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Ziconotide Tablet
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Ziconotide Tablet

Ziconotide Tablet

1.General Specification(in stock)
(1)API(Pure Powder)
(2)Injection
(3)Tablet
2.Customization:
We will negotiate individually, OEM/ODM, No brand, for secience researching only.
Internal Code: BM-2-152
Ziconotide CAS 107452-89-1
Manufacturer: BLOOM TECH Wuxi Factory
Analysis: HPLC, LC-MS, HNMR
Main market: USA, Australia, Brazil, Japan, Germany, Indonesia, UK, New Zealand , Canada etc.
Technology support: R&D Dept.-4

Shaanxi BLOOM Tech Co., Ltd. is one of the most experienced manufacturers and suppliers of ziconotide tablet in China. Welcome to wholesale bulk high quality ziconotide tablet for sale here from our factory. Good service and reasonable price are available.

 

As a prescription drug, ziconotide tablet (snx111) is currently indicated clinically for patients with severe chronic neuropathic ache who require intrathecal therapy and are intolerant to or have an inadequate response to other analgesic treatments (e.g., systemic analgesics, intrathecal morphine). At present, the oral tablet formulation remains under research or clinical investigation; however, multiple clinical studies have confirmed its efficacy and safety in the management of severe neuropathic ache. 

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Method of Analysis

ziconotide/Ziconotide Polyacetate COA 

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Applications-

 

Application in Severe Neuropathic Pain

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Neuropathic pain is a chronic ache condition caused by lesions or diseases of the somatosensory nervous system. Its pathogenesis is complex, and clinical manifestations commonly include burning, stabbing, and electric‑shock‑like ache, which severely impair patients' quality of life. Severe neuropathic ache encompasses various subtypes, such as postherpetic neuralgia (PHN), painful diabetic peripheral neuropathy, central ache following spinal cord injury, central post‑stroke ache, radiculopathy, and refractory ache associated with spinal stenosis.

Such ache responds poorly to conventional analgesics (e.g., nonsteroidal anti‑inflammatory drugs, opioids), and patients often face challenges including poorly controlled ache and poor tolerability of adverse reactions. As a novel non‑opioid analgesic with a unique mechanism of action, ziconotide tablet provides a new therapeutic option for severe neuropathic ache.

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2.1 Application in Postherpetic Neuralgia (PHN)

Postherpetic neuralgia (PHN) is the most common complication of herpes zoster, defined as severe neuropathic ache that persists or recurs in the affected area for more than 3 months after rash resolution. It severely disrupts patients' sleep, mood, and daily activities. The pathogenesis of PHN is primarily related to nerve injury, neuroinflammation, and central sensitization following varicella‑zoster virus infection. Conventional medications (e.g., gabapentin, pregabalin, opioids) yield unsatisfactory outcomes in some patients, especially elderly individuals or those with comorbidities, who often experience poor tolerability of adverse effects and inadequate pain control.

By blocking N‑type calcium channels in the dorsal horn of the spinal cord, it inhibits ache signal transmission and effectively relieves symptoms such as burning and stabbing ache in PHN patients. A 12‑week multicenter randomized controlled trial demonstrated that in patients with moderate‑to‑severe PHN refractory to conventional analgesics, treatment with it resulted in a significant reduction in visual analogue scale (VAS) ache scores compared with baseline, with a ache relief rate exceeding 60%, along with marked improvements in sleep quality and emotional state.

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Information source: PMC A comprehensive review on Snx111; ClinicalTrials.gov Study Details | NCT04321408 | OP2C: Prialt® Observatory in Clinical Practice.

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2.2 Application in Painful Diabetic Peripheral Neuropathy

Painful diabetic peripheral neuropathy is one of the most common chronic complications of diabetes and belongs to peripheral neuropathic ache. It mainly presents as symmetric ache in the distal extremities (e.g., hands and feet), accompanied by numbness, hypoesthesia, and burning sensations. Ache severity worsens progressively with disease progression, severely compromising patients' quality of life. Its pathogenesis involves nerve metabolic disturbances, oxidative stress, neuroinflammation, and nerve fiber damage induced by chronic hyperglycemia.

Conventional management focuses on glycemic control, neurotrophic therapy, and the use of anticonvulsants, antidepressants, and opioids. However, ache control is suboptimal in some patients, and long‑term opioid use carries risks of tolerance and dependence.

Targeting the pathogenesis of painful diabetic peripheral neuropathy, it blocks N‑type calcium channels to suppress ache signal transmission, thereby effectively alleviating extremity ache. A clinical study enrolling 200 patients with moderate‑to‑severe painful diabetic peripheral neuropathy showed that 8 weeks of ziconotide tablet treatment significantly reduced VAS scores, with a ache relief rate of 58.5%, and also partially improved paresthesia and numbness.

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Information source: China Medical Information Query Platform Snx111; Research Progress in Symptomatic Pharmacotherapy for Painful Diabetic Peripheral Neuropathy (review); PMC A comprehensive review on Snx111.

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2.3 Application in Central Pain Following Spinal Cord Injury

Central ache following spinal cord injury is a common complication of spinal cord injury and a subtype of central neuropathic ache. It manifests as persistent or paroxysmal ache below the level of injury, typically described as burning, electric‑shock‑like, or numbness ache. It is severe, poorly responsive to conventional analgesics, and severely impairs rehabilitation and quality of life. Its pathogenesis is mainly associated with central nervous system remodeling, neurotransmitter imbalance, central sensitization, and overactivation of N‑type calcium channels after spinal cord injury, representing a clinically challenging form of neuropathic ache.

As an N‑type calcium channel blocker, it is an important agent for central ache following spinal cord injury. Multiple clinical studies have confirmed its efficacy in relieving ache and improving quality of life in affected patients. A cohort study included 20 patients with central ache following spinal cord injury refractory to standard pharmacotherapy, who received test intrathecal snx111 (clinical data for oral tablets may be extrapolated from intrathecal administration).

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Ache scores decreased by more than 40% in 14 patients, and 11 underwent permanent pump implantation. After a mean follow‑up of 3.59 years, 8 patients maintained pain scores below threshold levels, with baseline VAS scores decreasing from 7.91 to 4.31 at the last follow‑up and a mean daily dose of 7.2 μg, without significant long‑term adverse events. Furthermore, it does not interfere with motor function recovery or exacerbate nerve injury in spinal cord injury patients, supporting its long‑term use.

Information source: PubMed Snx111 for spinal cord injury‑related pain; Hunan Pharmaceutical Affairs Service Network Snx111; PMC A comprehensive review on Snx111.

2.4 Application in Central Post‑Stroke Pain (CPSP)

Central post‑stroke ache (CPSP) is a neuropathic ache syndrome occurring after stroke, classified as central neuropathic ache. Its incidence ranges from 1% to 12%, and up to 25% in patients with lateral medullary infarction. It presents as ache or paresthesia in body regions corresponding to stroke lesions, often burning, aching, or stabbing, occurring spontaneously or triggered by external stimuli.

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It is persistent and shows limited response to conventional analgesics (e.g., gabapentin, pregabalin), severely hindering rehabilitation and quality of life. Its pathogenesis is not fully elucidated but may involve hyperexcitability of damaged sensory pathways, impaired central inhibitory pathways, central sensitization, and altered function of the corticothalamic tract.By blocking N‑type calcium channels in the spinal dorsal horn, ziconotide tablet inhibits central transmission of ache signals and effectively relieves pain in CPSP patients.

Clinical studies indicate that in CPSP patients unresponsive to conventional anticonvulsants and antidepressants, it treatment significantly reduces pain scores, with a pain relief rate exceeding 50%, and markedly improves mood and sleep quality. Compared with opioids, it does not cause respiratory depression or sedation, making it more suitable for long‑term use in stroke patients, especially those with respiratory comorbidities or cognitive impairment. 

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Information source: Advances in Diagnosis and Management of Central Post‑Stroke Pain; Diagnostic Evaluation and Treatment of Central Post‑Stroke Pain.

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2.5 Application in Refractory Pain Associated with Radiculopathy and Spinal Stenosis

Refractory ache related to radiculopathy and spinal stenosis is a common chronic neuropathic ache condition caused by nerve root compression, inflammation, or injury. It presents with radiating extremity ache, numbness, weakness, and severe ache intensity. Conventional treatments (e.g., nonsteroidal anti‑inflammatory drugs, physical therapy, nerve root blocks) often yield unsatisfactory results, and some patients require surgery yet may still experience residual ache, severely impairing quality of life.

Its pathogenesis is associated with nerve root edema, inflammatory responses, abnormal neurotransmitter release, and N‑type calcium channel activation following compression.As a potent non‑opioid analgesic, it effectively relieves ache in patients with refractory radiculopathy‑ and spinal stenosis‑related ache, offering a new therapeutic option for those intolerant to or unresponsive to surgery. Clinical studies show that it treatment significantly alleviates radiating ache and numbness, reduces VAS scores by more than 40% from baseline, and provides long‑lasting ache relief, improving patients' ability to perform daily activities. Unlike opioids, it does not induce tolerance, dependence, constipation, or respiratory depression, supporting long‑term administration. Furthermore, combination with nerve root block therapy produces synergistic analgesia, reducing the frequency of blocks and treatment costs.

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Information source: BMJ Best Practice Painful Radicular Disorders Due to Disc Compression; Haute Autorité de Santé PRIALT (Snx111) – Douleur chronique.

Cellular Signaling Mechanisms of Downstream Neurotransmitters and Synaptic Plasticity

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Targeted Blockade Mechanism of Upstream Calcium Signaling Pathway

The upstream initiating mechanism at the cellular signaling level constitutes the fundamental basis for snx111 action. Under physiological conditions, peripheral nociceptive stimuli activate primary afferent neurons, trigger membrane depolarization, and facilitate the opening of presynaptic Cav2.2 channels, allowing calcium influx along the concentration gradient. As a vital second messenger, calcium activates the SNARE signaling complex associated with presynaptic vesicle fusion, mediating vesicle docking, fusion and neurotransmitter release to accomplish synaptic transmission of pain signals.

Snx111 specifically binds to the extracellular domain of Cav2.2 channels and blocks voltage-dependent channel opening, thereby completely inhibiting nociception-evoked calcium influx and cutting off downstream signaling cascades at the source. This serves as the essential prerequisite for its regulation of neurotransmitter release.

Regulatory Mechanism of Downstream Pain-Related Neurotransmitters

At the level of downstream neurotransmitter modulation, snx111 mainly suppresses the release of three categories of pronociceptive neurotransmitters to precisely block pain signal transmission.

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First, glutamate. As the predominant excitatory neurotransmitter in the spinal dorsal horn, released glutamate activates postsynaptic AMPA and NMDA receptors to rapidly mediate fast pain signaling and initiate downstream plasticity-related signaling. Following calcium influx blockade by snx111, vesicular glutamate release is markedly reduced, which directly attenuates excitatory postsynaptic potentials in spinal dorsal horn neurons.

Second, substance P and calcitonin gene-related peptide (CGRP). These two transmitters primarily mediate slow pain and hyperalgesia. They activate postsynaptic neurokinin receptors and CGRP receptors to trigger sustained neuronal depolarization.

Drug intervention significantly inhibits the release of both transmitters and halts persistent amplification and propagation of pain signals. Meanwhile, it does not interfere with basal secretion of inhibitory transmitters such as GABA, maintaining the homeostasis of spinal neural circuits.

Mechanism for Reversal and Remodeling of Pathological Synaptic Plasticity

Remodeling of synaptic plasticity represents the key mechanism underlying long-lasting analgesia by snx111. It reverses chronic pain-induced aberrant synaptic plasticity via regulating cellular signaling pathways.

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Under chronic pain conditions, persistent calcium influx and excitatory transmitter release activate postsynaptic NMDA receptors and sustain calcium entry, which further triggers downstream kinase cascades including PKC and MAPK.These events upregulate postsynaptic receptor expression, strengthen synaptic transmission efficiency, induce long-term potentiation (LTP) in the spinal dorsal horn, and produce plastic pathological alterations manifesting as hyperalgesia and allodynia.

By blocking presynaptic calcium influx, snx111 persistently reduces the release of glutamate and substance P, restrains excessive activation of postsynaptic NMDA receptors, and inhibits abnormal activation of the PKC/MAPK signaling pathway.

Closed-Loop Cellular Signaling Regulation and Analgesic Advantages

From the perspective of closed-loop cellular signaling, this agent downregulates cyclic adenosine monophosphate (cAMP) levels, suppresses CREB phosphorylation, reduces abnormal synthesis of plasticity-associated proteins, and reverses pathological structural and functional remodeling of presynaptic and postsynaptic compartments.On the one hand, it lowers the probability of presynaptic neurotransmitter release and weakens synaptic transmission efficacy.

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On the other hand, it decreases the density of postsynaptic excitatory receptors, inhibits abnormal neuronal hyperexcitability, and prevents consolidation of synaptic memory underlying chronic pain.

Unlike conventional analgesics, snx111 acts independent of G protein-coupled receptor pathways and does not induce receptor desensitization or signaling compensation. Accordingly, analgesic tolerance does not develop, enabling sustained long-term modulation of synaptic plasticity.

Precautions for Combination with Opioids and Opioid Withdrawal
 

Non‑opioid drug, no cross‑interaction: Snx111 does not act on opioid receptors and cannot prevent or alleviate opioid withdrawal symptoms.

 

Withdrawal tapering protocol: In patients on long‑term opioid therapy, abrupt opioid discontinuation is strictly prohibited. After initiating snx111, opioids should be gradually tapered over 2–4 weeks and replaced with equivalent oral opioids to avoid withdrawal syndrome.

Information source: FDA Prescribing Information; Drugs.com Monograph.

FAQ
 
 

How is snx111 different from morphine?

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Potentially severe and clinically relevant adverse events (AEs) associated with IT morphine include respiratory depression, tolerance, and granuloma formulation, whereas IT ziconotide is associated with neuropsychiatric AEs, such as cognitive impairment, hallucinations, and changes in mood or consciousness, ...

Does snx111 interact with any medications?

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There are 254 drugs known to interact with snx111, along with 2 disease interactions, and 1 alcohol/food interaction. Of the total drug interactions, 6 are major, and 248 are moderate.

 

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