**Core Concept**
Ergosterol is a critical component of fungal cell membranes, playing a similar role to cholesterol in mammalian cells. Inhibiting ergosterol biosynthesis disrupts cell membrane integrity, ultimately leading to fungal cell death. Several antifungal agents target this pathway to exert their effects.

**Why the Correct Answer is Right**
Amphotericin B (Option C) does not inhibit ergosterol biosynthesis. Instead, it binds to ergosterol in the fungal cell membrane, forming pores that allow ions and small molecules to leak out, ultimately leading to cell death. This mechanism is distinct from the inhibition of ergosterol biosynthesis, which is the target for other antifungal agents.

**Why Each Wrong Option is Incorrect**
**Option A:** Ketoconazole is an imidazole antifungal that inhibits ergosterol biosynthesis by blocking the enzyme lanosterol 14α-demethylase, which is essential for converting lanosterol to ergosterol.

**Option B:** Fluconazole is a triazole antifungal that also inhibits ergosterol biosynthesis by blocking the same enzyme, lanosterol 14α-demethylase, as ketoconazole.

**Clinical Pearl / High-Yield Fact**
When choosing an antifungal agent, it's essential to understand the specific mechanism of action and potential side effects. For example, Amphotericin B can cause nephrotoxicity due to its binding to ergosterol in the cell membrane, making it essential to monitor renal function closely during treatment.

**✓ Correct Answer: C. Amphotericin B**