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etanercept (Qiangke)

✓ Approved

Shanghai Celgen · TNF · 重组蛋白

什么是 etanercept？

etanercept 是一种重组蛋白，由Shanghai Celgen研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intraarticular Injection、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名Qiangke
公司Shanghai Celgen
药物类别重组蛋白
分子靶点TNF
给药途径Injectable (Others), Intraarticular Injection, Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Shanghai Celgen

作用机制

分子靶点

etanercept 作用于 1 个分子靶点：

TNFtumor necrosis factor (TNFA, TNF-alpha)
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

etanercept 针对 5 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Musculoskeletal and connective tissue disordersAnkylosing spondylitis✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved
Musculoskeletal and connective tissue disordersPsoriatic arthropathy✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Musculoskeletal and connective tissue disordersJuvenile idiopathic arthritis✓ Approved

相关研究文献

PubMedAmerican journal of ophthalmology2026-10-23

Association Between Systemic TNF-α Inhibitor Use and Risk of Primary Open-Angle Glaucoma.

Hong Alexander T AT, Lin Forest F, Xu Benjamin Y BY, Weinreb Robert N RN

To evaluate the association between systemic tumor necrosis factor-alpha (TNF-α) inhibitor use and the long-term risk of primary open angle glaucoma (POAG), and to compare glaucoma risk among users of different TNF-α inhibitors. Retrospective, multicenter clinical cohort study. This retrospective, multicenter cohort study compared patients ≥40 years with and without TNF-α inhibitor use (2006-2026) using data from aggregated, de-identified electronic health records across 70 U.S. health care organizations. Patients prescribed TNF-α inhibitors (adalimumab, infliximab, etanercept, certolizumab pegol, or golimumab) were propensity matched (1:1) to controls without TNF-α inhibitor exposure based on demographics and systemic indications for TNF-a. Patients with a history of uveitis and related sequelae were excluded. New POAG diagnosis, identified by ICD-10 codes within 10 years of follow-up, was assessed using Cox proportional hazards models. Among 12,227 TNF-α inhibitor users and 1,354,651 controls, 11,915 matched pairs were analyzed (mean [SD] age 59 [10] years; 68% female). At 10 years, TNF-α inhibitor users were associated with a lower risk of POAG diagnosis compared to controls (2.0% vs. 3.3%; HR 0.70 [95% CI 0.59-0.82]; P<.001) In agent-specific analysis, adalimumab-users (n=4,962 per cohort) (HR 0.74 [0.57-0.96]) and infliximab users (n=2,134 per cohort; HR 0.68 [95% CI 0.47-0.97) were associated with a lower risk of POAG diagnosis compared to matched controls. No significant differences were observed in pairwise comparisons amongst TNF-α inhibitors. Systemic TNF-α inhibitor use, particularly adalimumab and infliximab, was associated with a modest but significant reduction in long-term POAG risk. These findings support a potential role of TNF-α-mediated inflammation in glaucomatous neurodegeneration.

PMID 42913929
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PubMedFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026-10-22

ADAR1 Inhibits ZBP1-Driven Neuronal Necroptosis After Intracerebral Hemorrhage.

Wang Shuoyang S, Bai Qingqing Q, Yu Dijing D, Wu Xiaodong X et al.

Necroptosis is a critical response to secondary brain injury following intracerebral hemorrhage (ICH). Z-DNA Binding Protein 1 (ZBP1) binds to dsRNA and promotes the activation of Receptor-Interacting Protein Kinase 3 (RIPK3). This study investigated whether Adenosine Deaminase Acting on RNA 1 (ADAR1) inhibits neuronal necroptosis after ICH. ADAR1-knockdown mice and ZBP1flox/flox/Thy1-Cre+/- mice were subjected to collagenase VII-induced ICH. Brain edema and neurobehavioral deficits were assessed. The expressions of ADAR1 and ZBP1 were investigated by qPCR, western blot, immunofluorescence, and ELISA. Protein interactions were performed using co-immunoprecipitation. ADAR1p150 was reduced in both ICH patients and mice. ZBP1 and ADAR1 both bound to dsRNA. ADAR1p150 suppressed ZBP1 activation, potentially through functional antagonism and dsRNA editing, although causality remains to be established. Knockout of ZBP1 resulted in increased ADAR1p150 expression and reduced brain edema. Etanercept and shRNA-mediated ADAR1 knockdown promoted ZBP1 expression. Complementation of the ADAR1 Zα truncation did not reduce ZBP1 in ADAR1-knockdown cells. The inhibitory effect of ADAR1 on ZBP1 was attenuated in ADAR1Zα-/- cells. These data show that the Zα domain is required for ADAR1 to suppress ZBP1, but they do not establish whether this suppression depends on RNA editing or on dsRNA binding alone.

PMID 42905946
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PubMedBiomarker research2026-10-22

Ex vivo JAK and TNF inhibitor-modulated immune signatures guide first-line therapy selection in rheumatoid arthritis.

Corrales Sagrario S, Pérez-Sánchez Carlos C, Cerdó Tomas T, Merlo Christian C et al.

Rheumatoid arthritis (RA) is a heterogeneous autoimmune disease for which selecting the most appropriate first targeted therapy remains challenging. We integrated ex vivo immune-cell functional assays, targeted proteomics, clinical outcomes, and a three-dimensional (3D) synovial model to identify treatment-associated molecular signatures and evaluate their relationship with subsequent response to Janus kinase inhibitors (JAKi) or tumour necrosis factor inhibitors (TNFi). Peripheral blood mononuclear cells and neutrophils from 48 b/tsDMARDs-naïve RA patients were cultured with autologous serum and treated ex vivo with Baricitinib or Etanercept to assess proliferation, adhesion, NETosis, and 92 inflammation-related proteins. The resulting JAKi- and TNFi-modulated protein signatures were subsequently evaluated in pretreatment serum from four independent RA treatment cohorts (n = 223; naïve and non-naïve). Unsupervised clustering was used to identify molecular subgroups, which were related to longitudinal DAS28-CRP outcomes at 3, 6, and 12 months. Logistic regression, neural network, and random forest models were evaluated using repeated nested cross-validation in naïve patients to discriminate treatment-specific 6-month remission outcomes. In a subset of naïve remission achievers, paired baseline and 6-month sera were applied to a 3D synovial micromass model. Ex vivo JAKi and TNFi comparably modulated immune cell functions but induced distinct protein signatures with limited overlap. When evaluated in pretreatment baseline serum, these signatures stratified b/tsDMARD-naïve patients into clusters with different baseline inflammatory profiles and treatment-specific ΔDAS28-CRP. High baseline expression of a drug-specific signature was associated with remission with the corresponding therapy and failure to achieve remission with the alternative treatment. Under repeated nested cross-validation, logistic regression showed the highest mean discrimination among the models, with an AUC of 0.70 (SD, 0.03; empirical 2.5th-97.5th percentile, 0.65-0.75) for distinguishing treatment-specific remission outcomes in b/tsDMARD-naïve RA. In remission achievers, 6-month sera from either therapy significantly reduced synovial lining thickness in 3D micromasses versus baseline. Ex vivo-derived JAKi- and TNFi-associated immune-related protein signatures, integrated within a machine-learning framework, showed moderate discriminatory ability for treatment-specific remission patterns in b/tsDMARD-naïve RA and, together with complementary evidence of reduced synovial lining thickness in remission achievers, support further investigation of biomarker-informed selection between JAKi and TNFi as first targeted therapies.

PMID 42907925
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PubMedCureus2026-10-20

Etanercept-Induced Cutaneous Necrotizing Vasculitis in a Patient With Rheumatoid Arthritis: A Case Report and Literature Review.

Nouri Chaimae C, Tahiri Latifa L, Rkain Hanan H, Kronbi Fatine F et al.

Tumor necrosis factor-alpha (TNF-α) inhibitors are effective therapies for rheumatoid arthritis (RA) but may rarely induce paradoxical autoimmune complications, including vasculitis. We report the case of a 53-year-old woman with seropositive RA and secondary Sjögren's syndrome who developed bilateral dependent petechial and purpuric lesions of the lower extremities after approximately 33 months of etanercept therapy at a dose of 25 mg twice weekly. At symptom onset, her RA was well controlled, with no clinical or ultrasonographic synovitis and a Disease Activity Score in 28 joints of 2.1. Skin biopsy demonstrated fibrinoid necrosis of dermal vessels, consistent with necrotizing angiitis. No gastrointestinal, renal, neurological, pulmonary, or ear, nose, and throat involvement was identified. The etiologic workup showed a normal complete blood count, preserved renal function, normal urinalysis and complement levels, negative anti-myeloperoxidase, anti-proteinase 3, anti-double-stranded DNA antibodies and cryoglobulins, and negative hepatitis B, hepatitis C, and human immunodeficiency virus serologies. Serum protein electrophoresis showed no monoclonal gammopathy. Antinuclear antibodies were weakly positive at a titer of 1:80 without clear pathological significance. Etanercept was permanently discontinued, and the active lesions resolved completely within approximately 20 days, leaving only residual hyperpigmented and cicatricial changes. No recurrence was documented during follow-up. Rechallenge was not performed, and tocilizumab was subsequently selected for RA control. The compatible latency, histological confirmation, positive dechallenge, sustained absence of recurrence, and lack of a more plausible alternative cause strongly supported the diagnosis of cutaneous necrotizing vasculitis probably induced by etanercept. This case highlights that anti-TNF-α-associated vasculitis may occur after prolonged treatment and requires systematic assessment for systemic involvement and competing autoimmune, infectious, and hematologic causes.

PMID 42899311
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PubMedFrontiers in pharmacology2026-10-15

Monoclonal antibodies associated IgA nephropathy or other nephropathies.

Miedziaszczyk Miłosz M, Kosiorowski Gracjan G, Kubasik Janusz J, Grabowski Tomasz T et al.

The use of monoclonal antibodies (mAbs) has revolutionized the treatment of autoimmune, inflammatory, and neoplastic diseases. However, accumulating evidence indicates that biologic therapies may be associated with renal adverse events, including various types of glomerulonephritis. The aim of this review was to summarize all reports available in the scientific literature regarding the occurrence of IgA nephropathy after monoclonal antibody treatment. Additionally, the risk of other glomerulonephritis after biologic therapy was discussed. IgA nephropathy (IgAN) is the most commonly reported glomerular lesion associated with monoclonal antibody therapy, particularly with TNF-α inhibitors such as infliximab, adalimumab, golimumab, and etanercept, as well as with immune checkpoint inhibitors targeting the PD-1 (pembrolizumab, nivolumab) and interleukin (ustekinumab) pathways. Proposed mechanisms include immune dysregulation with a shift toward Th2 and Th17-dependent responses, increased production of galactose-deficient IgA1, complement activation, formation of circulating immune complexes, and loss of immune tolerance. In some cases, drug discontinuation and glucocorticoid therapy have resulted in partial or complete disease remission, although progression to end-stage renal disease has also been reported. Due to the potential severity of these complications, initial and periodic monitoring of renal function and urinalysis are recommended in patients receiving monoclonal antibody therapy. Early recognition of renal involvement and prompt treatment modification can improve prognosis.

PMID 42876810
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PubMedCompendium of continuing education in dentistry (Jamesburg, N.J. : 1995)2026-10-13

Tumor Necrosis Factor-Alpha Inhibitors: Oral Health and Orthodontic Considerations.

Mahjour Neda N, Hersh Elliot V EV, Jeon Hyeran Helen HH, France Katherine K et al.

Autoimmune diseases affect approximately 4.6% of the US population and are frequently managed with immunomodulatory therapies, including tumor necrosis factor-alpha (TNF-α) inhibitors. These biologic agents, such as infliximab, adalimumab, etanercept, golimumab, and certolizumab pegol, target TNF-α, a key cytokine involved in inflammatory signaling and bone remodeling. While TNF-α inhibitors have demonstrated efficacy in reducing disease activity across a range of autoimmune conditions, their impact on oral health and orthodontic treatment remains underexplored. Clinical studies suggest that TNF-α inhibitors can affect oral health, potentially altering risk of periodontitis, oral infections, and caries. TNF-α also plays a central role in orthodontic tooth movement (OTM), and animal studies suggest that TNF-α inhibition, whether local or systemic, can significantly reduce OTM and root resorption by suppressing osteoclast activity and altering cytokine signaling. This review synthesizes the clinical pharmacology of TNF-α inhibitors, current knowledge of their systemic and oral effects, and their potential influence on OTM.

PMID 42867887
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