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Amphotericin B, a polyene antifungal antibiotic, has been produced from a strain of Streptomyces nodosus with an IC50 of 0.028–0.290 μg/ml.

In vitro: Amphotericin B was the most effective drug for treating many life-threatening fungal infections. In cells expressing TLR2 and CD14, amphotericin B induced signal transduction and inflammatory cytokine release. In primary murine macrophages and human cell lines expressing TLR2, CD14, and the adapter protein MyD88, amphotericin induced NF-κB-dependent reporter activity and cytokine release, whereas cells deficient in any of these failed to respond. Cells with TLR4 mutation were less responsive to amphotericin B stimulation than cells expressing normal TLR4 [1]. Amphotericin B could interact with cholesterol, the major sterol of mammal membranes, thus limiting the usefulness of Amphotericin B due to its relatively high toxicity [2]. Low AmB concentrations (≤ 0.1 μM) induced a polarization potential in KCl-loaded liposomes suspended in an iso-osmotic sucrose solution, indicating K+ leakage. AmB (＞ 0.1 μM) allowed cations and anions movements. LPs suspended in an iso-osmotic NaCl solution and exposed to AmB (0.05 μM) exhibited a nearly total collapse of the negative membrane potential, indicated that Na+ entered into the cells [3].

In vivo: Amphotericin B prolonged the incubation time and decreased PrPSc accumulation in the hamster scrapie model. Amphotericin B markedly resulted in reduction of PrPSc levels in mice with transmissible subacute spongiform encephalopathies (TSSE) [4].

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