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aztreonam lysine (Cayston / Corus 1020 / AZLI)

✓ Approved

Gilead Sciences, Inc. · 小分子 · 小分子

什么是 aztreonam lysine？

aztreonam lysine 是一种小分子，由Gilead Sciences, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Inhaled。

药物档案

商品名Cayston, Corus 1020, AZLI
公司Gilead Sciences, Inc.
药物类别小分子
给药途径Inhaled
状态Approved
来源： ClinicalTrials.gov, Gilead Sciences, Inc.

治疗适应症

aztreonam lysine 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsRespiratory tract infection✓ Approved
Infections and infestationsPneumonia pseudomonal✓ Approved
Respiratory, thoracic and mediastinal disordersBronchiectasisPhase III

相关研究文献

PubMedNature communications2026-06-13

Late-stage generation of 14C/3H-radiolabeled lysine residues via hydroformylation of peptides.

Schick Anika A, San Jose Gracia Marc M, Christian D Hammershøj Hans H, Broddefalk Johan J et al.

Peptides constitute a well-established and rapidly expanding field in the contemporary pharmaceutical drug landscape. Studies with 14C- or 3H-radiolabeled analogs are the gold standard for drug development, yet access to 14C-peptides is costly and limited to derivatization of the native structure with tags or lengthy multi-step syntheses. In this work, we report a platform that installs 14C- or 3H-radiolabeled lysine residues directly on solid-supported peptides. The workflow constitutes a mild, peptide-compatible hydroformylation process of allylglycine residues to generate labeled allysine, followed by reductive amination that furnishes radiolabeled lysine residues directly upon cleavage from the solid support. The hydroformylation setup can be tuned for flexible isotope introduction by using 14CO from solid precursors and 3H2 from standard tritium manifolds. We show that the optimized workflow tolerates diverse sequences and enables functionalization of peptides as complex as semaglutide analogs.

PMID 42285941
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PubMedJournal of experimental & clinical cancer research : CR2026-06-13

Inhibition of 5'-tiRNAGly restores anti-PD-1 immunotherapy efficacy via DLST-mediated OGDHL succinylation in gastric cancer.

Gu Xinliang X, Zhang Yu Y, Li Yang Y, Li Xun X et al.

Transfer RNA-derived small RNAs (tsRNAs) have been implicated in tumor progression and immune regulation in recent years. However, the specific role of tRNA halves (tiRNAs), a subclass of tsRNAs, in modulating immunotherapy response remains unexplored. In this study, 5'-tiRNAGly levels were examined in gastric cancer (GC) patients and found to be upregulated, especially in non-responders to anti-PD-1 therapy. Elevated 5'-tiRNAGly levels were also associated with diminished oxoglutarate dehydrogenase-like (OGDHL) expression. Further exploration revealed that 5'-tiRNAGly bound to DLST and promoted OGDHL destabilization, whereas targeted inhibition of 5'-tiRNAGly restored OGDHL stability through succinylation at lysine 910, enhanced tricarboxylic acid (TCA) cycle activity, and reduced glutamine-derived metabolic reprogramming. Additionally, 5'-tiRNAGly was found to decrease the activity of α-ketoglutarate dehydrogenase and inhibit succinylation of histone H3 at lysine 79 (H3K79suc), thereby downregulating PD-L1 transcription and reducing therapeutic responsiveness to PD-1 inhibitors. Conversely, restoration of this epigenetic modification upon 5'-tiRNAGly inhibition facilitated PD-L1 transcription, thereby sensitizing tumors to anti-PD-1 therapy. Our findings indicate that targeting 5'-tiRNAGly may represent a promising strategy to enhance responsiveness to anti-PD-1 therapy in GC patients.

PMID 42286727
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PubMedScandinavian journal of immunology2026-06-13

Virulence Factors of Porphyromonas gingivalis in Periodontitis and Rheumatoid Arthritis: Clinical Implications.

Daniela S Silva SS, Marta Kaminska K, Danuta Mizgalska M, Jan Potempa P et al.

Porphyromonas gingivalis (P. gingivalis), has been implicated in exacerbating inflammatory arthritis through its virulence factors. Understanding the role of these factors could inform strategies to mitigate both periodontal and synovial inflammation. This study aimed to investigate the prevalence of P. gingivalis virulence factors and their potential impact on disease activity in patients with periodontitis, rheumatoid arthritis (RA), or both conditions. Patients with RA (n = 22), RA plus periodontitis (n = 22), periodontitis (n = 10), and healthy controls (n = 35), were compared for C-reactive protein levels, anti-cyclic citrullinated peptide IgG, peptidylarginine-deiminase (PAD)2/4 activity and anti-P. gingivalis virulence-associated gingipain antibodies. All patients with periodontitis were compared for P. gingivalis, Tannerella forsythia and Prevotella intermedia colony-forming units, and gene variants of P. gingivalis, including PAD (P.PAD), major fimbriae (fimA), lysine-gingipain (kgp), and receptor antigen gene B (ragB). Higher mean clinical periodontal attachment loss was observed with P.PAD type 1 (p = 0.033). The major fimbriae and lysine-gingipain gene variants showed distinct distributions between groups. Anti-gingipain IgG levels showed positive correlations with RA disease activity. Despite limitations, this study supports a role for P. gingivalis in exacerbating periodontitis and RA underscoring the importance of P. gingivalis virulence factors in disease modulation and highlighting potential therapeutic strategies. Further research is needed to elucidate mechanistic pathways and develop effective interventions. Trial Registration: ISRCTN 17950307; https://doi.org/10.1186/ISRCTN17950307.

PMID 42286809
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PubMedExperimental & molecular medicine2026-06-13

Keratin 18 functions as a lactyltransferase to trigger necroptosis in diabetic kidney disease by modulating Fas transcription.

Zhao Qiao Q, Liu Xu X, Yang Yangliang Y, Meng Fufen F et al.

Diabetic kidney disease (DKD) is a type of chronic renal injury induced by diabetes mellitus and is characterized by persistent proteinuria and progressive decreases in the glomerular filtration rate. Recent studies have highlighted the significance of histone lactylation and necroptosis in the pathogenesis of DKD. We explored the mechanisms by which lactate-induced histone H3 lysine-18 lactylation (H3K18la) and H3K27la promote necroptosis in DKD. Lactate-induced H3K18la and H3K27la modulated Fas transcription, contributing to necroptosis and DKD progression. Moreover, keratin 18 (KRT18), identified as a lactyltransferase, regulated H3K18la and H3K27la levels, subsequently inducing Fas transcription and necroptosis. Furthermore, ginsenoside Rc (gRc) inhibited KRT18 lactyltransferase activity by competing for the lactate binding site in KRT18. Notably, gRc treatment reduced the KRT18, H3K18la, H3K27la, and Fas levels and alleviated necroptosis and renal dysfunction in DKD models. In conclusion, KRT18 functions as a lactyltransferase to induce Fas transcription and necroptosis. Moreover, inhibiting KRT18-mediated histone lactylation via gRc is a potential strategy for treating DKD.

PMID 42286157
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PubMedThe Journal of biological chemistry2026-06-13

Structural insights into histone mimicry by the small hepatitis delta antigen.

Hu Haiyun H, Lv Mengjiao M, Wang Xiaohui X, Shang Xinci X et al.

Hepatitis delta virus (HDV) is a satellite RNA virus that requires hepatitis B virus (HBV) for propagation but replicates its genome independently in the nucleus. The small form of the hepatitis delta antigen (S-HDAg) is essential for replication and is regulated by post-translational modifications. Acetylation at lysine 72 (K72ac) enables S-HDAg to interact with the bromodomain (BRD) of the host chromatin remodeler bromodomain adjacent to zinc finger domain protein 2B (BAZ2B) to promote viral replication. However, the structural basis for this interaction has remained elusive. Here, we provide structural and biophysical insights into this interaction through quantitative binding assays and X-ray crystallography. Isothermal titration calorimetry revealed that BRDs of BAZ2B and its close homolog BAZ2A bind to the viral peptide weakly, with BAZ2A-BRD exhibiting a modestly higher affinity. The crystal structure of BAZ2A-BRD in complex with the S-HDAg-K72ac peptide demonstrates an inverted binding orientation relative to canonical histone ligands, rationalizing the weak interaction. Mutagenesis studies confirmed the critical binding interface both in vitro and in cells. These findings elucidate the molecular mechanism by which HDV co-opts host BAZ2 bromodomains via a unique, weak-affinity interaction, providing a structural framework for understanding viral replication.

PMID 42285512
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PubMedFEMS microbiology letters2026-06-13

Fluorescent Protein Sensors Illuminate Cellular pH Changes in Enterobacter cloacae: Unravelling the Mechanisms of TolC-Dependent Acid Survival.

Chowdhury Sanchari S, Mohapatra Harapriya H

TolC is the outer membrane component of the tripartite RND efflux pump AcrAB-TolC. The underlying mechanism of TolC-dependent acid survival at physiological pH remains unclear. The present study aimed at understanding mechanism of TolC mediated acid survival in logarithmic phase culture of Enterobacter cloacae subsp. cloacae ATCC 13047 not preconditioned to acidic pH. Of the three distinct loci encoding tolC and tolC like proteins, only ECL_04363 (hereafter referred to as EctolC2) exhibited 86% identity with TolC protein from E. coli K12; deletion of which compromised survival at pH4.0. Tracking the periplasmic and cytoplasmic pH changes with fluorescent protein sensors indicated deletion of EctolC2 resulted in sustained cytoplasmic acidification and loss of pH homeostasis causing cell death. Exogenous supplementation of lysine significantly rescued acid induced lethality in EcΔtolC2 mutants. ΔmarRAB mutants exhibited slower death rate compared to Δrob mutants; underpinning role of the latter in upregulating EctolC2 at early time point of growth at pH4.0. Results of the study construe that EctolC2 provides reinforcement to the outer membrane preventing extreme acidification of the periplasm and thereby restoring cytoplasmic pH homeostasis. This study provides significant insight into mechanism of TolC dependent acid survival in E. cloacae.

PMID 42285540
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