Ziconotide Acetate Usages And Dosage

High Quality Ziconotide CAS:107452-89-1 Ziconotide Acetate Ziconotide Acetate In need in the throes of another for the treatment of severe chronic pain, nerve tissue is n-type calcium channel...
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High Quality Ziconotide CAS:107452-89-1 Ziconotide Acetate



Ziconotide Acetate In need in the throes of another for the treatment of severe chronic pain, nerve tissue is n-type calcium channel blockers.


Quick details of Ziconotide Acetate:

Product Name

Stock Ziconotide acetate CAS 107452-89-1

CAS No.

107452-89-1

Category

 API, peptide

Quality Standard

EP/USP

MFC102H172N36O32S7
MW2639.13

MSDS

Available

COA

Contact with me for updated version COA.

Sample

Available

MOQ

1g,1kg

Delivery Date

In 3 days

Place Of Origin

China

Application

Pharmaceutical raw materials

Packing : 1g/10g/50g100g/500g/1kg packed with Aluminum Foil Bag,Fluorinated Bottles,Glass Bottles,Plastic Bottles or as your special request. 

Remarks Our products are limited to scientific research and production use only .Our products will not be sold to countires and regions under administrative and patent protections.

 

What is Ziconotide Acetate?

Ziconotide (SNX-111; Prialt) is an atypical analgesic agent for the amelioration of severe and chronic pain. Derived from Conus magus, a cone snail, it is the synthetic form of an ω-conotoxin peptide.[1]

In December 2004 the Food and Drug Administration approved ziconotide when delivered as an infusion into the cerebrospinal fluid using an intrathecal pump system.


Ziconotide is a powerful analgesic drug that has a unique mechanism of action involving potent and selective block of N-type calcium channels, which control neurotransmission at many synapses. The analgesic efficacy of ziconotide likely results from its ability to interrupt pain signaling at the level of the spinal cord. Ziconotide is a peptidic drug and has been approved for the treatment of severe chronic pain in patients only when administered by the intrathecal route. Importantly, prolonged administration of ziconotide does not lead to the development of addiction or tolerance. The current review discusses the various studies that have addressed the in vitro biochemical and electrophysiological actions of ziconotide as well as the numerous pre-clinical studies that were conducted to elucidate its antinociceptive mechanism of action in animals. In addition, this review considers the pivotal Phase 3 (and other) clinical trials that were conducted in support of ziconotide's approval for the treatment of severe chronic pain and tries to offer some insights regarding the future discovery and development of newer analgesic drugs that would act by a similar mechanism to ziconotide but which might offer improved safety, tolerability and ease of use.


Application of Ziconotide Acetate:

Ziconotide's pharmacological effects have been investigated extensively in pre-clinical in vivo and in vitro models. Briefly, intrathecal ziconotide is a powerful antinociceptive drug in several animal models of chronic pain and it appears to have a completely novel mechanism of action that involves potent and selective block of pre-synaptic neuronal N-type calcium channels in the spinal cord. In fact, it is the only selective N-type channel blocker that is currently approved for clinical use. Evidence suggests that ziconotide delivers its antinociceptive efficacy by reducing the release of pronociceptive neurotransmitters in the dorsal horn of the spinal cord, thereby inhibiting pain signal transmission. Intrathecal ziconotide's clinical efficacy is consistent with the hypothesis that spinal N-type calcium channels are key regulators of nociceptive signaling in humans, although it is fair to say that its precise analgesic mechanism in humans remains unconfirmed at this time.


Future prospects and concluding remarks:

Ziconotide represents a great achievement for current pain therapy but despite its potent analgesic efficacy there remains significant opportunity for improvement. The opportunity derives primarily from the peptidic nature of the drug and its requirement for intrathecal administration in order to yield analgesic efficacy with reduced potential for systemic and central nervous system side-effects. Consequently, drug discovery researchers are considering various approaches to identify and develop novel orally active, N-type calcium channel-selective blockers that have the potential to be superior to ziconotide.


COA:


TEST ITEMSSPECIFICATIONS
AppearanceWhite  powder
Water Content(Karl Fischer)≤ 5.0%
Acetate Content(by HPLC)≤ 12.0%
Amino Acid Composition± 10% of theoretical
Purity(by HPLC)≥ 99.9%
Single Impurity(by HPLC)
 
≤ 1.0%
Peptide Content(by %N )≥ 80%
Assay(By Anhydrous, Acetic Acid-free )99~105.0%
Bacterial Endotoxins≤ 5EU/mg



Ziconotide Description:

Ziconotide has been described as a potent and long-lasting antinociceptive drug when administered by the intrathecal route. Experimental evidence of ziconotide's antinociceptive properties was first obtained in the early 1990s and since then extensive studies have been conducted to characterize its effects in multiple animal models of pain. It is also important to note that ziconotide can be efficacious under a variety of intrathecal dosing regimens, including single bolus injection and acute or chronic continuous infusion. Despite its potent efficacy, the therapeutic index of spinal ziconotide tends to be low and often its antinociceptive effects in animals are accompanied by motor deficits at higher doses. Although ziconotide does not easily cross the blood brain barrier in normal animals, it may cause hypotension if it enters the systemic circulation (Bowersox et al 1992; Wright et al 2000; Takahara et al 2002). This effect on blood pressure appears to be mediated at least partially by inhibition of sympathetic neurotransmission, probably as a result of N-type calcium channel blockade in sympathetic nerve terminals (Wang et al 1998).


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