Tinea capitis: Limited data available: Note: For Microsporum spp. infections, griseofulvin is preferred over terbinafine. If terbinafine is used, higher-dose regimens are preferred (Gupta 2003; Pierini 1998; Red Book [AAP 2018]; Ungpakorn 2004).
Standard-dose regimen: Children and Adolescents: Note: Dosing based on 4 to 6 mg/kg/day (Bar 2019; Bradley 2021; Gupta 2003; Red Book [AAP 2018]):
10 to <20 kg: Oral: 62.5 mg once daily.
20 to 40 kg: Oral: 125 mg once daily.
>40 kg: Oral: 250 mg once daily.
Duration of therapy: General: 6 weeks; Species-specific: Trichophyton tonsurans: 4 to 6 weeks; Microsporum canis: 6 to 12 weeks (Abdel-Rahman 2005; Bar 2019; Gupta 2003; Newland 2009; Red Book [AAP 2018]).
Higher-dose regimen (Abdel-Rahman 2005; Elewski 2008; Red Book [AAP 2018]): Children and Adolescents:
<25 kg: Oral: 125 mg once daily for 6 weeks.
25 to 35 kg: Oral: 187.5 mg once daily for 6 weeks.
>35 kg: Oral: 250 mg once daily for 6 weeks.
Onychomycosis: Limited data available (Gupta 1997b; Red Book [AAP 2018]): Children and Adolescents:
10 to 20 kg: Oral: 62.5 mg once daily for 6 weeks (fingernails) or 12 weeks (toenails).
>20 to 40 kg: Oral: 125 mg once daily for 6 weeks (fingernails) or 12 weeks (toenails).
>40 kg: Oral: 250 mg once daily for 6 weeks (fingernails) or 12 weeks (toenails).
There are no dosage adjustments provided in the manufacturer's labeling; however, clearance is decreased ~50% in adult patients with CrCl ≤50 mL/minute.
There are no pediatric-specific dosage adjustments provided in the manufacturer's labeling; use is contraindicated in adults with chronic or active hepatic disease.
(For additional information see "Terbinafine (systemic): Drug information")
Onychomycosis:
Continuous dosing: Oral: 250 mg once daily for 6 weeks (fingernail) or 12 weeks (toenail).
Pulsed dosing (alternative dosing method) (off-label): Oral: 250 mg once daily for 4 weeks, off for 4 weeks, then resume with 250 mg once daily for 4 weeks (Gupta 2013) or 250 mg twice daily for 1 week repeated every 4 weeks for 3 months (Takahata 2009; Yadav 2015). Note: Pulsed dosing is less effective but may reduce the risk of adverse effects, reduce cost, and improve patient compliance (Goldstein 2019).
Sporotrichosis, lymphocutaneous and cutaneous (alternative agent for patients who do not respond to itraconazole) (off-label use): Oral: 500 mg twice daily (IDSA [Kauffman 2007]). Treat for 2 to 4 additional weeks after all lesions have resolved; usual duration is 3 to 6 months (Chapman 2004; IDSA [Kauffman 2007]).
Tinea infections:
Dermatophyte folliculitis (tinea barbae, Majocchi granuloma) (off-label use): Oral: 250 mg once daily; duration is typically 2 to 6 weeks or until clinical resolution (Bonifaz 2003; Chou 2016; Gega 2010; Ilkit 2012; Jackson 2021; Wang 2018; Zhou 2017).
Tinea capitis (off-label use): Oral: 250 mg once daily for 4 to 6 weeks (El-Khalawany 2013; Gupta 2008; Treat 2020).
Tinea corporis/tinea cruris (alternative agent) (off-label use): Note: Alternative treatment for patients with extensive skin involvement or in whom topical therapy failed (Goldstein 2021).
Oral: 250 mg once daily for 1 to 2 weeks (del Palacio Hernandez 1990; Farag 1994; Gupta 2008; Voravutinon 1993).
Tinea pedis/tinea manuum (alternative agent) (off-label use): Note: Alternative treatment for patients with extensive skin involvement or in whom topical therapy failed (Goldstein 2021).
Oral: 250 mg once daily for 2 weeks (Bell-Syer 2012; Gupta 2008; Tausch 1998; White 1991).
There are no dosage adjustments provided in the manufacturer's labeling (has not been studied); however, clearance is decreased 50% in patients with CrCl ≤50 mL/minute.
Contraindicated in chronic or active hepatic disease.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling. [DSC] = Discontinued product
Tablet, Oral:
LamISIL: 250 mg [DSC]
Generic: 250 mg
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral:
LamISIL: 250 mg
Generic: 250 mg
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Lamisil: https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/020539s033lbl.pdf#page=11
Oral: Administer without regard to meals.
Oral: Administer without regard to meals.
Store below 25°C (77°F). Protect from light.
Treatment of onychomycosis of the toenail or fingernail due to susceptible dermatophytes (FDA approved in adults); has also been used in the treatment of tinea capitis.
Terbinafine may be confused with terbutaline
LamISIL may be confused with LaMICtal, Lomotil
Terbinafine may cause hepatotoxicity (ranging from mild and asymptomatic increased serum transaminases to hepatic failure) (Ref). Terbinafine liver injury may present as hepatocellular hepatitis or cholestatic hepatitis, with some cases progressing to vanishing bile duct syndrome (Ref). Most cases of hepatotoxicity are self-limited; although, persistent and severe hepatocellular injury cases have been reported, requiring discontinuation of therapy or in rare cases liver transplantation (Ref). Resolution may be delayed (eg, 3 to 6 months) following discontinuation of therapy (Ref). Acute hepatic failure due to terbinafine therapy is rare (Ref).
Mechanism: Non–dose-related; possible mechanisms include immunologic (part of a hypersensitivity reaction) or a metabolically mediated effect (formation of mono-GSH conjugate which binds to hepatobiliary proteins (Ref).
Onset: Varied; typically within the first 4 to 6 weeks of therapy (Ref).
Risk factors:
• HLA-A* 33:03 allele (Ref)
Severe cutaneous adverse reactions (SCARs), including Stevens Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) (Ref), drug reaction with eosinophilia and systemic symptoms (DRESS) (Ref) and acute generalized exanthematous pustulosis (AGEP) (Ref) have been reported. Other delayed cutaneous reactions include pityriasis rosea (Ref), lichenoid eruptions (Ref), symmetrical drug-related intertriginous and flexural erythema (SDRIFE) (Ref) and subacute cutaneous lupus erythematosus (SCLE) (Ref).
Mechanism: Non–dose-related; immunologic. Delayed hypersensitivity reactions including SCARs are T-cell-mediated (Ref).
Onset: Delayed hypersensitivity reactions: Varied; SCARs usually occur 1 to 8 weeks after initiation (Ref), although AGEP may have a more rapid onset within 2 days (Ross 2018); re-exposure usually results in symptoms within 1 to 4 days (Ref). SCLE generally occurs within 4 to 8 weeks after initiation (Ref).
Risk factors:
• Females (SCLE) (Ref)
• Cross-reactivity: Terbinafine, an allylamine antifungal, is structurally similar to naftifine; although, documented cross-reactivity has not been established. No cross-reactivity between terbinafine and naftifine was noted on patch tests (Ref).
Dysgeusia (including ageusia; bitter/sour > salty/sweet) (Ref) and altered sense of smell (including anosmia) may occur and severe cases resulting in decreased food intake, weight loss, anxiety, or depression have been reported. Resolution may be delayed (eg, several weeks to >1 year) following discontinuation of therapy or in some cases, disturbance may be permanent.
Mechanism: Not well known; possible mechanisms include receptor dysfunction through the inhibition of cytochrome P450-dependent enzyme or alteration of the cell structure or function of taste-related neurons through interference of the cholesterol biosynthesis pathway (Ref).
Onset: Delayed; mean onset of taste loss was 35 days (Ref).
Risk factors (taste disturbance):
• Age (>55 years) (Ref)
• History of taste loss (Ref)
• Low body mass index (<21 kg/m2) (Ref)
Thrombotic microangiopathy (TMA), including thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome, have been reported rarely (some fatal). Recurrent anemia and thrombocytopenia may occur within 2 weeks after discontinuation (Ref).
Mechanism: Non–dose-related; immunological (anti-ADAMTS-13 antibodies may be increased) (Ref).
Onset: Intermediate; in one case report, occurred within ~2 weeks after therapy initiation (Ref).
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
>10%: Nervous system: Headache (13%)
1% to 10%:
Dermatologic: Pruritus (3%), skin rash (6%), urticaria (1%)
Gastrointestinal: Diarrhea (6%), dysgeusia (3%; may be severe and result in weight loss, anxiety, and depression) (table 1) , dyspepsia (4%)
Drug (Terbinafine [Systemic]) |
Placebo |
Number of Patients (Terbinafine [Systemic]) |
Number of Patients (Placebo) |
---|---|---|---|
3% |
0.7% |
465 |
137 |
Hepatic: Increased serum transaminases (3%) (table 2)
Drug (Terbinafine [Systemic]) |
Placebo |
Number of Patients (Terbinafine [Systemic]) |
Number of Patients (Placebo) |
---|---|---|---|
3% |
1% |
465 |
137 |
Postmarketing:
Cardiovascular: Vasculitis
Dermatologic: Acute generalized exanthematous pustulosis (Zaouak 2019), alopecia (Cohen 2020, Richert 2001), bullous dermatitis (Gupta 1998a), cutaneous lupus erythematosus (Lorentz 2008), erythema multiforme (Carstens 1994, Todd 1995), exacerbation of psoriasis (Cohen 2020, Gupta 1998a), exfoliative dermatitis (Gupta 1998a), lichenoid eruption (Cohen 2020), pityriasis rosea (George 2015), psoriasiform eruption (Cohen 2020), skin photosensitivity (Kuo 2014), Stevens-Johnson syndrome (Cohen 2020), toxic epidermal necrolysis (Carstens 1994)
Gastrointestinal: Ageusia (Doty 2005), cholestasis (Kyriakidis 2017), pancreatitis, vomiting
Hematologic & oncologic: Agranulocytosis (Aguilar 2001, Ornstein 1998), anemia (Filanovsky 2015), hemolytic-uremic syndrome, pancytopenia (Kovacs 1994), severe neutropenia (Kovacs 1994, Shapiro 1999), thrombocytopenia (Filanovsky 2015), thrombotic microangiopathy (Filanovsky 2015), thrombotic thrombocytopenic purpura (Filanovsky 2015)
Hepatic: Cholestatic hepatitis (Kyriakidis 2017), hepatic failure (Song 2005), hepatic insufficiency, hepatocellular hepatitis (Kyriakidis 2017)
Hypersensitivity: Anaphylaxis, angioedema
Immunologic: Drug reaction with eosinophilia and systemic symptoms (Gupta 1998), serum sickness-like reaction
Nervous system: Altered sense of smell (Lareb Netherlands Pharmacovigilance Centre 2013), anosmia (Lareb Netherlands Pharmacovigilance Centre 2013), anxiety, depression, fatigue, hypoesthesia, malaise, paresthesia, vertigo
Neuromuscular & skeletal: Arthralgia, exacerbation of systemic lupus erythematosus (Cohen 2020), increased creatine phosphokinase in blood specimen, myalgia, rhabdomyolysis (Zhou 2020), systemic lupus erythematosus (Cohen 2020)
Ophthalmic: Decreased visual acuity, visual field defect
Otic: Auditory impairment, tinnitus
Respiratory: Flu-like symptoms
Miscellaneous: Fever
Hypersensitivity to terbinafine or any component of the formulation; chronic or active hepatic disease
Concerns related to adverse effects:
• Allylamine antifungal hypersensitivity: Use caution in patients sensitive to allylamine antifungals (eg, naftifine, butenafine); cross-sensitivity to terbinafine may exist.
• Ocular effects: Although rare, changes in the ocular lens and retina have been reported; discontinuation of therapy may be required.
Disease-related concerns:
• Autoimmune disease (Lupus): Precipitation or exacerbation of cutaneous or systemic lupus erythematosus has been observed; discontinue if signs and/or symptoms develop.
• Hepatic impairment: Use is contraindicated in patients with active or chronic hepatic disease; clearance is reduced by ~50% in hepatic cirrhosis.
• Renal impairment: Use with caution in patients with renal dysfunction (CrCl ≤50 mL/minute); clearance is reduced by ~50%.
Other warnings/precautions:
• Appropriate use: Due to potential toxicity, confirmation of diagnostic testing of nail or skin specimens prior to treatment of onychomycosis or dermatomycosis is recommended.
Substrate of CYP1A2 (minor), CYP2C19 (minor), CYP2C9 (minor), CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential; Inhibits CYP2D6 (moderate)
Ajmaline: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Ajmaline. Risk C: Monitor therapy
Amitriptyline: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Amitriptyline. CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Amitriptyline. Risk C: Monitor therapy
Amoxapine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Amoxapine. Risk C: Monitor therapy
Amphetamines: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Amphetamines. Management: Monitor for amphetamine toxicities (including serotonin syndrome) if used with a moderate CYP2D6 inhibitor. Initiate amphetamine therapy at lower doses, monitor frequently, and adjust doses as needed. Discontinue amphetamines if serotoinin syndrome occurs Risk C: Monitor therapy
ARIPiprazole: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of ARIPiprazole. Management: Monitor for increased aripiprazole pharmacologic effects. Aripiprazole dose adjustments may or may not be required based on concomitant therapy, indication, or dosage form. Consult full interaction monograph for specific recommendations. Risk C: Monitor therapy
ARIPiprazole Lauroxil: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of ARIPiprazole Lauroxil. Risk C: Monitor therapy
Atomoxetine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Atomoxetine. Risk C: Monitor therapy
Brexpiprazole: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Brexpiprazole. Management: If brexpiprazole is to be used together with both a moderate CYP2D6 inhibitor and a strong or moderate CYP3A4 inhibitor, the brexpiprazole dose should be reduced to 25% of the usual dose when treating indications other than major depressive disorder. Risk C: Monitor therapy
Carvedilol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Carvedilol. Risk C: Monitor therapy
ClomiPRAMINE: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of ClomiPRAMINE. CYP2D6 Inhibitors (Moderate) may increase the serum concentration of ClomiPRAMINE. Risk C: Monitor therapy
CloZAPine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of CloZAPine. Risk C: Monitor therapy
Codeine: CYP2D6 Inhibitors (Moderate) may diminish the therapeutic effect of Codeine. These CYP2D6 inhibitors may prevent the metabolic conversion of codeine to its active metabolite morphine. Risk C: Monitor therapy
CycloSPORINE (Systemic): Terbinafine (Systemic) may decrease the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
Desipramine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Desipramine. Risk C: Monitor therapy
Deutetrabenazine: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Deutetrabenazine. Risk C: Monitor therapy
Dextromethorphan: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Dextromethorphan. Risk C: Monitor therapy
Doxepin (Systemic): CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Doxepin (Systemic). Risk C: Monitor therapy
Doxepin (Topical): CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Doxepin (Topical). Risk C: Monitor therapy
DOXOrubicin (Conventional): CYP2D6 Inhibitors (Moderate) may increase the serum concentration of DOXOrubicin (Conventional). Risk X: Avoid combination
Eliglustat: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Eliglustat. Management: Eliglustat dose is 84 mg daily with CYP2D6 inhibitors. Use is contraindicated (COI) when also combined with strong CYP3A4 inhibitors. When also combined with a moderate CYP3A4 inhibitor, use is COI in CYP2D6 EMs or IMs and should be avoided in CYP2D6 PMs. Risk D: Consider therapy modification
Flecainide: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Flecainide. Risk C: Monitor therapy
Haloperidol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Haloperidol. Risk C: Monitor therapy
Iloperidone: CYP2D6 Inhibitors (Moderate) may decrease serum concentrations of the active metabolite(s) of Iloperidone. Specifically, concentrations of the metabolite P95 may be decreased. CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Iloperidone. Specifically, concentrations of the metabolite P88 may be increased. CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Iloperidone. Risk C: Monitor therapy
Imipramine: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Imipramine. Concentrations of desipramine may be increased. CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Imipramine. Risk C: Monitor therapy
Indoramin: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Indoramin. Risk C: Monitor therapy
Lofepramine: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Lofepramine. The active metabolite of lofepramine is desipramine. Risk C: Monitor therapy
Mequitazine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Mequitazine. Risk X: Avoid combination
Metoclopramide: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Metoclopramide. Risk C: Monitor therapy
Metoprolol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Metoprolol. Risk C: Monitor therapy
Nebivolol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Nebivolol. Risk C: Monitor therapy
Nortriptyline: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Nortriptyline. Risk C: Monitor therapy
Oliceridine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Oliceridine. Risk C: Monitor therapy
Olmutinib: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Olmutinib. Risk C: Monitor therapy
PARoxetine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of PARoxetine. Risk C: Monitor therapy
Perhexiline: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Perhexiline. Risk C: Monitor therapy
Perphenazine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Perphenazine. Risk C: Monitor therapy
Pimozide: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Pimozide. Risk C: Monitor therapy
Pitolisant: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Pitolisant. Risk C: Monitor therapy
Propafenone: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Propafenone. Risk C: Monitor therapy
Propranolol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Propranolol. Risk C: Monitor therapy
Protriptyline: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Protriptyline. Risk C: Monitor therapy
RifAMPin: May decrease the serum concentration of Terbinafine (Systemic). Risk C: Monitor therapy
RisperiDONE: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of RisperiDONE. Risk C: Monitor therapy
Saccharomyces boulardii: Antifungal Agents (Systemic, Oral) may diminish the therapeutic effect of Saccharomyces boulardii. Risk X: Avoid combination
Tamoxifen: CYP2D6 Inhibitors (Moderate) may decrease serum concentrations of the active metabolite(s) of Tamoxifen. Specifically, CYP2D6 inhibitors may decrease the metabolic formation of highly potent active metabolites. Management: Consider alternatives to the use of moderate CYP2D6 inhibitors with tamoxifen when possible, as the combination may be associated with reduced clinical effectiveness of tamoxifen. Risk D: Consider therapy modification
Tamsulosin: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Tamsulosin. Risk C: Monitor therapy
Tetrabenazine: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Tetrabenazine. Specifically, concentrations of the active alpha- and beta-dihydrotetrabenazine metabolites may be increased. Risk C: Monitor therapy
Thioridazine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Thioridazine. Risk X: Avoid combination
Timolol (Systemic): CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Timolol (Systemic). Risk C: Monitor therapy
TraMADol: CYP2D6 Inhibitors (Moderate) may decrease serum concentrations of the active metabolite(s) of TraMADol. CYP2D6 Inhibitors (Moderate) may increase the serum concentration of TraMADol. Risk C: Monitor therapy
Trimipramine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Trimipramine. Risk C: Monitor therapy
Valbenazine: CYP2D6 Inhibitors (Moderate) may increase serum concentrations of the active metabolite(s) of Valbenazine. Risk C: Monitor therapy
Vortioxetine: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Vortioxetine. Risk C: Monitor therapy
Zuclopenthixol: CYP2D6 Inhibitors (Moderate) may increase the serum concentration of Zuclopenthixol. Risk C: Monitor therapy
Published information related to the use of systemic terbinafine in pregnancy is limited (Gupta 1997a; Sarkar 2003).
Systemic therapy for the treatment of onychomycosis or tinea capitis is not recommended during pregnancy (Kaul 2017; Murase 2014).
AST/ALT prior to initiation, repeat if used >6 weeks; some experts have suggested that repeat testing at 6 weeks is unnecessary (Patel 2017); CBC (if used >6 weeks in immunocompromised patients).
Synthetic allylamine derivative that inhibits squalene epoxidase, a key enzyme in sterol biosynthesis in fungi. This results in a deficiency in ergosterol within the fungal cell membrane and results in fungal cell death.
Absorption: >70%.
Distribution: Distributed to sebum and skin predominantly.
Protein binding: Plasma: >99%.
Metabolism: Hepatic predominantly via CYP1A2, 3A4, 2C8, 2C9, and 2C19 to inactive metabolites.
Bioavailability: 40% (as a result of first-pass metabolism).
Half-life elimination: Terminal half-life: 200 to 400 hours; very slow release of drug from skin and adipose tissues occurs.
Effective half-life:
Children 5 to 11 years: 14.7 ± 4.3 hours (range: 9.8 to 25.7 hours) (Humbert 1998; Nejjam 1995).
Adults: ~36 hours.
Time to peak, plasma: Children and Adults: Within 2 hours (Abdel-Rahman 2005; manufacturer's labeling).
Excretion: Urine (80%, primarily as inactive metabolites); feces (20%) (Debruyne 2001).
Clearance:
Children 4 to 8 years: 1.41 ± 2.5 L/hour/kg (Abdel-Rahman 2005).
Adults: 0.47 ± 0.21 L/hour/kg (Abdel-Rahman 2005).
Renal function impairment: In CrCl ≤50 mL/minute, terbinafine clearance is decreased 50%.
Hepatic function impairment: In hepatic cirrhosis, terbinafine clearance is decreased 50%.
25 mg/mL Oral Suspension:
A 25 mg/mL oral suspension may be made using tablets. Crush twenty 250 mg tablets and reduce to a fine powder. Add small amount of a 1:1 mixture of Ora-Sweet and Ora-Plus and mix to a uniform paste; mix while adding the vehicle in geometric proportions to almost 200 mL; transfer to a calibrated bottle, rinse mortar with vehicle, and add quantity of vehicle sufficient to make 200 mL. Label "shake well" and "refrigerate". Stable 42 days.
Tablets (Terbinafine HCl Oral)
250 mg (per each): $12.67 - $13.08
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.