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At least 19 recordsLinked to original sources
PubMed1991

Effects of the 1-amino-adamantanes at the MK-801-binding site of the NMDA-receptor-gated ion channel: a human postmortem brain study.

Recent studies from our laboratory have provided evidence that the 1-amino-adamantane derivative memantine (1-amino-3,5-dimethyl-adamantane) binds to the MK-801-binding site of the N-methyl-D-aspartate (NMDA)-receptor-gated ion channel. This action has been suggested to account for the antiparkinsonian and antispastic activity of the drug. In the present investigation we have extended our work by testing a series of 1-amino-adamantanes, including amantadine (1-amino-adamantane) and memantine, for their ability to compete with [3H]MK-801 binding in membrane homogenates of postmortem human frontal cortex. The most potent substance (1-amino-3,5-diethyl-adamantane) had a Ki-value of 0.19 +/- 0.06 microM while the weakest substance (1-N-methyl-amino-adamantane) had a Ki-value of 21.72 +/- 1.63 microM. The Ki-value of amantadine was 10.50 +/- 6.10 microM. In agreement with our earlier investigation, the Ki-value of memantine was 0.54 +/- 0.23 microM. The results indicate that 1-amino-adamantanes, in general, may produce their pharmacological effects through an interaction with the NMDA-receptor-gated ion channel. The displacement of [3H]MK-801 binding thus may provide the basis to predict the antiparkinsonian and antispastic activity of novel substituted 1-amino-adamantanes and possibly of other drugs.

Adamantane↗
PubMed1992

[Effect of various adamantane compounds on the reproduction of Sindbis virus. Isolation and properties of a resistant strain].

Rimantadine and its structural analogs, i. e. amide of 1-adamantane carboxylic acid (AACA) and 1-adamantane acetic acid amide, were shown to be able to inhibit reproduction of Sindbis virus in culture Vero cells. AACA had the maximum antiviral activity. Subcultures of the initial sensitive population of Sindbis virus in the presence of AACA led to formation of mutants resistant to AACA as well as to rimantadine, adamantane acetic acid amide and ammonium chloride. The Sindbis virus population was heterogenous in sensitivity to AACA, which was evident from isolation of separate clones with various levels of sensitivity to the above mentioned compounds from the population. It was found that reproduction of the AACA sensitive and resistant strains of Sindbis virus differed: the latent period of the resistant strain was 2 hours longer than that of the sensitive strain. The same effect was observed in the comparative study on synthesis of the virus-specific RNA.

Animals↗
PubMed1978

[Electronoptical studies of the effect of 1-[p-(methylnitrosamino)-benzylidenamino]-adamantane on the fowl plague virus (FPV) in cell culture].

The adamantanamine derivative 1-[p-(methylnitrosamino)-benzylidenamino]-adamantane (MBAA) at a concentration of 40 microgram/ml demonstrated no effect on adsorption of fowl plague virus (FPV) on chick embryonal cells. The penetration of the virions took place by means of pinocytosis. In the final stages of penetration the virions became gradually disintegrated. Under the influence of MBAA, after break-down of the membrane of pinocytic vesicles a swollen part of the virus core remained in cytoplasm. The morphologically visible replication stages were completely blocked by MBAA. From these results it was concluded that the antiviral action of MBAA most probably depends on a block of virus replication between the final stages of the penetration process and the beginning of production of virus specific structural antigens.

Adamantane↗
PubMed1976

Phase transition in a lipid bilayer. II. Influence of adamantane derivatives.

The influence of thirty-four adamantane, protoadamantane, and homoadamantane derivatives on the phase transition characteristics of the bilayer in dipalmitoyl lecithin liposomes has been determined by differential scanning calorimetry. Each of these compounds induces a broadening of the phase transition profile of the lipid bilayer that is dependent upon the concentration of the solute and its molecular structure. The concentration--response curves obtained for these solutes suggest that the cage compound derivatives modify the phase properties and under some conditions may induce a phase separation in the doped bilayer. The relative activity sequences obtained for the compounds examined cannot be accounted for by simple considerations of lipid/water partition coefficients, substitution constants based on free energy relationships, or the relative polarities or sizes of substituent groups. The observations are consistent with the hypothesis that the position and orientation of a solute within the bilayer are critical factors in determining its relative potency. The position of a solute within the bilayer is significantly controlled by the presence of polar substituents and by the relative geometric relationships of these groups. For a given substituent group, the shape and size of the hydrocarbon cage becomes increasingly important. It is apparent that seemingly minor modifications in the structure of a solute can significantly alter its influence on the phase transition behavior of a bilayer.

Adamantane↗
PubMed1975

Biologically active polycycloalkanes. 1. Antiviral adamantane derivatives.

Convenient methods for the synthesis of 1-substituted 3-adamantyl chlorides and bromides (2), 1-adamantylphenols and -cresols (3), and 1-adamantylacetic (6) as well as 1,3-adamantanediacetic (11) acids are described. Several novel derivatives were synthesized from these key intermediates: adamantylcyclohexanols (4) and -cyclohexanones (5) from adamantylphenols (3), and esters (7,12, and 22), amides (13 and 18), thioamides (9 and 16), amidine (10), nitrile (15), and amines (14 and 17) from 1-adamantanecarboxylic (19) and -acetic (6) acids and 1,3-adamantanediacetic acid (11). Some adamantylpyrimidines (24) and -purines (25 and 26) were also prepared. Antiviral activities of the compounds obtained in this work and a series of new 1-adamantyl alkyl ketones synthesized before, together with those of some known adamantane derivatives, were tested in vitro on monolayer culture of chick ambryo fibroblasts against Newcastle disease virus.

Adamantane↗
PubMed1991

Modulation of glycine-activated membrane current by adamantane derivatives.

Pressure application of the inhibitory neurotransmitters glycine and GABA, respectively, evoked a Cl- current in spinal cord neurons of fetal mice in culture. Memantine, in low concentrations (0.3-5 microM) enhanced the glycine-mediated current at both negative and positive holding potentials. At concentrations of more than 5 microM, memantine increased the glycine-evoked current only when the membrane potential was positive. At negative potentials the current was inhibited. 3-isopropylamantadine and 3,5-diethylamantadine augmented the glycine-activated membrane current irrespective of the concentrations applied, whereas amantadine was ineffective. The GABA-activated Cl- current was not altered by the adamantanes. These data are evidence of a specific glycinergic interaction with putative antispastic agents and can explain some conflicting effects of memantine in experimentally induced seizures.

Adamantane↗
PubMed1976

[Inhibitory effect of alpha-methyl-1-adamantane methylamine hydrochloride (rimantadine) on RNA-dependent RNA polymerase induction in culture of cells, infected with influenza virus].

An anti-influenza preparation, rimantadine (alpha-methyl-1-adamantane methylamine hydrochloride) at concentrations of 10--25 mkg/ml depresses the RNA-dependent RNA polymerase induction in a culture of cells infected with influenza virus (fowl plague virus). The inhibitory effect is also observed 2 hours following cell infection. In vitro studies have demonstrated that rimantadine has no effect on the activity of virus-induced RNA-dependent RNA polymerase, as well as on that of RNA-dependent RNA polymerase associated with virus particles.

Adamantane↗
PubMed1975

[Antiviral chemotherapeutic agents. XVIII. Adamantane derivatives of amphetamine. Their potential interest as autonomic and antiparkinson agents].

Adamantane isologs of amphetamine, methamphetamine and pheniprazine and several derivatives were synthesized in order to study the influence of their more pronounced lipophilic characteristics on their biological properties. A preliminary examination of their toxicity, antiviral, CNS stimulant and antiparkinson activity is described. The adamantyl amphetamine, which proved active, will be further studied.

Adamantane↗
PubMed1976

Effect of adamantane derivatives on the activity of orthomyxovirus RNA-dependent RNA polymerase.

The effect of several adamantane derivatives on the activity of virion-associated RNA-dependent RNA polymerase of fowl plague virus (FPV) and influenza B virus was studied in vitro. Some of the derivatives inhibited the activity of the polymerase by 60 per cent. A correlation was established between the previously demonstrated capacity of these inhibitors to suppress orthomyxovirus reproduction in vivo and their ability to reduce the activity of virion-associated RNA-dependent RNA polymerase in vitro.

Adamantane↗
PubMed1976

Adamantane and protoadamantanealkanamines as potential anti-Parkinson agents.

The synthesis of 2-halo-1-adamantanemethanamines, 4-protoadamantanemethanamines, and 4-protoadamantaneamines is described. The anti-Parkinson activity of these amines in terms of reversal of reserpine-induced catalepsy in rats has been evaluated and compared with amantadine. 2-Bromo- and 2-chloro-1-adamantanemethanamines are shown to be twice as active as amantadine.

Adamantane↗
PubMed1977

Induction of the platelet release reaction by 1.3-dimethyl-5-aminoadamantane, a new adamantane derivative.

The amantadine derivative 1.3-dimethyl-5-aminoadamantane, D 145, induces in high concentrations of 2-10 mM the release reaction. Adenine nucleotides and 5-hydroxytryptamine (5-HT) are liberated to the same extent and in the same ratio as found after thrombin-induced release. The time course of release is very slow; maximal release is reached in 15-20 min. The process is temperature-dependent and dependent on energy derived from glycolysis and oxidative phosphorylation. Extracellular Ca++ does not promote the release process. D 145, in accordance with the mother-substance amantadine, inhibits 5-HT uptake non-competitively, KI = 0.15mM. In concentrations of 0.1-1 mM D 145 triggers only the liberation of 5-HT, adenine nucleotides are not liberated. The ADP induced platelet aggregation is completely inhibited after preincubation with a 1 mM solution of D 145.

Adamantane↗