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Terbinafine Hydrochloride

Terbinafine hydrochloride is a synthetic allylamine antifungal agent. Terbinafine is structurally and pharmacologically related to naftifine.

Mechanism of Action

The exact mechanism of action of terbinafine’s antifungal activity has not been fully determined.

The drug interferes with sterol biosynthesis by inhibiting the enzyme squalene monooxygenase (squalene 2,-epoxidase). The resulting accumulation of squalene (the usual substrate of the enzyme) in the cells, and decreased amounts of sterols, especially ergosterol, are both thought to contribute to the antifungal action of terbinafine.

Results from in vitro studies indicate that terbinafine may be fungicidal or fungistatic, depending on the concentration of the drug and the species tested, but the clinical importance of these in vitro findings are unknown.

Terbinafine Hydrochloride

The drug appears to be fungicidal against dermatophytes (e.g., Trichophyton spp., Epidermophyton spp., Microsporum spp.), but may be fungicidal or fungistatic against yeasts (e.g., Candida parapsilosis or C. albicans, respectively). The fungicidal effect of terbinafine may principally be related to the toxic accumulation of squalene, probably in combination with ergosterol depletion. Cellular death in several different fungi treated in vitro with terbinafine was always associated with a large increase in intracellular squalene concentrations, but not always with marked decreases in ergosterol, and a fungicidal effect is achieved in vitro in some fungi at terbinafine concentrations that do not completely prevent ergosterol biosynthesis.

Following doses 100 times greater than those that are fungicidal to dermatophytes, the drug achieves only 80% reductions in viable cell counts of some yeasts (e.g., C. albicans), and the fungistatic effect of terbinafine against C. albicans is thought to result from inhibition in ergosterol synthesis with resultant depletion of ergosterol. There may be a greater susceptibility of the hyphal or filamentous form than that of the yeast form of C. albicans to the disruptive effects of terbinafine and other (e.g., azole) antifungal agents on sterol biosynthesis, and the ability of terbinafine to suppress the invasive hyphal form of C. albicans may play an important role in its therapeutic efficacy against this organism. Squalene monooxygenase, similar to that contained in fungi, is involved in mammalian cholesterol synthesis; however, studies using rat liver indicate that the mammalian enzyme is 3 or 4 orders of magnitude (i.e., between 1000-10,000 times) less sensitive than the fungal enzyme to the effects of terbinafine.

The manufacturer states that inhibition of mammalian squalene monooxygenase would require terbinafine concentrations that are 4000-fold higher than those required for fungicidal activity in vitro.

Although azole antifungal agents, including imidazole derivatives (e.g., clotrimazole, econazole, ketoconazole, miconazole) and triazole derivatives (e.g., fluconazole, itraconazole) also appear to exert their antifungal activity by interfering with sterol biosynthesis, the mechanism of action of these antifungal agents differs from that of terbinafine and other allylamine derivatives. The allylamine derivatives appear to affect sterol biosynthesis at an earlier stage than do azole antifungal agents and do not appear to affect C-14 demethylation of sterol intermediates (e.g., lanosterol).

Also, the squalene epoxidase enzyme target of terbinafine and other allylamine derivatives is not a cytochrome P-450 type enzyme, and terbinafine and other allylamine derivatives have less effect on the microsomal cytochrome P-450 systems in the liver, adrenal glands, or testes than imidazole derivatives. Terbinafine does not appear to interfere with metabolism of certain antihistamines (e.g., astemizole [no longer commercially available in the US], terfenadine [no longer commercially available in the US]), cisapride, or benzodiazepines (e.g., midazolam, triazolam).

Spectrum Terbinafine is active in vitro against many fungi (including dermatophytic [e.g Trichophyton, Microsporum, Epidermophyton], filamentous [e.g Aspergillus], dimorphic [e.g., Blastomyces], and dematiaceous types) as well as yeasts, with an antifungal spectrum of activity similar to that of naftifine, although differences in specific in vitro and in vivo activity on weight and pharmacodynamic bases exist.

Terbinafine is active against most strains of T. rubrum and T. mentagrophytes in vitro and in vivo in clinical infections of the nail. Terbinafine usually is fungicidal in action against susceptible dermatophytes, Aspergillus, Blastomyces, Histoplasma, and certain other fungi and yeasts including C. parapsilosis but is only fungistatic against C. albicans; like naftifine, terbinafine may be fungicidal against C. albicans at high concentrations. Terbinafine is more active than azole antifungal agents, including imidazole derivatives (e.g., ketoconazole) or triazole derivatives (e.g., fluconazole, itraconazole) against dermatophytes (e.g., Epidermophyton floccosum, Microsporum spp., Trichophyton spp.) but is less active than these drugs against Candida spp.

Terbinafine is active in vitro against most strains of Epidermophyton floccosum, C. albicans, and Scopulariopsis brevicaulis. However, the efficacy of terbinafine in treating infections caused by these organisms has not been established in clinical studies, and it remains to be established whether in vitro susceptibility tests accurately reflect in vivo (clinical) activity for various fungi. SumMon®. For additional information on this drug until a more detailed monograph is developed and published, the manufacturer’s labeling should be consulted. It is essential that the labeling be consulted for detailed information on the usual cautions, precautions, and contraindications.


Terbinafine hydrochloride is administered orally. Although oral bioavailability of terbinafine (as determined by area under the plasma concentration-time curve [AUC]) may be increased (e.g., by 20%) when the drug is administered with food, such changes generally do not appear to be clinically important.

Because of the similarity in spelling between Lamisil® (the trade name for terbinafine hydrochloride) and Lamictal® (the trade name for lamotrigine, an anticonvulsant agent), several dispensing errors have been reported to the manufacturer of Lamictal® (GlaxoSmithKline).

These medication errors may be associated with serious adverse events either due to lack of appropriate therapy for seizures (e.g., in patients not receiving the prescribed anticonvulsant, lamotrigine, which may lead to status epilepticus) or, alternatively, to the risk of developing adverse effects (e.g., serious rash) associated with the use of lamotrigene in patients for whom the drug was not prescribed and consequently was not properly titrated.

Terbinafine Hydrochloride

Therefore, the manufacturer of Lamictal® cautions that extra care should be exercised in ensuring the accuracy of both oral and written prescriptions for Lamictal® and Lamisil®. The manufacturer also recommends that when appropriate, clinicians might consider including the intended use of the particular drug on the prescription in addition to alerting patients to carefully check the drug they receive and promptly bring any question or concern to the attention of the dispensing pharmacist.

The manufacturer also recommends that pharmacists assess the measures of avoiding dispensing errors and implement them as appropriate (e.g., placing drugs with similar names apart from one another in product storage areas, patient counseling).


Dosage of terbinafine hydrochloride is expressed in terms of terbinafine. The manufacturer states that safety and efficacy of terbinafine in children younger than 18 years of age have not been established. The usual adult dosage of terbinafine for the treatment of onychomycosis (tinea unguium) of the fingernail is 250 mg daily for a 6-week course.

Fingernail infections usually are reevaluated 18 weeks or longer after completion of therapy. The usual adult dosage of the drug for onychomycosis of the toenail also is 250 mg daily, but toenail infections generally respond inadequately to 6 weeks of therapy, requiring a continued course that extends to 12 weeks. Toenail infections usually are reevaluated 6-9 months after completion of therapy. Although more prolonged courses of therapy with the drug generally have not been shown to be substantially more effective in the treatment of these infections, some patients may benefit from extended and/or repeated courses of terbinafine therapy.

Patients should be advised that optimal clinical effect of terbinafine in the treatment of onychomycosis is delayed for several months after mycologic cure and completion of treatment because of the time required for outgrowth of healthy nail.

Because oral terbinafine is not recommended for patients with chronic or active liver disease and because there have been rare reports of liver failure in patients receiving the drug orally for the treatment of onychomycosis, the manufacturer recommends that liver function (ALT [SGPT] and AST [SGOT]) be evaluated prior to administration of oral terbinafine.

If biochemical or clinical signs of liver injury develop during terbinafine therapy, the drug should be discontinued. The drug also should be discontinued if a progressive rash or neutrophil count of 1000/mm3 or less develops since serious skin reactions (e.g., Stevens-Johnson syndrome, toxic epidermal necrolysis) and severe neutropenia have occurred rarely. Because decreases in absolute lymphocyte counts also can occur in patients receiving terbinafine, monitoring complete blood cell counts should be considered in patients receiving terbinafine for longer than 6 weeks, particuarly in those with known or suspected immunodeficiency.

Dosage in Renal and Hepatic Impairment

Clearance of terbinafine may be decreased substantially (e.g., by 50%) in patients with renal impairment (i.e., creatinine clearance of 50 mL/minute or less) or in those with preexisting liver disease (e.g., cirrhosis). Because use of terbinafine has not been studied adequately to date in such patients, the manufacturer states that the drug currently is not recommended in those with such dysfunction.


Terbinafine Hydrochloride Oral Tablets 250 mg (of terbinafine) Lamisil®,Novartis

Terbinafine: Susceptibility Factors


The pharmacokinetics of terbinafine and five known metabolites have been investigated in 12 children, (mean age 8 years; range 5-11 years), who took terbinafine 125 mg/day for 6-8 weeks for tinea capitis. The metabolism of terbinafine was similar to that observed in adults, and there were comparable steady-state plasma concentrations after administration of the same oral dose. Steady state was reached by day 21 with no further accumulation up to day 56.

Terbinafine was effective in all patients and safe and well tolerated over 56 days. In a randomized, double-blind comparison of terbinafine with itraconazole for 2 weeks for tinea capitis in Pakistani children (mean age 8 years), fever, body ache, and vertigo were seen with terbinafine in one patient each, and urticaria with itraconazole in two patients.

There were no significant changes in hematological and biochemical profiles. In an open assessment of the efficacy, safety, and tolerability of oral terbinafine 125-250 mg/day for 1, 2, and 4 weeks for tinea capitis in 132 Brazilian children aged 1-14 years, adverse events were reported in 10 patients.

The drug was prematurely withdrawn in one patient. In the post-treatment evaluation, two patients had abnormal bilirubin concentrations and eight patients had abnormal alkaline phosphatase activities; none was considered clinically relevant. In an open, non-comparative study of the use of terbinafine for 14 days to treat tinea capitis in 50 children and adolescents (mean age 7.6 years; range 24 months to 18 years), the clinical and mycological cure rates were 86%. The drug appeared to be well tolerated.

Two children had reversible neutropenia, thought to be due to a preceding viral illness; other adverse effects were not observed. In 14 children, aged 1-15 years, with Microsporum canis tinea capitis given oral terbinafine for 4 weeks, the recommended daily dose produced no response by week 4; the dose was doubled (to 250 mg/day) for a further 4-8 weeks in six patients and continued at the original dose in six patients.

Two patients withdrew. Four patients were cured after 8-12 weeks of treatment, and all had taken the doubled dose of terbinafine, except for one who had taken the usual adult dose of 250 mg/day from the start. Oral terbinafine was well tolerated by all but one patient, who had gastrointestinal disturbance and slightly raised transaminase activities during the first 4 weeks of treatment. In an open, prospective, uncontrolled study in 81 immunocompetent young children (aged 2-13 years) with tinea capitis due to Microsporum canis, oral terbinafine was given in dosages based on weight (62.5 mg for those weighing 10-20 kg and 125 mg for 20-40 kg), and applied topically to affected areas (1% cream bd). Treatment lasted for 4 weeks, followed by an 8-week observation (treatment-free) period.

All the subjects were assessed for efficacy and tolerability at 12 weeks. At 12 weeks: 32 had completely recovered, with no evidence of relapse during the observation period, and 21 had mycological cure but residual signs of infection. The effective cure rate was 65%. Terbinafine was well tolerated by these children: 75 had no adverse effects; the other six had abdominal pain, vomiting, generalized itching, local itching, and localized erythema. Hematological and biochemical parameters remained normal during the study.

Terbinafine: Side Effects

The allylamine derivative terbinafine can be used orally or topically. It is active against a broad range of fungi, including filamentous fungi and, to a lesser extent, yeastlike fungi. However, probably because of irreversible protein binding, its clinical usefulness is limited to the treatment of dermatophyte infections and perhaps lymphocutaneous sporotrichosis. Terbinafine acts by inhibiting the synthesis of fungal ergosterol at the level of squalene oxidase, leading to depletion of ergosterol and accumulation of toxic squalenes in the fungal cell membrane.


Numerous reviews and studies of the pharmacokinetics of terbinafine have appeared. Independent of food, its oral availability is 70-80%. With a single dose of 250 mg, plasma concentrations reach around 0.97 µg/ml after two hours. Apparent steady-state plasma concentrations are reached after 10-14 days after only two-fold accumulation, although the half-life is up to 3 weeks and microbiologically active concentrations can be measured in plasma for weeks to months after the last dose, which is consistent with slow redistribution from the peripheral tissues and fat. Protein binding is over 99% and the apparent volume of distribution over 2000 liters, high concentrations reaching adipose tissues, the dermis, epidermis, and nails. Less than 0.2% reaches the breast milk. After several weeks, no further accumulation of the compound occurs. In renal or hepatic failure, elimination is slowed. Terbinafine undergoes extensive and complex hepatic biotransformation involving at least seven CYP450 enzymes; none of its metabolites is mycologically active. Urinary excretion accounts for more than 70% and fecal elimination for 10% of total excretion; the extent of enterohepatic recycling is unknown. Children have a shorter half-life, a lower mean AUC, and a higher volume of distribution, reflecting their higher proportion of lipophilic tissues.

Comparative studies

The safety and efficacy of terbinafine 250 mg/day and itraconazole 200 mg/day given for 12 weeks for toenail onychomycosis have been compared in a randomized, double-blind study in 372 patients. Adverse events were reported in 39% of the terbinafine-treated patients and in 35% of the itraconazole-treated patients. The mean values of biochemical parameters of liver and kidney function did not change significantly. Terbinafine produced higher rates of clinical cure (76 versus 58%) and mycological cure (73 versus 46%) than itraconazole. In a randomized, double-blind comparison of terbinafine 250 mg/day with itraconazole 200 mg/day, administered for 12 weeks for toenail onychomycosis, mycological cure rates at the 36-week follow-up end-point (67 versus 61%) and the proportion of patients with adverse effects (23 versus 22%) were similar in both study arms. However, more patients taking terbinafine stopped treatment permanently because of treatment-related adverse events (8 versus 1%). In a double-blind, randomized, multicenter comparison of terbinafine (250 mg/day for 12 or 16 weeks) or itraconazole capsules (200 mg bd for 1 week every 4 weeks for 12 or 16 weeks), 236 patients reported at least one adverse event. All were within the known safety profile of both drugs, and there were no significant differences among the four treatment regimens. Continuous terbinafine was significantly more effective than intermittent itraconazole (mycological cure rates at week 72: 76, 81, 38, and 49%; significant for all comparisons between terbinafine and itraconazole).

General adverse effects

Terbinafine is usually well tolerated. Gastrointestinal complaints (dyspepsia, nausea, diarrhea) were the most common reasons for withdrawal. Abdominal pain and loss of taste were reported, as well as mild nervous system symptoms (headache and dizziness).

Terbinafine: Drug-Drug Interactions


Rifampicin 600 mg/day reduced terbinafine concentrations by about 50% by enzyme induction.


Theophylline is largely metabolized by CYP1A2 and terbinafine increases its half-life. In a randomized, crossover study in 12 healthy volunteers, terbinafine increased theophylline exposure by 16%, with a 14% reduction in clearance and a 24% increase in half-life. These pharmacokinetic changes may predispose individuals to accumulation of theophylline and unwanted toxicity. Caution should be taken in prescribing terbinafine for patients taking long-term theophylline.

Tricyclic antidepressants


Inhibition of CYP2D6 by terbinafine has been evaluated by assessing 48-hour concentration-time profiles of the tricyclic antidepressant desipramine in 12 healthy volunteers identified as extensive CYP2D6 metabolizers by genotyping and phenotyping. The pharmacokinetics were evaluated at baseline (50 mg oral desipramine given alone), steady state (after 250 mg oral terbinafine for 21 days), and 2 and 4 weeks after terbinafine withdrawal. The pharmacodynamics were evaluated before and 2 hours after each dose of desipramine, using Mini-Mental Status Examination and electroencephalography. Terbinafine inhibited CYP2D6 metabolism, as indicated by significant increases in desipramine Cmax and AUC and reductions in the Cmax and AUC of the CYP2D6-mediated metabolite, 2-hydroxydesipramine, both of which were still altered 4 weeks after terbinafine withdrawal. Caution should be exercised when co-prescribing terbinafine and drugs that are metabolized by CYP2D6, particularly those with a narrow therapeutic index.


  • A 51-year-old patient developed imipramine toxicity and increased plasma concentrations associated with the introduction of terbinafine, possibly due to inhibition of CYP2D6.


Metabolism by CYP2D6 is of major importance for the hydroxylation of nortriptyline, making it susceptible to competitive inhibition by terbinafine. Nortriptyline intoxication provoked by terbinafine has been reported. • A 74-year-old man taking a stable dose of nortriptyline for depression developed signs of nortriptyline intoxication 14 days after he started to take terbinafine. Nortriptyline serum concentrations were several times higher than the usual target range and fell to baseline after withdrawal of terbinafine. Re-challenge led to the same clinical and laboratory findings. • Nortriptyline intoxication secondary to terbinafine has been observed in a woman with a major depressive disorder. After rechallenge her serum nortriptyline concentration rose and the serum concentrations of its two hydroxylated metabolites fell. She had a normal genotype for CYP2D6, suggesting that this interaction can occur even in people without reduced CYP2D6 activity.


While terbinafine had no effect on warfarin in healthy volunteers, it can prolong the prothrombin time in some individuals, prompting intensification of laboratory control during terbinafine therapy. • A 71-year-old woman taking a stable dose of warfarin and cimetidine was treated with terbinafine, and 32 days later developed profuse intestinal bleeding associated with a prothrombin time of 120 seconds, suggestive of an interaction between warfarin and terbinafine, either directly or through the mediation of cimetidine (which can reduce terbinafine clearance by 33%). However, a contrasting case has also been reported. • A 68-year-old woman taking warfarin, glibenclamide, metformin, furosemide, and spironolactone was given terbinafine 250 mg/day and 4 weeks later required progressive increases in the warfarin dosage to maintain a therapeutic INR; after withdrawal of terbinafine, her warfarin requirements returned to baseline over 4 weeks, supporting enzyme induction with gradual onset and offset. Since a pharmacokinetic study of a single dose of warfarin in 26 healthy volunteers treated with terbinafine showed no significant interaction, and since a large postmarketing study of terbinafine did not find any cases of interaction of warfarin with terbinafine, the manufacturers and others have cautioned about any generalization regarding an interaction between terbinafine and warfarin.

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