TY - JOUR
T1 - The novel fungal Cyp51 inhibitor VT-1598 is efficacious in experimental models of central nervous system coccidioidomycosis caused by Coccidioides posadasii and Coccidioides immitis
AU - Wiederhold, Nathan P.
AU - Shubitz, Lisa F.
AU - Najvar, Laura K.
AU - Jaramillo, Rosie
AU - Olivo, Marcos
AU - Catano, Gabriel
AU - Trinh, Hien T.
AU - Yates, Christopher M.
AU - Schotzinger, Robert J.
AU - Garvey, Edward P.
AU - Patterson, Thomas F.
N1 - Funding Information:
This project utilized preclinical services funded by the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Department of Health and Human Services, under contracts HHSN272201100018I and HHSN272201000038I, Task Orders A28 and A98, respectively, to the University of Texas Health Science Center at San Antonio. The University of Arizona studies were funded by Viamet Pharmaceuticals,
Funding Information:
Inc., through a NIAID R21/R33 grant awarded to Viamet (AI 101497). VT-1598 and VT-1161 powder was provided by Viamet Pharmaceuticals, Inc.
Funding Information:
N.P.W. has received research support to the UT Health San Antonio from Astellas, bioMérieux, Cidara, F2G, Merck, and Viamet and has served on advisory boards for Merck, Astellas, Toyama, and Viamet. T.F.P. has received research grants to UT Health San Antonio from Astellas, Merck, and Revolution Medicines and has served as a consultant for Astellas, Gilead, Merck, Pfizer, Revolution Medicines, Toyama, Viamet, and Scynexis. L.K.N. has received travel support from Viamet Pharmaceuticals, Inc. C.M.Y., R.J.S., and E.P.G. are employees of Viamet Pharmaceuticals, Inc.
Publisher Copyright:
Copyright © 2018 American Society for Microbiology. All Rights Reserved.
PY - 2018/4
Y1 - 2018/4
N2 - Coccidioidal meningitis can cause significant morbidity, and lifelong antifungal therapy is often required. VT-1598 is a fungus-specific Cyp51 inhibitor that has potent in vitro activity against Coccidioides species. We evaluated the in vivo efficacy of VT-1598 in murine models of central nervous system coccidioidomycosis caused by C. posadasii and C. immitis. Infection was introduced via intracranial inoculation, and therapy began 48 h postinoculation. Oral treatments consisted of vehicle control, VT-1598, and positive controls of fluconazole in the C. immitis study and VT-1161 in the C. posadasii study. Treatment continued for 7 and 14 days in the fungal-burden and survival studies, respectively. Fungal burden was assessed in brain tissue collected 24 to 48 h posttreatment in the fungal-burden studies, on the days the mice succumbed to infection, or at prespecified endpoints in the survival studies. VT-1598 plasma concentrations were also measured in the C. posadasii study. VT- 1598 resulted in significant improvements in survival in mice infected with either species. In addition, the fungal burden was significantly reduced in the fungalburden studies. Plasma concentrations 48 h after dosing stopped remained above the VT-1598 MIC against the C. posadasii isolate, although levels were undetectable in the survival study after a 4-week washout. Whereas fungal burden remained suppressed after a 2-week washout in the C. immitis model, a higher fungal burden was observed in the survival arm of the C. posadasii model. This in vivo efficacy supports human studies to establish the utility of VT-1598 for the treatment of coccidioidomycosis.
AB - Coccidioidal meningitis can cause significant morbidity, and lifelong antifungal therapy is often required. VT-1598 is a fungus-specific Cyp51 inhibitor that has potent in vitro activity against Coccidioides species. We evaluated the in vivo efficacy of VT-1598 in murine models of central nervous system coccidioidomycosis caused by C. posadasii and C. immitis. Infection was introduced via intracranial inoculation, and therapy began 48 h postinoculation. Oral treatments consisted of vehicle control, VT-1598, and positive controls of fluconazole in the C. immitis study and VT-1161 in the C. posadasii study. Treatment continued for 7 and 14 days in the fungal-burden and survival studies, respectively. Fungal burden was assessed in brain tissue collected 24 to 48 h posttreatment in the fungal-burden studies, on the days the mice succumbed to infection, or at prespecified endpoints in the survival studies. VT-1598 plasma concentrations were also measured in the C. posadasii study. VT- 1598 resulted in significant improvements in survival in mice infected with either species. In addition, the fungal burden was significantly reduced in the fungalburden studies. Plasma concentrations 48 h after dosing stopped remained above the VT-1598 MIC against the C. posadasii isolate, although levels were undetectable in the survival study after a 4-week washout. Whereas fungal burden remained suppressed after a 2-week washout in the C. immitis model, a higher fungal burden was observed in the survival arm of the C. posadasii model. This in vivo efficacy supports human studies to establish the utility of VT-1598 for the treatment of coccidioidomycosis.
KW - Coccidioidal meningitis
KW - Coccidioides immitis
KW - Coccidioides posadasii
KW - Fluconazole
KW - Murine model
KW - VT-1598
UR - http://www.scopus.com/inward/record.url?scp=85044518976&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85044518976&partnerID=8YFLogxK
U2 - 10.1128/AAC.02258-17
DO - 10.1128/AAC.02258-17
M3 - Article
C2 - 29437615
AN - SCOPUS:85044518976
SN - 0066-4804
VL - 62
JO - Antimicrobial Agents and Chemotherapy
JF - Antimicrobial Agents and Chemotherapy
IS - 4
M1 - e02258-17
ER -