- 1. Name of the medicinal product
- 2. Qualitative and quantitative composition
- 3. Pharmaceutical form
- 4. Clinical particulars
- 4.1 Therapeutic indications
- 4.2 Posology and method of administration
- 4.3 Contraindications
- 4.4 Special warnings and precautions for use
- 4.5 Interaction with other medicinal products and other forms of interaction
- 4.6 Fertility, pregnancy and lactation
- 4.7 Effects on ability to drive and use machines
- 4.8 Undesirable effects
- 4.9 Overdose
- 5. Pharmacological properties
- 5.1 Pharmacodynamic properties
- 5.2 Pharmacokinetic properties
- 5.3 Preclinical safety data
- 6. Pharmaceutical particulars
- 6.1 List of excipients
- 6.2 Incompatibilities
- 6.3 Shelf life
- 6.4 Special precautions for storage
- 6.5 Nature and contents of container
- 6.6 Special precautions for disposal and other handling
- 7. Marketing authorisation holder
- 8. Marketing authorisation number(s)
- 9. Date of first authorisation/renewal of the authorisation
- 10. Date of revision of the text
PosologyA single 200 mg loading dose should be administered on Day 1, followed by 100 mg daily thereafter. Duration of treatment should be based on the patient's clinical response. In general, antifungal therapy should continue for at least 14 days after the last positive culture.
Duration of treatmentThere are insufficient data to support the 100 mg dose for longer than 35 days of treatment.Patients with renal and hepatic impairmentNo dosing adjustments are required for patients with mild, moderate, or severe hepatic impairment. No dosing adjustments are required for patients with any degree of renal insufficiency, including those on dialysis. ECALTA can be given without regard to the timing of haemodialysis (see section 5.2).
Other special populationsNo dosing adjustments are required for adult patients based on gender, weight, ethnicity, HIV positivity, or elderly (see section 5.2).
Paediatric populationThe safety and efficacy of ECALTA in children below 18 years have not been established. Currently available data are described in section 5.2 but no recommendation on a posology can be made.
Method of administrationFor intravenous use only.ECALTA should be reconstituted with water for injections to a concentration of 3.33 mg/mL and subsequently diluted to a concentration of 0.77 mg/mL. For instructions on reconstitution of the medicinal product before administration, see section 6.6.It is recommended that ECALTA be administered at a rate of infusion that does not exceed 1.1 mg/min (equivalent to 1.4 mL/min when reconstituted and diluted per instructions). Infusion associated reactions are infrequent when the rate of anidulafungin infusion does not exceed 1.1 mg/min (see section 4.4).ECALTA must not be administered as a bolus injection.
Hepatic effectsIncreased levels of hepatic enzymes have been seen in healthy subjects and patients treated with anidulafungin. In some patients with serious underlying medical conditions who were receiving multiple concomitant medicines along with anidulafungin, clinically significant hepatic abnormalities have occurred. Cases of significant hepatic dysfunction, hepatitis, and hepatic failure were uncommon in clinical trials. Patients with increased hepatic enzymes during anidulafungin therapy should be monitored for evidence of worsening hepatic function and evaluated for risk/benefit of continuing anidulafungin therapy.
Anaphylactic reactionsAnaphylactic reactions, including shock, were reported with the use of anidulafungin. If these reactions occur, anidulafungin should be discontinued and appropriate treatment administered.
Infusion-related reactionsInfusion-related adverse events have been reported with anidulafungin, including rash, urticaria, flushing, pruritus, dyspnea, bronchospasm and hypotension. Infusion-related adverse events are infrequent when the rate of anidulafungin infusion does not exceed 1.1 mg/min.Exacerbation of infusion-related reactions by co-administration of anaesthetics has been seen in a non-clinical (rat) study (see section 5.3). The clinical relevance of this is unknown. Nevertheless, care should be taken when co-administering anidulafungin and anaesthetic agents.
Fructose contentPatients with rare hereditary problems of fructose intolerance should not take this medicine.
Paediatric populationInteraction studies have only been performed in adults.
PregnancyThere are no data regarding the use of anidulafungin in pregnant women. Slight developmental effects have been observed in rabbits administered anidulafungin during pregnancy, in the presence of maternal toxicity (see section 5.3). The potential risk for humans is unknown. Therefore anidulafungin is not recommended in pregnancy.
Breast-feedingAnimal studies have shown excretion of anidulafungin in breast milk. It is not known whether anidulafungin is excreted in human breast milk. A decision on whether to continue/discontinue breast-feeding or therapy with anidulafungin should be made taking into account the benefit of breast-feeding to the child and the benefit of anidulafungin to the mother.
FertilityFor anidulafungin, there were no effects on fertility in studies conducted in male and female rats (see section 5.3).
Summary of the safety profileFifteen hundred sixty five (1565) subjects received single or multiple doses of intravenous anidulafungin in clinical trials: 1308 in Phase 2/3 trials (923 patients with candidaemia/invasive candidiasis, 355 patients with oral/oesophageal candidiasis, 30 patients with invasive aspergillosis), and 257 in Phase I studies. The safety profile of anidulafungin is based on 840 patients with candidaemia/invasive candidiasis receiving the recommended daily dose of 100 mg in 9 studies. Originally, in 3 studies (one comparative vs fluconazole, two non-comparative) 204 patients were studied; the mean duration of intravenous treatment in these patients was 13.5 days (range, 1 to 38 days) and 119 patients received ≥ 14 days of anidulafungin. In 6 additional studies (two comparative vs. caspofungin and four non-comparative), 636 patients including 53 neutropenic patients and 131 patients with deep tissue infection were studied; the mean durations of intravenous treatment in neutropenics patients and patients with deep tissue infection in these studies were 10.0 (range, 1 to 42 days) and 14.0 (range, 1 to 42 days) days, respectively. Adverse reactions were typically mild to moderate and seldom led to discontinuation. Infusion-related adverse reactions have been reported with anidulafungin in clinical studies, including flushing, hot flush, pruritus, rash, and urticaria, summarized in Table 1.
Tabulated list of adverse reactionsThe following table includes, the all-causality adverse reactions (MedDRA terms) from 840 subjects receiving 100 mg anidulafungin with frequency corresponding to very common (≥1/10), common (≥1/100 to <1/10), uncommon (≥1/1,000 to <1/100), rare (≥1/10,000 to <1/1,000), very rare (<1/10,000) and from spontaneous reports with frequency not known (cannot be estimated from the available data). Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness.Table 1. Table of Adverse Reactions
|System Organ Class||Very Common ≥ 1/10||Common ≥ 1/100 to < 1/10||Uncommon ≥ 1/1000 to <1/100||Rare ≥ 1/10,000 to <1/1,000||Very Rare < 1/10,000||Not Known|
|Blood and Lymphatic System Disorders||Coagulopathy|
|Immune System Disorders||Anaphylactic shock, anaphylactic reaction*|
|Metabolism and Nutrition Disorders||Hypokalaemia||Hyperglycaemia|
|Nervous System Disorders||Convulsion, headache|
|Vascular Disorders||Hypotension, hypertension||Flushing, hot flush|
|Respiratory, Thoracic and Mediastinal Disorders||Bronchospasm, Dyspnoea|
|Gastrointestinal Disorders||Diarrhoea, nausea||Vomiting||Abdominal pain upper|
|Hepatobiliary Disorders||Alanine aminotransferase increased, blood alkaline phosphatase increased, aspartate aminotransferase increased, blood bilirubin increased, cholestasis||Gamma-glutamyltransferase increased|
|Skin and Subcutaneous Tissue Disorders||Rash, pruritus||Urticaria|
|Renal and Urinary Disorders||Blood creatinine increased|
|General Disorders and Administration Site Conditions||Infusion site pain|
Reporting of suspected adverse reactionsReporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product.
United KingdomHealthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at www.mhra.gov.uk/yellowcard
IrelandHealthcare professionals are asked to report any suspected adverse reactions via HPRA Pharmacovigilance, Earlsfort Terrace, IRL - Dublin 2, Tel: +353 1 6764971, Fax: +353 1 6762517, Website: www.hpra.ieE-mail: firstname.lastname@example.org
Mechanism of actionAnidulafungin is a semi-synthetic echinocandin, a lipopeptide synthesised from a fermentation product of Aspergillus nidulans.Anidulafungin selectively inhibits 1,3-β-D glucan synthase, an enzyme present in fungal, but not mammalian cells. This results in inhibition of the formation of 1,3-β-D-glucan, an essential component of the fungal cell wall. Anidulafungin has shown fungicidal activity against Candida species and activity against regions of active cell growth of the hyphae of Aspergillus fumigatus.Activity in vitroAnidulafungin exhibited in-vitro activity against C. albicans, C. glabrata, C. parapsilosis, C. krusei and C. tropicalis. For the clinical relevance of these findings see Clinical efficacy and safety.Isolates with mutations in the hot spot regions of the target gene have been associated with clinical failures or breakthrough infections. Most clinical cases involve caspofungin treatment. However, in animal experiments these mutations confer cross resistance to all three echinocandins and therefore such isolates are classified as echinocandin resistant until further clinical experience are obtained concerning anidulafungin.The in vitro activity of anidulafungin against Candida species is not uniform. Specifically, for C. parapsilosis, the MICs of anidulafungin are higher than are those of other Candida species.A standardized technique for testing the susceptibility of Candida species to anidulafungin as well as the respective interpretative breakpoints has been established by European Committee on Antimicrobial Susceptibility Testing (EUCAST).Table 2. EUCAST Breakpoints
|Candida Species||MIC breakpoint (mg/L)|
|≤S (Susceptible)||>R (Resistant)|
|Other Candida spp.2||Insufficient evidence|
|1C. parapsilosis harbours an intrinsic alteration in the target gene, which is the likely mechanism for the higher MICs than with other Candida species. In the clinical trials the outcome for anidulafungin with C. parapsilosis was not statistically different from other species however, the use of echinocandins in candidaemia due to C. parapsilosis may not be regarded as therapy of first choice 2 EUCAST has not determined non-species related breakpoints for anidulafungin|
Clinical efficacy and safety
Candidaemia and other forms of Invasive CandidiasisThe safety and efficacy of anidulafungin were evaluated in a pivotal Phase 3, randomised, double-blind, multicentre, multinational study of primarily non-neutropenic patients with candidaemia and a limited number of patients with deep tissue Candida infections or with abscess-forming disease. Patients with Candida endocarditis, osteomyelitis or meningitis, or those with infection due to C. krusei, were specifically excluded from the study. Patients were randomised to receive either anidulafungin (200 mg intravenous loading dose followed by 100 mg intravenous daily) or fluconazole (800 mg intravenous loading dose followed by 400 mg intravenous daily), and were stratified by APACHE II score (≤20 and >20) and the presence or absence of neutropaenia. Treatment was administered for at least 14 and not more than 42 days. Patients in both study arms were permitted to switch to oral fluconazole after at least 10 days of intravenous therapy, provided that they were able to tolerate oral medication and were afebrile for at least 24 hours, and that the most recent blood cultures were negative for Candida species.Patients who received at least one dose of study medication and who had a positive culture for Candida species from a normally sterile site before study entry were included in the modified intent-to-treat (MITT) population. In the primary efficacy analysis, global response in the MITT populations at the end of intravenous therapy, anidulafungin was compared to fluconazole in a pre-specified two-step statistical comparison (non-inferiority followed by superiority). A successful global response required clinical improvement and microbiological eradication. Patients were followed for six weeks beyond the end of all therapy.Two hundred and fifty-six patients, ranging from 16 to 91 years in age, were randomised to treatment and received at least one dose of study medication. The most frequent species isolated at baseline were C. albicans (63.8% anidulafungin, 59.3% fluconazole), followed by C. glabrata (15.7%, 25.4%), C. parapsilosis (10.2%, 13.6%) and C. tropicalis (11.8%, 9.3%) - with 20, 13 and 15 isolates of the last 3 species, respectively, in the anidulafungin group. The majority of patients had Apache II scores ≤ 20 and very few were neutropenic.Efficacy data, both overall and by various subgroups, are presented below in Table 3.
|Table 3. Global success in the MITT population: primary and secondary endpoints|
|Anidulafungin||Fluconazole||Between group difference a ( 95% CI)|
|End of IV Therapy (1° endpoint)||96/127 (75.6%)||71/118 (60.2%)||15.42 (3.9, 27.0)|
|Candidaemia only||88/116 (75.9%)||63/103 (61.2%)||14.7 (2.5, 26.9)|
|Other sterile sitesb||8/11 (72.7%)||8/15 (53.3%)||-|
|Peritoneal fluid/IAc abscess||6/8||5/8|
|C. albicansd||60/74 (81.1%)||38/61 (62.3%)||-|
|Non-albicans speciesd||32/45 (71.1%)||27/45 (60.0%)||-|
|Apache II score ≤ 20||82/101 (81.2%)||60/98 (61.2%)||-|
|Apache II score > 20||14/26 (53.8%)||11/20 (55.0%)||-|
|Non-neutropenic (ANC, cells/mm3 > 500)||94/124 (75.8%)||69/114 (60.5%)||-|
|Neutropenic (ANC, cells/mm3 ≤ 500)||2/3||2/4||-|
|At Other Endpoints|
|End of All Therapy||94/127 (74.0%)||67/118 (56.8%)||17.24 (2.9, 31.6)e|
|2 Week Follow-up||82/127 (64.6%)||58/118 (49.2%)||15.41 (0.4, 30.4)e|
|6 Week Follow-up||71/127 (55.9%)||52/118 (44.1%)||11.84 (-3.4, 27.0)e|
|Table 4. Mortality|
|Overall study mortality||29/127 (22.8%)||37/118 (31.4%)|
|Mortality during study therapy||10/127 (7.9%)||17/118 (14.4%)|
|Mortality attributed to Candida infection||2/127 (1.6%)||5/118 (4.2%)|
Additional Data in Neutropenic PatientsThe efficacy of anidulafungin (200 mg intravenous loading dose followed by 100 mg intravenous daily) in adult neutropenic patients (defined as absolute neutrophil count ≤ 500 cells/mm3, WBC ≤ 500 cells/mm3 or classified by the investigator as neutropenic at baseline) with microbiologically confirmed invasive candidiasis was assessed in an analysis of pooled data from 5 prospective studies (1 comparative versus caspofungin and 4 open-label, non-comparative). Patients were treated for at least 14 days. In clinically stable patients, a switch to oral azole therapy was permitted after at least 5 to 10 days of treatment with anidulafungin. A total of 46 patients were included in the analysis. The majority of patients had candidemia only (84.8%; 39/46). The most common pathogens isolated at baseline were C. tropicalis (34.8%; 16/46), C. krusei (19.6%; 9/46), C. parapsilosis (17.4%; 8/46), C. albicans (15.2%; 7/46), and C. glabrata (15.2%; 7/46). The successful global response rate at End of Intravenous Treatment (primary endpoint) was 26/46 (56.5%) and End of All Treatment was 24/46 (52.2%). All-cause mortality up to the end of the study (6 Week Follow-up Visit) was 21/46 (45.7%).The efficacy of anidulafungin in adult neutropenic patients (defined as absolute neutrophil count ≤ 500 cells/mm3 at baseline) with invasive candidiasis was assessed in a prospective, double-blind, randomized, controlled trial. Eligible patients received either anidulafungin (200 mg intravenous loading dose followed by 100 mg intravenous daily) or caspofungin (70 mg intravenous loading dose followed by 50 mg intravenous daily) (2:1 randomization). Patients were treated for at least 14 days. In clinically stable patients, a switch to oral azole therapy was permitted after at least 10 days of study treatment. A total of 14 neutropenic patients with microbiologically confirmed invasive candidiasis (MITT population) were enrolled in the study (11 anidulafungin; 3 caspofungin). The majority of patients had candidemia only. The most common pathogens isolated at baseline were C. tropicalis (4 anidulafungin, 0 caspofungin), C. parapsilosis (2 anidulafungin, 1 caspofungin), C. krusei (2 anidulafungin, 1 caspofungin), and C. ciferrii (2 anidulafungin, 0 caspofungin). The successful global response rate at the End of Intravenous Treatment (primary endpoint) was 8/11 (72.7%) for anidulafungin and 3/3 (100.0%) for caspofungin (difference -27.3, 95% CI -80.9, 40.3); the successful global response rate at the End of All Treatment was 8/11 (72.7%) for anidulafungin and 3/3 (100.0%) for caspofungin (difference -27.3, 95% CI -80.9, 40.3). All-cause mortality up to the 6 Week Follow-Up visit for anidulafungin (MITT population) was 4/11 (36.4%) and 2/3 (66.7%) for caspofungin.Patients with microbiologically confirmed invasive candidiasis (MITT population) and neutropenia were identified in an analysis of pooled data from 4 similarly designed prospective, open-label, non-comparative studies. The efficacy of anidulafungin (200 mg intravenous loading dose followed by 100 mg intravenous daily) was assessed in 35 adult neutropenic patients defined as absolute neutrophil count ≤ 500 cells/mm3 or WBC ≤ 500 cells/mm3 in 22 patients or classified by the investigator as neutropenic at baseline in 13 patients. All patients were treated for at least 14 days. In clinically stable patients, a switch to oral azole therapy was permitted after at least 5 to 10 days of treatment with anidulafungin. The majority of patients had candidemia only (85.7%). The most common pathogens isolated at baseline were C. tropicalis (12 patients), C. albicans (7 patients), C. glabrata (7 patients), C. krusei (7 patients), and C. parapsilosis (6 patients). The successful global response rate at the End of Intravenous Treatment (primary endpoint) was 18/35 (51.4%) and 16/35 (45.7%) at the End of All Treatment. All-cause mortality by Day 28 was 10/35 (28.6%). The successful global response rate at End of Intravenous Treatment and End of All Treatment were both 7/13 (53.8%) in the 13 patients with neutropenia assessed by investigators at baseline.
Additional Data in Patients with Deep Tissue InfectionsThe efficacy of anidulafungin (200 mg intravenous loading dose followed by 100 mg intravenous daily) in adult patients with microbiologically confirmed deep tissue candidiasis was assessed in an analysis of pooled data from 5 prospective studies (1 comparative and 4 open-label). Patients were treated for at least 14 days. In the 4 open-label studies, a switch to oral azole therapy was permitted after at least 5 to 10 days of treatment with anidulafungin. A total of 129 patients were included in the analysis. Twenty one (16.3%) had concomitant candidemia. The mean APACHE II score was 14.9 (range, 2 44). The most common sites of infection included the peritoneal cavity (54.3%; 70 of 129), hepatobiliary tract (7.0%; 9 of 129), pleural cavity (5.4%; 7 of 129) and kidney (3.1%; 4 of 129). The most common pathogens isolated from a deep tissue site at baseline were C. albicans (64.3%; 83 of 129), C. glabrata (31.0%; 40 of 129), C. tropicalis (11.6%; 15 of 129), and C. krusei (5.4%; 7 of 129). The successful global response rate at the end of intravenous treatment (primary endpoint) and end of all treatment and all-cause mortality up to the 6 week follow-up visit is shown in Table 5.
|Table 5. Rate of Successful Global Responsea and All-Cause Mortality in Patients with Deep Tissue Candidiasis Pooled Analysis|
|MITT Population n/N (%)|
|Global Response of Success at EOIVTb|
|Peritoneal cavity||51/70 (72.9)|
|Hepatobiliary tract||7/9 (77.8)|
|Pleural cavity||6/7 (85.7)|
|Global Response of Success at EOTb||94/129 (72.9)|
|All-Cause Mortality||40/129 (31.0)|
|a A successful global response was defined as both clinical and microbiologic success b EOIVT, End of Intravenous Treatment; EOT, End of All Treatment|
General pharmacokinetic characteristicsThe pharmacokinetics of anidulafungin have been characterised in healthy subjects, special populations and patients. A low intersubject variability in systemic exposure (coefficient of variation ~25%) was observed. The steady state was achieved on the first day after a loading dose (twice the daily maintenance dose).
DistributionThe pharmacokinetics of anidulafungin are characterised by a rapid distribution half-life (0.5-1 hour) and a volume of distribution, 30-50 l, which is similar to total body fluid volume. Anidulafungin is extensively bound (>99%) to human plasma proteins. No specific tissue distribution studies of anidulafungin have been done in humans. Therefore, no information is available about the penetration of anidulafungin into the cerebrospinal fluid (CSF) and/or across the blood-brain barrier.
BiotransformationHepatic metabolism of anidulafungin has not been observed. Anidulafungin is not a clinically relevant substrate, inducer, or inhibitor of cytochrome P450 isoenzymes. It is unlikely that anidulafungin will have clinically relevant effects on the metabolism of drugs metabolised by cytochrome P450 isoenzymes.Anidulafungin undergoes slow chemical degradation at physiologic temperature and pH to a ring-opened peptide that lacks antifungal activity. The in vitro degradation half-life of anidulafungin under physiologic conditions is approximately 24 hours. In vivo, the ring-opened product is subsequently converted to peptidic degradants and eliminated mainly through biliary excretion.
EliminationThe clearance of anidulafungin is about 1 l/h. Anidulafungin has a predominant elimination half-life of approximately 24 hours that characterizes the majority of the plasma concentration-time profile, and a terminal half-life of 40-50 hours that characterises the terminal elimination phase of the profile.In a single-dose clinical study, radiolabeled (14C) anidulafungin (~88 mg) was administered to healthy subjects. Approximately 30% of the administered radioactive dose was eliminated in the faeces over 9 days, of which less than 10% was intact drug. Less than 1% of the administered radioactive dose was excreted in the urine, indicating negligible renal clearance. Anidulafungin concentrations fell below the lower limits of quantitation 6 days post-dose. Negligible amounts of drug-derived radioactivity were recovered in blood, urine, and faeces 8 weeks post-dose.
LinearityAnidulafungin displays linear pharmacokinetics across a wide range of once daily doses (15-130 mg).
Patients with fungal infectionsThe pharmacokinetics of anidulafungin in patients with fungal infections are similar to those observed in healthy subjects based on population pharmacokinetic analyses. With the 200/100 mg daily dose regimen at an infusion rate of 1.1 mg/min, the steady state Cmax and trough concentrations (Cmin) could reach approximately 7 and 3 mg/l, respectively, with an average steady state AUC of approximately 110 mgh/l.
WeightAlthough weight was identified as a source of variability in clearance in the population pharmacokinetic analysis, weight has little clinical relevance on the pharmacokinetics of anidulafungin.
GenderPlasma concentrations of anidulafungin in healthy men and women were similar. In multiple-dose patient studies, drug clearance was slightly faster (approximately 22%) in men.
ElderlyThe population pharmacokinetic analysis showed that median clearance differed slightly between the elderly group (patients ≥ 65, median CL = 1.07 l/h) and the non-elderly group (patients < 65, median CL = 1.22 l/h), however the range of clearance was similar.
EthnicityAnidulafungin pharmacokinetics were similar among Caucasians, Blacks, Asians, and Hispanics.
HIV positivityDosage adjustments are not required based on HIV positivity, irrespective of concomitant anti-retroviral therapy.
Hepatic insufficiencyAnidulafungin is not hepatically metabolised. Anidulafungin pharmacokinetics were examined in subjects with Child-Pugh class A, B or C hepatic insufficiency. Anidulafungin concentrations were not increased in subjects with any degree of hepatic insufficiency. Although a slight decrease in AUC was observed in patients with Child-Pugh C hepatic insufficiency, the decrease was within the range of population estimates noted for healthy subjects.
Renal insufficiencyAnidulafungin has negligible renal clearance (<1%). In a clinical study of subjects with mild, moderate, severe or end stage (dialysis-dependent) renal insufficiency, anidulafungin pharmacokinetics were similar to those observed in subjects with normal renal function. Anidulafungin is not dialysable and may be administered without regard to the timing of hemodialysis.
PaediatricThe pharmacokinetics of anidulafungin after at least 5 daily doses were investigated in 24 immunocompromised paediatric (2 to 11 years old) and adolescent (12 to 17 years old) patients with neutropenia. Steady state was achieved on the first day after a loading dose (twice the maintenance dose), and steady state Cmax and AUCss increase in a dose-proportional manner. Systemic exposure following daily maintenance dose of 0.75 and 1.5 mg/kg/day in this population were comparable to those observed in adults following 50 and 100 mg/day, respectively. Both regimens were well-tolerated by these patients.
ReconstitutionAseptically reconstitute each vial with 30 mL water for injections to provide a concentration of 3.33 mg/mL. The reconstitution time can be up to 5 mins. After subsequent dilution, the solution is to be discarded if particulate matter or discoloration is identified.
Dilution and infusionAseptically transfer the contents of the reconstituted vial(s) into an intravenous bag (or bottle) containing either 9 mg/mL (0.9%) sodium chloride for infusion or 50 mg/mL (5%) glucose for infusion obtaining an anidulafungin concentration of 0.77 mg/mL. The table below provides the volumes required for each dose.
Dilution requirements for ECALTA administration
|Dose||Number of vials of powder||Total reconstituted volume||Infusion volume A||Total infusion volumeB||Rate of infusion||Minimum duration of infusion|
|100 mg||1||30 mL||100 mL||130 mL||1.4 mL/min||90 min|
|200 mg||2||60 mL||200 mL||260 mL||1.4 mL/min||180 min|
|Date of first authorisation:||20 September 2007|
|Date of latest renewal:||23 August 2012|
Ramsgate Road, Sandwich, Kent, CT13 9NJ
+44 (0)1304 656 221
+44 (0)1304 616 161