Terbinafine hydrochloride (KWD 2019) is a synthetic allylamine derivative structurally related to naftifine. Terbinafine is active against dermatophytes.

SE:30 nM(ki)

Terbinafine (50 μM to 100 μM) inhibits only marginally the metabolism of ethoxycoumarin (CYP1A2), tolbutamide (CYP2C9), or ethynylestradiol, CsA, and cortisol. Terbinafine proves to be a potent inhibitor of the CYP2D6-mediated dextromethorphan O-demethylation and bufuralol 1-hydroxylation with IC50values of 0.2 μM and 0.25 μM, respectively. [1] Terbinafine is highly activ Aspergillus isolates (minimum inhibitory concentration [MIC] 0.01 to 2 mg/mL) with a primary fungicidal action (minimum fungicidal concentration [MFC] 0.02 to 4 mg/mL). [2] Terbinafine inhibits dextromethorphan O-demethylation with an apparent Ki ranging from 28 to 44 nM in human hepatic microsomes and averaging 22.4 nM for the heterologously expressed enzymes. [3] Terbinafine shows a very strong activity in vitro against Penicillium spp., Paecilomyces spp., Trichoderma spp., Acremonium spp. and Arthrographis spp. with GMs <1 mg/L. [4] Terbinafine decreases the levels of phosphorylated extracellular signal-regulated kinase (ERK). Terbinafine might cause a decrease of MEK, which in turn up-regulates p53 through the inhibition of ERK phosphorylation, and finally causes an increase of p21expression and cell-cycle arrest. [5]

Terbinafine demonstrates efficacy both as a topical application and through oral administration in experimental dermatophytoses. Notably, in guinea pigs infected with fungi, a significant decrease in skin temperature is observed after the fourth terbinafine treatment[6].