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Antibiotics · SSTI · 11 slides

Faropenem in skin and soft tissue infections.

An invited talk at PUNJ SURG 2026, Ludhiana: where an oral penem fits after parenteral therapy for skin and soft tissue infections.

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Contents · 3 parts

Why faropenem

Slide 1: Faropenem in skin and soft tissue infections
01 / 11

Faropenem in skin and soft tissue infections

Faropenem in Skin and Soft Tissue Infections (SSTI)

Dr Prateek Gupta

Assistant Professor, Department of General Surgery Dayanand Medical College and Hospital, Ludhiana

prateekguptasurgery.com

01-11-2026

Slide 2: The gap it fills
02 / 11

The gap it fills

ESBLs

Since 1983, ESBLs have defeated third-generation cephalosporins; producers are often multidrug resistant

Carbapenems

Drugs of choice for ESBL infections — but parenteral only

Discharge

Patients leaving hospital with SSTIs need an oral antibiotic

Shaikh S et al. 2015; Dalhoff A et al. 2006; WHO fact sheet: Antibiotic resistance

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Slide 3: Faropenem: a penem antibiotic
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Faropenem: a penem antibiotic

Belongs to the penem class Structure similar to carbapenems Resistant to β-lactamases due to its unique structure

Contraindication

Hypersensitivity to any component or to drugs of the same class; anaphylaxis to β-lactams

Approved formulations in India

Indications: respiratory tract (upper and lower), urinary tract (uncomplicated and complicated), skin and soft tissue, and gynaecological infections

Prescribing information, faropenem (Feb 2009)

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FormulationDosing
200 mg tabletThree times a day
300 mg ER tabletTwice a day

Spectrum and activity

Slide 4: Broad spectrum, including anaerobes
04 / 11

Broad spectrum, including anaerobes

Lower MICs and greater activity than most third-generation cephalosporins.

Woodcock JM et al., J Antimicrob Chemother 1997;39:35–43

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OrganismMIC90 (mg/L)Note
Enterobacteriaceae48–32× more active than cefuroxime; Serratia 32
MSSA0.12Considerable activity
Group A/B streptococci, S. milleri0.06Good activity
S. pneumoniae (incl. some quinolone-R)0.25Good activity
E. faecalis2More active than comparators
H. influenzae, M. catarrhalis1Good activity
Anaerobes: C. perfringens, B. fragilis—≈ metronidazole / clindamycin; ≈ co-amoxiclav
P. aeruginosa, S. maltophilia128Weak activity
Slide 5: MIC90 vs comparators (mg/L)
05 / 11

MIC90 vs comparators (mg/L)

Active against E. coli and Klebsiella spp., including ESBL-producing strains, and P. mirabilis.

Schurek KN et al., Expert Rev Anti Infect Ther 2007;5(2):185–98

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OrganismFaropenemAmox-clavCefuroximeImipenem
S. aureus (MS)0.1222≤0.5
S. aureus (MR)>3216>3232
S. pyogenes0.030.03≤0.015≤0.008
S. pneumoniae0.250.54≤0.5
E. coli1168≤0.5
K. pneumoniae28>321
P. mirabilis42>322
Acinetobacter spp.>3232>320.25
P. aeruginosa>32>16>32>8
Slide 6: Activity against resistant strains
06 / 11

Activity against resistant strains

β-lactamase stability

Highly stable to group 2b, TEM-1, SHV-1, TEM-3, TEM-9, ESBL (2be) and S. aureus β-lactamases

Woodcock JM et al., JAC 1997

vs cephalosporins

Erythromycin- and clindamycin-resistant S. pneumoniae: MIC50 0.06 mg/L — 2× (cefotaxime) to 66× (cefixime) lower than cephalosporins

Schmitz FJ et al., JAC 2001;48:141–56

MDR isolates, China

141 isolates, 16 hospitals: E. faecalis fully susceptible; one resistant E. coli; three resistant K. pneumoniae. All E. faecium, P. aeruginosa and A. baumannii resistant.

Feng XW et al., Infect Microbes Dis 2020

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Slide 7: Additional properties
07 / 11

Additional properties

Low inoculum effect

Significantly less inoculum effect on bactericidal activity against S. pneumoniae. (Inoculum effect: MIC rises as the bacterial load rises — typical of β-lactams with β-lactamase producers.)

Boswell FJ et al., JAC 2002;50:525–32

Post-antibiotic effect

Growth suppression after brief exposure: 0.7–2.6 h against S. aureus, S. pneumoniae and E. coli

Gettig JP et al., Ann Pharmacother 2008;42:80–90

Pro-host effect

Enhances neutrophil killing: myeloperoxidase activation → superoxide production → faster bacterial killing

Sato K et al., JAC 1999;44:337–41

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Clinical use

Slide 8: Oral step-down therapy
08 / 11

Oral step-down therapy

All carbapenems are parenteral; faropenem medoxomil (ester prodrug) is oral, with 70–80% bioavailability Candidate for IV-to-oral switch and step-down, e.g. after ertapenem Good activity against MSSA, streptococci and certain anaerobes No clinically relevant activity against MRSA

Pharmacokinetics

Well absorbed; no food effect Low volume of distribution Found in sputum, tonsil tissue, sinus mucosa Metabolised by renal DHP-I; excreted mainly in urine 300 mg: peak urine concentration 55.6 µg/mL at 2 h

Dalhoff A et al., Biochem Pharmacol 2006; Schurek KN et al., Expert Rev Anti Infect Ther 2007

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Slide 9: Special populations and interactions
09 / 11

Special populations and interactions

Special populations

Pregnancy: safety not established; only if benefit outweighs risk Lactation: excreted in breast milk Infants: safety not established Elderly: prolonged half-life; start at 150 mg and monitor; stop if diarrhoea; risk of vitamin K-deficiency bleeding

Drug interactions

Sodium valproate: lower valproic acid levels; seizures may recur Furosemide: increased kidney toxicity Imipenem–cilastatin: raises faropenem blood levels

Prescribing information, faropenem

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Slide 10: Faropenem in SSTIs
10 / 11

Faropenem in SSTIs

Phase III: faropenem medoxomil 300 mg BID (n = 298) vs amoxicillin–clavulanate 625 mg TID (n = 295), 7 days; test of cure 7–14 days post-therapy

Bite-wound pathogens

405 aerobic and anaerobic isolates from dog (99), cat (108), human (191) and other animal (7) bites

All isolates inhibited by ≤0.125 mg/L MIC ranges and MIC90s similar to co-amoxiclav More active than fluoroquinolones against most anaerobes

Schurek KN et al., Expert Rev Anti Infect Ther 2007; Goldstein EJ et al., JAC 2002;50:411–20

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OutcomeFaropenemAmox–clav
Clinical cure91.1%91.2%
Microbiological eradication91.6%90.6%
Slide 11: Thank you
11 / 11

Thank you

Dr Prateek Gupta · prateekguptasurgery.com

Sources and image credits

Sources are cited at the foot of each slide, as listed below.

    Sources

    • [1] Shaikh S et al. 2015; Dalhoff A et al. 2006; WHO fact sheet: Antibiotic resistance
    • [2] Prescribing information, faropenem (Feb 2009)
    • [3] Woodcock JM et al., J Antimicrob Chemother 1997;39:35–43
    • [4] Schurek KN et al., Expert Rev Anti Infect Ther 2007;5(2):185–98
    • [5] Woodcock JM et al., JAC 1997
    • [6] Schmitz FJ et al., JAC 2001;48:141–56
    • [7] Feng XW et al., Infect Microbes Dis 2020
    • [8] Boswell FJ et al., JAC 2002;50:525–32
    • [9] Gettig JP et al., Ann Pharmacother 2008;42:80–90
    • [10] Sato K et al., JAC 1999;44:337–41
    • [11] Dalhoff A et al., Biochem Pharmacol 2006; Schurek KN et al., Expert Rev Anti Infect Ther 2007
    • [12] Prescribing information, faropenem
    • [13] Schurek KN et al., Expert Rev Anti Infect Ther 2007; Goldstein EJ et al., JAC 2002;50:411–20