Early investigational antibiotics for the treatment of acute exacerbations of chronic bronchitis

ABSTRACT

Introduction: Acute exacerbations in patients with chronic bronchitis are a leading cause of hospitalizations and death. Bacteria contribute significantly to such exacerbations. The aim of this review was to explore the potential role of investigational antibiotics in the treatment of these episodes.

Areas covered: The available literature in PubMed database, in websites related to investigational drugs and in websites of the producing companies has been searched. The in vitro activity against pathogens involved in acute exacerbations of chronic bronchitis and the pharmacokinetic profile of antibiotics currently under development were taken into consideration for inclusion in the review.

Expert opinion: Several novel antimicrobial agents have completed preclinical and Phase I studies and were well-tolerated. Further investigation is mandatory in order to evaluate their future in treatment of chronic bronchitis exacerbations and discover potential advantages compared to already approved antimicrobials.

KEYWORDS:

• Bacterial exacerbations
• chronic bronchitis
• novel antibiotics
• in vitro activity
• pharmacokinetic profile

Article highlights

• Bacterial pathogens are implicated in the 25-50% of AECB.

• Gepotidacin, TP-271, WCK-4873 and WCK-2349/WCK-771 have in vitro activity against a broad spectrum of bacteria implicated in AECB.

• WCK-2349/WCK-771 has sufficient penetration to respiratory tract.

• Several early investigational drugs either lack in vitro activity against pathogens involved in AECB or are no longer in the line of development.

• Further research is warranted in order to assess potential superiority of new antibiotics compared to already approved ones.

This box summarizes key points contained in the article.

Declaration of interest

M. Falagas has participated in advisory boards of Achaogen, AstraZeneca, Infectopharm, Tetraphase, Pfizer, and Xellia; received lecture honoraria from Cipla, Merck, Sanofi and Novartis; and received research support from Angelini, Astellas, Rokitan, and Shionogi. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Additional information

Funding

This paper was not funded.