Clarithromycin

FLORHAM PARK, N.J., Sept. 01, 2026 (GLOBE NEWSWIRE) -- Phathom Pharmaceuticals, Inc. (Nasdaq: PHAT), a biopharmaceutical company focused on commercializing and developing novel treatments for gastrointestinal (GI) diseases, announced today that members of its management team are scheduled to participate in the following upcoming investor conferences in September: 2026 Cantor Global Healthcare Conference in New York, NY Date: Wednesday, September 9, 2026 Fireside Chat: 10:55 am EDT Management to participate in one-on-one meetings throughout the conference H.C. Wainwright 28th Annual Global Investment Conference in New York, NY Date: Tuesday, September 15, 2026 Fireside Chat: 3:30 pm EDT Management to participate in one-on-one meetings throughout the conference To access the live webcast and archived recordings of each event, visit the News & Events section of the Phathom website at . Recordings will be available for 90 days following the conclusion of each meeting. About Phathom Pharmaceuticals, Inc. Phathom Pharmaceuticals is a biopharmaceutical company focused on the commercialization and development of novel treatments for gastrointestinal diseases. Phathom has in-licensed the exclusive rights to vonoprazan, a first-in-class potassium-competitive acid blocker (PCAB) for the U.S., Europe and Canada. Phathom currently markets vonoprazan in the United States as VOQUEZNA ® (vonoprazan) tablets for the relief of heartburn associated with Non-Erosive GERD in adults, the healing and maintenance of healing of Erosive GERD in adults and relief of associated heartburn, and as part of VOQUEZNA ® DUAL PAK ® (vonoprazan tablets, amoxicillin capsules) and VOQUEZNA ® TRIPLE PAK ® (vonoprazan tablets, amoxicillin capsules, clarithromycin tablets) for the treatment of H. pylori infection in adults. For more information about Phathom, visit the company’s website at and follow on LinkedIn and X . MEDIA CONTACT Nick Benedetto 1-877-742-8466 media@phathompharma.com INVESTOR CONTACT Eric Sciorilli 1-877-742-8466 ir@phathompharma.com © 2026 Phathom Pharmaceuticals. All rights reserved. VOQUEZNA, VOQUEZNA DUAL PAK, VOQUEZNA TRIPLE PAK, Phathom Pharmaceuticals, and their respective logos are registered trademarks of Phathom Pharmaceuticals, Inc.

A senolytic drug already in clinical development for oncology sharply reduced bacterial burden in preclinical models of notoriously treatment-resistant Mycobacterium abscessus infection by eliminating senescent host macrophages rather than targeting the pathogen directly, according to research published August 18 in Nature Communications. The findings identify cellular senescence as a disease-promoting host response in chronic intracellular infection and raise the prospect of host-directed therapies that operate independently of conventional antimicrobial resistance mechanisms. The work was led by corresponding authors Edoardo Scarpa and Loris Rizzello at the National Institute of Molecular Genetics "Romeo and Enrica Invernizzi" (INGM) and the University of Milan's Department of Pharmaceutical Sciences, in collaboration with the Emerging Bacterial Pathogens Unit at IRCCS San Raffaele Scientific Institute and other Italian institutions. Mycobacterium abscessus (Mab), a nontuberculous mycobacterium that causes chronic pulmonary disease, is intrinsically resistant to many antibiotics and notoriously difficult to eradicate. The researchers found that chronic intracellular Mab infection drives murine alveolar-like macrophages into a stable senescent state through pathogen-induced DNA damage. The effect required live, replicating bacteria: propiolactone-fixed Mab failed to induce comparable markers of DNA double-strand breaks. Bulk RNA sequencing and reanalysis of spatial transcriptomics data from infected mouse lung tissue further showed transcriptome-wide upregulation of senescence-associated gene programs and their spatial enrichment in infected regions. Infected senescent macrophages also developed a senescence-associated secretory phenotype (SASP), characterized by factors including TNF-α, IL-6, IL-1α, and matrix metalloproteinases. Conditioned-media experiments showed that these secreted factors were sufficient to induce senescence in naïve, uninfected neighboring cells. The effect was also evident spatially: approximately 85.7% of uninfected cells within 60 µm of Mab-positive cells were positive for senescence-associated β-galactosidase (SA-β-gal). The resulting SASP environment increased the permissiveness of neighboring cells to subsequent Mab infection, suggesting that infection-induced senescence may help create and expand a cellular niche favorable to bacterial persistence. Key findings were also validated in human monocyte-derived macrophages from healthy donors. The researchers next tested navitoclax (ABT-263), an inhibitor of the anti-apoptotic proteins BCL-2, BCL-XL, and BCL-W with established senolytic activity. Senescent cells can become dependent on these survival pathways, making them particularly susceptible to apoptosis following navitoclax treatment. In chronically infected macrophages, navitoclax produced an approximately 2.3 log10 reduction in intracellular colony-forming units (CFUs) across at least seven biological replicates, an effect comparable in magnitude to the standard-of-care antibiotic clarithromycin. Importantly, navitoclax did not increase extracellular bacterial counts, suggesting that apoptotic elimination of infected senescent cells did not simply release viable Mab into the surrounding environment. The effect extended to an in vivo model. In C57BL/6N mice with chronic respiratory Mab infection, oral navitoclax at 50 mg/kg/day reduced pulmonary bacterial burden compared with vehicle control, with the experiment independently repeated twice. The findings build on evidence that senescence may represent a therapeutically actionable host response in other chronic infections. A 2025 Nature Communications study from Johns Hopkins showed that navitoclax improved treatment outcomes in mouse models of pulmonary tuberculosis when used alongside antibiotic therapy, reducing bacterial burden, lung damage, and fibrosis. There are important differences between the studies. In the tuberculosis work, navitoclax showed no direct activity against Mycobacterium tuberculosis and did not reduce bacterial burden when given alone, with its benefit emerging as an adjunct to conventional antibiotics. The new Mab study provides evidence that senescent macrophages themselves form a permissive niche for infection and that eliminating those cells can substantially reduce intracellular bacterial burden. Clinical investigation of senolytic approaches in infectious disease nevertheless remains extremely limited. DASAHIVCURE (NCT05527418), a Phase II study of dasatinib in recent HIV-1 infection, has been cited in the senolytics literature as a rare example of a potentially senolytic agent being investigated in an infectious-disease setting. No comparable clinical trial of senolytic therapy for a bacterial infection had been identified as of August 2026. For Mab pulmonary disease itself, clinical development remains centered on antimicrobial regimens. Among the most advanced efforts is FORMaT (NCT04310930), a Phase II/III adaptive platform trial sponsored by the University of Queensland that is evaluating antibiotic treatment strategies for Mab pulmonary disease. The new study is entirely preclinical, and substantial barriers remain before senolytic therapy could be tested clinically against Mab infection. Navitoclax has a well-established risk of thrombocytopenia resulting from BCL-XL inhibition in platelets, which has complicated its development in oncology. The drug has been evaluated in studies including the Phase III TRANSFORM-2 trial (NCT04468984) in relapsed or refractory myelofibrosis, where its BCL-2-family inhibition is being exploited as an anticancer mechanism rather than for its senolytic properties. Whether more selective senolytic strategies could spare platelets while retaining activity against the survival pathways required by infected senescent macrophages remains unresolved. No IND application or registered clinical trial for navitoclax as a senolytic treatment for an infectious disease had been identified as of August 2026. The authors position senolysis as a potential host-directed adjunct to antibiotics rather than a replacement for antimicrobial therapy. By targeting a host-cell state that appears to favor bacterial persistence, such an approach could complement conventional drugs without depending directly on the pathogen's antimicrobial susceptibility. Spot something wrong? Report an issue with this article