Drug Monograph

Isavuconazonium Sulfate (Cresemba)

isavuconazonium sulfate — prodrug of isavuconazole

Second-Generation Triazole Antifungal·Oral (Capsules) / Intravenous
Pharmacokinetic Profile
Half-Life
~130 hours (range 85–130 h); supports once-daily dosing
Metabolism
Prodrug cleaved by plasma esterases to isavuconazole; then CYP3A4, CYP3A5, and UGT
Protein Binding
>99% (albumin)
Bioavailability
~98% (oral); no clinically relevant food effect
Volume of Distribution
308–542 L; extensive tissue distribution
Clinical Information
Drug Class
Second-Generation Triazole Antifungal (prodrug)
Available Doses
186 mg capsules (= 100 mg isavuconazole); 74.5 mg capsules (= 40 mg); 372 mg IV vial (= 200 mg)
Route
Oral (capsules), IV; bioequivalent and interchangeable
Renal Adjustment
No adjustment required; no cyclodextrin vehicle (unlike voriconazole IV)
Hepatic Adjustment
Mild-moderate (Child-Pugh A/B): no adjustment. Severe (Class C): no data; monitor closely
Pregnancy
May cause fetal harm (animal data); advise contraception
Lactation
Unknown excretion in human milk; weigh benefit vs risk
Schedule / Legal Status
Prescription only (non-scheduled)
Generic Available
No (brand Cresemba only)
QTc Effect
Shortens QTc (unique among azoles); contraindicated in familial short QT syndrome
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
Invasive aspergillosisIV: adults and pediatrics ≥1 year; Capsules: adults and pediatrics ≥6 years (≥16 kg)First-lineFDA Approved
Invasive mucormycosisIV: adults and pediatrics ≥1 year; Capsules: adults and pediatrics ≥6 years (≥16 kg)MonotherapyFDA Approved

Isavuconazonium sulfate is the water-soluble prodrug of isavuconazole, a broad-spectrum triazole antifungal approved by the FDA in 2015. The SECURE trial demonstrated non-inferiority to voriconazole for invasive aspergillosis with significantly fewer drug-related adverse events, particularly in skin, ocular, and hepatobiliary categories. Unlike voriconazole, isavuconazole has activity against Mucorales, making it the only azole with FDA approval for both invasive aspergillosis and invasive mucormycosis. Key practical advantages include near-complete oral bioavailability (~98%) without food effect, linear pharmacokinetics, no cyclodextrin vehicle in the IV formulation (safe in renal impairment), and once-daily maintenance dosing after a loading period.

Off-Label Uses

Antifungal prophylaxis in high-risk immunocompromised patients — emerging data as alternative to posaconazole. Evidence quality: Moderate (growing)

Invasive candidiasis — in vitro activity and PK/PD modeling support use; limited clinical data. Evidence quality: Low

Cryptococcosis — in vitro activity documented; clinical data limited. Evidence quality: Low

Dose

Dosing

Adult Dosing — Same for All Approved Indications

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Invasive aspergillosis — IV372 mg (= 200 mg isavuconazole) IV q8h × 6 doses (48 h)372 mg IV once daily372 mg/dayInfuse over minimum 1 hour via in-line filter; start maintenance 12–24 h after last loading dose
No cyclodextrin vehicle — safe in renal impairment
Invasive aspergillosis — oralTwo 186 mg capsules (= 200 mg) PO q8h × 6 doses (48 h)Two 186 mg capsules once daily372 mg/daySwallow whole; do not crush, chew, or open; no food restriction
IV and oral are bioequivalent; no additional loading dose when switching
Invasive mucormycosis — IV or oral372 mg q8h × 6 doses (same as IA)372 mg once daily372 mg/daySame dosing as invasive aspergillosis; duration based on clinical and mycological response

Pediatric Dosing

PopulationLoading DoseMaintenance DoseMaximum DoseNotes
IV: ≥1 year10 mg/kg (as isavuconazonium sulfate) IV q8h × 6 doses10 mg/kg IV once daily372 mg per individual doseWeight-based dosing; max any single dose = 372 mg
Start maintenance 12–24 h after last loading dose
Capsules: ≥6 years (≥16 kg)Weight-based dosing using 74.5 mg and/or 186 mg capsules per PI tables; max any single dose = 372 mg
Clinical Pearl — Simplified Dosing Advantage

Isavuconazonium has the simplest dosing regimen among the mold-active triazoles. The same dose is used for both invasive aspergillosis and mucormycosis, with no dose adjustments needed for renal impairment, mild-to-moderate hepatic impairment, age, or food intake. The IV and oral formulations are bioequivalent, and no additional loading dose is required when switching between them. This contrasts sharply with voriconazole (non-linear PK, CYP2C19 polymorphism, mandatory TDM) and posaconazole (three non-interchangeable formulations, food-dependent absorption for suspension). The loading regimen of 6 doses over 48 hours achieves near-steady-state concentrations rapidly given the drug’s long half-life (~130 h).

PK

Pharmacology

Mechanism of Action

Isavuconazonium sulfate is a water-soluble prodrug that is rapidly hydrolyzed by plasma esterases to the active moiety isavuconazole and an inactive cleavage product. Isavuconazole inhibits fungal lanosterol 14α-demethylase (CYP51), the same target as other triazoles, blocking ergosterol synthesis and disrupting the fungal cell membrane. Its spectrum covers Aspergillus species (including A. fumigatus, A. niger, A. flavus, A. terreus), Candida species, Cryptococcus neoformans, and critically the Mucorales order (Rhizopus, Mucor, Lichtheimia), which distinguishes it from voriconazole. Unlike voriconazole, isavuconazole displays linear pharmacokinetics with low inter- and intra-patient variability, and its water-soluble prodrug formulation eliminates the need for cyclodextrin solubilizing agents in the IV formulation.

ADME Profile

ParameterValueClinical Implication
Absorption~98% absolute oral bioavailability; Tmax ~2–3 h; no clinically relevant food effectIV-to-oral switch without dose adjustment; capsules can be taken with or without food; can also be administered via nasogastric tube (IV solution reconstituted)
DistributionVd 308–542 L; protein binding >99% (predominantly albumin); wide tissue distributionExtensive penetration into lungs, liver, and other tissues; high protein binding means free-drug fraction is very low (~0.6–1.7%); may be affected in hypoalbuminemic patients
MetabolismProdrug cleaved by plasma esterases; isavuconazole metabolized by CYP3A4, CYP3A5, then UGT; linear PKLinear pharmacokinetics (unlike voriconazole) mean dose-proportional exposure changes; moderate CYP3A4 inhibitor (fewer drug interactions than voriconazole or posaconazole)
Eliminationt½ ~130 h (range 85–130 h); primarily fecal elimination; <1% unchanged in urine; not removed by hemodialysisVery long half-life supports once-daily maintenance dosing; loading regimen needed to achieve therapeutic levels quickly; no renal dose adjustment needed (no cyclodextrin in IV)
SE

Side Effects

Adverse event data below are from 403 adult patients treated with isavuconazonium in the Phase 3 SECURE and VITAL trials. In the SECURE trial, isavuconazole demonstrated significantly fewer drug-related adverse events compared with voriconazole, particularly in skin (33% vs 42%), ocular (15% vs 27%), and hepatobiliary (9% vs 16%) categories.

≥10%Very Common
Adverse EffectIncidenceClinical Note
Nausea26%Most common GI complaint; generally manageable; consider antiemetics
Vomiting25%May impair oral dosing; can switch to IV if persistent
Diarrhea22%Common in immunocompromised population; evaluate for infectious etiology
Headache17%Generally mild; responds to simple analgesics
Elevated liver chemistry tests16%Generally reversible; did not require discontinuation in most cases
Hypokalemia14%Correct before therapy; important given QTc-shortening effect
Constipation13%May be multifactorial in immunocompromised patients
Dyspnea12%Evaluate for underlying pulmonary disease progression
Cough12%Distinguish from underlying pulmonary infection
Peripheral edema11%Assess for cardiac and renal causes
Back pain10%Generally self-limiting
SeriousSerious (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Hepatotoxicity (hepatitis, cholestasis, hepatic failure including fatal cases)Uncommon; severe cases reported with azoles as a classDays to weeksMonitor LFTs at baseline and during therapy; discontinue if clinical hepatitis or jaundice develops; reported mainly in patients with serious underlying conditions
QTc shorteningConcentration-related effect; unique among azolesDuring therapyContraindicated in familial short QT syndrome; no QTc prolongation observed (advantage over voriconazole and posaconazole)
Exfoliative cutaneous reactionsRareVariableDiscontinue if exfoliative skin reaction develops
Infusion-related reactions (IV)Uncommon; dyspnea, chills, dizziness, paresthesia, hypoesthesiaDuring infusionDiscontinue infusion if reaction occurs
Embryo-fetal toxicityAnimal data: skeletal abnormalities, perinatal mortalityDuring pregnancyAdvise effective contraception; verify pregnancy status before initiating; do not use in pregnancy unless life-threatening infection with no alternative
DiscontinuationDiscontinuation Rates
Phase 3 Trials (403 patients)
Low overall
Most common reasons: Confusional state (0.7%), acute renal failure (0.7%), increased bilirubin (0.5%), convulsion (0.5%), dyspnea (0.5%), vomiting (0.5%)
SECURE Trial Comparison
Fewer vs voriconazole
Significantly fewer drug-related adverse events and drug discontinuations compared to voriconazole
Tolerability Advantage Over Voriconazole

In the SECURE trial, isavuconazole demonstrated significantly fewer adverse events compared with voriconazole in several key categories: skin disorders (33% vs 42%, p=0.037), ocular disorders (15% vs 27%, p=0.002), and hepatobiliary disorders (9% vs 16%, p=0.016). Notably, isavuconazole does not cause the visual disturbances characteristic of voriconazole (~21% with voriconazole), does not cause photosensitivity or phototoxicity, and shortens rather than prolongs the QTc interval. These advantages make isavuconazole an attractive alternative for patients intolerant of voriconazole.

Int

Drug Interactions

Isavuconazole is a substrate of CYP3A4 and CYP3A5, and a moderate inhibitor of CYP3A4. Its interaction profile is generally less complex than voriconazole (which inhibits CYP2C19, CYP2C9, CYP3A4) or posaconazole (strong CYP3A4 inhibitor). However, the bidirectional CYP3A4 interaction still creates important contraindications with strong inducers and inhibitors.

MajorStrong CYP3A4 Inhibitors (ketoconazole, high-dose ritonavir)
MechanismCYP3A4 inhibition significantly increases isavuconazole plasma concentrations
EffectIncreased risk of isavuconazole toxicity
ManagementConcomitant use is contraindicated
FDA PI
MajorStrong CYP3A4 Inducers (rifampin, carbamazepine, St. John’s wort, long-acting barbiturates)
MechanismCYP3A4 induction significantly decreases isavuconazole concentrations
EffectLoss of antifungal efficacy; breakthrough infections
ManagementConcomitant use is contraindicated
FDA PI
ModerateTacrolimus
MechanismCYP3A4 inhibition increases tacrolimus exposure
EffectPotential nephrotoxicity and neurotoxicity
ManagementMonitor tacrolimus trough concentrations and adjust dose as needed; effect is more modest than with voriconazole or posaconazole
FDA PI
ModerateCyclosporine
MechanismModerate CYP3A4 inhibition may increase cyclosporine levels
EffectPotential nephrotoxicity
ManagementMonitor cyclosporine levels; dose adjustment may be necessary
FDA PI
ModerateSirolimus
MechanismModerate CYP3A4 inhibition increases sirolimus exposure
EffectSirolimus toxicity
ManagementMonitor sirolimus levels and adjust dose; NOT contraindicated (unlike voriconazole and posaconazole)
FDA PI
ModerateLopinavir/ritonavir (low-dose ritonavir)
MechanismCYP3A4 inhibition increases isavuconazole levels
EffectIncreased isavuconazole exposure; potential toxicity
ManagementUse with caution; monitor for isavuconazole-related adverse effects
FDA PI
ModerateMidazolam / CYP3A4-metabolized benzodiazepines
MechanismModerate CYP3A4 inhibition increases midazolam exposure
EffectProlonged sedation
ManagementConsider dose reduction; use lorazepam (glucuronidated) as an alternative
FDA PI
MinorWarfarin
MechanismNo clinically significant interaction in PK studies
EffectMinimal impact on INR
ManagementStandard monitoring; advantage over voriconazole which significantly increases warfarin effect
FDA PI
Mon

Monitoring

  • Hepatic Function (LFTs)Baseline; during therapy
    Routine
    Elevated liver chemistry tests reported in 16% of patients. Generally reversible and did not require discontinuation. Severe hepatic reactions have been reported as a class effect with azole antifungals. Discontinue if clinical hepatitis or jaundice develops.
  • Electrolytes (K+, Mg2+)Baseline; periodically
    Routine
    Hypokalemia reported in 14% of patients. Correct before and during therapy. Important given the unique QTc-shortening effect of isavuconazole.
  • Therapeutic Drug MonitoringNot routinely required
    Trigger-based
    Due to high oral bioavailability (~98%), linear PK, and no food effect, routine TDM is generally not needed. Consider TDM in critical illness, suspected malabsorption, drug interactions, or treatment failure. An exposure-toxicity relationship has been suggested in some studies.
  • Calcineurin Inhibitor / mTOR Inhibitor LevelsAt initiation and during therapy
    Routine
    Isavuconazole moderately increases tacrolimus, cyclosporine, and sirolimus levels. Monitor trough concentrations and adjust doses accordingly. The effect is less pronounced than with voriconazole or posaconazole.
  • Dermatologic AssessmentAs needed
    Trigger-based
    Exfoliative cutaneous reactions have been reported. Discontinue if severe skin reaction develops. Unlike voriconazole, isavuconazole does not cause photosensitivity or photocarcinogenesis.
CI

Contraindications & Cautions

Absolute Contraindications

  • Hypersensitivity to isavuconazole or isavuconazonium sulfate
  • Coadministration with strong CYP3A4 inhibitors (ketoconazole, high-dose ritonavir [400 mg q12h]) — significantly increase isavuconazole levels
  • Coadministration with strong CYP3A4 inducers (rifampin, carbamazepine, St. John’s wort, long-acting barbiturates) — significantly reduce isavuconazole levels
  • Familial short QT syndrome — isavuconazole shortens QTc in a concentration-related manner

Relative Contraindications (Specialist Input Recommended)

  • Pregnancy — may cause fetal harm based on animal studies (skeletal malformations, perinatal mortality); advise effective contraception
  • Severe hepatic impairment (Child-Pugh C) — no data available; monitor for adverse reactions if use is necessary

Use with Caution

  • Concurrent immunosuppressants (tacrolimus, sirolimus, cyclosporine) — moderate CYP3A4 inhibition increases levels
  • Hepatic impairment (mild-moderate) — lower clearance observed; no dose adjustment required but monitor LFTs
  • Drug particulates from IV formulation — in-line filter required; insoluble isavuconazole precipitate may form after dilution
FDA Safety Warning QTc Shortening, Hepatic Reactions, and Embryo-Fetal Toxicity

Isavuconazole shortens the QTc interval in a concentration-related manner, which is unique among triazole antifungals. It is contraindicated in patients with familial short QT syndrome. Hepatic adverse reactions including elevations in ALT, AST, alkaline phosphatase, and total bilirubin have been reported and are generally reversible. Severe hepatic reactions including cholestasis and hepatic failure (including fatal cases) have been reported with azole antifungals in patients with serious underlying conditions. Based on animal data, isavuconazonium may cause fetal harm — effective contraception should be used during treatment.

Pt

Patient Counselling

Purpose of Therapy

Isavuconazonium (Cresemba) is a newer antifungal medication used to treat serious fungal infections of the lungs and other organs, including Aspergillus and Mucor infections. It is started with a loading dose over the first two days and then taken once daily. The capsule and IV forms work equally well, and your doctor may switch between them during your treatment.

How to Take

Swallow capsules whole — do not chew, crush, dissolve, or open them. Capsules can be taken with or without food. Take your daily dose at roughly the same time each day. If switching from IV to capsules, no additional loading dose is needed.

Nausea & Vomiting
Tell patientNausea and vomiting are common (about 1 in 4 patients). These are usually manageable and tend to improve over time. Anti-nausea medication can be used if needed.
Call prescriberIf vomiting is severe or prevents keeping the capsules down; the IV form may be substituted.
Liver Health
Tell patientBlood tests to monitor liver function are required during treatment. Most liver test changes are mild and reverse on their own.
Call prescriberImmediately if you notice yellowing of the skin or eyes, dark urine, persistent nausea, unusual tiredness, or upper abdominal pain.
Drug Interactions & Pregnancy
Tell patientSome medications can dangerously increase or decrease the effect of isavuconazonium. Always inform all healthcare providers you are taking this medication. Animal studies suggest this medicine may harm an unborn baby — reliable contraception is essential during treatment.
Call prescriberBefore starting any new medication, herbal supplement, or over-the-counter product. Immediately if pregnancy is suspected.
Skin Reactions
Tell patientUnlike some other antifungal medications, isavuconazonium does not typically cause sun sensitivity or vision changes. However, skin peeling reactions have been rarely reported.
Call prescriberIf you develop any new rash, skin peeling, or blistering.
Ref

Sources

Regulatory (PI / SmPC)
  1. Astellas Pharma US, Inc. CRESEMBA (isavuconazonium sulfate) Prescribing Information (revised 2025). U.S. Food and Drug Administration. accessdata.fda.govCurrent PI including adult and pediatric dosing (expanded in 2023/2025 for pediatric patients ≥1 year IV, ≥6 years oral), safety data from Phase 3 trials, and updated drug interaction information.
  2. Astellas Pharma US, Inc. CRESEMBA (isavuconazonium sulfate) Prescribing Information (original 2015 approval). accessdata.fda.govOriginal FDA approval label establishing indications for invasive aspergillosis and mucormycosis in adults, dosing regimen, and comprehensive safety profile from SECURE and VITAL trials.
Key Clinical Trials
  1. Maertens JA, Raad II, Marr KA, et al. Isavuconazole versus voriconazole for primary treatment of invasive mould disease caused by Aspergillus and other filamentous fungi (SECURE): a phase 3, randomised-controlled, non-inferiority trial. Lancet. 2016;387(10020):760-769. doi:10.1016/S0140-6736(15)01159-9Landmark double-blind RCT demonstrating isavuconazole non-inferiority to voriconazole for IA (42-day mortality 18.6% vs 20.2%) with significantly fewer drug-related adverse events.
  2. Marty FM, Ostrosky-Zeichner L, Cornely OA, et al. Isavuconazole treatment for mucormycosis: a single-arm open-label trial and case-control analysis. Lancet Infect Dis. 2016;16(7):828-837. doi:10.1016/S1473-3099(16)00071-2VITAL trial establishing efficacy of isavuconazole in mucormycosis (37 patients); 42-day all-cause mortality 33% in primary treatment comparable to amphotericin B matched controls (39%).
  3. Patterson TF, Thompson GR 3rd, Denning DW, et al. Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the IDSA. Clin Infect Dis. 2016;63(4):e1-e60. doi:10.1093/cid/ciw326IDSA aspergillosis guideline recommending isavuconazole alongside voriconazole as first-line treatment for invasive aspergillosis.
Mechanistic / Basic Science
  1. Shirley M, Scott LJ. Isavuconazole: a review in invasive aspergillosis and mucormycosis. Drugs. 2016;76(17):1647-1657. doi:10.1007/s40265-016-0652-6Comprehensive review of isavuconazole’s mechanism, spectrum, PK properties, and clinical trial results at the time of FDA approval.
  2. Andes DR, Ghannoum MA, Mukherjee PK, et al. Outcomes by MIC values for patients treated with isavuconazole or voriconazole for invasive aspergillosis in the phase 3 SECURE and VITAL trials. Antimicrob Agents Chemother. 2019;63(1):e01634-18. doi:10.1128/AAC.01634-18Pooled MIC-outcome analysis from SECURE and VITAL, showing no relationship between MIC <16 mcg/mL and clinical outcomes for either isavuconazole or voriconazole.
Pharmacokinetics / Special Populations
  1. Desai A, Kovanda L, Kowalski D, Lu Q, Townsend R, Bonate PL. Population pharmacokinetics of isavuconazole from phase 1 and phase 3 (SECURE) trials in adults and target attainment in patients with invasive infections due to Aspergillus and other filamentous fungi. Antimicrob Agents Chemother. 2016;60(9):5483-5491. doi:10.1128/AAC.02819-15Population PK model establishing Vd 308–542 L, CL 2.4–4.1 L/h, near-complete bioavailability, and half-life of 84.5–117.0 h in the SECURE trial population.
  2. Kovanda LL, Desai AV, Lu Q, et al. Isavuconazole population pharmacokinetic analysis using nonparametric estimation in patients with invasive fungal disease (results from the VITAL study). Antimicrob Agents Chemother. 2016;60(8):4568-4576. doi:10.1128/AAC.00514-16VITAL study PK analysis showing mean bioavailability of 96.6% (median 98.2%), mean clearance 2.5 L/h, and consistent PK across different IFD types and underlying disease groups.
  3. Desai A, Helmick M, Heo N, et al. Pharmacokinetics and bioequivalence of isavuconazole administered as isavuconazonium sulfate intravenous solution via nasogastric tube or orally in healthy subjects. Antimicrob Agents Chemother. 2021;65(9):e00442-21. doi:10.1128/AAC.00442-21Bioequivalence study demonstrating that IV solution given via NG tube achieves equivalent exposure to oral capsules, establishing an alternative route for patients who cannot swallow.
  4. Huang H, Xie H, Chaphekar N, et al. A physiologically based pharmacokinetic analysis to predict the pharmacokinetics of intravenous isavuconazole in patients with or without hepatic impairment. Antimicrob Agents Chemother. 2021;65(5):e02032-20. doi:10.1128/AAC.02032-20PBPK model confirming 98% oral bioavailability, long half-life, and reduced clearance in hepatic impairment, with no data for Child-Pugh C patients.