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AZ

aztreonam lysine (Cayston / Corus 1020 / AZLI)

✓ Approved

Gilead Sciences, Inc. · Small Molecule · Small Molecule

What is aztreonam lysine?

aztreonam lysine is a small molecule developed by Gilead Sciences, Inc.. It is approved for therapeutic indications via inhaled.

Drug Profile

Brand NamesCayston, Corus 1020, AZLI
CompanyGilead Sciences, Inc.
Drug ClassSmall Molecule
RouteInhaled
StatusApproved
Sources: ClinicalTrials.gov, Gilead Sciences, Inc.

Therapeutic Indications

aztreonam lysine is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsRespiratory tract infection✓ Approved
Infections and infestationsPneumonia pseudomonal✓ Approved
Respiratory, thoracic and mediastinal disordersBronchiectasisPhase III

Related Research Articles

PubMedNature communications2026-10-15

Antagonistic roles of histone H3 lysine methyltransferases dictate tumor immune surveillance.

Gladstein Amy C AC, Charles Solomon Akino Mercy AM, Poltorack Carson D CD, Venkatesh Sharan S et al.

SETD2 is a critical tumor suppressor in lung cancer that catalyzes histone H3 lysine 36 (H3K36) trimethylation. Oncogenic histone H3 alleles, including H3K36M, causally drive cancer formation by dominantly inhibiting SETD2 and other H3K36 methyltransferases. Here we show that expression of the H3K36M oncogene paradoxically suppresses tumor growth in KRAS-driven lung cancer by promoting transcription of repetitive elements and accumulation of cytoplasmic dsRNA, activating antiviral-like immune clearance. Unexpectedly, all attendant effects of H3K36M expression require SETD2 activity despite widespread loss of H3K36 trimethylation. Reducing H3K36 dimethylation through genetic or pharmacologic attenuation of NSD2 phenocopies H3K36M expression, revealing NSD2 as the relevant target through which H3K36M triggers immune activation. Mechanistically, H3K36M expression or NSD2 attenuation reveals a SETD2-dependent mechanism that limits EZH2-mediated repression of repetitive elements, enabling dsRNA accumulation and immune activation. These findings establish opposing roles for NSD2- and SETD2-dependent H3K36 methylation in lung tumor immunity and reveal an NSD2-SETD2-EZH2 axis that can be targeted to modulate viral mimicry and immune surveillance in cancer.

PMID 42875424
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PubMedDrug delivery and translational research2026-10-15

In vitro, ex vivo and in vivo evaluation of polyelectrolyte nanogels for mucosal vaccines.

Bonaccorso Angela A, Corteggio Annunziata A, D'Apice Luciana L, Cardamone Antonio A et al.

Nasal administration is investigated as an effective mucosal site suitable for non-invasive vaccine delivery and able to elicit both systemic and mucosal immunity. Delivery of proteins across the epithelial barrier is a key point to induce an immune response. In this framework, nanogels are properly designed to present the delivered antigen to the immune system, promoting their targeting to specific immune populations. Nanogels for nasal administration based on dextran sulfate and ϵ-poly-L-lysine have been prepared by polyelectrolyte complexation. To unlock the potential of mucosal vaccination, we evaluated nanogel for their ability to enhance antigen delivery across mucus barriers and promote immune activation. Using fluorescein-labelled ovalbumin as a model antigen, we investigated how nanogel governs antigen transport, cellular uptake, and presentation. Produced results showed that nanogel combines favourable physicochemical properties with mucoadhesive behaviour, enabling efficient interaction with the mucus layer. This translates into enhanced uptake and controlled intracellular trafficking in murine Bone Marrow-derived-Dendritic Cells, ultimately promoting effective antigen cross-presentation. Importantly, intranasal administration in vivo revealed prolonged antigen retention within the airway mucosa compared to the free antigen, indicating sustained local antigen availability. In addition, studies in human monocyte-derived macrophages provided preliminary information on the inflammatory response and intracellular fate of the nanogels in a human-relevant system. Together, these findings contribute to the preliminary preclinical characterization of the nanogel platform, while further studies are required to establish its immunogenicity and vaccine efficacy.

PMID 42875718
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PubMedFrontiers in microbiology2026-10-15

Preoperative gut microbial and metabolic signatures associated with postoperative Hirschsprung-associated enterocolitis in short-segment Hirschsprung disease.

Zhang Minzhong M, Gong Yiming Y, Zhang Tian T

Hirschsprung-associated enterocolitis (HAEC) is a major postoperative complication of Hirschsprung disease (HSCR), but whether preoperative gut microbial and metabolic alterations are associated with its subsequent development remains unclear. This prospective cohort study investigated whether preoperative gut microbial and metabolic profiles are associated with postoperative HAEC in children with short-segment Hirschsprung disease (S-HSCR). Sixty-two children with S-HSCR were enrolled, and preoperative fecal samples were collected before pull-through surgery for 16S rRNA gene sequencing, targeted short-chain fatty acid (SCFA) analysis, and untargeted metabolomic profiling. Patients were followed for 3 years after surgery and classified according to the occurrence of postoperative HAEC. During follow-up, 27 patients developed postoperative HAEC. Compared with patients who remained HAEC-free, those who subsequently developed HAEC showed reduced microbial diversity, a lower Gut Microbiome Health Index, a higher Microbiome Dysbiosis Index, and distinct microbial community composition before surgery. Differential abundance analyses identified depletion of several anaerobic commensals and potential SCFA-producing taxa, together with enrichment of potentially pro-inflammatory taxa such as Escherichia-Shigella. Co-occurrence network analysis revealed reduced microbial interaction complexity and connectivity in the HAEC cohort. An exploratory random forest model based on preoperative microbial signatures achieved an area under the curve of 0.80 for predicting postoperative HAEC. Children who later developed HAEC also had significantly lower fecal levels of butyric acid, valeric acid, and total SCFAs. Exploratory untargeted metabolomic analysis yielded preliminary signals across several metabolic pathways, including lysine-related metabolism. Children with S-HSCR who subsequently develop postoperative HAEC already exhibit distinct preoperative microbial dysbiosis and metabolic alterations. These findings suggest that early-life disruption of the gut microbiota and host-microbe metabolic balance may contribute to HAEC susceptibility.

PMID 42876518
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PubMedRedox biology2026-10-14

HDAC1-mediated SUCLA2 lysine β-hydroxybutyrylation modulates myocardial mitochondrial function in sepsis-induced heart dysfunction.

Wen Ri R, Ning Wanshan W, Huang Xin-Mei XM, Hao Peng-Hui PH et al.

Lysine β-hydroxybutyrylation (Kbhb) is associated with energy regulation and mitochondrial function, and its role in sepsis-induced heart dysfunction has not been elucidated. Reveals the extensive effects of Kbhb in sepsis-induced heart dysfunction and identifies the potential targets. A septic heart dysfunction rat model was induced by lipopolysaccharide intraperitoneal injection. Proteomic and β-hydroxybutyrylomic analyses were conducted to assess alterations in Kbhb between cardiac tissues from the control and lipopolysaccharide rats. Putative regulatory proteins were identified by leveraging a multifaceted hybrid learning framework combined with protein language models. Lysine to arginine (R) mutation was made to mimic decreased Kbhb levels. Transcriptomic analysis was further performed to predict the potential downstream mechanisms. Succinate-CoA Ligase ADP-Forming Subunit Beta (SUCLA2) was selected because of its role in mitochondrial function, and the Kbhb level at the K444 site was significantly different. Decreased Kbhb level at K444 of SUCLA2 was confirmed in septic cardiac tissues and lipopolysaccharide-treated H9c2 cardiomyocytes using specific antibody. SUCLA2K444R mutant reversed the protective effects of SUCLA2WT on mitochondrial function in lipopolysaccharide-treated H9c2 cardiomyocytes, accompanied by decreased succinyl-CoA synthetase activity, reduced mitochondrial membrane potential, suppressed adenosine triphosphate production, and increased reactive oxygen species accumulation. The aggravating effects of the SUCLA2K444R mutant on septic heart dysfunction were confirmed in vivo using the specific promoter. Mechanistically, histone deacetylase 1 inhibited SUCLA2 Kbhb at K444 residue. Reduced SUCLA2 Kbhb level at K444 site aggravates myocardial mitochondrial dysfunction, leading to sepsis-induced heart dysfunction. This study reveals a novel function of Kbhb in sepsis-induced heart dysfunction and elucidates the mechanism of SUCLA2 K444 Kbhb.

PMID 42874129
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PubMedFood chemistry2026-10-14

Simultaneous determination of eight free- or cross-linked advanced glycation end products in different processed meat products based on UPLC-MS/MS.

Ru Sumei S, Li Jiaxin J, Lu Yingshuang Y, Zhang Yan Y et al.

A universal ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method was developed for the simultaneous detection of eight free- or cross-linked advanced glycation end products (AGEs), including Nε-carboxymethyllysine, Nε-carboxyethyllysine, Nδ-(5-hydro-5-methyl-4-imidazolon-2-yl)ornithine, glyoxal-derived hydroimidazolone, methylglyoxal lysine dimer, glyoxal lysine dimer, pyrraline and argpyrimidine. This method achieved the separation and quantification of the eight AGEs substances within 16 min. All analytes exhibited high correlation coefficients (R2 > 0.999) within their respective linear ranges. Limits of detection and quantification in reconstituted solution were 0.8-2.5 and 2.5-5.5 μg/L, corresponding to 0.08-0.25 and 0.25-0.55 mg/kg in samples. Respectively. Method validation was performed using crispy fried pork as a blank matrix. The recovery rates ranged from 85.5% to 122.0%, with acceptable intra-day and inter-day precision. This method was successfully applied to the detection of AGEs in 30 different representative meat products, providing technical support for the research on the formation and control of AGEs.

PMID 42874394
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PubMedEMBO reports2026-10-14

Interspecies regulation of virulence through gingipain inhibition by a Tannerella forsythia serpin.

Książek Mirosław M, Benedyk-Machaczka Małgorzata M, Mizgalska Danuta D, Sochaj-Gregorczyk Alicja A et al.

Periodontitis is driven by dysbiotic microbial communities in which Porphyromonas gingivalis (Pg) acts as a keystone pathogen through its caspase-like fold (Clan CD) proteases, gingipains. Tannerella forsythia (Tf), another member of the periodontal pathogenic community, uniquely produces the broad-spectrum serpin termed miropin, yet its biological significance as an inhibitor in periodontal inflammation remains unclear. Here, we demonstrate that miropin directly inhibits the lysine-specific gingipain Kgp and the calpain-like protease Tpr produced by Pg, forming irreversible covalent inhibitory complexes. While recombinant native miropin impairs Pg growth, an engineered variant targeting both lysine- and arginine-specific gingipains entirely abolishes bacterial growth in a defined medium. In vivo, recombinant miropin reduces Pg virulence and, when co-infected with wild-type Tf, prevents lethal infection and significantly reduces alveolar bone loss, but not when co-infected with a miropin-deficient mutant. Protection is associated with inhibition of gingipain activity and normalization of the RANKL/OPG ratio in periodontal tissues. These findings identify miropin as a potent interspecies virulence modulator and challenge the prevailing view of Tf as an exclusively pathogenic member of the oral microbiome.

PMID 42870048
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