Cubicin is the first of a new class of antibiotics for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) and methicillin-sensitive Staphylococcus aureus (MSSA) known as the cyclic lipopeptides.1 It is indicated in the UK for the treatment in adults of complicated skin and soft tissue infections (cSSTIs) and of right-sided infective endocarditis (RIE) due to Staphylococcus aureus and Staphylococcus aureus bacteraemia (SAB) when associated with RIE or with cSSTI.1,2
 

Cubicin was launched in the UK in March 2006 and received a positive Scottish Medicines Consortium (SMC) ruling for its use in treating cSSTIs in April 2006.3

Cubicin has a novel mode of action (MOA) and works by binding to and penetrating the cell membrane causing cell death.2 While most other antibiotics used to treat MRSA work by preventing growth of bacteria, Cubicin is ‘bactericidal’ meaning that it quickly kills the bacteria cells, eliminating the infection.2 Cubicin’s unique mode of action is important as it means there is no cross resistance to existing classes of antibiotics and that resistance may be slow to emerge.4,5 Resistance to antibiotics is a major concern to healthcare professionals and so an agent which minimizes the likelihood of resistance developing is an important addition to the available treatment options.
 

Cubicin represents a valuable first line treatment option in situations where it is important to begin effective treatment as quickly as possible but where the susceptibility of the infecting organism to antibiotics is not yet known – so called empirical therapy.  This is because it is active in vitro against a broad range of Gram positive bacteria, including6,7:

• Staphylococci
• Streptococci
• Enterococci
• MRSA
• Methicillin-resistant Staphylococcus epidermidis (MRSE)
• Glycopeptide-intermediate Staphylococcus aureus (GISA) and Staphylococcus epidermidis (GISE)
• Vancomycin-resistant Staphylococcus aureus (VRSA)
• Vancomycin-resistant enterococci (VRE)
• Linezolid or quinupristin/dalfopristin-resistant Staphylococci and enterococci
  

Cubicin is as effective as the current first-line treatment for MRSA, vancomycin, offering an important empirical treatment option for clinicians.1,8 In clinical studies Cubicin achieved clinical success rates (defined as cure or improvement of clinical symptoms) of 69% versus 67% compared to vancomycin.8
 

In addition to equivalent efficacy, Cubcin has a faster onset of action than alternative treatments – in clinical trials 63% of patients were successfully treated in seven days with Cubicin compared to 33% with comparator antibiotics (e.g. vancomycin).1 Treating patients as quickly as possible is an important goal in MRSA management as delay of appropriate treatment has been shown to increase morbidity and mortality.9 Cubicin’s rapid onset of action therefore has the potential to offer a significant clinical benefit.

Cubicin is administered via a once daily 30 minute infusion at a dose of 4mg/kg and no dose adjustment is needed for most patients meaning it may be more suitable for difficult to manage patients such as those with renal impairment or the elderly.2

Cubicin has a safety and tolerability profile comparable with antibiotics such as vancomycin however serum drug monitoring is not required, thus reducing the burden on healthcare professionals. The main side effects associated with Cubicin were mostly reported in clinical trials as being ‘mild’ or ‘moderate’ and include constipation, nausea and headache.1,2  

1. Arbeit RD, Maki D, Tally FP, et al. The safety and efficacy of daptomycin for the treatment of complicated skin and skin-structure infections. Clin Infect Dis 2004; 38: 1673-81
2. Novartis UK. Cubicin (daptomycin) Summary of Product Characteristics
3. Scottish Medicines Consortium. March 2006. Available at: http://www.scottishmedicines.org.uk/smc/files/daptomycin_Cubicin_(248-06).pdf
4. Silverman JA et al. Correlation of Daptomycin Bactericidal Activity and Membrane Depolarization in Staphylococcus aureus. Antimicrobial Agents and Chemotherapy 2003; 47: 2538-2544
5. Stratton CW. Dead bugs don’t mutate: susceptibility issues in the emergence of bacterial resistance. Emerg Infect Dis 2003; 9: 10-16
6. Ginsburg I. The role of bacteriolysis in the pathophysiology of inflammation, infection and post-infectious sequelae. APMIS 2002; 110:753-770
7. Fass RY and Helsel VL. In vitro activity of LY146032 against staphylococci, streptococci, and eterococci. Antimicrob Agents Chemother 1986;30781-784
8. Novartis data on file. EPAR 2006. Scientific discussion
9. Lode H. Management of serious nosocomial bacterial infections: do current therapeutic options meet the need? Clin Microbiol Infect 2005; 11: 778-87