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We report Pranlukast (PRK) as a novel allosteric inhibitor of\n                    <jats:italic>Mtb<\/jats:italic>\n                    's arginine biosynthetic enzyme, Ornithine acetyltransferase (\n                    <jats:italic>Mt<\/jats:italic>\n                    ArgJ). PRK treatment remarkably abates the survival of free as well as macrophage\u2010internalized\n                    <jats:italic>Mtb<\/jats:italic>\n                    , and shows enhanced efficacy in combination with standard\u2010of\u2010care drugs. Notably, PRK also reduces the 5\u2010lipoxygenase (5\u2010LO) signaling in the infected macrophages, thereby surmounting an enhanced response against intracellular pathogen. Further, treatment with PRK alone or with rifampicin leads to significant decrease in\n                    <jats:italic>Mtb<\/jats:italic>\n                    burden and tubercular granulomas in\n                    <jats:italic>Mtb<\/jats:italic>\n                    \u2010infected mice lungs. Taken together, this study demonstrates a novel allosteric inhibitor of\n                    <jats:italic>Mt<\/jats:italic>\n                    ArgJ, which acts as a dual\u2010edged sword, by targeting the intracellular bacteria as well as the bacterial pro\u2010survival signaling in the host. PRK is highly effective against\n                    <jats:italic>in\u00a0vitro<\/jats:italic>\n                    and\n                    <jats:italic>in\u00a0vivo<\/jats:italic>\n                    survival of\n                    <jats:italic>Mtb<\/jats:italic>\n                    and being an FDA\u2010approved drug, it shows a potential for development of advanced combinatorial therapy against tuberculosis.\n                  <\/jats:p>","DOI":"10.15252\/emmm.201708038","type":"journal-article","created":{"date-parts":[[2018,2,26]],"date-time":"2018-02-26T20:10:21Z","timestamp":1519675821000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":46,"title":["An allosteric inhibitor of Mycobacterium tuberculosis ArgJ: Implications to a novel combinatorial therapy"],"prefix":"10.1038","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4381-5990","authenticated-orcid":false,"given":"Archita","family":"Mishra","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashalatha S","family":"Mamidi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raju S","family":"Rajmani","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ananya","family":"Ray","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajanya","family":"Roy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2466-2514","authenticated-orcid":false,"given":"Avadhesha","family":"Surolia","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2018,2,26]]},"reference":[{"key":"BFEMMM201708038_CR2","doi-asserted-by":"crossref","first-page":"e1343","DOI":"10.1038\/cddis.2014.313","volume":"5","author":"N Aguil\u00f3","year":"2014","unstructured":"Aguil\u00f3 N, Uranga S, Marinova D, Mart\u00edn C, Pardo J (2014) Bim is a crucial regulator of apoptosis induced by Mycobacterium tuberculosis. 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