Disease relevance of Antelepsin

• Stiff-man syndrome and clonazepam [1].
• Clonazepam and branchial myoclonus [2].
• In contrast, ethosuximide, trimethadione, valproic acid, and low concentrations of clonazepam are anticonvulsant drugs that act predominantly against Metrazol and absence seizures; these agents are ineffective or inhibit accumulation of only cyclic GMP [3].
• Blepharospasm: successful treatment with clonazepam [4].
• Successful treatment of two cases of intention tremor with clonazepam [5].

Psychiatry related information on Antelepsin

• Clomipramine and clonazepam in cataplexy [6].
• Early coadministration of clonazepam with sertraline for panic disorder [7].
• Successful treatment of restless legs with clonazepam [8].
• Clonazepam treatment of adolescents with neuroleptic-induced akathisia [9].
• The authors describe the first five patients enrolled in an open clinical trial of clonazepam as a maintenance treatment in lithium-refractory bipolar disorder [10].

High impact information on Antelepsin

• The selective PBR ligands 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxamide (PK11195) and 4' chlorodiazepam (Ro5-4864), but not the centrally acting benzodiazepine ligand clonazepam, induced dose-dependent apoptosis in HSC [11].
• This benzodiazepine binding site is of the peripheral type, based on the relative potencies of Ro5-4864 and clonazepam in competing for [3H]diazepam binding [12].
• Startle disease, or hyperekplexia: response to clonazepam and assignment of the gene (STHE) to chromosome 5q by linkage analysis [13].
• Treatment with clonazepam resulted in complete and lasting improvement of the myoclonus [14].
• Successful treatment of primary reading epilepsy with clonazepam [15].

Chemical compound and disease context of Antelepsin

• Clinical, biochemical, and physiological features distinguishing myoclonus responsive to 5-hydroxytryptophan, tryptophan with a monoamine oxidase inhibitor, and clonazepam [16].
• The combination of sodium valproate, clonazepam and primidone (3 patients), or piracetam, clonazepam and primidone (3 patients), or the four drugs together (3 patients) was necessary to provide substantial relief of myoclonus [17].
• Both drugs significantly reduced dyskinetic movements: clonazepam had a stronger effect on orofacial dyskinesia, and phenobarbital was more effective for limbs and axial movements [18].
• Seizure management in acute hepatic porphyria: risks of valproate and clonazepam [19].
• Its chief uses are in status epilepticus, in which intravenous clonazepam may replace diazepam as the drug of first choice, and in the minor motor seizures of childhood, particularly petit mal absences, the Lennox-Gastaut syndrome and infantile spasms [20].

Biological context of Antelepsin

• The kinetics of clonazepam serum protein binding were studied in three umbilical cord serum and three adult serum specimens [21].
• The applicability of a pharmacokinetic model for drug interactions by enzyme induction was tested by chronic dosing situation using carbamazepine (Tegretol) as the inducer and clonazepam (Clonopin) as the drug affected [22].
• Clonazepam serum protein binding during development [21].
• Clonazepam acetylation in fast and slow acetylators [23].
• The epileptic patients had focal and stimulus-elicitable myoclonus with enlarged somatosensory evoked potentials and enhanced long-loop reflexes, and they responded well to anticonvulsants, especially clonazepam and valproic acid [24].

Anatomical context of Antelepsin

• Removal of extramitochondrial Na(+) or inhibition of mitochondrial Na(+)/Ca(2+) exchange with clonazepam blocked mitochondrial Ca(2+) efflux and resulted in a net accumulation of Ca(2+) by the mitochondria [25].
• Using drug incubation in chick-embryo hepatocyte culture, we found that porphyrin was increased by carbamazepine, clonazepam, and valproate [26].
• The unbound fraction (means +/- SE) of clonazepam was 17.3% +/- 0.7% in umbilical cord serum and 13.9% +/- 0.2% in adult serum (P less than 0.01) [21].
• The permeability across the blood-brain barrier of phenobarbital, phenytoin, clonazepam, and diazepam was determined in a total of 29 patients with the double-indicator dilution method [27].
• In addition, the systemic administration of clonazepam produced a decrease in the Bmax of [3H]DPAT binding to 5-HT1A sites in the hippocampus [28].

Associations of Antelepsin with other chemical compounds

• Short-term augmentation of fluoxetine with clonazepam in the treatment of depression: a double-blind study [29].
• Arterial and venous concentrations of phenobarbital, phenytoin, clonazepam, and diazepam after rapid intravenous injections [30].
• Arterial and venous concentrations of phenobarbital, phenytoin, clonazepam, and diazepam were followed for 12 hr after a rapid intravenous injection [30].
• Conversely, the CBR agonist clonazepam and the CBR antagonist flumazenil did not affect testosterone secretion [31].
• Sodium valproate and clonazepam in the treatment of intractable epilepsy [32].

Gene context of Antelepsin

• However, clonazepam, which does not have an affinity to PBR, did not affect adipose differentiation and proliferation of hMSCs [33].
• MoCo deficiency should be considered in the differential diagnosis of neonatal hyperekplexia, particularly in the instances of refractoriness to clonazepam, an early demise in infancy or the evidence of no mutations in the GLRA1 gene [34].
• Adjunctive clonazepam treatment of tic symptoms in children with comorbid tic disorders and ADHD [35].
• The i.p. injection of the 5-HT1A receptor agonists, buspirone (1 mg/kg) or 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino(tetralin) (0.05 and 0.1 mg/kg) or benzodiazepine (clonazepam, 1 mg/kg) significantly reduced or suppressed the emotional stress-induced increase of colonic spike bursts [36].
• Clonazepam-induced intestinal motor disturbances are linked to central nervous system release of cholecystokinin in rats [37].

Analytical, diagnostic and therapeutic context of Antelepsin

• Plasma levels of clonazepam were measured by electron-capture gas-liquid chromatography and those of carbamazepine and its epoxide metabolite by gas chromatographic-chemical ionization-mass spectrometry [22].
• Plasmapheresis (seven patients) and corticosteroids or other immunosuppressant medication (eight patients) did not help; one improved dramatically after treatment with clonazepam [38].
• After treatment in a double-blind manner with vehicle, imipramine (5 and 15 mg/kg, 7 days), and clonazepam (5 mg/kg, 3 days), the response to BMI microinjection into the DMH was once again recorded [39].
• Effects of treatment with imipramine and clonazepam on an animal model of panic disorder [39].
• Although her EEG was normal, the episodes were compatible with complex partial seizures and ceased after carbamazepine and clonazepam were reinstituted [40].

References