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

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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PubMedJAC-antimicrobial resistance2026-05-25

Therapeutic strategies for multi-resistant Escherichia coli in urinary tract infections-a cause for concern.

Unni Rekha R, Varghese Ruby R, Arakal Benita B, Padmanabhan Lochana L et al.

Antimicrobial resistance (AMR) is a serious and growing public health concern driven by multiple factors. Urinary tract infection (UTI) is one of the infections commonly associated with AMR, and more than 80% of UTIs are caused by Escherichia coli. MDR E. coli is a significant problem that requires urgent intervention, particularly in complicated UTIs (cUTIs) with underlying comorbidities. Although prevalence rates of MDR E. coli vary globally, it remains a critical clinical and economic challenge on every continent. The majority of MDR E. coli strains produce ESBLs, followed by AmpC enzymes, making them generally resistant to penicillins, cephalosporins and aztreonam. While there are some therapeutic options for uncomplicated UTIs (uUTIs), choices are limited for cUTIs, with carbapenems being the mainstay of treatment. However, carbapenem resistance is on the rise, severely impeding clinical regimens. With very few options available, combinations of antimicrobial agents for synergistic activity are increasingly relied upon for carbapenem-resistant E. coli. This situation has compelled the search for novel antimicrobial agents, which are slowly entering the market, although not as quickly as AMR is spreading worldwide. Current focus is shifting towards alternative antimicrobial therapies that exhibit broad-spectrum bactericidal activity and immunomodulatory effects, considered for both preventive and therapeutic strategies. A multi-disciplinary approach combining novel antimicrobials, innovative therapies and robust infection control measures will be essential to effectively manage MDR E. coli in uUTIs and cUTIs and mitigate the global threat of antibiotic resistance.

PubMedbioRxiv : the preprint server for biology2026-05-25

Epigenetic maintenance of PRC2-repressed chromatin requires RTT109 but not H3K56 acetylation.

Yap Rochelle E RE, Ebot-Ojong Felicia F, Ameri-Solanky Abigail J AJ, Lewis Zachary A ZA

In animals, plants, and some fungi, Polycomb Repressive Complex 2 (PRC2) catalyzes trimethylation of histone H3 lysine 27 (H3K27me3) to establish transcriptionally repressed chromatin. Here, we identify the histone acetyltransferase RTT109 as a key regulator of PRC2-repressed domains in the model fungus Neurospora crassa . Although RTT109 interacts with the VPS75 homolog Nucleosome Assembly Factor 2 (NAF-2), we show that proper structure and function of PRC2-methylated chromatin require RTT109 catalytic activity but are independent of NAF-2 and H3K56 acetylation. We further demonstrate that H3K27me3 can be stably propagated over multiple rounds of mitosis in the absence of sequence-specific PRC2 targeting, and that RTT109 is essential for maintenance of the repressed state. These findings uncover a replication-linked mechanism for epigenetic memory and establish RTT109 as a key regulator of Polycomb-mediated chromatin inheritance.

PubMedActa biochimica et biophysica Sinica2026-05-25

Metabolic reprogramming promotes AR-V7 splicing via SRSF2 lactylation in castration-resistant prostate cancer.

Zhu Wenkai W, Xu Jingran J, Batur Jesur J, Wang Zhenda Z et al.

Metabolic alterations are a hallmark of cancer, yet their direct influence on oncogenic splicing remains unclear. This study demonstrates that castration-resistant prostate cancer (CRPC) exhibits enhanced glycolysis compared to hormone-sensitive disease, resulting in elevated lactate and increased global protein lactylation. Lactylomic profiling identifies the splicing factor SRSF2 as a key target, modified at a conserved lysine (K36). SRSF2 lactylation competes with ubiquitination, thereby stabilizing the protein and enabling it to promote the alternative splicing of androgen receptor (AR) pre-mRNA into the AR-V7 variant, a major driver of CRPC development. Functional assays confirm that both LDHA and SRSF2 are critical for CRPC cell proliferation, migration, and tumor growth, and their high expression correlates with poor patient prognosis. Our work establishes a direct mechanistic link between glycolysis and oncogenic splicing via protein lactylation, nominating the LDHA/SRSF2/AR-V7 axis as a therapeutic target.

PubMedActa biochimica et biophysica Sinica2026-05-25

Sti1 participates in the dynamics of protein aggregation triggered by glucose signaling in Saccharomyces cerevisiae.

Chen Jiawei J, Zhou Jiayu J, Sun Keren K, Zhang Hanlin H et al.

Environmental changes put stress on living organisms. We find that nutrient starvation induces dynamic protein aggregations in yeast cells, and many chaperones are involved in this process. Among them, Sti1/HOP, the co-chaperone of Hsp70 and Hsp90, plays roles in the formation of protein quality control (PQC) compartments and protein stasis (or proteostasis) maintenance, and it co-localizes to insoluble protein deposits (IPOD) by liquid-liquid phase separation (LLPS). Notably, the subcellular localization and cytoplasmic aggregation of Sti1 are rigorously regulated by the PQC machinery, including Ssa1/Hsp70 and Hsp82/Hsp90. On the other hand, STI1 deletion abolishes cytoplasmic aggregation of chaperones, including Ssa1, Hsp42 and Hsp104. These results reveal an interdependent model of chaperone-mediated aggregate formation. Furthermore, lysine 9 (K9) of Sti1 is identified as a critical residue governing its cytoplasmic condensation through a potential post-translational modification.

PubMedTranslational cancer research2026-05-25

Lysine crotonylation-related long non-coding RNAs: a novel prognostic framework for gastric carcinoma.

Hu Hao H, Zhao Hegui H, Yao Daiyi D, Tang Qulai Q et al.

Despite advances in oncology, gastric carcinoma (GC) persists as a major contributor to global cancer mortality. Lysine crotonylation (Kcr) has emerged as a pivotal post-translational modification governing gene transcription and chromatin dynamics. Yet, the specific impact of crotonylation-related long non-coding RNAs (lncRNAs) on the clinical prognosis and immune landscape of GC remains to be elucidated. Therefore, this study aimed to construct a novel prognostic framework based on Kcr-related lncRNAs and comprehensively investigate its association with the immune landscape in GC. RNA sequencing profiles and corresponding clinical metadata were acquired from The Cancer Genome Atlas (TCGA). Through co-expression analysis, we screened for lncRNAs associated with crotonylation modifications. We then constructed a novel prognostic signature using a stepwise approach comprising univariate Cox regression, least absolute shrinkage and selection operator (LASSO) regularization, and multivariate Cox regression. The predictive performance of this model was evaluated via Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves. Furthermore, we explored correlations between the risk signature and the tumor microenvironment (TME), tumor mutation burden (TMB), and therapeutic response. Finally, in vitro assays were conducted to investigate the biological function of UBOX5-AS1 in GC cell lines. Our research established a novel predictive framework centered on nine lncRNAs associated with crotonylation. The study findings demonstrated that patients classified as high-risk faced considerably poorer overall and progression-free survival rates than those in the low-risk category. While this risk assessment tool demonstrates standalone prognostic capabilities, its predictive power substantially increases when integrated with established clinical parameters. Functional enrichment analyses indicated an association between these identified lncRNAs and cancer-related signaling cascades. Furthermore, the risk score correlated with multiple TME characteristics, including immune cell infiltration patterns, extracellular matrix remodeling, and tumor mutational burden. Notably, low-risk patients displayed reduced indices of tumor immune dysfunction and exclusion, suggesting enhanced responsiveness to immunotherapeutic interventions. Additionally, the model accurately predicted patient sensitivity to specific chemotherapeutic agents like afatinib and dasatanib. Finally, our experimental evidence suggests UBOX5-AS1 as critical in promoting GC cell growth and advancement. We developed a signature of lncRNAs linked to crotonylation that offers dependable prognostic insights and characterizes the immune microenvironment within GC. However, additional investigation is necessary to confirm its practical applications in clinical settings.

PubMedJournal of cellular and molecular medicine2026-05-25

Salvianolic Acid B Inhibited LH2 Expression to Reduce Collagen Synthesis in Pulmonary Fibrosis.

Shao Songjun S, Rao Shanshan S, Hu Silu S, Zhang Yabin Y et al.

Collagen deposition and scar formation are hallmark features of fibrotic diseases. Lysyl hydroxylase 2 (PLOD2/LH2), a key collagen-modifying enzyme, catalyses lysine hydroxylation at telopeptide sites to promote pyridinoline cross-link formation, thereby enhancing collagen stability and matrix stiffness. However, the mechanisms regulating LH2 in pulmonary fibrosis (PF) are not fully understood. Here, we identify Salvianolic acid B (SAB) as a potent antifibrotic compound that targets LH2-associated collagen cross-linking. LH2 expression was markedly increased in alveolar epithelial cells and fibroblasts during PF, and its silencing attenuated TGF-β1-induced fibrotic protein expression. SAB reduced LH2 protein levels and significantly alleviated fibrotic remodelling, as evidenced by restored lung architecture and reduced collagen deposition. Mechanistically, the antifibrotic effects of SAB and LH2 were associated with inhibition of epithelial-mesenchymal transition (EMT), fibroblast-to-myofibroblast transition (FMT), and the Wnt/β-catenin signalling pathway. This study indicates that pharmacological inhibition of LH2 by SAB effectively disrupts collagen cross-linking and fibrotic progression, offering a promising therapeutic avenue for pulmonary fibrosis.

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