omega conotoxin MVIIA - CAS 107452-89-1

omega conotoxin MVIIA - CAS 107452-89-1 Catalog number: BADC-00172

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ω conotoxin MVIIA (omega conotoxin MVIIA) has been isolated from the venom of the cone Conus magus. Omega-conotoxins act at presynaptic membranes, they bind and block voltage-sensitive calcium channels (VSCC).

ADCs Cytotoxin
Product Name
omega conotoxin MVIIA
Catalog Number
Molecular Formula
Molecular Weight
omega conotoxin MVIIA

Ordering Information

Catalog Number Size Price Quantity
BADC-00172 1 mg $598
ω conotoxin MVIIA (omega conotoxin MVIIA) has been isolated from the venom of the cone Conus magus. Omega-conotoxins act at presynaptic membranes, they bind and block voltage-sensitive calcium channels (VSCC).
Ziconotide; Prialt
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-methylsulfanylethyl)-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-tetracosazatricyclo[,68]pentaoctacontan-24-yl]acetic acid
Canonical SMILES
1.60±0.1 g/cm3(Predicted)
Soluble in water
Melting Point
>187°C (dec.)
Mechanism Of Action
Ziconotide/ is a N-type calcium channel blocker (NCCB). Voltage-sensitive calcium channel (VSCC) conduction plays a major role in the transmission of pain. The N-type VSCC's are found in high concentrations in the dorsal root ganglion cells responsible for the spinal processing of pain. Ziconotide selectively and reversibly binds to and blocks these channels without interacting with other ion channels or cholinergic, monoaminergic or mu and delta-opioid receptors. Ziconotide thus inhibits the spinal signalling of pain.
In Vitro
Nifedipine and omega-agatoxin IVA dose dependently (IC50 values of 10 nM and 0.7 nM, respectively) blocked most of the release, whereas omega-conotoxin MVIIA (IC50 = 5 nM) caused partial blockage.
In Vivo
In pithed rats, omega-conotoxin MVIIA preferentially suppressed the sympathetic nerve stimulation-induced pressor response, whereas cilnidipine suppressed the pressor response induced by sympathetic nerve stimulation and angiotensin II. In anesthetized rats, cilnidipine or omega-conotoxin MVIIA decreased mean blood pressure, while heart rate was decreased by omega-conotoxin MVIIA, but slightly increased by cilnidipine.
Clinical Trial Information
NCT NumberCondition Or DiseasePhaseStart DateSponsorStatus
NCT01373983Peripheral NeuropathyPhase 42014-12-30University Hospital, LinkoepingCompleted
NCT03321955Neuropathic PainPhase 42021-01-12Albany Medical CollegeCompleted
NCT01992562Painful MyelopathyPhase 42018-09-18Aaron BosterWithdrawn (Logistical issues with study process and recruitment)
NCT00996983PainPhase 22021-03-05National Cancer Institute, NaplesActive, not recruiting
NCT00002160HIV InfectionsPhase 22005-06-24NeurexCompleted
ADCs Cytotoxin
white powder.
Room temperature, or blue ice upon request.
Store at -20°C
1.Clinical Uses of Intrathecal Therapy and Its Placement in the Pain Care Algorithm.
Pope JE1, Deer TR2, Bruel BM3, Falowski S4. Pain Pract. 2016 Feb 23. doi: 10.1111/papr.12438. [Epub ahead of print]
Intrathecal drug delivery is an effective treatment option for patients with severe chronic pain who have not obtained adequate analgesia from more conservative therapies (eg, physical therapy, systemic opioids, nonsteroidal anti-inflammatory drugs, antidepressants, and anticonvulsants). This review focuses on, but is not limited to, the 2 agents currently approved by the U.S. Food and Drug Administration for intrathecal analgesia: preservative-free morphine and ziconotide (a nonopioid, selective N-type calcium channel blocker). We describe the appropriate use of intrathecal therapy in the management of severe chronic pain, based on current best practices. Topics addressed here include patient selection, trialing, dosing and titration, adverse event profiles, long-term management, intrathecal therapy for cancer-related pain, and the placement of intrathecal therapy in the pain care algorithm. In appropriately selected patients with chronic pain, intrathecal therapy can provide substantial pain relief with improved functioning and quality of life.
2.Intrathecal Ziconotide: Dosing and Administration Strategies in Patients With Refractory Chronic Pain.
McDowell GC 2nd1, Pope JE2. Neuromodulation. 2016 Feb 9. doi: 10.1111/ner.12392. [Epub ahead of print]
INTRODUCTION: Ziconotide is a non-opioid analgesic for intrathecal (IT) administration. The aim of this review is to provide a comprehensive and clinically relevant summary of the literature on dosing and administration with IT ziconotide in the management of refractory chronic pain, and to describe novel dosing strategies intended to improve clinical outcomes.
3.ZiconotideMonotherapy: A Systematic Review of Randomised Controlled Trials.
Brookes ME1, Eldabe S, Batterham A. Curr Neuropharmacol. 2016 Feb 10. [Epub ahead of print]
INTRODUCTION: Chronic neuropathic pain is difficult to treat and is often refractory to most modalities of treatment. Ziconotide is a novel, potent, non-opioid, calcium channel blocking agent which has been shown in clinical trials to be effective in treating chronic neuropathic pain.
4.Delivery of ziconotide to cerebrospinal fluid via intranasal pathway for the treatment of chronic pain.
Manda P1, Kushwaha AS1, Kundu S2, Shivakumar HN3, Jo SB1, Murthy SN4. J Control Release. 2016 Feb 28;224:69-76. doi: 10.1016/j.jconrel.2015.12.044. Epub 2015 Dec 28.
The purpose of the current study was to investigate the plausibility of delivery of ziconotide to the cerebrospinal fluid (CSF) via intranasal administration. Ziconotide was administered either in the form of solution or Kolliphor P 407 gels (KP 407) intranasally in Sprague-Dawley rats. The effect of incorporation of chitosan in the formulation was also investigated. Time course of drug in the CSF was investigated by collecting CSF from cisterna magna. Pharmacokinetics of ziconotide in CSF following intrathecal and intravenous (i.v.) administration of ziconotide was investigated. Upon intrathecal administration the elimination rate constant of ziconotide in CSF was found to be 1.01±0.34h(-1). The Cmax and Tmax of ziconotide in CSF following intravenous administration were found to be 37.78±6.8ng/mL and ~2h respectively. The time required to attain maximum concentration (Tmax) in CSF was less upon intranasal administration (15min) compared to i.

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