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Mycamine (Micafungin Sodium) - Description and Clinical Pharmacology



Mycamine is a sterile, lyophilized product for intravenous (IV) infusion that contains micafungin sodium. Micafungin sodium is a semisynthetic lipopeptide (echinocandin) synthesized by a chemical modification of a fermentation product of Coleophoma empetri F-11899. Micafungin inhibits the synthesis of 1, 3-beta-D-glucan, an integral component of the fungal cell wall.

Each single-use vial contains 50 mg or 100 mg micafungin sodium, 200 mg lactose, with citric acid and/or sodium hydroxide (used for pH adjustment). Mycamine must be diluted with 0.9% Sodium Chloride Injection, USP, or 5% Dextrose Injection, USP [see Dosage and Administration (2)]. Following reconstitution with 0.9% Sodium Chloride Injection, USP, the resulting pH of the solution is between 5-7.

Micafungin sodium is chemically designated as:

Pneumocandin A0,1-[(4R,5R)-4,5-dihydroxy-N 2-[4-[5-[4-(pentyloxy)phenyl]-3-isoxazolyl]benzoyl]-L-ornithine]-4-[(4S)-4-hydroxy-4-[4-hydroxy-3-(sulfooxy)phenyl]-L-threonine]-, monosodium salt.

The chemical structure of micafungin sodium is:

The empirical/molecular formula is C56H70N9NaO23S and the formula weight is 1292.26.

Micafungin sodium is a light-sensitive, hygroscopic white powder that is freely soluble in water, isotonic sodium chloride solution, N,N-dimethylformamide and dimethylsulfoxide, slightly soluble in methyl alcohol, and practically insoluble in acetonitrile, ethyl alcohol (95%), acetone, diethyl ether and n-hexane.


Mechanism of Action

Micafungin is a member of the echinocandin class of antifungal agents [see Clinical Pharmacology ] _Refi4i_section_id_914a92f5-5b2a-44d1-9d.



The pharmacokinetics of micafungin were determined in healthy subjects, hematopoietic stem cell transplant recipients, and patients with esophageal candidiasis up to a maximum daily dose of 8 mg/kg body weight.

The relationship of area under the concentration-time curve (AUC) to micafungin dose was linear over the daily dose range of 50 mg to 150 mg and 3 mg/kg to 8 mg/kg body weight.

Steady-state pharmacokinetic parameters in relevant patient populations after repeated daily administration are presented in Table 7.

Table 7. Pharmacokinetic Parameters of Micafungin in Adult Patients



Dose (mg)

Pharmacokinetic Parameters

(Mean ± Standard Deviation)



AUC0-24 1






Patients with IC 2

[Day 1]







[Steady State]







HIV 3 - Positive

Patients with EC 4 [Day 1]



















[Day 14 or 21]





















[Day 7]





per kg






















1 AUC 0-infinity is presented for day 1; AUC 0-24 is presented for steady state.
2 candidemia or other Candida Infections
3 human immunodeficiency virus
4 esophageal candidiasis
5 hematopoietic stem cell transplant

Pediatric Patients 4 months of age and older

Micafungin pharmacokinetics in 229 pediatric patients 4 months through 16 years of age were characterized using population pharmacokinetics. Micafungin exposure was dose proportional across the dose and age range studied.

Table 8. Summary (Mean +/- Standard Deviation) of Micafungin Pharmacokinetics in Pediatric Patients 4 Months of Age and older (Steady-State)

Body weight group


Dose 1

Cmax.ss 2

(mcg·h /mL)



30 kg or less



7.1 +/- 4.7

55 +/- 16

12.5 +/- 4.6

0.328 +/- 0.091


14.2 +/- 9.3

109 +/- 31


21.3 +/- 14.0

164 +/- 47

Greater than 30 kg



8.7 +/- 5.6

67 +/- 17

13.6 +/- 8.8

0.241 +/- 0.061


17.5 +/- 11.2

134 +/- 33


23.0 +/- 14.5

176 +/- 42

1 Or the equivalent if receiving the adult dose (50, 100, or 150 mg)
2 Derived from simulations from the population PK model.
3 Derived from the population PK model

Special Populations

Adult Patients with Renal Impairment

Mycamine does not require dose adjustment in patients with renal impairment. A single 1-hour infusion of 100 mg Mycamine was administered to 9 adult subjects with severe renal impairment (creatinine clearance less than 30 mL/min) and to 9 age-, gender-, and weight-matched subjects with normal renal function (creatinine clearance greater than 80 mL/min). The maximum concentration (Cmax) and AUC were not significantly altered by severe renal impairment.

Since micafungin is highly protein bound, it is not dialyzable. Supplementary dosing should not be required following hemodialysis.

Adult Patients with Hepatic Impairment

  • •A single 1-hour infusion of 100 mg Mycamine was administered to 8 adult subjects with moderate hepatic impairment (Child-Pugh score 7-9) and 8 age-, gender-, and weight-matched subjects with normal hepatic function. The Cmax and AUC values of micafungin were lower by approximately 22% in subjects with moderate hepatic impairment compared to normal subjects. This difference in micafungin exposure does not require dose adjustment of Mycamine in patients with moderate hepatic impairment.
  • •A single 1-hour infusion of 100 mg Mycamine was administered to 8 adult subjects with severe hepatic impairment (Child-Pugh score 10-12) and 8 age-, gender-, ethnic- and weight-matched subjects with normal hepatic function. The mean Cmax and AUC values of micafungin were lower by approximately 30% in subjects with severe hepatic impairment compared to normal subjects. The mean Cmax and AUC values of M-5 metabolite were approximately 2.3-fold higher in subjects with severe hepatic impairment compared to normal subjects; however, this exposure (parent and metabolite) was comparable to that in patients with systemic Candida infection. Therefore, no Mycamine dose adjustment is necessary in patients with severe hepatic impairment.


The mean ± standard deviation volume of distribution of micafungin at terminal phase was 0.39 ± 0.11 L/kg body weight when determined in adult patients with esophageal candidiasis at the dose range of 50 mg to 150 mg.

Micafungin is highly (greater than 99%) protein bound in vitro, independent of plasma concentrations over the range of 10 to 100 mcg/mL. The primary binding protein is albumin; however, micafungin, at therapeutically relevant concentrations, does not competitively displace bilirubin binding to albumin. Micafungin also binds to a lesser extent to α1-acid-glycoprotein.


Micafungin is metabolized to M-1 (catechol form) by arylsulfatase, with further metabolism to M-2 (methoxy form) by catechol-O-methyltransferase. M-5 is formed by hydroxylation at the side chain (ω-1 position) of micafungin catalyzed by cytochrome P450 (CYP) isozymes. Even though micafungin is a substrate for and a weak inhibitor of CYP3A in vitro, hydroxylation by CYP3A is not a major pathway for micafungin metabolism in vivo. Micafungin is neither a P-glycoprotein substrate nor inhibitor in vitro.

In four healthy volunteer studies, the ratio of metabolite to parent exposure (AUC) at a dose of 150 mg/day was 6% for M-1, 1% for M-2, and 6% for M-5. In patients with esophageal candidiasis, the ratio of metabolite to parent exposure (AUC) at a dose of 150 mg/day was 11% for M-1, 2% for M-2, and 12% for M-5.


The excretion of radioactivity following a single intravenous dose of 14C-micafungin sodium for injection (25 mg) was evaluated in healthy volunteers. At 28 days after administration, mean urinary and fecal recovery of total radioactivity accounted for 82.5% (76.4% to 87.9%) of the administered dose. Fecal excretion is the major route of elimination (total radioactivity at 28 days was 71% of the administered dose).


Mechanism of Action

Micafungin inhibits the synthesis of 1, 3-beta-D-glucan, an essential component of fungal cell walls, which is not present in mammalian cells.

Drug Resistance

There have been reports of clinical failures in patients receiving Mycamine therapy due to the development of drug resistance. Some of these reports have identified specific mutations in the FKS protein component of the glucan synthase enzyme that are associated with higher MICs and breakthrough infection.

Activity In Vitro and In Clinical Infections

Micafungin has been shown to be active against most isolates of the following Candida species, both in vitro and in clinical infections:

Candida albicans
Candida glabrata
Candida guilliermondii
Candida krusei
Candida parapsilosis
Candida tropicalis

Susceptibility Testing Methods

The interpretive standards for micafungin against Candida species are applicable only to tests performed using Clinical Laboratory and Standards Institute (CLSI) microbroth dilution reference method M27-A3 for minimum inhibitory concentration (MIC; based on partial inhibition endpoint) and CLSI disk diffusion reference method M44-A2; both MIC and zone diameter results are read at 24 hours.

When available, the clinical microbiology laboratory should provide the results of in vitro susceptibility test results for antimicrobial drug products used in resident hospitals to the physician as periodic reports that describe the susceptibility profile of pathogens. These reports should aid the physician in selecting an antifungal drug product for treatment. The techniques for Broth Microdilution and Disk Diffusion are described below.

Broth Microdilution Technique

Quantitative methods are used to determine antifungal MICs. These MICs provide estimates of the susceptibility of Candida species to antifungal agents. MICs should be determined using a standardized CLSI procedure1,2. Standardized procedures are based on a microdilution method (broth) with standardized inoculum concentrations and standardized concentrations of micafungin powder. The MIC values should be interpreted according to the criteria provided in Table 9.

Disk Diffusion Technique

Qualitative methods that require measurement of zone diameters also provide reproducible estimates of the susceptibility of Candida species to antifungal agents. The CLSI procedure3 uses standardized inoculum concentrations and paper disks impregnated with 10 mcg of micafungin to test the susceptibility of Candida species to micafungin at 24 hours. Disk diffusion interpretive criteria are provided in Table 9.

Table 9. Susceptibility Interpretive Criteria for Micafungin


Broth Microdilution MIC (mcg/mL)
at 24 hours

Disk Diffusion at 24 hours

(Zone diameters in mm)



Intermediate (I)





Intermediate (I)



Candida albicans

≤ 0.25


≥ 1

≥ 22


≤ 19

Candida tropicalis

≤ 0.25


≥ 1

≥ 22


≤ 19

Candida krusei

≤ 0.25


≥ 1

≥ 22


≤ 19

Candida parapsilosis

≤ 2


≥ 8

≥ 16


≤ 13

Candida guilliermondii

≤ 2


≥ 8

≥ 16


≤ 13

Candida glabrata

≤ 0.06


≥ 0.25

Not Applicable 1

Not Applicable

Not Applicable

MIC: minimum inhibitory concentration

1 Disk diffusion zone diameters have not been established for this strain/antifungal agent combination.

A report of “Susceptible” indicates that the isolate is likely to be inhibited if the antimicrobial compound in the blood reaches the concentrations usually achievable.

The “Intermediate” category implies that an infection due to the isolate may be appropriately treated in body sites where the drug is physiologically concentrated or when a high dosage of drug is used. The “Resistant” category implies that the isolates are not inhibited by the concentrations of the drug usually achievable with normal dosage schedules and clinical efficacy of the drug against the pathogen has not been reliably shown in treatment studies.

Quality Control

Standardized susceptibility test procedures require the use of quality control organisms to monitor and ensure the accuracy and precision of supplies and reagents used in the assay, and the technique of the individual performing the test1, 2, 3. Standard micafungin powder and 10 mcg disks should provide the following range of values noted in Table 10.

Table 10. Acceptable Quality Control Ranges for Micafungin to be Used in Validation of Susceptibility Test Results

QC strains

Broth microdilution (MIC in mcg/mL) at 24- hour

Disk Diffusion

(Zone diameter in mm) at 24-hour

Candida parapsilosis ATCC 1 22019

0.5 – 2.0

14 – 23

Candida krusei ATCC 6258

0.12 – 0.5

23 – 29

Candida tropicalis ATCC 750

Not Applicable 2

24 – 30

Candida albicans ATCC 90028

Not Applicable

24 – 31

MIC: minimum inhibitory concentration

1 ATCC is a registered trademark of the American Type Culture Collection.
2 Quality control ranges have not been established for this strain/antifungal agent combination.


Carcinogenesis, Mutagenesis, Impairment of Fertility

Hepatic carcinomas and adenomas were observed in a 6-month intravenous toxicology study with an 18-month recovery period of micafungin sodium in rats designed to assess the reversibility of hepatocellular lesions.

Rats administered micafungin sodium for 3 months at 32 mg/kg/day (corresponding to 8 times the highest recommended human dose [150 mg/day], based on AUC comparisons), exhibited colored patches/zones, multinucleated hepatocytes and altered hepatocellular foci after 1 or 3 month recovery periods, and adenomas were observed after a 21-month recovery period. Rats administered micafungin sodium at the same dose for 6 months exhibited adenomas after a 12-month recovery period; after an 18-month recovery period, an increased incidence of adenomas was observed, and additionally, carcinomas were detected. A lower dose of micafungin sodium (equivalent to 5 times the human AUC) in the 6-month rat study resulted in a lower incidence of adenomas and carcinomas following 18 months recovery. The duration of micafungin dosing in these rat studies (3 or 6 months) exceeds the usual duration of Mycamine dosing in patients, which is typically less than 1 month for treatment of esophageal candidiasis, but dosing may exceed 1 month for Candida prophylaxis.

Although the increase in carcinomas in the 6-month rat study did not reach statistical significance, the persistence of altered hepatocellular foci subsequent to Mycamine dosing, and the presence of adenomas and carcinomas in the recovery periods suggest a causal relationship between micafungin sodium, altered hepatocellular foci, and hepatic neoplasms. Whole-life carcinogenicity studies of Mycamine in animals have not been conducted, and it is not known whether the hepatic neoplasms observed in treated rats also occur in other species, or if there is a dose threshold for this effect.

Micafungin sodium was not mutagenic or clastogenic when evaluated in a standard battery of in vitro and in vivo tests (i.e., bacterial reversion - S. typhimurium, E. coli; chromosomal aberration; intravenous mouse micronucleus).

Male rats treated intravenously with micafungin sodium for 9 weeks showed vacuolation of the epididymal ductal epithelial cells at or above 10 mg/kg (about 0.6 times the recommended clinical dose for esophageal candidiasis, based on body surface area comparisons). Higher doses (about twice the recommended clinical dose, based on body surface area comparisons) resulted in higher epididymis weights and reduced numbers of sperm cells. In a 39-week intravenous study in dogs, seminiferous tubular atrophy and decreased sperm in the epididymis were observed at 10 and 32 mg/kg, doses equal to about 2 and 7 times the recommended clinical dose, based on body surface area comparisons. There was no impairment of fertility in animal studies with micafungin sodium.

Animal Toxicology and/or Pharmacology

High doses of micafungin sodium (5 to 8 times the highest recommended human dose, based on AUC comparisons) have been associated with irreversible changes to the liver when administered for 3 or 6 months, and these changes may be indicative of pre-malignant processes [see Nonclinical Toxicology].

Reproductive Toxicology Studies

Micafungin sodium administration to pregnant rabbits (intravenous dosing on days 6 to 18 of gestation) resulted in visceral abnormalities and abortion at 32 mg/kg, a dose equivalent to about four times the recommended dose based on body surface area comparisons. Visceral abnormalities included abnormal lobation of the lung, levocardia, retrocaval ureter, anomalous right subclavian artery, and dilatation of the ureter.


Adult Treatment of Candidemia and Other Candida Infections

Two dose levels of Mycamine were evaluated in a randomized, double-blind study to determine the efficacy and safety versus caspofungin in patients with invasive candidiasis and candidemia.  Patients were randomized to receive once daily intravenous infusions (IV) of Mycamine, either 100 mg/day or 150 mg/day or caspofungin (70 mg loading dose followed by 50 mg maintenance dose).  Patients in both study arms were permitted to switch to oral fluconazole after at least 10 days of intravenous therapy, provided they were non-neutropenic, had improvement or resolution of clinical signs and symptoms, had a Candida isolate which was susceptible to fluconazole, and had documentation of 2 negative cultures drawn at least 24 hours apart. Patients were stratified by APACHE II score (20 or less or greater than 20) and by geographic region.  Patients with Candida endocarditis were excluded from this analysis. Outcome was assessed by overall treatment success based on clinical (complete resolution or improvement in attributable signs and symptoms and radiographic abnormalities of the Candida infection and no additional antifungal therapy) and mycological (eradication or presumed eradication) response at the end of IV therapy.  Deaths that occurred during IV study drug therapy were treated as failures.

 In this study, 111/578 (19.2%) of the patients had baseline APACHE II scores of greater than 20, and 50/578 (8.7%) were neutropenic at baseline (absolute neutrophil count less than 500 cells/mm3). Outcome, relapse and mortality data are shown for the recommended dose of Mycamine (100 mg/day) and caspofungin in Table 11.

Table 11. Efficacy Analysis: Treatment Success in Patients in Study 03-0-192 with Candidemia and other Candida Infections

Mycamine 100 mg/day

n (%)

% treatment difference


Caspofungin 70/50 mg/day 1

n (%)

Treatment Success at End of IV Therapy 2

135/191 (70.7)


(-2.0, 16.3)

119/188 (63.3)

Success in Patients with Neutropenia at Baseline

14/22 (63.6)

5/11 (45.5)

Success by Site of Infection


116/163 (71.2)

103/161 (64)


4/5 (80)

5/9 (55.6)

Acute Disseminated 3

6/13 (46.2)

5/9 (55.6)




























     Intraabdominal abscess



Chronic Disseminated




4/6 (66.7)

2/5 (40)

Success by Organism 4

     C. albicans

57/81 (70.4)

45/73 (61.6)

     C. glabrata

16/23 (69.6)

19/31 (61.3)

     C. tropicalis

17/27 (63)

22/29 (75.9)

     C. parapsilosis

21/28 (75)

22/39 (56.4)

     C. krusei

5/8 (62.5)

2/3 (66.7)

     C. guilliermondii



     C. lusitaniae

2/3 (66.7)


Relapse through 6 Weeks 5


49/135 (36.3)

44/119 (37)

     Culture confirmed relapse



     Required systemic antifungal therapy



     Died during follow-up



     Not assessed



Overall study mortality

58/200 (29)

51/193 (26.4)

     Mortality during IV therapy

28/200 (14)

27/193 (14)

1 70 mg loading dose on day 1 followed by 50 mg/day thereafter (caspofungin)
2 All patients who received at least one dose of study medication and had documented invasive candidiasis or candidemia. Patients with Candida endocarditis were excluded from the analyses.
3 A patient may have had greater than 1 organ of dissemination
4 A patient may have had greater than 1 baseline infection species
5 All patients who had a culture confirmed relapse or required systemic antifungal therapy in the post treatment period for a suspected or proven Candida infection. Also includes patients who died or were not assessed in follow-up.

In two cases of ophthalmic involvement assessed as failures in the above table due to missing evaluation at the end of IV treatment with Mycamine, therapeutic success was documented during protocol-defined oral fluconazole therapy.

Adult Treatment of Esophageal Candidiasis

In two controlled trials involving 763 patients with esophageal candidiasis, 445 adults with endoscopically-proven candidiasis received Mycamine, and 318 received fluconazole for a median duration of 14 days (range 1-33 days).

Mycamine was evaluated in a randomized, double-blind study which compared Mycamine 150 mg/day (n = 260) to intravenous fluconazole 200 mg/day (n = 258) in adults with endoscopically-proven esophageal candidiasis. Most patients in this study had HIV infection, with CD4 cell counts less than 100 cells/mm3. Outcome was assessed by endoscopy and by clinical response at the end of treatment. Endoscopic cure was defined as endoscopic grade 0, based on a scale of 0-3. Clinical cure was defined as complete resolution in clinical symptoms of esophageal candidiasis (dysphagia, odynophagia, and retrosternal pain). Overall therapeutic cure was defined as both clinical and endoscopic cure. Mycological eradication was determined by culture, and by histological or cytological evaluation of esophageal biopsy or brushings obtained endoscopically at the end of treatment. As shown in Table 12, endoscopic cure, clinical cure, overall therapeutic cure, and mycological eradication were comparable for patients in the Mycamine and fluconazole treatment groups.

Table 12. Endoscopic, Clinical, and Mycological Outcomes for Esophageal Candidiasis at End-of-Treatment

Treatment Outcome 1


150 mg/day


200 mg/day

% Difference 2

(95% CI)

n = 260

n = 258

Endoscopic Cure

228 (87.7%)

227 (88.0%)

-0.3% (-5.9, +5.3)

Clinical Cure

239 (91.9%)

237 (91.9%)

0.06% (-4.6, +4.8)

Overall Therapeutic Cure

223 (85.8%)

220 (85.3%)

0.5% (-5.6, +6.6)

Mycological Eradication

141/189 (74.6%)

149/192 (77.6%)

-3.0% (-11.6, +5.6)

1 Endoscopic and clinical outcome were measured in modified intent-to-treat population, including all randomized patients who received 1 or more doses of study treatment. Mycological outcome was determined in the per protocol (evaluable) population, including patients with confirmed esophageal candidiasis who received at least 10 doses of study drug, and had no major protocol violations.
2 Calculated as Mycamine – fluconazole

Most patients (96%) in this study had Candida albicans isolated at baseline. The efficacy of Mycamine was evaluated in less than 10 patients with Candida species other than C. albicans, most of which were isolated concurrently with C. albicans.

Relapse was assessed at 2 and 4 weeks post-treatment in patients with overall therapeutic cure at end of treatment. Relapse was defined as a recurrence of clinical symptoms or endoscopic lesions (endoscopic grade greater than 0). There was no statistically significant difference in relapse rates at either 2 weeks or through 4 weeks post-treatment for patients in the Mycamine and fluconazole treatment groups, as shown in Table 13.

Table 13. Relapse of Esophageal Candidiasis at Week 2 and through Week 4 Post-Treatment in Patients with Overall Therapeutic Cure at the End of Treatment



150 mg/day

n = 223


200 mg/day

n = 220

% Difference 1

(95% CI)

Relapse 2 at

Week 2

40 (17.9%)

30 (13.6%)

4.3% (-2.5, 11.1)

Relapse Through Week 4 (cumulative)

73 (32.7%)

62 (28.2%)

4.6% (-4.0, 13.1)

1 Calculated as Mycamine – fluconazole; N = number of patients with overall therapeutic cure (both clinical and endoscopic cure at end-of-treatment);
2 Relapse included patients who died or were lost to follow-up, and those who received systemic anti-fungal therapy in the post-treatment period

In this study, 459 of 518 (88.6%) patients had oropharyngeal candidiasis in addition to esophageal candidiasis at baseline. At the end of treatment 192/230 (83.5%) Mycamine treated patients and 188/229 (82.1%) of fluconazole treated patients experienced resolution of signs and symptoms of oropharyngeal candidiasis. Of these, 32.3% in the Mycamine group, and 18.1% in the fluconazole group (treatment difference = 14.2%; 95% confidence interval [5.6, 22.8]) had symptomatic relapse at 2 weeks post-treatment. Relapse included patients who died or were lost to follow-up, and those who received systemic antifungal therapy during the post-treatment period. Cumulative relapse at 4 weeks post-treatment was 52.1% in the Mycamine group and 39.4% in the fluconazole group (treatment difference 12.7%, 95% confidence interval [2.8, 22.7]).

Prophylaxis of Candida Infections in Hematopoietic Stem Cell Transplant Recipients

In a randomized, double-blind study, Mycamine (50 mg IV once daily) was compared to fluconazole (400 mg IV once daily) in 882 [adult (791) and pediatric] patients undergoing an autologous or syngeneic (46%) or allogeneic (54%) stem cell transplant. All pediatric patients, except 2 per group, received allogeneic transplants. The status of the patients’ underlying malignancy at the time of randomization was: 365 (41%) patients with active disease, 326 (37%) patients in remission, and 195 (22%) patients in relapse. The more common baseline underlying diseases in the 476 allogeneic transplant recipients were: chronic myelogenous leukemia (22%), acute myelogenous leukemia (21%), acute lymphocytic leukemia (13%), and non-Hodgkin’s lymphoma (13%). In the 404 autologous and syngeneic transplant recipients the more common baseline underlying diseases were: multiple myeloma (37.1%), non-Hodgkin's lymphoma (36.4%), and Hodgkin's disease (15.6%). During the study, 198 of 882 (22.4%) transplant recipients had proven graft-versus-host disease; and 475 of 882 (53.9%) recipients received immunosuppressive medications for treatment or prophylaxis of graft-versus-host disease.

Study drug was continued until the patient had neutrophil recovery to an absolute neutrophil count (ANC) of 500 cells/mm3 or greater or up to a maximum of 42 days after transplant. The average duration of drug administration was 18 days (range 1 to 51 days). Duration of therapy was slightly longer in the pediatric patients who received Mycamine (median duration 22 days) compared to the adult patients who received Mycamine (median duration 18 days).

Successful prophylaxis was defined as the absence of a proven, probable, or suspected systemic fungal infection through the end of therapy (usually 18 days), and the absence of a proven or probable systemic fungal infection through the end of the 4-week post-therapy period. A suspected systemic fungal infection was diagnosed in patients with neutropenia (ANC less than 500 cells/mm3); persistent or recurrent fever (while ANC less than 500 cells/mm3) of no known etiology; and failure to respond to at least 96 hours of broad spectrum antibacterial therapy. A persistent fever was defined as four consecutive days of fever greater than 38ºC. A recurrent fever was defined as having at least one day with temperatures 38.5ºC or higher after having at least one prior temperature higher than 38ºC; or having two days of temperatures higher than 38ºC after having at least one prior temperature higher than 38ºC. Transplant recipients who died or were lost to follow-up during the study were considered failures of prophylactic therapy.

Successful prophylaxis was documented in 80.7% of adult and pediatric Mycamine recipients, and in 73.7% of adult and pediatric patients who received fluconazole (7.0% difference [95% CI = 1.5, 12.5]), as shown in Table 14, along with other study endpoints. The use of systemic antifungal therapy post-treatment was 42% in both groups.

The number of proven breakthrough Candida infections was 4 in the Mycamine and 2 in the fluconazole group.

The efficacy of Mycamine against infections caused by fungi other than Candida has not been established.

Table 14. Results from Clinical Study of Prophylaxis of Candida Infections in Hematopoietic Stem Cell Transplant Recipients

Outcome of Prophylaxis


50 mg/day

(n = 425)


400 mg/day

(n = 457)

Success 1

343 (80.7%)

337 (73.7%)


82 (19.3%)

120 (26.3%)

All Deaths  2

Proven/probable fungal infection prior to death

18 (4.2%)

1 (0.2%)

26 (5.7%)

3 (0.7%)

Proven/probable fungal infection (not resulting in death) 

6 (1.4%)

8 (1.8%)

Suspected fungal infection 3

53 (12.5%)

83 (18.2%)

Lost to follow-up

5 (1.2%)

3 (0.7%)

1 Difference (Mycamine – fluconazole): +7.0% [95% CI=1.5, 12.5]
2 Through end-of-study (4 weeks post-therapy)
3 Through end-of-therapy

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