Drug Database
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

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PubMedNature metabolism2026-09-05

UBE2N deficiency contributes to MASH development via p62-regulated mitophagy and PANoptosis.

Wang Feng F, Lee Jin J, Park Jeong-Su JS, Huang Meizhou M et al.

K63-linked ubiquitination (K63) is closely associated with the interaction, intracellular trafficking or activity of tagged proteins. However, its role during metabolic dysfunction-associated steatohepatitis (MASH) is largely unknown. Here we show that UBE2N, a ubiquitin-conjugating enzyme that specializes in creating K63, is downregulated by THAP11 in human and mouse hepatocytes with MASH. While hepatocyte-specific Ube2n deficiency exacerbates western diet-induced MASH and fibrosis via PANoptosis and impaired mitophagy, its overexpression reverses these pathological phenotypes and restores hepatic homeostasis. Mechanistically, UBE2N increases PARKIN-mediated K63-p62 at lysine 420, promoting K63-p62 translocation into damaged mitochondria for mitophagic clearance. Ube2n deficiency, conversely, induces cytoplasmic p62 accumulation and NRF2 hyperactivation, driving PANoptosis. Additional Sqstm1 deletion mitigates Ube2n deletion-induced pathologies, highlighting the importance of p62 accumulation for MASH progression. Thus, our results demonstrate that hepatocyte UBE2N is essential for regulation of metabolic stress-mediated mitophagy and PANoptosis, and that p62 is a proof-of-concept target for treating MASH and fibrosis.

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PubMedInternational journal of molecular medicine2026-09-04

Research progress on lysine acetylation (Review).

Zhang Minghui M, Zhang Yuqi Y, Yin Haoxin H, Yan Junyuan J et al.

Lysine acetylation is recognized as a critical and reversible post‑translational modification that is essential for numerous cellular functions and biological processes. The dynamic interplay between lysine acetylation and deacetylation to regulates a wide spectrum of processes, including histone modification, gene expression, cell cycle progression, DNA repair and signal transduction. Emerging evidence has demonstrated that the dysregulation of lysine acetylation is strongly associated with multiple diseases, including cancer, cardiovascular diseases, chronic inflammatory diseases and neurological diseases. These alterations can modify gene expression and disrupt cellular homeostasis. The present review aimed to highlight the biological functions of lysine acetyltransferases and lysine deacetylases, their contributions to disease pathogenesis, and the interplay the crosstalk of lysine acetylation with other post‑translational modifications. Drawing on the latest research findings, the therapeutic potential of targeting acetylation pathways is discussed, with the aim of providing new insight into the development of innovative treatment strategies and clinical applications.

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PubMedJournal of proteome research2026-09-04

Hyperlactate-Associated Lysine Lactylome Remodeling in Laryngeal Squamous Cell Carcinoma.

Zhang Dan D, Li Xinglan X, Li Huan H, Wang Liang L et al.

Laryngeal squamous cell carcinoma (LSCC) lacks reliable biomarkers, and the roles of lactate metabolism and lysine lactylation (Kla) remain largely unknown. We profiled the lysine lactylome of LSCC, paired it with adjacent normal tissues, and integrated the data with quantitative proteomic and transcriptomic analyses. LSCC exhibited a hyperlactate-associated phenotype characterized by dysregulated lactate-related genes (LRGs), altered protein abundance, increased tissue lactate, and globally increased Kla levels. Data-independent acquisition mass spectrometry (DIA-MS) identified 1616 Kla sites on 1468 peptides from 688 proteins, with most differential sites being upregulated in tumors. Differentially lactylated proteins were enriched in cell-matrix adhesion, cell migration, chromatin remodeling, and gene-regulatory processes and were clustered into cytoskeletal and nuclear regulatory modules. Multiple Kla sites were also detected on the core histones. Immunoblotting and tissue microarray analyses confirmed increased pan-Kla expression in the LSCC. Pan-Kla levels were independent of sex and age but positively correlated with the tumor stage and lymph-node metastasis. These findings provide a systematic resource for hyperlactate-associated lactylome remodeling in LSCCs and identify candidate Kla-related molecular features associated with clinicopathological progression for future functional and clinical evaluation.

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PubMedProceedings of the National Academy of Sciences of the United States of America2026-09-04

Lysine iminylation derived from ω-3 polyunsaturated fatty acids.

Zhang Bingsen B, Hsieh Yu-Heng YH, Bales Tyler R TR, Butler Scott D SD et al.

Protein posttranslational modifications (PTMs) play a central role for regulating protein function and cellular processes, with many PTMs arising from reactions with electrophilic metabolites. Here we extend the known landscape of PTMs with the identification of "lysine C3-iminylation," the conjugation of protein lysine residues with propionaldehyde. To stabilize iminylation for mass spectrometric analyses and distinguish it from other isomeric PTMs, we developed a fixation and stable-isotope labeling approach based on parallel reduction of proteome with sodium borohydride and borodeuteride. Analyses of protein hydrolysates confirmed the presence of C3-iminylation in Caenorhabditis elegans and mouse. Additionally, proteomics results demonstrated specificity of this PTM in vitro and in vivo and revealed C3-iminylation in proteins related to critical metabolic pathways. Importantly, collective evidence from isotope tracing as well as genetic, dietary, and pharmacological manipulation experiments uncovered that C3-iminylation originates from cytochrome P450 (CYP)-mediated oxidation of omega-3 fatty acids. Correspondingly, C3-iminylation levels were elevated in C. elegans daf-2(e1370) mutants, an aging model, in which CYP activity is generally increased. These findings not only expand our understanding of the biochemical diversity of PTMs but also underscore the complex interplay between lipid metabolism and protein modifications, enabling further exploration of their biological and clinical implications.

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PubMedFrontiers in endocrinology2026-09-04

Metabolic-epigenetic crosstalk in latent autoimmune diabetes in adults: potential roles of lactate-induced histone lactylation in immune regulation and pancreatic β-cell fate.

Zhang Wen W, Wang Xiaoran X, He Bing B, Xia Yongliang Y et al.

Latent autoimmune diabetes in adults (LADA) is clinically between type 2 and type 1 diabetes with progressive autoimmune loss of β-cells and variable insulin dependence. Lactate was once thought to be a glucan byproduct and is now recognized as a signaling enzyme regulating gene expression via lysine lactylation. One of these marks is histone H3 lysine 18 lactylation (H3K18la), which is enriched at active enhancers and links immune genes. We examined literature and systematically distinguished direct LADA evidence from inferences from studies of type 1 diabetes, β-cell biology, autoimmune disease, and cancer. Present data posits elevated lactate and H3K9la in cell dedifferentiation, and H3K18la has stronger mechanistic support in immune regulation and enhancer activity. Cell-type-specific validation in longitudinal LADA cohorts and disease-specific experiments is lacking. We consider H3K18la a biologically plausible mechanism of LADA pathogenesis rather than an established driver. We emphasize that biomarker development or therapeutic translation will require strict LADA-specific evidence.

PMID 42694315
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PubMedPesticide biochemistry and physiology2026-09-04

Kojic acid and ε-poly-L-lysine suppress potato common scab and remodel the tuber-associated microbiome.

Nie Fengjie F, He Zexue Z, Zhang Li L, Zhang Yu Y et al.

Potato common scab (PCS) is an economically important soil-borne disease whose occurrence is governed not only by pathogen virulence but also by the disease-associated microbiome and soil environment. However, studies on natural bioactive compounds have primarily focused on direct pathogen inhibition, whereas their roles in microbiome remodeling remain largely unexplored. Here, we investigated the antibacterial activity of kojic acid (KA) and ε-poly-L-lysine (ε-PL) against Streptomyces scabies and evaluated their effects on PCS severity and the tuber-associated microbiome. Both KA and ε-PL significantly inhibited the growth of Streptomyces scabies G9, with ε-PL exhibiting stronger in vitro antibacterial activity. Both treatments disrupted hyphal ultrastructure, increased membrane permeability, and triggered extensive transcriptional reprogramming involving cell envelope organization, central metabolism, membrane transport, and genetic information processing. Net-house and field trials showed that both compounds substantially reduced disease severity; significant yield increases were observed in the net-house trial, whereas no significant yield differences were detected among treatments in the field trial. Microbiome analyses revealed that both compounds improved the physicochemical properties and enzyme activities of tuber-associated soil, reshaped the composition and predicted functional profiles of the tuber-associated bacterial community, and reduced the relative abundance of pathogen-associated Streptomyces taxa. Correlation analyses revealed significant associations among soil environmental factors, pathogen-associated Streptomyces taxa, and disease occurrence. Collectively, these findings indicate that KA and ε-PL suppress PCS in association with direct antibacterial activity and remodeling of the tuber-associated bacterial community. This study provides insights into the potential roles of natural bioactive compounds in pathogen suppression and microbiome modulation.

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