Advantages
- A promising new drug candidate for triazole-resistant pulmonary aspergillosis, a condition for which effective treatments are currently lacking.
- A repositioning drug made by changing the formulation of Luliconazole, a generic topical antifungal drug.
- A combination of drugs that are already being used in clinical settings, and Luliconazole is effective at low doses, reducing the risk of side effects.
Current Stage and Key Data
- In vitro evaluation: Combined administration of itraconazole and a low-dose Luliconazole against 11 strains of triazole-resistant A. fumigatus. Synergy in drug sensitivity confirmed via the checkerboard method.
- In vivo evaluation: Demonstrated significant extension of survival in a triazole-resistant A. fumigatus silkworm infection model compared to untreated or monotherapy groups.
Partnering Model
- Technical evaluation, patent licensing, or collaborative R&D in coordination with the developing university.
- Target partners: Pharmaceutical or biotech companies focused on antifungal drug development and/or drug repositioning strategies.
Background
Pulmonary aspergillosis is a fungal infection caused by the Aspergillus species, classified into invasive, chronic, and allergic bronchopulmonary forms. Chronic pulmonary aspergillosis, in particular, often affects patients with underlying respiratory conditions or immunodeficiency, impacting over 3 million people worldwide with a poor 5-year survival rate of 50–60%. The emergence of A. fumigatus strains resistant to triazoles, the primary first-line treatment, has become a critical global issue. With mortality rates for resistant infections reaching up to 90%, the WHO categorized A. fumigatus in its 2022 Fungal Priority Pathogens List as a "Critical Priority Group," necessitating urgent research and development.
We discovered that triazole antifungal drugs exert their antifungal effects primarily by inhibiting Cyp51B, and that Luliconazole, an imidazole antifungal drug used as a topical medication for tinea and other conditions, primarily inhibits Cyp51A, leading to the present invention.
Principal Investigator
Hidetaka Majima (Medical Mycology Research Center, Chiba University)
Patents and References
- PCT patent pending