Disease relevance of Lamisil

• Terbinafine and fulminant hepatic failure [1].
• SF 86-327, the most effective of these compounds so far, is highly active in vitro against a wide range of fungi and exceeds clinical standards in the oral and topical treatment of guinea pig dermatophytoses [2].
• Treatment of seborrhoeic dermatitis with oral terbinafine [3]?
• Terbinafine for black piedra [4].
• Desipramine toxicity with terbinafine [5].

Psychiatry related information on Lamisil

• Terbinafine was well tolerated, although one patient developed erectile dysfunction while receiving treatment [6].
• Patient self-assessment also favoured terbinafine, with 65% evaluating it as good to very good, compared with 58% for itraconazole [7].
• RESULTS: After 9 months of treatment, the mycological cure rates were 22/34 (64.7%) for the terbinafine-only group and 30/34 (88.2%) for the combination therapy group (p<0.05) [8].
• Lamisil has the distinct advantage of producing good results in a short time period, making patient compliance less of a problem [9].
• Age and sex were often significant explanatory variables, and further analysis of change scores at 12 weeks revealed that females treated with terbinafine + debridement reported significantly less improvement in the physical activities problems (p = 0.0021) and overall problem (p = 0.0112) scores [10].

High impact information on Lamisil

• The quadruple mutant, however, was more sensitive to terbinafine, an inhibitor of Erg1p, than the are1are2 strain suggesting that the presence of TAG and/or intact lipid particles has an additional protective effect [11].
• Overexpression/selection using the sterol synthesis inhibitors terbinafine (TBF, targeting squalene epoxidase) and itraconazole (ITZ, targeting lanosterol C(14)-demethylase) yielded nine new resistance loci [12].
• Rat SE cDNA was isolated by selecting yeast transformants expressing rat cDNA in the presence of transformants expressing rat cDNA in the presence of terbinafine, an inhibitor specific for fungal SE [13].
• (vi) Treatment of S. cerevisiae with azole or terbinafine resulted in transcriptional upregulation of genes FKS2 and PMR1 known to be Ca2+ regulated [14].
• Terbinafine hepatotoxicity resulting in chronic biliary ductopenia and portal fibrosis [15].

Chemical compound and disease context of Lamisil

• Available studies show that the efficacy of itraconazole appears to be greater than that of griseofulvin, but similar to or lower than that of terbinafine in patients with dermatophyte onychomycosis or cutaneous fungal infections [16].
• A rabbit model of coccidioidal meningitis was used to compare the therapeutic efficacies of terbinafine (TBF) and fluconazole (FCZ) [17].
• Additionally, oral terbinafine is more effective than ketoconazole 200 mg/day in tinea corporis/cruris [18].
• We report the effects of ketoconazole and the bistriazole ICI 195,739 acting alone or in combination with the allylamine terbinafine (Lamisil) on murine models of Chagas' disease [19].
• On the other hand, topical amorolfine and topical or oral terbinafine were ineffective for tinea unguium, although these drugs eradicated or reduced the fungal burden of plantar skin [20].

Biological context of Lamisil

• Terbinafine had no statistically significant effect on the pharmacokinetics of alfentanil [21].
• CONCLUSIONS: Terbinafine inhibits CYP2D6 sufficiently to produce a discordance between genotype and phenotype for the enzyme [22].
• Terbinafine is well tolerated after oral or topical administration and has a relatively low potential for drug interactions [18].
• By contrast, our in vitro data showed that the 50% inhibitory concentration of terbinafine against rat P. carinii is 3.7 microg/ml, a level that cannot be clinically achieved in serum [23].
• Terbinafine resistance in these T. rubrum clinical isolates appears to be due to a single amino acid substitution in SE [24].

Anatomical context of Lamisil

• Measurable concentrations of terbinafine were achieved in sebum and hair samples within the first week of administration and by week 3 in stratum corneum and nail samples [25].
• Inhibition of human vascular endothelial cells proliferation by terbinafine [26].
• Terbinafine is well absorbed from the gastrointestinal tract, and the time to reach effective concentrations in nail is 1 to 2 weeks [27].
• Terbinafine at 3 microM induced more limited ultrastructural damage to the amastigotes consistent with increased vacuolization of the cells and the appearance of occasional autophagic vacuoles [28].
• The uptake of terbinafine into skin and testis tissues was described by a PB-PK model which incorporates a membrane permeability rate limitation [29].

Associations of Lamisil with other chemical compounds

• We evaluated terbinafine and itraconazole against 30 isolates of Penicillium marneffei using a modification of the National Committee for Clinical Laboratory Standards broth macrodilution MIC testing protocol for yeasts [30].
• The in vitro activities of fluconazole or voriconazole plus terbinafine were evaluated against 20 Candida isolates by the checkerboard, time-kill, and Etest methods [31].
• Synthesis and structure-activity relationships of side-chain-substituted analogs of the allylamine antimycotic terbinafine lacking the central amino function [32].
• In vitro activities of terbinafine against Aspergillus species in comparison with those of itraconazole and amphotericin B [33].
• Naftifine had a lower potency (IC50, 114.6 nM) than terbinafine [34].

Gene context of Lamisil

• Terbinafine inhibits CYP2D6 [27].
• In vitro and in vivo studies of the anticancer action of terbinafine in human cancer cell lines: G0/G1 p53-associated cell cycle arrest [35].
• Terbinafine resistance in a pleiotropic yeast mutant is caused by a single point mutation in the ERG1 gene [36].
• Absence of effect of terbinafine on the activity of CYP1A2, NAT-2, and xanthine oxidase [37].
• We report that ROX1 deletion resulted in 2.5- to 16-fold-lower susceptibilities to azoles and terbinafine [38].

Analytical, diagnostic and therapeutic context of Lamisil

• Mycological cure rates achieved with terbinafine generally improve after treatment cessation, reflecting the drug's fungicidal mechanism of action and its residual effect in tissue [18].
• Both oral and topical terbinafine have been very well tolerated in clinical trials to date, with only minor adverse effects reported [39].
• Bioassay for SF 86-327, a new antifungal agent [40].
• Fatal hepatic veno-occlusive disease associated with terbinafine in a liver transplant recipient [41].
• In the first patient all abnormalities have disappeared, but in the second patient alkaline phosphatase, aminotransferase and gamma-glutamyl transferase levels have remained elevated (follow up 3 months after cessation of treatment with terbinafine) [42].

References