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interleukin-2 (Interking)

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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

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相关研究文献

PubMedCells2026-07-27

Interleukin-1β and Interleukin-6 Signaling Differentially Regulate ABC Transporter Activity and Amyloid-β Handling in Primary Porcine Brain Endothelial Cells.

Razmi Ahmad H AH, Penny Jeffrey I JI

Impaired amyloid-β clearance at the blood-brain barrier (BBB) contributes to Alzheimer's disease (AD), yet the regulation of endothelial transport processes under neuroinflammatory conditions remains incompletely understood. Here, we investigated the time-dependent effects of interleukin-1β (IL-1β), interleukin-6 (IL-6) classical signaling directly via the membrane-bound IL-6 receptor, and IL-6 trans-signaling via the IL-6 /soluble IL-6 receptor complex (IL-6/sIL-6r) on ATP-binding cassette (ABC) transporter activity and expression in primary porcine brain endothelial cells (PBECs), and assessed intracellular accumulation of amyloid-β(1-42). Cytokine exposure did not affect PBEC viability. IL-1β induced a robust, time-dependent increase in ABCB1 activity and expression, whereas IL-6 produced a transient enhancement that was not sustained at 72 h. In contrast, IL-6 trans-signaling elicited a delayed but sustained increase in ABCB1 function and expression. IL-1β increased ABCG2 activity and expression at early time points, while IL-6 and IL-6/sIL-6r had minimal effects. Notably, IL-1β and IL-6 trans-signaling increased ABCC5 activity without detectable changes in protein expression. Cytokine-induced transporter modulation was associated with reduced intracellular amyloid-β accumulation. Pharmacological inhibition of ABC transporters increased intracellular amyloid-β levels, supporting a role for these transporters in endothelial amyloid-β handling. However, as transendothelial amyloid-β transport was not directly assessed, these findings should be interpreted as changes in intracellular amyloid-β accumulation rather than direct evidence of altered BBB clearance. These findings demonstrate signaling- and time-dependent regulation of BBB ABC transporters and reveal distinct effects of IL-6 classical signaling and IL-6 trans-signaling on endothelial transporter regulation. Collectively, these results highlight signaling context as an important determinant of BBB transport responses under neuroinflammatory conditions.

PMID 42505383
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PubMedCranio : the journal of craniomandibular practice2026-07-27

Cytokines and biomarkers of bone resorption and cartilage degeneration in synovial fluid of patients with temporomandibular joint osteoarthritis: A scoping review.

Torres Catalina C, Vera Darco D, Solar Melissa M, Fuentes Del Campo Aler A

Osteoarthritis of the temporomandibular joint is characterized by joint tissue degeneration. However, the synthesized and categorized information regarding biomarkers present in synovial fluid samples from patients who have not been treated for this disease is scarce. This review aims to provide an overview of inflammatory cytokines, bone, and cartilage degeneration biomarkers relevant to this temporomandibular disorder (TMD). Following JBI and PRISMA-ScR guidelines, 26 studies from five databases were analyzed, identifying 45 biomarkers. Inflammatory cytokines (interleukin 1 beta, interleukin 6, tumor necrosis factor alpha), cartilage degeneration markers (matrix metalloproteinases), and bone resorption markers (receptor activator of nuclear factor kappa-B ligand, osteoprotegerin) were most frequently reported. Vascular endothelial growth factor was associated with cartilage degeneration and bone resorption. These biomarkers may aid in disease characterization; however, further standardized clinical studies are required for validation and comparison with other TMDs.

PMID 42504100
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PubMedCells2026-07-27

Monoclonal Antibodies Directed Against IL-5 in the Treatment of Pediatric Asthma.

Fainardi Valentina V, Carbone Roberta R, Buono Enrico Vito EV, Menzella Marialaura M et al.

Severe treatment-resistant asthma (STRA) in children is often sustained by type 2 inflammation and eosinophil-dependent airway disease that persists despite optimized inhaled therapy and the mitigation of modifiable factors. This review summarizes the clinical and translational evidence on monoclonal antibodies targeting the interleukin-5 (IL-5) axis (anti-IL-5 and anti-IL-5Rα) available in pediatric severe asthma. PubMed/MEDLINE was searched up to January 2026 for English-language studies in patients aged 0-18 years addressing mepolizumab and benralizumab, including randomized trials, high-quality observational studies, meta-analyses, and international guidance. Mepolizumab has the most robust pediatric data, showing consistent reductions in exacerbations and blood eosinophils, and improvements in symptom control and quality of life, with safety broadly comparable to adults. The pediatric evidence for benralizumab is more limited but shows rapid eosinophil depletion, improved outcomes in selected children, and acceptable safety; further trials are ongoing. Overall, IL-5-directed biologics represent a key add-on option for carefully selected children with severe eosinophilic asthma, while pediatric-specific predictors of response, comparative effectiveness, and standardized long-term monitoring and stopping criteria remain priorities.

PMID 42505356
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PubMedImmunological investigations2026-07-27

The Microglial NLRP3 Inflammasome in Multiple Sclerosis: Bridging Innate Immunity, Chronic Inflammation, and IFN-β Response.

Koyya Prathyusha P, Alavilli Hemasundar H, Pandrangi Santhi Latha SL, Manthari Ram Kumar RK

Background: Multiple sclerosis (MS) is a chronic neurodegenerative and demyelinating disease that is marked by chronic inflammation of the central nervous system (CNS). Although interferon-β (IFN-β) remains one of the pillars of treatment for relapsing-remitting MS (RRMS), inconsistencies in the responses of patients signify the necessity to comprehend the immunopathological processes.Objectives: The NLRP3 (NOD-like receptor family pyrin domain-containing 3) inflammasome, an intracellular signaling platform controlling the activation of caspase-1 and the maturation of interleukin-1β (IL-1β) and interleukin-18 (IL-18) has been of considerable interest among emerging molecular actors. Microglia, the native CNS macrophage, are the center stage of tissue damage and repair.Results: Demyelination and axonal degeneration in neuroinflammation are linked to the role of aberrant activity of the microglial NLRP3 inflammasome. In addition, it is also suggested that an inhibition of inflammasome by IFN-β can be observed in a mechanistic interaction between NLRP3 signaling and response to treatment.Conclusion: In this literature review, the presented data summarize the existing information about the contribution of NLRP3 to the pathogenesis of MS disease, microglial activation, and IFN-β regulation, and how this pathway can be applied to shape personalized treatment approaches.

PMID 42505028
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PubMedCurrent oncology (Toronto, Ont.)2026-07-27

Real-World Tumor-Infiltrating Lymphocyte Therapy for Metastatic Melanoma: Treatment Delivery, Immune Reconstitution, and Cardiac Monitoring During High-Dose IL-2.

Aboelatta Mohamed A MA, Zarka Jabra J, Tchatchua Nika N, Aboelatta Noureldin A NA et al.

Background/Objectives: Tumor-infiltrating lymphocyte (TIL) therapy is an important option for patients with metastatic melanoma progressing after standard systemic therapy, but real-world data on treatment delivery, toxicity monitoring, and immune recovery remain limited. We evaluated clinical outcomes, treatment tolerance, immune reconstitution, and cardiac biomarker dynamics across three Mayo Clinic sites. Methods: We retrospectively analyzed adults with metastatic melanoma who received lymphodepleting chemotherapy followed by TIL infusion and high-dose interleukin-2 (IL-2) between April 2024 and December 2025. Clinical outcomes, treatment delivery, and adverse events were assessed. Longitudinal immune monitoring included CD4 and CD8 T-cell counts, CD4:CD8 ratio, and immunoglobulin G (IgG) at baseline and follow-up. In a prespecified cardiac sub-cohort, high-sensitivity troponin (hs-Tn) was measured during IL-2 administration to evaluate associations with cardiac events and IL-2 interruption. Results: Thirty-six patients underwent TIL infusion. The objective response rate was 50.0%, including complete responses in 13.9%, and the disease control rate was 72.2%. Median progression-free survival was 3.61 months, and median overall survival was 12.94 months. M1d disease was associated with inferior overall survival on univariable analysis (HR 6.55, 95% CI 2.03-21.17; p = 0.002), with attenuation after multivariable adjustment. Receipt of ≥3 IL-2 doses was associated with longer overall survival on univariable analysis (HR 0.20, 95% CI 0.06-0.64; p = 0.007), but this association also attenuated after adjustment. Longitudinal immune monitoring demonstrated persistent CD4 lymphopenia through 6 months, sustained inversion of the CD4:CD8 ratio, and declining IgG at months 3 and 6. In the cardiac sub-cohort (24 patients; 87 IL-2 doses), post-dose hs-Tn ≥15 ng/L was associated with clinically significant cardiac events (OR 9.6, 95% CI 1.5-60.6; p = 0.016) and IL-2 interruption (OR 3.4, 95% CI 1.1-10.7; p = 0.036). For cardiac events, hs-Tn ≥15 ng/L had 100% sensitivity and 100% negative predictive value. Conclusions: In routine practice, TIL therapy was feasible and active in metastatic melanoma. M1d disease identified a subgroup with poor survival, peri-dose hs-Tn showed promise as a tool to support safer IL-2 delivery, and prolonged CD4 suppression with IgG decline suggests that recovery after TIL therapy extends beyond initial hematologic reconstitution. These findings support prospective validation of biomarker-guided IL-2 monitoring and extended post-treatment immune surveillance.

PMID 42505181
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PubMedCurrent oncology (Toronto, Ont.)2026-07-27

Interleukin-1β Gene (IL-1B) rs16944 (-511 C > T) Promoter Polymorphism Is Associated with Cutaneous Melanoma Susceptibility, Stage, and Anatomical Localization in a Northern Italian Case-Control Study.

Cauci Sabina S, Buligan Cinzia C, Nacci Patrizia P, Petris Gianluca G et al.

Immunity plays critical roles in cutaneous melanoma. We investigated the association between the pro-inflammatory interleukin-1β gene (IL-1B) rs16944 (-511 C > T) promoter single nucleotide polymorphism (SNP) and cutaneous melanoma susceptibility and clinical features. This observational case-control study included 133 patients with cutaneous melanoma and 900 healthy controls from Northeastern Italy. The rs16944 C > T polymorphism was determined by genomic DNA restriction fragment analysis. The IL-1B rs16944 C allele (OR = 1.44, p = 0.014) and CC genotype (OR = 1.48, p = 0.037) were associated with modestly higher odds of melanoma. Among melanoma patients, the CC genotype was associated with Stage I disease (OR = 2.45, p = 0.016) and Breslow thickness ≤ 0.75 mm (OR = 2.27, p = 0.049), whereas it was less frequent in Stage IV melanoma (OR = 0.37, p = 0.029). The CT genotype was associated with Stage IV melanoma (OR = 3.03, p = 0.014) and with lower-limb (OR = 2.45, p = 0.038) and lower-extremity (OR = 3.09, p = 0.005) melanoma. These divergent associations are exploratory and do not establish disease trajectory or a functional effect of rs16944; mechanistic interpretation remains uncertain because IL-1β expression or activity was not measured in this cohort. To our knowledge, this is the first report of an association between a genetic polymorphism and lower-limb/lower-extremity melanoma. These exploratory findings require confirmation in independent cohorts.

PMID 42505240
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