Evidence map›Paper›PMID 23913123›Full record

ArticleNature medicine2013

Discovery of Q203, a potent clinical candidate for the treatment of tuberculosis.

Kevin Pethe, Pablo Bifani, Jichan Jang, Sunhee Kang, Seijin Park, Sujin Ahn, Jan Jiricek, Juyoung Jung, Hee Kyoung Jeon, Jonathan Cechetto and 45 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 272 papers.

0numbers the graph read from it
0cells of the map it votes in
272citing papers in PubMed
20.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

272 citing papers in PubMed, 600 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. The Mycobacterial cyt-Journal of medicinal chemistry · 2026
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Journal of bacteriology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Imidazo[1,2‑ACS omega · 2026
    Review
  19. Article
  20. Article

212 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

55 authors at 10 institutions in 5 countries.

Kevin Pethe1] Institut Pasteur Korea, Sampyeong-dong, Seongnam-si, Gyeonggi-do, Korea. [2].
Pablo Bifani
Jichan Jang
Sunhee Kang
Seijin Park
Sujin Ahn
Jan Jiricek
Juyoung Jung
Hee Kyoung Jeon
Jonathan Cechetto
Thierry Christophe
Honggun Lee
Marie Kempf
Mary Jackson
Anne J Lenaerts
Ha Pham
Victoria Jones
Min Jung Seo
Young Mi Kim
Mooyoung Seo
Jeong Jea Seo
Dongsik Park
Yoonae Ko
Inhee Choi
Ryangyeo Kim
Se Yeon Kim
SeungBin Lim
Seung-Ae Yim
Jiyoun Nam
Hwankyu Kang
Haejin Kwon
Chun-Taek Oh
Yoojin Cho
Yunhee Jang
Junghwan Kim
Adeline Chua
Bee Huat Tan
Mahesh B Nanjundappa
Srinivasa P S Rao
Whitney S Barnes
René Wintjens
John R Walker
Sylvie Alonso
Saeyeon Lee
Jungjun Kim
Soohyun Oh
Taegwon Oh
Ulf Nehrbass
Sung-Jun Han
Zaesung No
Jinhwa Lee
Priscille Brodin
Sang-Nae Cho
Kiyean Nam
Jaeseung Kim
Institut Pasteur Korea · KRNovartis (Singapore) · SGColorado State University · USGenomics Institute of the Novartis Research Foundation · USQurient (South Korea) · KRYonsei University · KRCentre Hospitalier Universitaire d'Angers · FRChungnam National University · KRNational University of Singapore · SGUniversité Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

New therapeutic strategies are needed to combat the tuberculosis pandemic and the spread of multidrug-resistant (MDR) and extensively drug-resistant (XDR) forms of the disease, which remain a serious public health challenge worldwide. The most urgent clinical need is to discover potent agents capable of reducing the duration of MDR and XDR tuberculosis therapy with a success rate comparable to that of current therapies for drug-susceptible tuberculosis. The last decade has seen the discovery of new agent classes for the management of tuberculosis, several of which are currently in clinical trials. However, given the high attrition rate of drug candidates during clinical development and the emergence of drug resistance, the discovery of additional clinical candidates is clearly needed. Here, we report on a promising class of imidazopyridine amide (IPA) compounds that block Mycobacterium tuberculosis growth by targeting the respiratory cytochrome bc1 complex. The optimized IPA compound Q203 inhibited the growth of MDR and XDR M. tuberculosis clinical isolates in culture broth medium in the low nanomolar range and was efficacious in a mouse model of tuberculosis at a dose less than 1 mg per kg body weight, which highlights the potency of this compound. In addition, Q203 displays pharmacokinetic and safety profiles compatible with once-daily dosing. Together, our data indicate that Q203 is a promising new clinical candidate for the treatment of tuberculosis.

Indexed as

Adenosine TriphosphateAnimalsCell ProliferationDisease Models, AnimalDrug Evaluation, PreclinicalElectron Transport Complex IIIExtensively Drug-Resistant TuberculosisImidazolesMiceMice, Inbred BALB CMycobacterium tuberculosisPiperidinesPyridinesRatsRats, Sprague-DawleyAdenosine TriphosphateElectron Transport Complex IIIImidazolesPiperidinesPyridinestelacebec

Identifiers

PMID23913123
OpenAlexW2092679747

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.