ASP2397 Is a Novel Natural Compound That Exhibits Rapid and Potent Fungicidal Activity against Aspergillus Species through a Specific Transporter

Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifu...

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Published inAntimicrobial agents and chemotherapy Vol. 63; no. 10
Main Authors Nakamura, Ikuko, Ohsumi, Keisuke, Takeda, Shinobu, Katsumata, Kiyomitsu, Matsumoto, Satoru, Akamatsu, Souichiro, Mitori, Hikaru, Nakai, Toru
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.10.2019
Subjects
Antifungal Agents
Aspergillus
Aspergillus fumigatus
Coordination Complexes
Fungal Proteins
Peptides, Cyclic
Pharmacology
antifungal agent
fungicidal
aspergillosis
siderophore
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Abstract Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against (including azole-sensitive and azole-resistant isolates), , and at an MIC range of 1 to 4 μg/ml in human serum. Time-kill curve experiments showed that ASP2397 reduced germinated conidia of by more than 1 log CFU within 6 h. In addition, ASP2397 inhibited hyphal elongation from germinated conidia of , , and more rapidly than voriconazole. Under conditions of delayed treatment initiation in an IPA mouse model, ASP2397 had efficacy superior to that of posaconazole, with 100% survival and over 1 log CFU/g reduction in lung fungal burden. Histopathological investigation of lungs also showed that ASP2397 markedly suppressed disease progression. To clarify its mechanism of action, we generated a UV-induced mutant of with low susceptibility to ASP2397. The mutant had a point mutation in the siderophore transporter gene , which is absent in mammalian cells. These findings suggest that ASP2397 may improve clinical treatment options for IPA.
AbstractList Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against Aspergillus fumigatus (including azole-sensitive and azole-resistant isolates), A. terreus, and A. flavus at an MIC range of 1 to 4 μg/ml in human serum. Time-kill curve experiments showed that ASP2397 reduced germinated conidia of A. fumigatus by more than 1 log10 CFU within 6 h. In addition, ASP2397 inhibited hyphal elongation from germinated conidia of A. fumigatus, A. terreus, and A. flavus more rapidly than voriconazole. Under conditions of delayed treatment initiation in an IPA mouse model, ASP2397 had efficacy superior to that of posaconazole, with 100% survival and over 1 log10 CFU/g reduction in lung fungal burden. Histopathological investigation of lungs also showed that ASP2397 markedly suppressed disease progression. To clarify its mechanism of action, we generated a UV-induced mutant of A. fumigatus with low susceptibility to ASP2397. The mutant had a point mutation in the siderophore transporter gene sit1, which is absent in mammalian cells. These findings suggest that ASP2397 may improve clinical treatment options for IPA.
Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against (including azole-sensitive and azole-resistant isolates), , and at an MIC range of 1 to 4 μg/ml in human serum. Time-kill curve experiments showed that ASP2397 reduced germinated conidia of by more than 1 log CFU within 6 h. In addition, ASP2397 inhibited hyphal elongation from germinated conidia of , , and more rapidly than voriconazole. Under conditions of delayed treatment initiation in an IPA mouse model, ASP2397 had efficacy superior to that of posaconazole, with 100% survival and over 1 log CFU/g reduction in lung fungal burden. Histopathological investigation of lungs also showed that ASP2397 markedly suppressed disease progression. To clarify its mechanism of action, we generated a UV-induced mutant of with low susceptibility to ASP2397. The mutant had a point mutation in the siderophore transporter gene , which is absent in mammalian cells. These findings suggest that ASP2397 may improve clinical treatment options for IPA.
Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against Aspergillus fumigatus (including azole-sensitive and azole-resistant isolates), A. terreus , and A. flavus at an MIC range of 1 to 4 μg/ml in human serum. ABSTRACT Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against Aspergillus fumigatus (including azole-sensitive and azole-resistant isolates), A. terreus , and A. flavus at an MIC range of 1 to 4 μg/ml in human serum. Time-kill curve experiments showed that ASP2397 reduced germinated conidia of A. fumigatus by more than 1 log 10 CFU within 6 h. In addition, ASP2397 inhibited hyphal elongation from germinated conidia of A. fumigatus , A. terreus , and A. flavus more rapidly than voriconazole. Under conditions of delayed treatment initiation in an IPA mouse model, ASP2397 had efficacy superior to that of posaconazole, with 100% survival and over 1 log 10 CFU/g reduction in lung fungal burden. Histopathological investigation of lungs also showed that ASP2397 markedly suppressed disease progression. To clarify its mechanism of action, we generated a UV-induced mutant of A. fumigatus with low susceptibility to ASP2397. The mutant had a point mutation in the siderophore transporter gene sit1 , which is absent in mammalian cells. These findings suggest that ASP2397 may improve clinical treatment options for IPA.
Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against Aspergillus fumigatus (including azole-sensitive and azole-resistant isolates), A. terreus , and A. flavus at an MIC range of 1 to 4 μg/ml in human serum. Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug with rapid-onset and potent fungicidal activity is needed. The novel cyclic hexapeptide ASP2397 (currently known as VL-2397) exhibited antifungal activity against Aspergillus fumigatus (including azole-sensitive and azole-resistant isolates), A. terreus , and A. flavus at an MIC range of 1 to 4 μg/ml in human serum. Time-kill curve experiments showed that ASP2397 reduced germinated conidia of A. fumigatus by more than 1 log 10 CFU within 6 h. In addition, ASP2397 inhibited hyphal elongation from germinated conidia of A. fumigatus , A. terreus , and A. flavus more rapidly than voriconazole. Under conditions of delayed treatment initiation in an IPA mouse model, ASP2397 had efficacy superior to that of posaconazole, with 100% survival and over 1 log 10 CFU/g reduction in lung fungal burden. Histopathological investigation of lungs also showed that ASP2397 markedly suppressed disease progression. To clarify its mechanism of action, we generated a UV-induced mutant of A. fumigatus with low susceptibility to ASP2397. The mutant had a point mutation in the siderophore transporter gene sit1 , which is absent in mammalian cells. These findings suggest that ASP2397 may improve clinical treatment options for IPA.
Author Katsumata, Kiyomitsu
Nakamura, Ikuko
Matsumoto, Satoru
Takeda, Shinobu
Ohsumi, Keisuke
Akamatsu, Souichiro
Mitori, Hikaru
Nakai, Toru
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Keywords antifungal agent
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aspergillosis
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Citation Nakamura I, Ohsumi K, Takeda S, Katsumata K, Matsumoto S, Akamatsu S, Mitori H, Nakai T. 2019. ASP2397 is a novel natural compound that exhibits rapid and potent fungicidal activity against Aspergillus species through a specific transporter. Antimicrob Agents Chemother 63:e02689-18. https://doi.org/10.1128/AAC.02689-18.
Present address: Satoru Matsumoto, Clinical Trial Testing Department, LSI Medience Co., Tokyo, Japan; Souichiro Akamatsu, Infectious Disease Unit, Department of Medical Innovations, New Drug Research Division, Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan.
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Snippet Current therapies against invasive pulmonary aspergillosis (IPA) have a limited cure rate. Given that a delay in treatment initiation may be fatal, a new drug...
SourceID pubmedcentral
proquest
crossref
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pubmed
SourceType Open Access Repository
Aggregation Database
Index Database
SubjectTerms Antifungal Agents
Aspergillus
Aspergillus fumigatus
Coordination Complexes
Fungal Proteins
Peptides, Cyclic
Pharmacology
Title ASP2397 Is a Novel Natural Compound That Exhibits Rapid and Potent Fungicidal Activity against Aspergillus Species through a Specific Transporter
URI https://www.ncbi.nlm.nih.gov/pubmed/31405853
https://journals.asm.org/doi/10.1128/AAC.02689-18
https://search.proquest.com/docview/2272735722
https://pubmed.ncbi.nlm.nih.gov/PMC6761492
Volume 63
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