What other options are available for difficult to treat candida auris fungemia besides micafungin and amphotericin B? Is there any data to add flucytosine or alternative antifungal for persistent fungemia?

Comment by InpharmD Researcher

Current CDC guidance recommends an echinocandin as initial therapy and liposomal amphotericin B for echinocandin resistance or lack of improvement after 5 days; fosmanogepix or ibrexafungerp may be considered through expanded access for pan-resistant infections. In a single-arm phase 2 study of 9 patients with C. auris candidemia, fosmanogepix achieved treatment success in 88.9% at the end of therapy and 66.7% at 2-week follow-up, with 88.9% survival at Day 30. In contrast, published clinical evidence for ibrexafungerp specifically in C. auris infection remains limited to preliminary reports, with additional evidence derived primarily from broader invasive candidiasis studies and in vitro susceptibility testing. No clinical data support the addition of flucytosine for persistent fungemia; available evidence is limited to in vitro studies demonstrating synergy or partial synergy with anidulafungin and predominantly indifferent but nonantagonistic interactions with micafungin, amphotericin B, or voriconazole. Overall, fosmanogepix has limited direct clinical evidence as an alternative therapy, whereas clinical evidence supporting ibrexafungerp or flucytosine-containing regimens for difficult-to-treat or persistent C. auris fungemia remains limited.

Background

According to 2024 CDC recommendations, an echinocandin is the preferred initial treatment for Candida auris infection in adults and children aged ≥2 months; available options include anidulafungin, caspofungin, and micafungin. Liposomal amphotericin B (5 mg/kg IV daily) should be considered when susceptibility testing indicates echinocandin resistance or when the patient does not improve after 5 days of echinocandin therapy. For infections caused by pan-resistant isolates, the investigational antifungals fosmanogepix or ibrexafungerp may be considered through expanded-access programs, although the CDC states that treatment recommendations for echinocandin-resistant and pan-resistant infections are based on limited evidence. The guidance does not discuss adding flucytosine or provide data supporting flucytosine-containing combination therapy for persistent C. auris fungemia. [1]

With the growing concerns of multi-resistant Candida species, such as Candida auris and some Candida glabrata isolates, and the limited number of antifungal drug classes, recent reviews discussed the ongoing efforts on the development of novel antifungal agents. Ibrexafungerp, a triterpenoid derived from enfumafungin, inhibits the (1,3)-beta-D-glucan synthase. As such, despite its structural difference from echinocandins, both therapeutic classes exhibit fungicidal antifungal activity via the same target. Additionally, as ibrexafungerp has been observed to bind to different binding sites on the target enzyme and only partially overlaps with that of echinocandins, ibrexafungerp can maintain antifungal activity against a majority of FKS-mutant echinocandin resistant isolates. Compared to echinocandins in vitro, ibrexafungerp exerts minimum inhibitory concentrations (MICs) for Candida spp. that are relatively higher compared to other echinocandins, except for C. parapsilosis. Murine models also demonstrated oral administration to be effective in treating invasive candidiasis caused by different Candida spp., including C. auris and C. glabrata FKS-mutant isolates. Available clinical data pertaining to the clinical use of ibrexafungerp in various fungal infections are primarily limited to phase II trials. One ongoing open-label phase III study (NCT 03363841) aims to evaluate the efficacy, safety, tolerability, and pharmacokinetics of oral ibrexafungerp as an emergency use treatment for patients with a documented C. auris infection. While published results are currently unavailable, based on preliminary findings from a conference report, one review states infections were completely resolved (culture negative) in two cases after treatment with ibrexafungerp, including a case with difficult-to-treat C. auris that persisted after treatment with fluconazole and micafungin. The use of ibrexafungerp against C.auris infections and echinocandin-resistant isolates requires further validation in clinical settings. [2], [3], [4], [5], [6]

A phase 2, randomized, open-label, multicenter study evaluated the safety and efficacy of two dosing regimens of oral ibrexafungerp (formerly SCY-078) following initial echinocandin therapy in non-neutropenic patients with invasive candidiasis. A diagnosis of invasive candidiasis required a positive blood culture or positive culture from another normally sterile site for Candida, collected prior to the start of echinocandin treatment; patients with Candida endocarditis, endophthalmitis, osteomyelitis, meningitis, or chronic disseminated candidiasis were potential candidates for inclusion, as well as patients who received > 10 days of echinocandin therapy prior to enrollment. Patients who were eligible received initial therapy with an echinocandin for 3-10 days. Those who were clinically stable, afebrile for at least 24 hours, had negative blood cultures for at least 48 hours, and could receive oral medications were randomized 1:1:1 to receive oral ibrexafungerp 1,000 mg on day 1 followed by 500 mg daily; oral ibrexafungerp 1,250 mg on day 1 followed by 750 mg daily, or standard of care (oral fluconazole 800 mg, as a single dose, on day 1 followed by 400 mg once daily or intravenous micafungin 100 mg once daily, as per in vitro susceptibility results). Population pharmacokinetic analysis observed that an ibrexafungerp 750 mg regimen is predicted to achieve the target exposure in approximately 85% of the population. Rates of adverse events were similar between the ibrexafungerp groups and the fluconazole group. All groups had similar favorable response rates: 86% for ibrexafungerp 750 mg vs.71% for both fluconazole and ibrexafungerp 500 mg. Of note, the frequency of different Candida isolates and antifungal susceptibility was not reported within the population. [7]

A 2020 in vitro study investigated the susceptibility of pan-resistant C.auris isolates to ibrexafungerp and other antifungal agents. The study highlighted that prior laboratory tests on ibrexafungerp demonstrated its broad effectiveness against various Candida species, including fluconazole-resistant C. albicans and C. auris. In addition to ibrexafungerp, the study examined several other antifungal drugs, namely fluconazole, voriconazole, itraconazole, isavuconazole, posaconazole, anidulafungin, caspofungin, micafungin, amphotericin B, and flucytosine. The results indicated that all five pan-resistant C. auris isolates exhibited susceptibility to ibrexafungerp, with low MICs ranging from 0.12 to 1. Among the 195 C. auris isolates with varying degrees of antifungal resistance, the average ibrexafungerp MIC was determined to be 0.407 mcg/mL. Notably, one C. auris isolate showed a higher ibrexafungerp MIC of 8. The range of ibrexafungerp MICs observed in this study aligns well with serum concentrations achievable according to previous preclinical pharmacokinetic and pharmacodynamic investigations, as well as murine models of disseminated candidiasis. The study emphasized the remarkable characteristics of C. auris, such as its nearly universal resistance to fluconazole, as well as unusually elevated resistance to azoles, echinocandins, and amphotericin B. The exact mechanisms underlying these resistance patterns remain unclear. The findings of this study underscore the need for further comprehensive assessments of ibrexafungerp, including expanded clinical trials, to gain deeper insights into its therapeutic potential for combating C. auris infections. [8]

Another 2020 study evaluated the in vitro activity of ibrexafungerp against C. auris isolates, including those that were both highly fluconazole- and echinocandin-resistant, compared to six comparator antifungal agents (anidulafungin, micafungin, amphotericin B, fluconazole, voriconazole, and isavuconazole); in vitro activity against C. albicans and C. glabrata were tested as well. Three C. auris reference strains, and 122 C. auris, 16 C. albicans, and 16 C. glabrata isolates were included. Ibrexafungerp MICs against the 122 C. auris isolates ranged from 0.06 to 2 mg/L, with an MIC50 of 0.5 mg/L, showing uniform susceptibility. Eight isolates displayed high MICs to anidulafungin (4 to 32 mg/L) and micafungin (32 mg/L); these isolates harbored fks alterations and all displayed wild-type susceptibility to ibrexafungerp (MIC 0.25 mg/L [n= 3] or 0.5 mg/L [n= 5]). Except for one isolate, all were fluconazole-resistant and showed variable susceptibility to voriconazole and isavuconazole. Against the C. albicans and C. glabrata isolates, modal MICs of ibrexafungerp were 0.06 mg/L and 0.25 mg/L, respectively. [9]

Literature Review

A search of the published medical literature revealed 4 studies investigating the researchable question:

Level of evidence

C - Multiple studies with limitations or conflicting results Read more→

Please see Tables 1-4 for your response.

Clinical Efficacy and Safety of a Novel Antifungal, Fosmanogepix, in Patients with Candidemia Caused by Candida auris: Results from a Phase 2 Trial
Design	Multicenter, open-label, single-arm study N= 9
Objective	To assess the efficacy and safety of fosmanogepix in patients with candidemia and/or invasive candidiasis caused by Candida auris, with limited antifungal treatment options
Study Groups	All patients (n= 9)
Inclusion Criteria	Eligible participants were ≥18 years, with established candidemia and/or invasive candidiasis caused by C. auris, cultured within 120 h (for candidemia) or 168 h (for invasive candidiasis without candidemia) with accompanying clinical signs and limited treatment options
Exclusion Criteria	Severe or moderate hepatic impairment, concomitant use of strong CYP inhibitors, life expectancy <7 days, diagnosis of C. krusei infection, deep-seated Candida-related infections requiring >42 days of treatment, pregnancy or lactation
Methods	Participants were enrolled at 2 South African sites and received fosmanogepix within 12 hours of enrollment. A 1,000-mg IV loading dose was administered over 3 hours twice on Day 1, 12 hours apart, followed by 600 mg IV over 3 hours once daily. From Day 4, clinically stable participants able to swallow tablets could switch to oral fosmanogepix 800 mg once daily; however, all enrolled participants received IV therapy exclusively. Treatment continued for 14 days after bloodstream clearance, defined as 2 consecutive negative blood cultures, and for up to 42 days. An independent data review committee assessed treatment success at the end of study treatment (EOST) and at 2- and 4-week follow-up. Blood cultures, mycological outcomes, survival, treatment-emergent adverse events (TEAEs), pharmacokinetics, and in vitro antifungal susceptibility were evaluated. All participants had candidemia without deep-seated invasive candidiasis and had received ≥1 dose of an echinocandin for ≤4 days before fosmanogepix; no other antifungal class was administered before study treatment.
Duration	December 2019 to October 2020
Outcome Measures	Primary: Treatment success at EOST Secondary: Day 30 survival, time to first negative blood culture, mycological outcomes
Baseline Characteristics		All patients (n= 9)
	Mean age, years (range)	49.8 ± 17.7 (21 to 76)
	Age, years <65 yrs >=65 yrs	7 (77.8%) 2 (22.2%)
	Female	3 (33.3%)
	Race Black or African American White Asian	5 (55.6%) 3 (33.3%) 1 (11.1%)
	Mean BMI, kg/m2	28.11 ± 6.6
	Mean APACHE II score	12.7 ± 6.4
	ICU	9 (100.0%)
	Abbreviations: BMI, body mass index; ICU, intensive care unit.
Results		Fosmanogepix (n= 9)
	Treatment Success at EOST [95% CI]	8 (88.9%) [51.8 to 99.7]
	Sustained treatment success 2 weeks after EOST [95% CI]	6 (66.7%) [29.9% to 92.5%]
	Treatment Failure	1 (11.1%)
	Survival at Day 30	8 (88.9%)
	Mycological eradication at EOST	6 (66.7%)
	Indeterminate mycological outcome at EOST	2 (22.2%)
	Mycological recurrence at EOST/early follow-up	1 (11.1%)
	Eradication during combined 2- and 4-week follow-up	7 (77.8%)
Adverse Events	All participants experienced a treatment-emergent adverse event (TEAE); however, none were considered treatment related. The most common TEAEs were pyrexia, constipation, multiple organ dysfunction syndrome, pneumonia, pruritus, hypertension, and hypotension. Two deaths, both unrelated to FMGX treatment, were reported.
Study Author Conclusions	In conclusion, FMGX was safe and well-tolerated and demonstrated activity in participants with candidemia caused by C. auris. Based on the results from this pilot study, as well as a previously completed Phase 2 study in patients with candidemia, FMGX has the potential to be a safe and effective treatment option for patients with candidemia/invasive candidiasis.
Critique	This prospective study provides direct clinical evidence for fosmanogepix in critically ill patients with C. auris candidemia, with outcomes independently assessed and supported by isolate susceptibility testing. However, the uncontrolled sample was limited to 9 patients from 2 South African sites, all likely infected with Clade III isolates and briefly exposed to an echinocandin beforehand; therefore, the study does not establish comparative efficacy or specifically evaluate fosmanogepix as add-on therapy for persistent fungemia, and it provides no data regarding flucytosine.

Table 1 References:
[11] Vazquez JA, Pappas PG, Boffard K, et al. Clinical efficacy and safety of a novel antifungal, fosmanogepix, in patients with candidemia caused by Candida auris: results from a phase 2 trial. Antimicrob Agents Chemother. 2023;67(5):e01419-22. doi:10.1128/aac.01419-22

Managing Candida auris Fungemias: The Results of a Prospective and International Study
Design	Prospective, international study N= 162
Objective	To prospectively assess patient characteristics, outcomes, and therapeutic approaches for Candida auris fungemias
Study Groups	All patients (n= 162)
Inclusion Criteria	Patients monitored prospectively between 15 April 2024 and 15 October 2024, aged 16 years or older, with positive blood cultures for C. auris
Exclusion Criteria	Not specified
Methods	Patients were prospectively enrolled from 34 referral centers across Türkiye, India, Saudi Arabia, Egypt, Bahrain, Bangladesh, and Afghanistan. Demographic, clinical, laboratory, comorbidity, antifungal susceptibility, treatment, blood-culture clearance, and 30-day mortality data were collected through a web-based case report form. Blood cultures were obtained at least every 48 hours after initial C. auris detection until negative results were confirmed. Isolates were identified using MALDI-TOF mass spectrometry, Vitek 2 Compact, Vitek 2 plus polymerase chain reaction, or the BD Phoenix system. Antifungal susceptibility testing (AFST) used CLSI broth microdilution or Vitek 2 Compact, with CDC tentative breakpoints where available. Appropriate treatment was defined as a regimen containing ≥1 antifungal with confirmed in vitro activity against the isolate. Multidrug resistance was defined as resistance to 2 antifungal agents across the azole, polyene, and echinocandin classes; pandrug resistance was resistance to all 3 classes. Mortality risk factors were evaluated using univariate analyses and stepwise multiple binary logistic regression. No patients were reported to have received flucytosine for treatment; flucytosine was evaluated only through in vitro MIC testing.
Duration	15 April 2024 to 15 October 2024
Outcome Measures	Primary: 30-day all-cause mortality after initial positive blood culture for C. auris
Baseline Characteristics		All patients (n= 162)
	Age, median years (range)	66 (16 to 96)
	Charlson Comorbidity Index	4.1 ± 2.2
	Highest body temperature, °C	37.7 ± 0.93
	Mean arterial pressure, mmHg	89 ± 15.8
	SOFA score	7.2 ± 4.9
Results	Among 162 patients with Candida auris fungemia, 30-day all-cause mortality was 56.2% (91/162), and the median time to blood-culture negativity was 7 days (interquartile range [IQR] 4 to 14). Echinocandins were administered to 89.5% of patients; mortality was 46.8% with micafungin, 54.2% with caspofungin, and 62.5% with anidulafungin, although treatments were not randomized. Inadequate treatment was associated with 90.9% mortality versus 55.6% with adequate empirical treatment and 56.2% with culture-guided treatment (overall p= 0.041); adjusted analysis also associated lack of appropriate antifungal treatment with increased mortality (odds ratio [OR] 11.258; 90% confidence interval [CI] 1.302 to 97.310; p= 0.065). Flucytosine demonstrated an MIC50 of 0.5 µg/mL and an MIC90 of 64 µg/mL among 52 isolates, but no patients received flucytosine; therefore, the study provided no clinical efficacy or safety data supporting its addition for persistent fungemia.
Adverse Events	Not specified
Study Author Conclusions	Optimizing therapy for C. auris fungemia involves early strain identification, prompt echinocandin use, surveillance, proper catheter management, effective source control particularly in abdominal surgery, monitoring deep-seated candidal complications, and recognizing thrombocytopenia as a critical warning sign.
Critique	This large, prospective, international cohort provides clinically relevant treatment, susceptibility, clearance, and mortality data and supports echinocandins, particularly micafungin, anidulafungin, and caspofungin, as the principal active treatments in this population. However, treatment was not randomized, only 52 isolates underwent flucytosine testing, no patient was reported to receive flucytosine, and antifungal treatment durations were not reported; therefore, the study provides in vitro flucytosine data but no clinical evidence supporting its addition for persistent C. auris fungemia.

Table 2 References:
[12] Erdem H, akir-Yildirim S, Ankarali H, et al. Managing Candida auris fungemias: the results of a prospective and international study. Antimicrob Agents Chemother. 2025;69(8):e00358-25. doi:10.1128/aac.00358-25

Heightened Efficacy of Anidulafungin When Used in Combination with Manogepix or 5-Flucytosine against Candida auris In Vitro
Design	In vitro study using checkerboard assays and microfluidics-assisted imaging N= 25 isolates
Objective	To examine the efficacy of anidulafungin in combination with manogepix or 5-flucytosine against drug-resistant and susceptible Candida auris isolates
Study Groups	Drug-resistant C. auris isolates (n= 11) Susceptible C. auris isolates (n= 14)
Inclusion Criteria	Clinical C. auris isolates belonging to clades I, III, and IV, isolated from various sites (blood, urine, respiratory tract, skin)
Exclusion Criteria	None specified
Methods	Twenty-five clinical C. auris isolates from 6 patients underwent EUCAST broth microdilution susceptibility testing against anidulafungin, amphotericin B, fluconazole, voriconazole, 5-flucytosine, fosmanogepix, and manogepix. MICs were defined as the lowest concentrations producing 90% growth inhibition for amphotericin B and 50% inhibition for the other agents relative to drug-free controls. Eleven isolates with differing susceptibility profiles were selected for triplicate checkerboard combination assays. Drug interactions were categorized by fractional inhibitory concentration index (FICI) as synergistic (≤0.5), partially synergistic (>0.5 to <1), additive (1), indifferent (>1 to <4), or antagonistic (>4); response-surface analyses using the Bliss independence model were also performed. The two most promising combinations—anidulafungin plus 5-flucytosine and anidulafungin plus manogepix—were further evaluated using live-cell microfluidic imaging of multidrug-resistant isolate B12663. Colony-area changes were used to calculate doubling times.
Duration	Susceptibility and checkerboard assays: 24-hour incubation at 37°C. Microfluidic experiment: 4-hour growth period followed by antifungal exposure; the protocol specified 20 hours of perfusion, while the doubling-time analysis shown in Figure 4 was based on 16 hours of treatment after the initial 4-hour growth period.
Outcome Measures	Antifungal MIC distribution, MIC50/MIC90, and percentage of resistant isolates; FICI and interaction classification for each combination; change in individual-agent MICs during combination treatment; change in CFU/mL relative to starting inoculum and monotherapy; colony doubling time and colony area during microfluidic imaging
Baseline Characteristics	Among the 25 clinical Candida auris isolates obtained from 6 patients in the United States, 18 (72%) belonged to the South Asian clade, 5 (20%) to the South African clade, and 2 (8%) to the South American clade. Eight isolates (32%) were blood-derived. Overall, 96% of isolates were resistant to fluconazole, 40% to voriconazole, and 32% to anidulafungin; amphotericin B resistance was classified in 96%, although MIC clustering around the tentative 2-mg/L breakpoint limited the reliability of this classification. Eleven isolates with differing susceptibility profiles, including 9 South Asian and 2 South African isolates, were selected for combination testing.
Results	Manogepix and 5-flucytosine demonstrated the greatest single-agent potency, with MIC50/MIC90 values of 0.008/0.03 mg/L and 0.25/0.25 mg/L, respectively. Anidulafungin plus manogepix demonstrated synergy or partial synergy against all 11 isolates, while anidulafungin plus 5-flucytosine demonstrated synergy or partial synergy against 10 of 11 isolates; these combinations reduced anidulafungin MICs by median values of 3 and 2 log2-fold, respectively. Compared with anidulafungin monotherapy, the manogepix and 5-flucytosine combinations reduced CFU/mL by 3.6 and 2.1 log10-fold, respectively. In multidrug-resistant isolate B12663, anidulafungin plus manogepix increased doubling time from 2.75 to 9.50 hours and reduced colony area by 96.5%, whereas anidulafungin plus 5-flucytosine increased doubling time from 3.19 to 4.90 hours and reduced colony area by 63.5% versus the respective partner-agent monotherapies (p< 0.001 for both doubling-time comparisons).
Adverse Events	Not applicable (in vitro study)
Study Author Conclusions	In summary, combinations of anidulafungin with manogepix or 5-flucytosine show the highest potential against the tested C. auris isolates. Further studies are needed to determine the mechanisms that underlie these drug interactions and to evaluate their efficacy and safety in a murine model as well as whether these combinations also protect against the development of resistance.
Critique	The use of triplicate checkerboard assays, response-surface analyses, and live-cell microfluidic imaging provided internally consistent evidence that anidulafungin plus manogepix or 5-flucytosine had greater in vitro activity than the corresponding monotherapies. However, this study evaluated only 11 isolates in combination experiments, included isolates from multiple anatomical sites rather than exclusively fungemia isolates, and provided no clinical efficacy or safety outcomes; therefore, it supports these combinations as investigational options but does not establish their effectiveness for persistent C. auris fungemia in patients.

Table 3 References:
[13] John LLH, Thomson DD, Bicanic T, et al. Heightened efficacy of anidulafungin when used in combination with manogepix or 5-flucytosine against Candida auris in vitro. Antimicrob Agents Chemother. 2023;67(6):e01645-22. doi:10.1128/aac.01645-22

In Vitro Antifungal Combination of Flucytosine with Amphotericin B, Voriconazole, or Micafungin against Candida auris Shows No Antagonism
Design	In vitro study N= 15 isolates
Objective	To evaluate the in vitro interaction between flucytosine and either amphotericin B, micafungin, or voriconazole against Candida auris isolates
Study Groups	Not applicable
Inclusion Criteria	Candida auris isolates from various origins, including clinical isolates from India and control/type strains from Korea and Japan
Exclusion Criteria	Not applicable
Methods	Interactions between flucytosine and amphotericin B, micafungin, or voriconazole were evaluated using a checkerboard microdilution method based on the European Committee on Antimicrobial Susceptibility Testing reference technique. Final tested concentrations were 0.008 to 0.5 μg/mL for flucytosine, 0.008 to 4 μg/mL for amphotericin B, 0.004 to 2 μg/mL for micafungin, and 0.008 to 4 μg/mL for voriconazole. Plates were incubated at 37°C and read spectrophotometrically using a 50% growth-inhibition endpoint for drugs alone and in combination. Candida parapsilosis ATCC 22019 and Candida krusei ATCC 6258 served as quality controls. Experiments were performed in duplicate, with similar results between replicates; therefore, results from one replicate were reported in the MIC tables. Interactions were classified using the fractional inhibitory concentration index (FICI): synergy, ≤0.5; indifference, >0.5 to ≤4; and antagonism, >4. Response-surface analysis using the Bliss independence model was also performed to visualize drug interactions.
Duration	Not applicable
Outcome Measures	MIC ranges for each antifungal alone and in combination; fold changes in MICs when agents were combined; FICI values and corresponding classification as synergistic, indifferent, or antagonistic; and confirmation of selected interactions using Bliss response-surface modeling
Baseline Characteristics	The study included 15 molecularly identified Candida auris isolates. Of these, 12 (80%) were clinical isolates collected from Indian patients between 2009 and 2011, 2 (13.3%) were control/type strains collected in Korea between 2004 and 2006, and 1 (6.7%) was a type strain collected in Japan in 2009. Patient-level demographic characteristics were not reported because this was an in vitro study.
Results	Flucytosine, amphotericin B, micafungin, and voriconazole alone demonstrated MIC ranges of 0.125 to 1, 0.25 to 1, 0.125 to 0.5, and 0.03 to 4 μg/mL, respectively. Combining flucytosine with amphotericin B, micafungin, or voriconazole generally produced indifferent interactions; synergy was observed only against the Japanese type strain CBS 10913 with flucytosine plus amphotericin B or micafungin. No antagonism was observed with any combination, including flucytosine plus voriconazole.
Adverse Events	Not applicable
Study Author Conclusions	Overall, although the three combinations showed mainly indifferent interactions, we observed that flucytosine can be used in combination with other drugs without risk of antagonism. In summary, we demonstrated that there is no antagonism when flucytosine is combined in vitro with amphotericin B, voriconazole, or micafungin.
Critique	The duplicate testing, use of a standardized EUCAST-based method, and concordant FICI and Bliss-model findings strengthen the internal reliability of the in vitro results. However, synergy was limited to a single, relatively susceptible type strain, the isolates represented only the East and South Asian clades, and the study provided no clinical evidence regarding bloodstream clearance, survival, safety, dosing, or efficacy in persistent C auris fungemia; therefore, it primarily supports the absence of in vitro antagonism rather than an established clinical benefit from adding flucytosine.

Table 4 References:
[14] Bidaud AL, Botterel F, Chowdhary A, Dannaoui E. In vitro antifungal combination of flucytosine with amphotericin B, voriconazole, or micafungin against Candida auris shows no antagonism. Antimicrob Agents Chemother. 2019;63(12):e01393-19. doi:10.1128/AAC.01393-19