropyl)-16-carbamoyl-71-[(1R)-1-hydroxyethyl]-7,39,77-tris(hydroxymethyl)-27-[(4-hydroxyphenyl)methyl]-48-methyl-33-(2-methylpropyl)-30-[2-(methylsulfanyl)ethyl]-2,5,8,11,14,23,26,29,32,35,38,41,44,47,50,53,56,59,62,69,72,75,78,85-tetracosaoxo-18,19,65,66,81,82-hexathia-3,6,9,12,15,22,25,28,31,34,37,40,43,46,49,52,55,58,61,70,73,76,79,84-tetracosaazatricyclo[40.37.4.2^{21,68}]pentaoctacontan-24-yl]acetic acid
SMILES: [H][C@]12CSSC[C@]3([H])NC(=O)[C@H](CCCCN)NC(=O)[C@H](C)NC(=O)CNC(=O)[C@H](CCCCN)NC(=O)CNC(=O)[C@H](CCCCN)NC(=O)[C@@H](N)CSSC[C@]([H])(NC(=O)[C@]([H])(CSSC[C@H](NC(=O)[C@H](CCCCN)NC(=O)CNC(=O)[C@H](CO)NC(=O)[C@H](CCCNC(N)=N)NC1=O)C(N)=O)NC(=O)[C@H](CC(O)=O)NC(=O)[C@H](CC1=CC=C(O)C=C1)NC(=O)[C@H](CCSC)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CCCNC(N)=N)NC(=O)[C@H](CO)NC3=O)C(=O)N[C@@]([H])([C@@H](C)O)C(=O)NCC(=O)N[C@@H](CO)C(=O)N2

References

Synthesis Reference

Avi Tovi, Chaim Eidelman, Shimon Shushan, Shai Elster, Alon Hagi, Alexander Ivchenko, Gabriel-Marcus Butilca, Gil Zaoui, Eleonora Alterman, Leah Bar-Oz, Tehila Gadi. "Methods for the production of peptide having a c-terminal amide." Patent WO2006119388A2, issued November 09, 2006.

General References

Skov MJ, Beck JC, de Kater AW, Shopp GM: Nonclinical safety of ziconotide: an intrathecal analgesic of a new pharmaceutical class. Int J Toxicol. 2007 Sep-Oct;26(5):411-21. [Article]
Miljanich GP: Ziconotide: neuronal calcium channel blocker for treating severe chronic pain. Curr Med Chem. 2004 Dec;11(23):3029-40. [Article]
McGivern JG: Ziconotide: a review of its pharmacology and use in the treatment of pain. Neuropsychiatr Dis Treat. 2007 Feb;3(1):69-85. [Article]
Olivera BM, Gray WR, Zeikus R, McIntosh JM, Varga J, Rivier J, de Santos V, Cruz LJ: Peptide neurotoxins from fish-hunting cone snails. Science. 1985 Dec 20;230(4732):1338-43. doi: 10.1126/science.4071055. [Article]
Olivera BM, Cruz LJ, de Santos V, LeCheminant GW, Griffin D, Zeikus R, McIntosh JM, Galyean R, Varga J, Gray WR, et al.: Neuronal calcium channel antagonists. Discrimination between calcium channel subtypes using omega-conotoxin from Conus magus venom. Biochemistry. 1987 Apr 21;26(8):2086-90. doi: 10.1021/bi00382a004. [Article]
Valentino K, Newcomb R, Gadbois T, Singh T, Bowersox S, Bitner S, Justice A, Yamashiro D, Hoffman BB, Ciaranello R, et al.: A selective N-type calcium channel antagonist protects against neuronal loss after global cerebral ischemia. Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7894-7. doi: 10.1073/pnas.90.16.7894. [Article]
Bourinet E, Zamponi GW: Block of voltage-gated calcium channels by peptide toxins. Neuropharmacology. 2017 Dec;127:109-115. doi: 10.1016/j.neuropharm.2016.10.016. Epub 2016 Oct 15. [Article]
Park J, Luo ZD: Calcium channel functions in pain processing. Channels (Austin). 2010 Nov-Dec;4(6):510-7. doi: 10.4161/chan.4.6.12869. Epub 2010 Nov 1. [Article]
Patel R, Montagut-Bordas C, Dickenson AH: Calcium channel modulation as a target in chronic pain control. Br J Pharmacol. 2018 Jun;175(12):2173-2184. doi: 10.1111/bph.13789. Epub 2017 Apr 26. [Article]
Simms BA, Zamponi GW: Neuronal voltage-gated calcium channels: structure, function, and dysfunction. Neuron. 2014 Apr 2;82(1):24-45. doi: 10.1016/j.neuron.2014.03.016. [Article]
Wang F, Yan Z, Liu Z, Wang S, Wu Q, Yu S, Ding J, Dai Q: Molecular basis of toxicity of N-type calcium channel inhibitor MVIIA. Neuropharmacology. 2016 Feb;101:137-45. doi: 10.1016/j.neuropharm.2015.08.047. Epub 2015 Sep 4. [Article]
Deer TR, Pope JE, Hanes MC, McDowell GC: Intrathecal Therapy for Chronic Pain: A Review of Morphine and Ziconotide as Firstline Options. Pain Med. 2019 Apr 1;20(4):784-798. doi: 10.1093/pm/pny132. [Article]
Sanford M: Intrathecal ziconotide: a review of its use in patients with chronic pain refractory to other systemic or intrathecal analgesics. CNS Drugs. 2013 Nov;27(11):989-1002. doi: 10.1007/s40263-013-0107-5. [Article]
Bourinet E, Altier C, Hildebrand ME, Trang T, Salter MW, Zamponi GW: Calcium-permeable ion channels in pain signaling. Physiol Rev. 2014 Jan;94(1):81-140. doi: 10.1152/physrev.00023.2013. [Article]
Evans AR, Nicol GD, Vasko MR: Differential regulation of evoked peptide release by voltage-sensitive calcium channels in rat sensory neurons. Brain Res. 1996 Mar 18;712(2):265-73. doi: 10.1016/0006-8993(95)01447-0. [Article]
Maggi CA, Tramontana M, Cecconi R, Santicioli P: Neurochemical evidence for the involvement of N-type calcium channels in transmitter secretion from peripheral endings of sensory nerves in guinea pigs. Neurosci Lett. 1990 Jul 3;114(2):203-6. doi: 10.1016/0304-3940(90)90072-h. [Article]
Smith MT, Cabot PJ, Ross FB, Robertson AD, Lewis RJ: The novel N-type calcium channel blocker, AM336, produces potent dose-dependent antinociception after intrathecal dosing in rats and inhibits substance P release in rat spinal cord slices. Pain. 2002 Mar;96(1-2):119-27. doi: 10.1016/s0304-3959(01)00436-5. [Article]
FDA Approved Drug Products: Prialt (ziconotide) solution [Link]

External Links

KEGG Drug: D06363
PubChem Substance: 347910345
ChemSpider: 17291932
RxNav: 68503
ChEMBL: CHEMBL4594214
Wikipedia: Ziconotide

Clinical Trials

Clinical Trials

Phase	Status	Purpose	Conditions	Count
4	Completed	Not Available	Peripheral neuropathy	1
4	Completed	Treatment	Neuropathic Pain	1
4	Withdrawn	Treatment	Painful Myelopathy / Painful Neuropathy	1
3	Completed	Treatment	Pain	2
2	Active Not Recruiting	Treatment	Cancer / Intractable Pain / Neuropathic Pain / Pain	1
2	Completed	Treatment	Cancer / Human Immunodeficiency Virus (HIV) Infections / Pain	1
Not Available	Completed	Not Available	Patients With Severe Chronic Pain	1
Not Available	Recruiting	Not Available	Refractory Pains	1

Pharmacoeconomics

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Form	Route	Strength
Injection, solution	Intrathecal	100 ug/1mL
Injection, solution	Intrathecal	100 μg/ml
Injection, solution	Intrathecal	100 MICROGRAMMI/ML
Injection, solution	Intrathecal	25 μg/ml
Injection, solution	Intrathecal	25 ug/1mL
Injection, solution	Intrathecal	25 MICROGRAMMI/ML

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)
US5859186	No	1999-01-12	2011-12-30
US5364842	No	1994-11-15	2016-12-30
US8653033	No	2014-02-18	2024-10-01
US8765680	No	2014-07-01	2024-10-01
US9707270	No	2017-07-18	2024-10-01

Properties

State

Solid

Experimental Properties

Not Available

Predicted Properties

Property	Value	Source
Water Solubility	2.36 mg/mL	ALOGPS
logP	-2	ALOGPS
logP	-23	Chemaxon
logS	-3	ALOGPS
pKa (Strongest Acidic)	3.41	Chemaxon
pKa (Strongest Basic)	12.18	Chemaxon
Physiological Charge	6	Chemaxon
Hydrogen Acceptor Count	43	Chemaxon
Hydrogen Donor Count	42	Chemaxon
Polar Surface Area	1133.84 Å²	Chemaxon
Rotatable Bond Count	38	Chemaxon
Refractivity	671.2 m³·mol^-1	Chemaxon
Polarizability	265.03 Å³	Chemaxon
Number of Rings	4	Chemaxon
Bioavailability	0	Chemaxon
Rule of Five	No	Chemaxon
Ghose Filter	No	Chemaxon
Veber's Rule	No	Chemaxon
MDDR-like Rule	Yes	Chemaxon

Predicted ADMET Features

Not Available

Spectra

Mass Spec (NIST): Not Available
Spectra: Not Available

Targets

Build, predict & validate machine-learning models

Use our structured and evidence-based datasets to unlock new
insights and accelerate drug research.

Learn more

Use our structured and evidence-based datasets to unlock new insights and accelerate drug research.

Learn more

Details1. Voltage-dependent N-type calcium channel subunit alpha-1B

Kind: Protein
Organism: Humans
Pharmacological action: Yes
Actions: Inhibitor

General Function: Voltage-gated calcium channel activity
Specific Function: Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hor...
Gene Name: CACNA1B
Uniprot ID: Q00975
Uniprot Name: Voltage-dependent N-type calcium channel subunit alpha-1B
Molecular Weight: 262493.84 Da

References

Olivera BM, Cruz LJ, de Santos V, LeCheminant GW, Griffin D, Zeikus R, McIntosh JM, Galyean R, Varga J, Gray WR, et al.: Neuronal calcium channel antagonists. Discrimination between calcium channel subtypes using omega-conotoxin from Conus magus venom. Biochemistry. 1987 Apr 21;26(8):2086-90. doi: 10.1021/bi00382a004. [Article]
Valentino K, Newcomb R, Gadbois T, Singh T, Bowersox S, Bitner S, Justice A, Yamashiro D, Hoffman BB, Ciaranello R, et al.: A selective N-type calcium channel antagonist protects against neuronal loss after global cerebral ischemia. Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7894-7. doi: 10.1073/pnas.90.16.7894. [Article]
Bourinet E, Zamponi GW: Block of voltage-gated calcium channels by peptide toxins. Neuropharmacology. 2017 Dec;127:109-115. doi: 10.1016/j.neuropharm.2016.10.016. Epub 2016 Oct 15. [Article]
Park J, Luo ZD: Calcium channel functions in pain processing. Channels (Austin). 2010 Nov-Dec;4(6):510-7. doi: 10.4161/chan.4.6.12869. Epub 2010 Nov 1. [Article]
Patel R, Montagut-Bordas C, Dickenson AH: Calcium channel modulation as a target in chronic pain control. Br J Pharmacol. 2018 Jun;175(12):2173-2184. doi: 10.1111/bph.13789. Epub 2017 Apr 26. [Article]
Wang F, Yan Z, Liu Z, Wang S, Wu Q, Yu S, Ding J, Dai Q: Molecular basis of toxicity of N-type calcium channel inhibitor MVIIA. Neuropharmacology. 2016 Feb;101:137-45. doi: 10.1016/j.neuropharm.2015.08.047. Epub 2015 Sep 4. [Article]
Bourinet E, Altier C, Hildebrand ME, Trang T, Salter MW, Zamponi GW: Calcium-permeable ion channels in pain signaling. Physiol Rev. 2014 Jan;94(1):81-140. doi: 10.1152/physrev.00023.2013. [Article]
FDA Approved Drug Products: Prialt (ziconotide) solution [Link]

Details2. Voltage-dependent P/Q-type calcium channel subunit alpha-1A

Kind: Protein
Organism: Humans
Pharmacological action: No
Actions: Inhibitor
Curator comments: The reported inhibition was low, even at relatively high peptide concentrations; this interaction is unlikely to play a substantial role in vivo.

General Function: Voltage-gated calcium channel activity
Specific Function: Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hor...
Gene Name: CACNA1A
Uniprot ID: O00555
Uniprot Name: Voltage-dependent P/Q-type calcium channel subunit alpha-1A
Molecular Weight: 282362.39 Da

References

Wang F, Yan Z, Liu Z, Wang S, Wu Q, Yu S, Ding J, Dai Q: Molecular basis of toxicity of N-type calcium channel inhibitor MVIIA. Neuropharmacology. 2016 Feb;101:137-45. doi: 10.1016/j.neuropharm.2015.08.047. Epub 2015 Sep 4. [Article]

Drug created at March 19, 2008 16:21 / Updated at September 25, 2021 23:52

Ziconotide

Identification

Structure for Ziconotide (DB06283)

Pharmacology

Interactions

Products

Categories

Chemical Identifiers

References

Clinical Trials

Pharmacoeconomics

Properties

Spectra

Targets

References

References