Skip to main content

Be ready for invasive fungal infections (IFIs)

Lady looking upwards happily

I Am… AmBisome®

In a changing landscape of fungal pathogens, AmBisome® is ready to help you take on invasive fungal infections (IFIs) with confidence.1-5

3D image of yellow liposome

STAY ONE STEP AHEAD OF IFIs WITH AMBISOME®

  • Broad-spectrum of in vitro activity against the most common fungal pathogens, including those causing rare and difficult-to-treat infections2-4,6
  • Fungicidal activity* against most clinically important yeasts and moulds2,4,5,7,8
  • Reduced toxicity vs. conventional amphotericin B formulations5,9-16
  • Lower potential for pharmacokinetic DDIs vs. azoles - Amphotericin B is not know to be a substrate nor an inhbitor of the CYP450 enzyme system†7,17,18
  • Improved tissue penetration vs. conventional amphotericin B19
  • Low risk of resistance7,20-23
  • Well established tolerability and safety profile**5
  • Over three decades of clinical experience24

I AM… EFFECTIVE AGAINST A BROAD SPECTRUM OF CLINICALLY RELEVANT FUNGAL PATHOGENS2-4,7

AmBisome® has a broad spectrum of in vitro activity against the most common fungal pathogens, including those causing rare and difficult-to-treat infections (e.g. azole-resistant strains)2-4,6

Additionally, AmBisome® demonstrates fungicidal activity against most clinically important yeasts and moulds, including:2,4,5,7,8

  • A multitude of Candida species, including both C. albicans and non-albicans species
  • Aspergillus fumigatus and Aspergillus flavus
  • Mucorales
  • Cryptococcus neoformans
  • Histoplasma capsulatum
Man wearing red shirt looking pensive

Treat promptly and treat broad with AmBisome®

Be ready for IFIs by choosing to treat promptly with AmBisome®’s broad-spectrum activity.

I AM… ESTABLISHED FOR THE TREATMENT OF IFIs IN A VARIETY OF HIGH-RISK PATIENT POPULATIONS14,25-33

The efficacy of AmBisome® has been established in a variety of at-risk patient populations, including those with:

Icon of blood droplet
Haematological
disorders14,25,26,32,33
Icon of stem cell transplantation
Stem cell transplantations
(allogenic/autologous)25
Icon of solid organ transplant
Solid organ
transplants25,26
Icon of HIV / AIDs
HIV/AIDS25,27-29
Icon of neutropenia
Neutropenia14,25,32,33
Icon of Diabetes melitus
Diabetes mellitus26
Icon of hospital bed and IV bag
Critical conditions in the ICU31
Icon of pancreas
Pancreatitis26
Icon of blood cells and pathogens
Sepsis or septic shock31
Image of nurse changing IV bag

I AM… ASSOCIATED WITH A LOWER POTENTIAL FOR PHARMACOKINETIC DRUG-DRUG INTERACTIONS VS. AZOLES†,7,17,18

Amphotericin B is not known to be a substrate nor an inhibitor of the CYP450 enzyme system. 7,17,18 Drugs that are known to have pharmacodynamic interactions with amphotericin B may also interact with AmBisome®.5,7,18,34

DDIs for amphotericin B are mostly related to nephrotoxicity and electrolyte disturbances, which may be augmented by co-administered drugs with similar renal side effects. Resultant changes may reduce clearance or alter the efficacy/toxicity of co-administered drugs that undergo renal elimination.5,7,18,34 Regular monitoring of renal function is recommended in patients receiving AmBisome® in conjunction with any nephrotoxic medications, and appropriate potassium supplementation may be required.5

Close-up of doctor’s and patient’s hands

For patients on multiple medications, consider the risk of DDIs.

Learn more about the interactions of AmBisome® and other antifungals with treatments commonly used in patients most at risk of developing IFIs.

I Am… the liposomal form of amphotericin B that sets me apart from other conventional forms of amphotericin B9,13,35

The liposomal delivery of AmBisome® reduces toxicity vs. other forms of amphotericin B, whilst retaining antifungal action.5,9-16 AmBisome® has a targeted liposomal delivery system (a liposome bilayer) that encapsulates amphotericin B, minimising adverse effects on host tissues and significantly reducing frequency of infusion-related reactions (P<0.001), nephrotoxic effects (P<0.001) and hypokalaemia (P=0.02) in febrile neutropenic patients vs. conventional amphotericin B.**9,14,36

AmBisome® also demonstrates improved tissue penetration with sustained drug levels and activity in key target tissues including the brain, lungs, kidneys, liver, and spleen vs. conventional amphotericin B.19

See how AmBisome®'s mechanism of action can help to reduce toxicity compared with conventional amphotericin B.

Image of vials with yellow fluid

Choose a treatment that has a well established tolerability and safety profile**5

Discover in more detail how AmBisome®’s liposomal delivery reduces nephrotoxicity vs. conventional amphotericin B and find out about adverse events associated with AmBisome®

Microscopic photo of Aspergillus on blue background

I AM… ASSOCIATED WITH A LOW RISK OF RESISTANCE7,20-23

Resistance to azoles and echinocandins is increasing worldwide due to widespread prophylaxis use, amongst other things7,37-40, which has led to a variety of rare and resistant breakthrough infections.38,41 After more than 50 years of clinical use, acquired resistance to amphotericin B, the active ingredient in AmBisome®, has rarely been reported.7,20-23

Watch the video below to see how AmBisome® may help to overcome the challenge of antifungal resistance.

Microscopic photo of blue stained fungal pathogens

Take action in the face of growing resistance.

Discover how AmBisome® can help you stay one step ahead of IFIs in a changing IFI landscape.

I Am… indicated in a broad range of iFIs5

AmBisome® is indicated in adults and children aged 1 month to 18 years for:5

  • The treatment of severe systemic and/or deep mycoses
  • The treatment of visceral leishmaniasis in immunocompetent patients, including both adults and children
  • The empirical treatment of presumed fungal infections in febrile neutropenic patients, where the fever has failed to respond to broad-spectrum antibiotics and appropriate investigations have failed to define a bacterial or viral cause

Infections successfully treated with AmBisome® include: disseminated candidiasis, aspergillosis, mucormycosis, chronic mycetoma, cryptococcal meningitis and visceral leishmaniasis.5

AmBisome® should not be used to treat the common clinically inapparent forms of fungal disease that show only positive skin or serological tests.5

Close-up of doctor’s and patient’s hands

Initiate broad-spectrum fungicidal treatment promptly, to reduce mortality risk.4,45-50

Early diagnosis and prompt treatment of IFIs in high-risk patients is key to ensuring favourable outcomes.45,46,51,52

I AM... HELPING YOU TAKE ON IFIs WITH CONFIDENCE5

The dose of AmBisome® must be adjusted to the specific requirements of each patient. For more information on starting doses and escalation recommendations, please refer to the Summary of Product Characteristics.5

No adjustments in dose or frequency are required with AmBisome® in:5

  • Elderly patients
  • Patients with hepatic disorders
  • Paediatric patients¥
  • Patients with renal impairment¥¥

I Am… AmBisome®, ready to help you fight the next suspected IFI5

Footnotes

*Based on in vitro data, the clinical relevance is unknown.

**Double-blind, randomised trial comparing AmBisome® (initial dose of 3 mg/kg/day) and cAMB (0.6 mg/kg/day) as empiric antifungal therapy in adults and children (2-80 years) with persistent neutropenia (< 500/mm3) and fever despite >5 days empirical antibacterial therapy. The total number of patients was 687, of whom almost half (n=333) had acute leukemia. Treatment success (primary efficacy endpoint), was defined as a composite of five criteria: survival for seven days after initiation of the study drug; resolution of fever during the period of neutropenia; successful treatment of any base-line fungal infection, if present; the absence of breakthrough fungal infections during administration of the study drug or within seven days after the completion of treatment; and the absence of premature discontinuation of the study drug because of toxicity or lack of efficacy.14

Please refer to the AmBisome® SmPC and the SmPC of concomitant medications for a full list of DDIs prior to prescribing to ensure minimal interaction. No specific interaction studies have been performed with AmBisome®. However, recommendations in the prescribing information are based on the known DDI profile of amphotericin B and interactions that may be of clinical significance.5

§AmBisome® is indicated for empiric therapy in the treatment of suspected IFIs in febrile neutropenic patients where the fever has failed to respond to broad spectrum antibiotics and appropriate investigations have failed to define a bacterial or viral cause5

No data are available on which to make a dose recommendation for patients with hepatic impairment.

¥AmBisome® is not recommended for use in children below 1 month old due to lack of data on safety and efficacy.5

¥¥AmBisome® has been administered to a large number of patients with pre-existing renal impairment at starting doses ranging from 1-3 mg/kg/day in clinical trials and no adjustment in dose or frequency of administration was required. AmBisome® has been shown to be substantially less toxic than conventional amphotericin B, particularly with respect to nephrotoxicity, however, renal adverse events may still occur. In particular, caution should be exercised when prolonged therapy is required. Regular laboratory evaluation of serum electrolytes, particularly potassium and magnesium, as well as renal, hepatic and haematopoietic function should be performed, at least once weekly. If clinically significant reduction in renal functioning, or worsening of other parameters occurs, consideration should be given to dose reduction, treatment interruption or discontinuation.5

References

  1. Lamoth F et al. Clin Infect Dis. 2017;64(11):1619-1621.
  2. Lass-Flörl C et al. Antimicrob Agents Chemother. 2008;52(10):3637-3641.
  3. Almyroudis NG et al. Antimicrob Agents Chemother. 2007;51(7):2587-2590.
  4. Chandrasekar P. J Antimicrob Chemother. 2011;66:457-465.
  5. AmBisome® Summary of Product Characteristics (UK).
  6. Manavathu EK et al. J Antimicrob Chemother. 2000;46:229-234. 26.
  7. Nett JE and Andes DR. Infect Dis Clin North Am. 2016;30:51-83.
  8. Meletiadis J et al. Antimicrob Agents Chemother. 2007;51(9):3329-3337.
  9. Adler-Moore J and Proffitt RT. J Antimicrob Chemother. 2002;49(Suppl. 1):21-30.
  10. Keady S and Panesae P. EJHP Practice. 2010;16(3):78-80.
  11. Falci DR et al. Mycoses. 2015;58:104-112.
  12. Stone NR et al. Drugs. 2016;76(4):485-500.
  13. Adler-Moore JP et al. Med Mycol. 2016;54(3):223-231.
  14. Walsh TJ et al. N Engl J Med. 1999;340:764-71.
  15. Ullmann A et al. Clin Infect Dis. 2006;43:e29-38.
  16. Wingard JR et al. Clin Infect Dis. 2000;31:1155-1163.
  17. Vadlapatla RK et al. Expert Opin Drug Metab Toxicol. 2014;10(4):561-580.
  18. Chau MM et al. Internal Medicine Journal. 2021;51(Suppl. 7):37-66.
  19. Adler-Moore JP et al. Curr Opin Investig Drugs. 2003;4(2):179-185.
  20. Messer SA et al. Diagnos Microbiol Infect Dis. 2020;97:115007.
  21. Mesa-Arango AC et al. Front Microbiol. 2012;3:286.
  22. Vallejo C et al. Rev Esp Quimioter. 2013;26(4):378-386.
  23. Vincent BM et al. PLoS Biol. 2013;11(10):e1001692.
  24. AmBisome® Summary of Product Characteristics (Ireland). Available at: https://www.medicines.org.uk/emc/product/1022/smpc#gref [Last accessed: December 2022].
  25. Cornely OA et al. Clin Infect Dis. 2007;44(10):1289-1297.
  26. Kuse E-R et al. Lancet. 2007;369(9572):1519-1527.
  27. Hamill RJ et al. Clin Infect Dis. 2010;51(2):225-232.
  28. Wheat LG et al. Antimicrob Agents Chemother. 2001;45(8):2354-2357.
  29. Johnson PC et al. Ann Intern Med. 2002;137(2):105-109.
  30. Wheat J et al. Medicine (Baltimore). 2018;97(13):e0245.
  31. Álvarez-Lerma F et al. J Chemother. 2009;21(3):330-337.
  32. Walsh TJ et al. N Engl J Med. 2002;346(4):225-234.
  33. Walsh TJ et al. N Engl J Med. 2004;351(14):1391-1402.
  34. Lewis RE. Mayo Clin Proc. 2011;86(8):805-817.
  35. Walker L et al. MBio. 2018;9(1):e02383–17
  36. Laurent A et al. Burns Open. 2020;4:110-116.
  37. Perlin DS et al. Lancet Infect Dis. 2017;17(12):e383–e392.
  38. van der Linden JWM et al. Emerg Infect Dis. 2015;21(6):1041-1044.
  39. Pfaller MA et al. Open Forum Infect Dis. 2019;6(Suppl. 1):S79-s94.
  40. Arendrup MC. Clin Microbiol Infect. 2014;20(Suppl. 6):42-44.
  41. Lass-Flörl C and Cuenca-Estrella M. J Antimicrob Chemother. 2017;72(Suppl. 1):i5-11.
  42. Verweij PE. Drug Resist Updat. 2015;21–22:30–40.
  43. Verweij PE et al. Clin Infect Dis. 2016;62(3):362–368.
  44. Pfaller MA et al. J Clin Microbiol. 2012;50(6):2040–2046.
  45. Pappas PG et al. Nat Rev Dis Primers. 2018;11;4:18026.
  46. Morrell M et al. Antimic Ag Chem. 2005:49(9):3640-45.
  47. Bassetti M et al. Crit Care. 2014;18(4):458.
  48. ESICM/ESCMID task force on practical management of invasive candidiasis in critically ill patients. Martin Loeches et al. Intensive Care Med. 2019;45(6):789-805.
  49. Tashiro M et al. J Infect Chemother. 2021;S1341-321X(21)00174-4.
  50. Nivoix Y et al. Clin Infect Dis. 2008;47(9):1176-1184.
  51. Chatelon J et al. Adv Ther. 2019;36:3308-3320.
  52. Pagano L and Mayor S. Future Sci OA. 2018;14;4(6):FSO307.

Date of preparation: December 2022. Job code: IHQ-AMB-0801.