Quinidine sulfate
(Synonyms: Chinidin Sodium, Pitayine Sodium, β-quinine Sodium, (+)-quinidine Sodium) 目录号 : GC25812Quinidine (Chinidin, Pitayine, β-quinine, (+)-quinidine) acts as a blocker of voltage-gated sodium channels, also an antimuscarinic and antimalarial.
Cas No.:6591-63-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Quinidine (Chinidin, Pitayine, β-quinine, (+)-quinidine) acts as a blocker of voltage-gated sodium channels, also an antimuscarinic and antimalarial.
Quinidine selectively reduces the proliferation of merlin-deficient HMM cell lines by causing a G0/G1 arrest, whereas the proliferation rates of merlinexpressing HMM cell lines remain unchanged. In addtion to its function as a channel blocker, quinidine is an inhibitor of a specific isoform of the cytochrome P450 family (CYP2D6), which is involved in the detoxification and metabolism of multiple commonly prescribed drugs as well as numerous endogenous substrates[1].
Quinidine is a potent and selective inhibitor of P450db and that quinidine can inhibit the in vivo metabolism of debrisoquine in humans. Quinidine is an inhibitor of amphetamine metabolism in vivo[2].
[1] Tsuruo T, et al. Cancer Res. 1984, 44(10):4303-7. [2] David E Moody, et al. Journal of Analytical Toxicology. 1990, 14: 311-317.
| Cas No. | 6591-63-5 | SDF | Download SDF |
| 别名 | Chinidin Sodium, Pitayine Sodium, β-quinine Sodium, (+)-quinidine Sodium | ||
| 分子式 | C40H48N4O4.H2SO4.2H2O | 分子量 | 648.83 |
| 溶解度 | 储存条件 | Store at -20°C | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.5412 mL | 7.7062 mL | 15.4124 mL |
| 5 mM | 0.3082 mL | 1.5412 mL | 3.0825 mL |
| 10 mM | 0.1541 mL | 0.7706 mL | 1.5412 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Dextromethorphan/Quinidine sulfate for pseudobulbar affect
Drugs Today (Barc) 2008 Sep;44(9):661-8.PMID:19137121DOI:10.1358/dot.2008.44.9.1258664.
A new agent containing a combination of dextromethorphan (DM) and quinidine (Q) is currently under development for the treatment of pseudobulbar affect (PBA). PBA is a disorder of emotional regulation, characterized by uncontrollable outbursts of laughing and/or crying that are disproportionate to the emotions being experienced. The pathophysiology of PBA is currently unknown, although the disorder is thought to occur exclusively in the setting of neurological disease. The most influential theory on PBA posits that emotional outbursts are being generated autonomously in the brain stem due to loss of regulatory control by the frontal lobe. Although rarely life-threatening, PBA can have significant impact on patient quality of life, and thus merits treatment. There are currently no approved treatments for PBA. Several agents have been found to be effective in small placebo-controlled trials and case series, with the most commonly used agents being tricyclic antidepressants and selective serotonin reuptake inhibitors. Both these treatments are inexpensive and relatively low-risk, although the quality and quantity of data available on their efficacy are not optimal. DM has several pharmacological mechanisms of action relevant to the brain. It is an N-methyl-D-aspartate (NMDA) receptor antagonist, which prompted investigators to study its potential for slowing progression in amyotrophic lateral sclerosis (ALS), where glutamate toxicity is thought to be a factor. The combination agent DM/Q was developed to slow the metabolism of DM by P450 2D6 enzymes in the liver. DM/Q was not effective in slowing ALS progression, but patients noted that it helped to control their emotional outbursts, suggesting it might be useful as a treatment for PBA. DM is also a sigma-1 receptor agonist. These receptors are widely distributed in the brain, but probably most heavily in the limbic system, suggesting that DM may exert its emotion-controlling effects via these receptors. The endogenous ligands for sigma-1 receptors are not altogether known, although they appear to include gonadal steroids. DM/Q was recently shown to be effective in reducing the severity of PBA in two large studies of ALS and multiple sclerosis, which are probably the most common neurological settings. These are the largest treatment studies of PBA ever done. The agent was safe and relatively well tolerated. Further studies are being conducted to see if efficacy can be maintained with lower doses of quinidine. If DM/Q is approved by the U.S. Food and Drug Administration for treatment of PBA, it would be the first agent approved for this purpose. Currently, the antidepressants are probably the most attractive pharmacologic options for treatment of PBA. The choice of whether to use DM/Q in this setting will likely depend on individual patient factors as well as cost.
AVP-923, a combination of dextromethorphan hydrobromide and Quinidine sulfate for the treatment of pseudobulbar affect and neuropathic pain
IDrugs 2010 Apr;13(4):254-65.PMID:20373255doi
AVANIR Pharmaceuticals Inc, under license from Irisys Research & Development, is developing AVP-923 (Zenvia, Neurodex) for the treatment of pseudobulbar affect (PBA; in collaboration with Medison Pharma Ltd) and neuropathic pain associated with diabetic peripheral neuropathy. PBA, the main indication of AVP-923, is a neurological disorder characterized by uncontrollable and unpredictable episodes of laughing and/or crying. AVP-923 consists of a combination of the NMDA antagonist/sigma1 receptor agonist dextromethorphan hydrobromide (DM) and the cytochrome P450 2D6 (CYP2D6) enzyme inhibitor Quinidine sulfate (Q). DM has been under investigation for several years as a neuroprotective agent in stroke, neurosurgery and amyotrophic lateral sclerosis (ALS); however, it is rapidly metabolized by CYP2D6, reducing the drug's bioavailability at neuronal targets. The inclusion of Q inhibits the rapid first-pass metabolism of DM to increase systemic concentrations of the drug in the plasma and, in theory, increase the potential efficacy. The initial clinical data for AVP-923 in the treatment of PBA demonstrated the combination was effective, but exhibited significant side effects. Of particular concern to the FDA were increased QTc intervals reported in patients dosed with a 30-/30-mg dose of DM/Q. A subsequent phase III clinical trial assessing a lower dose of AVP-923 (20 or 30 mg DM/10 mg Q) for the treatment of PBA in patients with ALS or multiple sclerosis was implemented by AVANIR and demonstrated a favorable safety profile of AVP-923 while maintaining efficacy. Pending approval of the data from the FDA, AVP-923 would be the first FDA-approved treatment for PBA.
Quinidine photosensitivity
Arch Dermatol 1975 Nov;111(11):1440-3.PMID:128321doi
Photodermatitis occurring in three patients taking oral Quinidine sulfate cleared when the drug was discontinued and recurred when it was readministered. The dermatitis was experimentally reproduced with long-wave ultraviolet light (UV-A, 320-400 nm) in these three patients, who also exhibited a decreased minimal erythema dose (MED) to hot quartz irradiation. Patients taking quinidine who had no dermatitis exhibited normal MEDs and normal response to UV-A. Normal subjects injected intradermally with quinidine and irradiated with UV-A showed no reaction. These observations indicate that the photosensitive dermatitis to quinidine that occurred in the three patients is idiosyncratic and that the UV-A is at least partially responsible for the development of the dermatitis that correlates with the absorption of quinidine in the UV-A range. Quinidine must be considered among the drugs that can produce photosensitive dermatitis.
Quinidine-induced agranulocytosis
JAMA 1977 Aug 22;238(8):884-6.PMID:577979doi
In a 75-year-old man, agranulocytosis and septicemia developed after eight weeks of Quinidine sulfate therapy. An IgG antibody requiring the presence of quinidine was shown by complement-dependent leukocytotoxicity and leukoagglutination reactions. The antibody did not cross-react with quinine and was active against WBCs obtained from normal subjects and from the patient himself.
Relative bioavailability of quinidine gluconate and Quinidine sulfate in healthy volunteers
J Clin Pharmacol 1979 May-Jun;19(5-6):261-9.PMID:469022DOI:10.1002/j.1552-4604.1979.tb02479.x.
A comparison of the bioavailability of Quinidine sulfate to quinidine gluconate tablets in a single-dose randomized cross-over design with 20 healthy volunteers shows that the sulfate salt is more rapidly absorbed and provides significantly greater peak concentrations 1 hour after administration as compared to the peak levels achieved with the gluconate salt at approximately 5 hours after administration. When adjusted for the actual amount of quinidine contained in each tablet, there was no significant difference in the amount of quinidine bioavailable. Since quinidine gluconate absorption is significantly slower than Quinidine sulfate, a combination of the two dosage forms may be utilized in providing the loading dose. Based on the computer modeling and the clinical data accumulated by this laboratory (unpublished) over the past four years, quinidine gluconate, in the dosage form utilized in this study, provides more constant blood levels with smaller differences between the Cpmax and Cpmin than the sulfate when administered every 6 or 8 hours. Further controlled clinical studies are needed to confirm these observations in patients.