若生智能
Drug Database
IN

interleukin-2 (Interking)

✓ Approved

Shenzhen Neptunus · IL2RA · 重组蛋白

什么是 interleukin-2？

interleukin-2 是一种重组蛋白，由Shenzhen Neptunus研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名Interking
公司Shenzhen Neptunus
药物类别重组蛋白
分子靶点IL2RA
给药途径Injectable (Others), Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Shenzhen Neptunus

作用机制

分子靶点

interleukin-2 作用于 1 个分子靶点：

IL2RAinterleukin 2 receptor subunit alpha (IL2R, TCGFR)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

interleukin-2 针对 15 个适应症，涉及 4 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Adenosquamous cell lung cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Bladder cancer✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Breast cancer✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsLeprosy✓ Approved

注册免费账户还可查看另外 10 个适应症

免费注册查看全部适应症 →

相关研究文献

PubMedCellular signalling2026-06-13

Berberine alleviates hypersensitivity pneumonitis-like lung inflammation by restoring TFEB-dependent autophagic flux and neutrophil homeostasis.

Xie Weidong W, Deng Wei W, Zhang Jing J, Chang Shuai S et al.

Hypersensitivity pneumonitis (HP) is an immune-mediated interstitial lung disease caused by inhaled environmental antigens, and effective targeted therapies remain limited. Berberine (BBR) has established anti-inflammatory activity, but its role in HP is unclear. Here, we combined network pharmacology with experimental validation to investigate the therapeutic potential and mechanism of BBR in HP. We identified 38 overlapping targets between BBR and HP, with network analysis highlighting tumor necrosis factor (TNF), interleukin 1 beta (IL1β), interleukin 6 (IL6), B-cell lymphoma/leukemia-2 (BCL2) and caspase 3 (CASP3). Functional enrichment implicated TNF signaling, apoptosis and autophagy, suggesting that disruption of cellular homeostasis is central to HP progression and may be targeted by BBR. In a 1,3-β-glucan (β-glucan)-induced model of HP-like lung inflammation, BBR markedly reduced pulmonary inflammatory responses and increased autophagy-related protein expression in neutrophil-dominant lesions. In β-glucan-stimulated differentiated HL-60 cells, BBR attenuated inflammatory injury, limited apoptosis and preserved cellular function. Mechanistically, BBR restored defective autophagic flux by promoting transcription factor EB (TFEB) nuclear translocation, thereby improving neutrophil homeostasis and reducing inflammatory damage. These findings identify TFEB-dependent restoration of autophagic flux as a key mechanism underlying the protective effects of BBR in experimental HP-like lung inflammation and support BBR as a potential therapeutic candidate for HP.

PMID 42285189
阅读全文 →
PubMedImmunity2026-06-13

Interleukin 23 promotes a pro-inflammatory Th17 cell state by stabilizing RORγt and suppressing glucocorticoid receptor activity.

Yang Dandan D, Huang Linglin L, Yang Jianfei J, Etxezarreta-Arrastoa Oier O et al.

Interleukin 23 receptor (IL-23R) signaling is critical for the generation of pro-inflammatory CD4+ IL-17-producing T helper cells (Th17) that can drive autoimmune tissue inflammation, but the underlying mechanisms are not clear. We integrated phosphoproteomic and transcriptomic data downstream of IL-23R and IL-12 receptor (IL-12R), which share a common subunit, to identify mechanisms engaged specifically by IL-23. We identified chromodomain helicase DNA-binding protein 1 (CHD1), an epigenetic regulator, and the glucocorticoid receptor (GR), a transcription factor (TF), as mediators of IL-23R signaling. IL-23R activation promoted CHD1 interaction with TF STAT3 and co-binding at the TF RORγt locus to enforce a pro-inflammatory Th17 state. Conversely, IL-23R signaling altered phosphorylation of the GR, thereby preventing its activation and nuclear translocation, ultimately impairing GR-driven inhibition of pro-inflammatory Th17 gene programs. Our findings uncover two mechanisms by which IL-23 promotes a pro-inflammatory Th17 cell state, offering potential therapeutic targets for treating Th17-driven autoimmune tissue inflammation and restoring homeostasis.

PMID 42285104
阅读全文 →
PubMedJHEP reports : innovation in hepatology2026-06-13

Interleukin-8-Driven Monocyte Activation in Primary Sclerosing Cholangitis: Insights from Single-Cell Analysis and Humanized Immune System Mice.

Heyerick Lander L, De Vos Zenzi Z, Baekelandt Aline A, De Muynck Kevin K et al.

Primary sclerosing cholangitis (PSC) is an immune-mediated liver disease with an incompletely understood pathogenesis. Monocyte/macrophage cell dysregulation has been suggested to contribute, although their functional relevance remains insufficiently understood. The main aim of this study was to identify peripheral myeloid cell populations involved in PSC pathogenesis and assess the therapeutic potential of targeting associated inflammatory signalling pathways. Additionally, we sought to enhance translational relevance through the application of a humanized immune system (HIS) mouse model. Peripheral blood mononuclear cells from PSC and ulcerative colitis patients and from healthy controls were profiled using cellular indexing of transcriptomes and epitopes by sequencing. Inflammatory signalling via the IL-8:CXCR1/2 axis was further evaluated in both conventional and HIS mouse models of cholestatic liver disease. Our data show that PSC patients exhibit a population of circulatory CXCL8+CD14+ monocytes with upregulated proinflammatory signalling. Serum concentrations of the proinflammatory cytokine IL-8, encoded by CXCL8, were increased in PSC patients (p<0.001) and associated with poor prognosis. PSC patients with high IL-8 concentrations (≥ 27.8 pg/mL) at baseline had a significantly worse transplant-free survival in comparison to patients with low IL-8 concentrations (logrank hazard ratio 6.12, 95% CI 1.68-22.33). Intrahepatic IL-8+ macrophages were expanded during disease progression (p<0.05). Pharmacologic Cxcr1 antagonism in conventional rodent immune system and antibody-mediated IL-8 neutralization in HIS mice reduced cholestatic liver injury. A circulatory CXCL8+CD14+ monocyte subset and intrahepatic IL-8+ macrophages were identified as potential contributors to PSC pathogenesis. HIS mouse models could mark a significant advance in translational research on human immune responses. Targeting the IL-8:CXCR1/2 axis may represent a promising therapeutic strategy and urges further investigation.

PMID 42285508
阅读全文 →
PubMedBasic research in cardiology2026-06-13

Aortic baroreceptor afferents as sensors for systemic inflammation.

Brognara Fernanda F, Castania Jaci Airton JA, Machado Mirele Resende MR, de Oliveira Neto José Teles JT et al.

Neuroimmune communication is essential for regulating inflammation and maintaining cardiovascular homeostasis, but the role of sensory pathways in this process is poorly understood. Arterial baroreceptors are typically defined as mechanoreceptors essential for arterial pressure homeostasis and have been associated with modulation of the immune response. However, their role in sensing systemic inflammation remains unknown. Here, we establish the molecular profile of the rat aortic depressor nerve (ADN) as an immune-competent tissue and investigate its response to lipopolysaccharide (LPS)-induced endotoxemia. Using analysis of gene expression, total protein quantification, and immunofluorescence assay, we demonstrate that the ADN, from male Sprague-Dawley rats (7-8 weeks old), constitutively expresses key components for innate immune signalling, including Toll-like receptor 4 (TLR4), MyD88, and phosphorylated NF-κB, indicating a state of constant immunological vigilance. LPS administration induced an inflammatory response within the ADN, upregulating gene expression of NF-κB, interleukin-6, and type I interleukin 1 receptor, and it also increased the ADN electrical activity. Notably, the increase in nerve firing occurred while the animals were experiencing systemic hypotension and also during the diastolic phase, indicating that this response is not from the mechanosensory reflex. Furthermore, we characterized the progression of this immune response in the nodose ganglion and aortic arch, identifying a coordinated neuroimmune sensory axis. These findings reposition arterial baroreceptors from purely mechanoreceptors to integrative immunosensors that actively detect and respond to systemic inflammation. This novel neuroimmune circuit represents a critical link between inflammation and cardiovascular system, offering a novel therapeutic target for treating cardiovascular and inflammatory conditions.

PMID 42286138
阅读全文 →
PubMedTranslational research : the journal of laboratory and clinical medicine2026-06-13

A novel spontaneous rat model of chronic kidney disease with mitochondrial dysfunction driven by thioredoxin insufficiency.

Ohmori Iori K IK, Ouchida Mamoru M, Hada Yoshiko Y, Uchida Haruhito A HA et al.

Chronic kidney disease (CKD) is a global health burden with high prevalence and poor prognosis. Although oxidative stress and mitochondrial dysfunction have been implicated in its pathogenesis, in vivo causal evidence remains limited. Thioredoxin (Trx), encoded by Txn1, is a redox-active protein that plays a central role in controlling oxidative stress and maintaining intracellular redox homeostasis. To address this gap, we investigated the lifelong phenotypes of Txn1-F54L mutant rats harboring approximately one-third of the normal Trx activity. These rats were generated via N-ethyl-N-nitrosourea mutagenesis and validated by clustered regularly interspaced palindromic repeat (CRISPR)/CRISPR-associated protein 9 genome editing. Comprehensive analyses included biochemical testing, histopathology, immunohistochemistry, transmission electron microscopy, RNA-sequencing, western blotting, and cytokine profiling. Txn1-F54L mutant rats spontaneously developed progressive CKD, with median survival times of 110-119 days for homozygotes and 303-346 days for heterozygotes. Their clinical features-elevated blood urea nitrogen, hypoalbuminemia, hypercholesterolemia, hypertension, and arterial medial sclerosis-closely resembled those of human CKD. Histopathological evaluation revealed extensive tubular injury, interstitial fibrosis, and glomerulosclerosis. Transcriptomic profiling identified 3,418 differentially expressed genes significantly enriched in immune activation and fibrosis pathways. Mitochondrial dysfunction was prominent in proximal tubules, accompanied by oxidative stress accumulation and concurrent activation of regulated cell death pathways (apoptosis, necroptosis, and pyroptosis). Elevated serum levels of interleukin-1β, interleukin-6, and interferon-γ indicated systemic inflammation. Our findings demonstrate that lifelong Trx deficiency induces oxidative stress-mediated mitochondrial dysfunction and regulated cell death, leading to inflammation and progressive CKD. This study establishes the Txn1 mutant rat as a valuable spontaneous CKD model, providing translational insights and a platform for developing therapeutic strategies targeting oxidative stress-induced pathways.

PMID 42285432
阅读全文 →
PubMedBiochemical and biophysical research communications2026-06-13

β-Sitosterol protects human chondrocytes from IL-1β -induced damage by inhibiting ferroptosis.

Zhang Le L, Kong Xiaochuan X, Hong Gang G, Zheng Yinfeng Y et al.

To investigate the effect of β-Sitosterol on interleukin (IL)-1β-induced chondrocyte injury and the related mechanism. An osteoarthritis model was constructed by treating immortalized human cartilage cells with IL-1β. The identity and purity of β-Sitosterol were confirmed by FTIR, 1H NMR, 13C NMR, RP-HPLC-ELSD, and UPLC-MS before cell experiments. The optimal concentrations of IL-1β and β-Sitosterol for treating cells were determined by qPCR and CCK8 assay. The cells were divided into three groups: Control group, Model group, and Model+β-Sitosterol group. Cell viability was detected by CCK8 assay. The mRNA expression of IL-18, IL-1β and tumor necrosis factor-α (TNF-α) was detected by qPCR. Collagen type II alpha 1 chain (COL2A1) and matrix metalloproteinase 13 (MMP13) expression was detected by immunofluorescence. Reactive oxygen species (ROS) and mitochondrial membrane potential were detected by flow cytometry. Malondialdehyde (MDA), Glutathione (GSH) and Fe2+ were detected by ELISA and biochemical test. Mitochondrial structure was observed by transmission electron microscopy, and the protein expression of ferroptosis related factors was detected by Western blot. After induction of chondrocytes with IL-1β, the cell viability was decreased, the gene expression of inflammatory cytokines was increased, the proportion of cells with reduced ROS content and mitochondrial membrane potential were increased, MDA and Fe2+ content were increased, and GSH content was decreased. Mitochondrial structure showed ferroptosis-like changes. The expression of COL2A1, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), total nuclear factor erythroid 2-related factor 2 (NRF2), and nuclear NRF2 was decreased. MMP13, ANO6, and p-p38/p38 levels were increased. Treatment of chondrocytes with β-Sitosterol could reverse these changes induced by IL-1β. Spectrally confirmed, high-purity β-Sitosterol alleviated IL-1β-induced chondrocyte injury by suppressing inflammatory activation, extracellular matrix degradation, mitochondrial dysfunction, and ferroptosis-related oxidative damage, suggesting its potential as a candidate compound for osteoarthritis intervention.

PMID 42284994
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多interleukin-2