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4-Aminopyridine

The Experts below are selected from a list of 198 Experts worldwide ranked by ideXlab platform

Guo Hong – 1st expert on this subject based on the ideXlab platform

  • Synthesis of Molecularly Imprinted Microspheres Polymer with 4-Aminopyridine as Template and the Study of Their Binding Characteristics
    Chemical Research in Chinese Universities, 2020
    Co-Authors: Guo Hong

    Abstract:

    The molecularly imprinted microspheres using 4 aminopyridine as template were prepared with precipitation polymerization. The batch way was used to investigate the selectively binding ability of the microspheres for 4 aminopyridine. The effects of different amount of solvent and initiator on the shape and the size of the particles were studied. The substrate selectivity of the polymer was investigated. The results showed that the imprinted polymer exhibited a high affinity for 4 aminopyridine among the tested compounds.

  • Studies on the Binding Nature in Molecularly Imprinted Polymer Selective for 4-Aminopyridine
    Chemical Research in Chinese Universities, 2020
    Co-Authors: Guo Hong

    Abstract:

    A molecularly imprinted polymer was prepared using 4 aminopyridine as template. The bulk polymer obtained was ground up, sieved and investigated in equilibrium binding experiments to evaluate the binding characteristics of the 4 aminopyridine imprinted polymer. Scatchard analysis showed that two classes of binding sites were produced in the polymer matrix and their dissociation constants were calculated to be 6.0 μmol/L and 1.2 mmol/L respectively, by utilizing the model of multiple independent classes of binding sites. The substrate selectivity of the polymer was investigated. The results showed that the imprinted polymer exhibited much higher affinity for 4 aminopyridine among the tested compounds. \{ 1H NMR\} studies and the analysis of the resonance structure of 4 aminopyridine indicated that the selective binding interaction between the template and binding sites in the polymer arose from their ionic interaction.

J. C. Koetsier – 2nd expert on this subject based on the ideXlab platform

  • 4-Aminopyridine Is Superior to 3,4-Diaminopyridine in the Treatment of Patients With Multiple Sclerosis
    JAMA Neurology, 1994
    Co-Authors: C. H. Polman, F. W. Bertelsmann, R. De Waal, H.a.m. Van Diemen, B.m.j. Uitdehaag, A. C. Van Loenen, J. C. Koetsier

    Abstract:

    Objective: To compare the efficacy and toxicity of 4-Aminopyridine and 3,4-diaminopyridine in patients with multiple sclerosis. Design: Intervention study with a before-after design and a randomized, double-blind, crossover design. Setting: University referral center. Patients: Twenty-four patients with definite multiple sclerosis who had been treated in a previous clinical trial with 4-Aminopyridine. Interventions: Nonresponders to treatment with 4-Aminopyridine (14 patients) were treated with 3,4-diaminopyridine in a 4-week, open-label trial with doses up to 1.0 mg/kg of body weight (before-after design). Responders to treatment with 4-Aminopyridine (10 patients) participated in a comparative study of 6 weeks’ duration with 4-Aminopyridine and 3,4-diaminopyridine according to a randomized, double-blind, double-crossover design. Main Outcome Measures: Neurophysiologic variables for nonresponders, neurologic functions and symptoms on a visual analogue scale for responders, and side effects for both groups. Results: Toxicity profiles of 4-Aminopyridine and 3,4-diaminopyridine were different, and systemic tolerability was reduced for 3,4-diaminopyridine. 4-Aminopyridine was more effective than 3,4-diaminopyridine, especially for ambulation, fatigue, and overall daily functioning. Conclusion: Our data suggest that, concerning both efficacy and side effects, 4-Aminopyridine is superior to 3,4-diaminopyridine in the treatment of patients with multiple sclerosis.

  • 4-Aminopyridine in the Treatment of Patients With Multiple Sclerosis: Long-term Efficacy and Safety
    JAMA Neurology, 1994
    Co-Authors: C. H. Polman, F. W. Bertelsmann, A. C. Van Loenen, J. C. Koetsier

    Abstract:

    Objective: To study the long-term efficacy and safety of 4-Aminopyridine in patients with multiple sclerosis. Design: Case series, follow-up varying from 6 to 32 months. Setting: University referral center. Patients: Thirty-one patients with definite MS, 23 of them being exposed to long-term administration (6 to 32 months) of 4-Aminopyridine, since they showed a favorable initial response to the drug. Interventions: Long-term oral treatment with 4-Aminopyridine in daily doses of up to 0.5 mg/kg of body weight. Main Outcome Measures: Neurologic functions and symptoms as reported by the patients; side effects. Results: Twenty of 23 patients who showed a favorable initial response benefited from long-term administration. Ambulation and fatigue (each in 13 patients) and visual function (in five patients) were most frequently reported to be improved. Three major side effects did occur during a follow-up of 406 patient months: a generalized epileptic seizure in two patients and hepatitis in one. Conclusions: Although a substantial proportion of patients with multiple sclerosis seem to benefit from long-term administration of 4-Aminopyridine, additional studies are needed to clarify the exact value of the drug.

Yu Huang – 3rd expert on this subject based on the ideXlab platform

  • 4-Aminopyridine-induced phasic contractions in rat caudal epididymis are mediated through release of noradrenaline.
    European Journal of Pharmacology, 1995
    Co-Authors: Yu Huang

    Abstract:

    Abstract 4-Aminopyridine, a K+ channel blocker, evoked phasic contractions in the caudal duct of the rat epididymis. The 4-Aminopyridine-induced contractile response was either inhibited or prevented by the α1-adrenoceptor antagonists, prazosin (IC50 = 2.7 nM) and benoxathian (IC50 = 14.6 nM). Blockers (1 μM) of α2-adrenoceptors and purinoceptors but not of β-adrenoceptors or muscarinic receptors caused a small but statistically significant reduction of the 4-Aminopyridine-induced response. 4-Aminopyridine lost its ability to induce contractions after noradrenergic nerves had been destroyed by 6-hydroxydopamine. In addition, protriptyline and xylamine, blockers of noradrenaline uptake, also inhibited the 4-Aminopyridine-induced contractile response. However, other putative K+ channel blockers (tetraethylammonium ion, quinine, quinidine and glibenclamide) did not cause the muscle to contract. These findings demonstrate that the 4-Aminopyridine-induced release of noradrenaline and adenosine 5′-triphosphate as co-transmitters results from membrane depolarization due to 4-Aminopyridine blockade of K+ channels in noradrenergic nerve terminals. The 4-Aminopyridine-sensitive K+ channels might thus play a physiological role in regulating the nerve membrane potential and neurotransmission in the rat caudal epididymis.

  • BaCl2‐ and 4‐aminopyridine‐evoked phasic contractions in the rat vas deferens
    British Journal of Pharmacology, 1995
    Co-Authors: Yu Huang

    Abstract:

    1. The actions of BaCl2 and 4-Aminopyridine, blockers of K+ channels, on the mechanical activity of the epididymal half of the rat vas deferens were investigated. 2. Both BaCl2 and 4-Aminopyridine dose-dependently evoked phasic contractions. High extracellular potassium (35-40 mM) caused a tonic contraction but abolished the BaCl2- and 4-Aminopyridine-induced phasic activity and reduced the BaCl2-induced sustained component of contraction, but increased the 4-Aminopyridine-induced tonic contraction. 3. Omission of calcium from the extracellular medium totally abolished the 4-Aminopyridine-induced response but only reduced the mean amplitude of phasic contractions induced by BaCl. 4. Procaine (10 mM), an inhibitor of internal calcium release, completely abolished the phasic activity and reduced the sustained contraction induced by BaCl2. The remaining tone was abolished by nifedipine (1 microM). 5. Tetraethylammonium (1 mM) suppressed the amplitude of the BaCl2-induced phasic contractions, and induced a biphasic increase in tonic tension. 6. The BaCl2-induced responses were resistant to prazosin (1 microM), yohimbine (3 microM), propranolol (3 microM) or atropine (3 microM); in contrast, the 4-Aminopyridine-induced activity was effectively inhibited by prazosin (1 microM) attenuated by yohimbine (1 microM) and atropine (1 microM) but not by propranolol (3 microM). The 4-Aminopyridine-induced response was abolished by pretreatment of the vas deferens with 6-hydroxydopamine (0.5 mM). 7. The results indicate that the BaCl2-evoked activity in the vas deferens was mainly due to blockade of Ba(2+)-sensitive K+ channels on the smooth muscle plasma membrane. Subsequent calcium entry through the depolarized plasma membrane was needed to trigger generation of phasic contractions. 4-Aminopyridine-induced action, however, was largely mediated by neurotransmitters released from the depolarized nerve terminals as a result of blockade of K+ channels.