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lysine salicylate (lysine salicylate / Dolorosan)

✓ Approved

VUFB · 小分子 · 小分子

什么是 lysine salicylate？

lysine salicylate 是一种小分子，由VUFB研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名lysine salicylate, Dolorosan
公司VUFB
药物类别小分子
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, VUFB

治疗适应症

lysine salicylate 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Gastrointestinal disordersAbdominal pain✓ Approved

相关研究文献

PubMedInternational journal of general medicine2026-09-11

Exploration of the Immune Microenvironment of Melanoma and Construction of Prognostic Models Based on the Expression Profile of Lysine Crotonylation-Related Genes.

Li Chen C, Cui Xinyu X, Yang Yong Y, Li Xiaoyang X et al.

Melanoma is highly invasive with poor advanced-stage prognosis and remarkable heterogeneity of the tumor immune microenvironment. Lysine crotonylation regulates tumor progression and immune processes, yet its role in melanoma remains unclear. This study aims to explore the value of crotonylation-related genes in melanoma. Transcriptomic data of 471 melanoma samples from the TCGA database were utilized. Consensus clustering was performed based on 2971 crotonylation-related genes. Differential analysis, WGCNA and LASSO regression were combined to construct a prognostic model, followed by analyses of the immune microenvironment and drug sensitivity. Molecular docking and cellular experiments were adopted to investigate the core gene SEPTIN1. Melanoma patients were classified into two subtypes (C1 and C2). Patients in the high-risk group of the established prognostic model exhibited shorter overall survival. SEPTIN1 was correlated with prognosis, immune microenvironment and TMZ response. TMZ could downregulate the expression of SEPTIN1, and overexpression of SEPTIN1 reversed the anti-tumor effect of TMZ. Expression signatures of crotonylation-related genes can be applied to molecular subtyping, immune microenvironment dissection and prognostic stratification of melanoma, providing potential clues for individualized diagnosis and treatment of melanoma.

PMID 42723965
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PubMedNature communications2026-09-11

The metabolic and anatomical complexity of root microhabitats modulate their interaction with the microbiota.

Frene Juan P JP, Custódio Valéria V, Rouco Helena H, Martinez-Jarquin Sandra S et al.

Plant roots constantly communicate with their microbiota, adapting their anatomy to facilitate microbial colonisation under abiotic stresses. Microbes, in turn, can reshape root anatomy once they establish. However, the mechanisms that coordinate this interplay remain largely unknown. Working with the aquatic plant family Lemnaceae, we reveal that the inherent complexity of root anatomy determines root plasticity in response to microbial colonisation. This microbiota-driven anatomical plasticity enhances plant survival in nutrient-competitive environments. By combining synthetic root models with real roots, we also find that anatomical plasticity is associated with metabolic reprogramming during microbial establishment. Moreover, we identify a plant metabolite, N6,N6,N6-Trimethyl-L-lysine, that regulates anatomical plasticity in response to microbial colonisation. Our work generalizes the importance of microhabitat complexity for microbiome recruitment under challenging environmental conditions.

PMID 42722645
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PubMedMicrobiome2026-09-11

Integrated landscape of salivary metagenome and multi-biofluid metabolome characterizes a microbial-metabolic axis in upper gastrointestinal cancer progression.

Zhang Shuai S, Zhang Nan N, Zhang Xiaofeng X, Liu Yanxiu Y et al.

Upper gastrointestinal cancer (UGIC) imposes a major global health burden, yet the stage-specific molecular changes along the microbial-metabolic axis remain limited understood. We aimed to delineate this molecular landscape across UGIC progression and evaluate its potential as non-invasive methods for precision screening. Derived from a multi-center population-based UGIC screening program, we enrolled 420 individuals, stratified into normal, low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and UGIC (n = 105 per group). Integrated salivary metagenomics and paired salivary/plasma metabolomics were performed to capture local and systemic dysregulation. We uncovered distinct stage-specific divergence during UGIC progression: profound remodeling of the salivary microbiota (104 differential species) and salivary metabolomics (80 differential metabolites) initiated early at the LGIN stage, whereas plasma metabolic dysregulation (40 differential metabolites) peaked significantly later at the HGIN stage. Integrative analysis revealed salivary microbiota related more closely with salivary metabolome than plasma metabolome. Moreover, statistical evidence suggested that dysbiotic salivary microbiota was associated with altered lysine- and tryptophan-related catabolic pathways converging on Acetyl-CoA-related metabolic nodes, supporting a potential metabolic mechanism in precancerous lesions. Finally, the discriminative model integrating metagenomic and metabolomic markers demonstrated promising diagnostic performance in distinguishing these precancerous lesions (LGIN: area under the curve [AUC] = 0.83; HGIN: AUC = 0.77) and UGIC (AUC = 0.76) from normal. This study characterizes a stage-specific microbial-metabolic axis that facilitates the comprehensive understanding of UGIC pathogenesis. These multi-biofluid signatures offer a promising non-invasive triage strategy for detecting precancerous lesions and optimizing endoscopic resource allocation. Video Abstract.

PMID 42723112
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PubMedTranslational cancer research2026-09-11

Construction and validation of a β-hydroxybutyrylation-related molecular model for predicting prognosis of papillary thyroid carcinoma.

An Xiaoxiao X, Li Biao B, Zhai Baowei B

Papillary thyroid carcinoma (PTC) usually has a favorable prognosis, yet a subset of patients develops persistent, recurrent, or biologically aggressive disease. The clinical relevance of lysine β-hydroxybutyrylation (Kbhb)-related transcriptional programs in PTC remains unclear. Accordingly, this study aimed to characterize Kbhb-related molecular heterogeneity in PTC, construct a prognostic signature, and explore its association with the tumor microenvironment (TME). Transcriptomic and clinical data from PTC samples within The Cancer Genome Atlas Thyroid Carcinoma (TCGA-THCA) cohort were analyzed to identify Kbhb-related differentially expressed genes (DEGs), define molecular subtypes, construct a prognostic signature, and characterize tumor microenvironmental features. Single-cell RNA-sequencing data from PTC were further used to explore the cellular distribution of representative genes. We identified 51 Kbhb-related DEGs in PTC and defined two Kbhb molecular subtypes. The Kbhb_C2 subtype showed shorter progression-free interval (PFI) and a more immune- and stroma-enriched microenvironment. A six-gene prognostic signature comprising TARID, CDSN, PIMREG, KLRC1, SYT13, and NPR3 was then established. High-risk patients had significantly worse PFI in the full, training, and testing cohorts, with 1-, 3-, and 5-year areas under the curve (AUCs) of 0.715, 0.793, and 0.771, respectively, in the full cohort. High-risk tumors also exhibited higher stromal, immune, and ESTIMATE scores, altered immune infiltration, and increased expression of multiple immune checkpoint molecules. Single-cell analysis confirmed distinct cell-type-specific expression patterns of representative genes. Kbhb-related transcriptional programs define clinically relevant molecular heterogeneity in PTC and are closely associated with prognosis and TME remodeling. The identified six-gene signature provides a biologically interpretable framework for risk stratification in PTC.

PMID 42724419
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PubMedJournal of thoracic disease2026-09-11

Single-cell and machine learning identify a trihydroxybutyrylation-related prognostic signature in esophageal cancer.

Zhang Qun Q, Li Duojie D, Yin Hongmei H, Zhu Chaomang C et al.

Esophageal squamous cell carcinoma (ESCC) is a highly aggressive malignancy with a poor prognosis. This study identifies malignant epithelial subtypes and establishes prognostic biomarkers through single-cell transcriptomics and integrative machine learning approaches. We re-analyzed the single-cell RNA sequencing data (GSE188900) and identified malignant epithelial cells using inferCNV. Differentially expressed genes (DEGs) among malignant epithelial subtypes were identified and intersected with lysine β-hydroxybutyrylation (Kbhb)-related genes. Candidate genes were screened using Cox, least absolute shrinkage and selection operator (LASSO), and extreme gradient boosting (XGBoost) to construct a random survival forest (RSF) prognostic model. Model performance was validated in GSE53625, TCGA-ESCC, and GSE53624 cohorts. Finally, the expression of prognostic genes was detected by quantitative polymerase chain reaction (qPCR). Single-cell RNA sequencing identified three distinct malignant epithelial cells in ESCC. Among them, the Malignant2 subtype exhibited stemness-related characteristics, initiated tumor differentiation, and was potentially regulated by the transcription factor (TF) SOX11. There were 659 genes identified by intersecting Malignant2-related DEGs with Kbhb-related genes. Based on these genes, a seven-gene prognostic model was constructed, and a corresponding risk score was calculated. Correlation analysis showed that the risk score was positively associated with tumor stage. qPCR results confirmed that the expression patterns of the prognostic genes were consistent with the computational analysis. The enrichment of Kbhb-related genes in the Malignant2 subtype suggests a potential link between metabolic reprogramming and epigenetic regulation in ESCC progression. We identified distinct malignant epithelial subtypes in ESCC and developed a seven-gene prognostic signature based on Kbhb-related genes. This model demonstrated robust predictive performance and was significantly associated with tumor stages.

PMID 42724740
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PubMedTranslational pediatrics2026-09-11

Decreased H3K79 acetylation and dysregulation of neurodevelopmental genes in fetal down syndrome.

Ye Shuai S, Bai Baoling B, Zhao Zhuran Z, Wang Li L et al.

Down syndrome (DS), the most prevalent chromosomal disorder caused by trisomy 21, manifests intellectual disability and cognitive dysfunction. Cumulative studies confirm epigenetic pathways including DNA methylation and non-coding RNAs drive DS pathological progression. Histone post-translational modifications (PTMs) are core epigenetic regulators of fetal brain development. However, genome-wide PTM alterations and their downstream functions in fetal DS brains remain poorly characterized, leaving a key gap in revealing epigenetic mechanisms underlying DS neurodevelopmental defects. To address this, we aimed to establish the first comprehensive landscape of histone PTMs in fetal DS cortex and investigate whether specific PTM changes contribute to aberrant neurodevelopmental gene expression. Fetal cortexs from control and DS groups were subjected to global histone modification profiling via high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). We detected mono-, di-, and tri-methylation, acetylation, homocysteinylation and malonylation on all four core histones (H2A, H2B, H3, H4). Chromatin immunoprecipitation sequencing (ChIP-seq) was used to map genomic binding profiles of H3 lysine 79 acetylation (H3K79ac). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to quantify mRNA levels of candidate neurodevelopmental genes. HPLC-MS/MS analysis identified 172 distinct histone PTMs in control fetal cortices and 168 PTMs in DS fetal cortical samples. Quantitative comparison of 22 quantifiable histone PTMs revealed that H3K79ac showed the most prominent reduction in DS samples, with a 34% decrease (P<0.05). Chromatin immunoprecipitation (ChIP)-seq verified specific H3K79ac occupancy at the genomic loci of three vital neurodevelopmental genes: TNFSF13B, NXPH1 and CAMK4. Correspondingly, qRT-PCR revealed aberrant transcription levels of these three genes in DS fetal cortices. This study establishes the first quantitative landscape of histone PTMs in in DS fetal cortical tissues. We demonstrate that depleted H3K79ac acts as a candidate epigenetic driver of DS neuropathology by disrupting the transcription of critical neurodevelopmental genes. This work reveals a novel epigenetic mechanism and a promising therapeutic target for DS-related neurodevelopmental disorders.

PMID 42724460
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