FLOMOXEF is a broad-spectrum oxacephem (oxacephalosporin) antibiotic. Flomoxef exhibits a broad spectrum of antibacterial activity against G(+), G(-) and even anaerobes such as Staphylococcus sp., Escherichia coli, and Bacteroides sp., and it can be used singly to treat infection caused by aerobes and anaerobes (Mixed infection) effectively. Flomoxef belongs to the cephamycin, so it is very stable against β-lactamase as well as Extended Spectrum β-lactamase (ESBL), a novel resistance induced by Enterobacteriaceae. There is no Oxyimino group in the structure of Flomoxef, so it won’t derive ESBL and it is also effective for the treatment to ESBL infection. No disulfiram-like reaction and less incidence of vitamin K deficiency than that of Latamoxef.
Indications: The following infections caused by Flomoxef sodium susceptible strains: Staphylococcus spp., Streptococcus spp.(excluding Enterobacter), Streptococcus pneumoniae, Branhamella catarrhalis, Neisseria gonorrhoeae, E. coli, Klebsiella spp., Proteus spp., Influenzae spp., Peptostreptococcus spp.、Bacteroides spp.。ex. Septicemia, Cholecystitis,, Cholangitis, Peritonitis, Bronchitis, Bronchiectasis, AECB, Pyelonephritis, Cystitis, Prostatitis, Pyelonephritis, Pneumonia.
Mechanism of action: The antibacterial action of Flomoxef sodium results from the inhibition of bacterial cell wall synthesis, and this action is bactericidal. Flomoxef sodium has binding-affinity for penicillin-binding proteins (PBP), and demonstrates antibacterial activity, especially by showing inhibiting action to mullein-crosslinking enzymes.
Dosage: Adult: 1g Q8H~1g Q6H. Children: 100mg/kg/day, in 3 to 4 divided doses. The dosage should be adjusted according to the age of patient and severity of the symptoms. In refractory or severe infections, the dose my be increased to 2g Q8H for adults, and 200mg/kg/day for children.
Administration of Flomoxef to renal patients: When creatinine clearance are 80, 80-50, 50-25, 25-5, and <5 ml/min, the doses are 4, 3, 2, 1, and 0.5g/day, respectively. Hemodialysis:In patients undergoing hemodialysis, a 1g dose of parenteral Flomoxef may be administered at the end respectively of each hemodialysis session.
ADVERSE REACTIONS A. HEMATOLOGIC EFFECTS 1. EOSINOPHILIA occurs infrequently in patients receiving FLOMOXEF; however, no clinical symptoms have occurred as a result (Hosoda et al, 1987; Iwai et al, 1991; Kanegae et al, 1987; Sekiguchi et al, 1987; Yanagishima et al, 1987). 2. A 9-month-old girl developed NEUTROPENIA 5 days after treatment with flomoxef for purulent cervical lymphadenitis. Flomoxef was withdrawn on day 8 when she was found to have neutropenia with 1% neutrophils. Assays for antibodies to various viruses were negative. The neutropenia persisted and was shown to be autoimmune in nature. As granulocyte-bound IgG decreased over the next 8 months, absolute neutrophil counts increased. The authors suggested that the persistent autoimmune neutropenia was triggered by the antibiotic (Taniuchi et al, 2000). 3. Slight and transient reductions in erythrocyte count, hemoglobin, hematocrit, and leukocyte count have been reported rarely with FLOMOXEF (Ohta et al, 1987). B. COAGULATION DEFECTS 1. SUMMARY: FLOMOXEF has not been associated with bleeding disorders. In one study, treatment with intravenous FLOMOXEF 2 g once or twice daily in five and six healthy male volunteers, respectively, for 8 days, did not cause any significant changes in prothrombin time (PT), coagulation factors II, VII, IX, or X, in fibrinogen levels, activated partial thromboplastin time (APTT), platelet counts, bleeding time, or collagen- and ADP-induced platelet aggregation (Uchida & Matsubara, 1991). PT, PTT, and fibrinogen remained in the normal range in all 10 adult patients treated with FLOMOXEF 1 gm imtramuscularly every 12 hours (for 5 days) for chronic bronchitis. Factors II & VII & Xg protein c, protein S, and AT III were not depleted (Cazzola et al, 1993). 2. In another series, an inhibitory effect on VITAMIN K metabolism was observed with FLOMOXEF, although this effect was less pronounced than with MOXALACTAM. In contrast with MOXALACTAM, no interference with platelet function occurred with FLOMOXEF. Monitoring of prothrombin time is probably unnecessary except in patients who are suspected of having low vitamin K stores (Andrassy et al, 1991). 3. Transient THROMBOCYTOSIS occurs infrequently in patients receiving FLOMOXEF; however, this effect has been mild and transient, and resolves upon discontinuation of therapy (Higashino et al, 1987; Iwai et al, 1991; Okada & Furukawa, 1987; Yanagishima et al, 1987). 4. One study evaluated the in-vitro antiplatelet effects of some old and new cephalosporins including FLOMOXEF. FLOMOXEF was found to have the potential to affect human platelet aggregation adversely only at high concentrations which are not achievable in vivo (Cazzola et al, 1993). C. GASTROINTESTINAL EFFECTS 1. LOOSE STOOLS have occurred in some patients receiving FLOMOXEF therapy (Andrassy et al, 1991; Sekiguchi et al, 1987). 2. STOMATITIS and numbness of the tongue occurred in one patient receiving FLOMOXEF for the treatment of respiratory tract infection; symptoms improved with cessation of therapy (Takagi et al, 1987). D. LIVER 1. Asymptomatic elevation in serum hepatic transaminases occurs infrequently in patients receiving FLOMOXEF; however, this has not resulted in clinical hepatotoxicity (Kanegae et al, 1987; Kuroki et al, 1987; Ohta et al, 1987; Yanagishima et al, 1987). E. SKIN 1. RASH occurs infrequently in patients receiving FLOMOXEF; symptoms improve with cessation of therapy (Higashino et al, 1987; Takagi et al, 1987). 2. URTICARIA occurred in one patient receiving FLOMOXEF 1 g twice a day for the treatment of urinary tract infection; this effect was slight and transient (Ohta et al, 1987). F. OTHER 1. DISULFIRAM-LIKE REACTIONS FLOMOXEF has not been shown to interfere with ethanol metabolism, and has not been reported to cause DISULFIRAM-like reactions (Uchida & Matsubara, 1991).
DRUG INTERACTIONS DRUG-DRUG COMBINATIONS A. AMINOGLYCOSIDES 1. Summary: Concomitant administration of aminoglycosides and cephalosporins could theoretically have additive nephrotoxic effects. Several cases have been reported that describe nephrotoxic symptoms due to the interaction of aminoglycoside antibiotics and cephalothin (Tvedegaard, 1976; Kleinknecht et al, 1973; Klastersky et al, 1975; Cabanillas et al, 1975; Tobias et al, 1976; Gillett et al, 1976). Further case reports or controlled studies documenting the concurrent use of aminoglycosides with cephalosporins are necessary to determine the extent of this interaction. 2. Adverse Effect: an increased risk of nephrotoxicity 3. Clinical Management: Coadministration of aminoglycoside antibiotics with cephalosporins could produce additive nephrotoxic effects. Use of these agents should be avoided in patients with prior renal insufficiency. If coadministration of these two antibiotic classes is necessary, patients should be monitored for evidence of nephrotoxicity.
Flomoxef (INN) is an oxacephem antibiotic.
It has been classified as second-generation[1] and fourth-generation.[2]
References
- ^ Masuda Z, Kurosaki Y, Ishino K, Yamauchi K, Sano S (April 2008). "Pharmacokinetic analysis of flomoxef in children undergoing cardiopulmonary bypass and modified ultrafiltration". Gen Thorac Cardiovasc Surg 56 (4): 163–9. doi:10.1007/s11748-007-0208-5. PMID 18401677.
- ^ Ito M, Ishigami T (1991). "The meaning of the development of flomoxef and clinical experience in Japan". Infection. 19 Suppl 5: S253–7. doi:10.1007/bf01645536. PMID 1783441.
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Antibacterials: cell envelope antibiotics (J01C-J01D)
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| Intracellular |
- Inhibit peptidoglycan subunit synthesis and transport: NAM synthesis inhibition (Fosfomycin)
- DADAL/AR inhibitors (Cycloserine)
- bactoprenol inhibitors (Bacitracin)
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| Glycopeptide |
- Inhibit PG chain elongation: Vancomycin# (Oritavancin
- Telavancin)
- Teicoplanin (Dalbavancin)
- Ramoplanin
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β-lactams/
(Inhibit PBP
cross-links) |
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| Other |
- polymyxins/detergent
- depolarizing
- Hydrolyze NAM-NAG
- Gramicidin
- Isoniazid
- Teixobactin
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- #WHO-EM
- ‡Withdrawn from market
- Clinical trials:
- †Phase III
- §Never to phase III
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Index of bacterial disease
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| Description |
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| Disease |
- Gram-positive firmicutes
- Gram-positive actinobacteria
- Gram-negative proteobacteria
- Gram-negative non-proteobacteria
- Cholera
- Tuberculosis
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| Treatment |
- Antibiotics
- cell wall
- nucleic acid
- mycobacteria
- protein synthesis
- other
- Antibodies
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