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omega conotoxin MVIIA - CAS 107452-89-1

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Category
ADCs
Product Name
omega conotoxin MVIIA
Catalog Number
107452-89-1
CAS Number
107452-89-1
Description
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).
Molecular Weight
2639.2
Molecular Formula
C102H172N36O32S7
COA
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MSDS
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Tag
ADCs Cytotoxin
Structure
CAS 107452-89-1 omega conotoxin MVIIA
Specification
Purity
97% (HPLC)
Appearance
white powder.
Application
ADCs Cytotoxin
Storage
stable in freeze-dried state. In solution, keep at -20 °C.
Solubility
water, saline.
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Reference Reading
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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