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interleukin-2 (Interking)

✓ Approved

Shenzhen Neptunus · IL2RA · Recombinant Proteins

What is interleukin-2?

interleukin-2 is a recombinant proteins developed by Shenzhen Neptunus. It is approved for therapeutic indications via injectable (others) or intravenous (iv) or subcutaneous injection.

Drug Profile

Brand NamesInterking
CompanyShenzhen Neptunus
Drug ClassRecombinant Proteins
Molecular TargetIL2RA
RouteInjectable (Others), Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Shenzhen Neptunus

Mechanism of Action

Molecular Targets

interleukin-2 acts on 1 molecular target:

IL2RAinterleukin 2 receptor subunit alpha (IL2R, TCGFR)
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Therapeutic Indications

interleukin-2 is developed for 15 unique indications across 4 therapeutic areas.

Therapeutic AreaConditionPhase
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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Related Research Articles

PubMedFrontiers in immunology2026-07-25

Epstein-Barr virus reactivation triggers selective IL-6/IL-10 axis inflammation and CD3+CD8+ T-cell activation leading to severe leukopenia, hyperinflammatory shock, and myocardial injury: a case report.

Chen Yong Y, Wang Jie J, Yao Qiuju Q, Zhong Junhui J et al.

Reactivation of Epstein-Barr virus (EBV) can lead to life-threatening complications beyond hemophagocytic lymphohistiocytosis (HLH). We report a case of severe EBV reactivation in a 24-year-old female. She had persistent high fever, severe leukopenia, hyperinflammatory shock, and myocardial injury, but lacked typical HLH features. Laboratory tests showed elevated proportions of CD3+CD8+ T cells and increased interferon-γ (IFN-γ), interleukin-6 (IL-6), interleukin-10 (IL-10), and high-sensitivity troponin. Interleukin-2 (IL-2) and tumor necrosis factor-α (TNF-α) levels were normal. The inflammatory pathway may be involved as follows: EBV infects B cells and activates specific CD8+ T cells. These T cells mainly secrete IFN-γ without concurrent IL-2 or TNF-α release, resulting in moderate macrophage activation and IL-6/IL-10-related inflammation. This mechanism differs fundamentally from the uncontrolled inflammation in HLH. With glucocorticoids and ganciclovir treatment, the patient's symptoms and laboratory markers rapidly and completely resolved. This case highlights the heterogeneity of EBV inflammatory response: clinicians should recognize its atypical manifestations, differentiate it from HLH, and provide individualized treatment based on immunophenotypic profiles.

PMID 42500678
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PubMedMedicine2026-07-25

Assessing the rosacea potential pathogenic risks of cinnamaldehyde in daily skin care products and cosmetics using network toxicology and molecular docking with experimental validation.

Huang Hao H, Wen Ju J, Feng Junrong J, Zhang Zhihong Z et al.

Rosacea, a chronic inflammatory skin disorder, severely impairs patients' quality of life and imposes substantial medical burdens. Existing treatments are hampered by unsatisfactory therapeutic effects and high recurrence rates, driving urgent research into novel pathogenic mechanisms. As a common spice and cosmetic preservative, cinnamaldehyde's safety risks in rosacea patients remain poorly characterized. This study aimed to integrate network toxicology with in vitro cellular assays to clarify its pathogenic roles and molecular pathways, providing novel theoretical support for its adverse impacts on rosacea sufferers. First, we predicted the target genes of cinnamaldehyde using the PubChem, SwissTargetPrediction, SuperPred, and ChEMBL databases. Second, we obtained relevant targets for rosacea using the GeneCards and CTD databases and identified the intersection targets with toxic substances. Then, we constructed a protein-protein interaction network of the core toxic substance combination using the STRING database and performed Gene Ontology functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis to predict possible mechanisms. Subsequently, molecular docking validation of the active ingredients with the main targets was performed using AutoDock Vina software. Finally, cinnamaldehyde was added to the rosacea-like cellular model in HaCaT cells to assess its effects and molecular mechanisms by Cell Counting Kit-8, reverse transcription quantitative polymerase chain reaction, and enzyme-linked immunosorbent assay. Database screening revealed 43 overlapping targets between the 195 predicted targets of cinnamaldehyde and the 1889 disease-related targets for rosacea, which included notable proteins such as prostaglandin‑endoperoxide synthase 2 (cyclooxygenase‑2; PTGS2), matrix metallopeptidase 9 (MMP9), and epidermal growth factor receptor (EGFR). Protein-protein interaction analysis identified PTGS2 as a pivotal hub protein, while Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis indicated that interleukin-17 signaling and lipid metabolism are vital mechanisms involved in rosacea. Molecular docking studies demonstrated strong binding affinities between cinnamaldehyde and the identified core targets. Furthermore, cell culture experiments confirmed that cinnamaldehyde exacerbates rosacea by upregulating the expression of PTGS2, MMP9, and EGFR, along with increasing the production of inflammatory cytokines such as interleukin-8 and interleukin-1 beta. In summary, our findings elucidate the potential pathogenic mechanisms by which cinnamaldehyde may induce rosacea, highlighting the roles of the core targets PTGS2, MMP9, and EGFR in mediating inflammation. This research provides new scientific insights that could inform preventive strategies and therapeutic interventions aimed at managing the toxicity associated with rosacea.

PMID 42499056
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PubMedJPGN reports2026-07-25

Successful treatment of eosinophilic esophagitis with upadacitinib prescribed for atopic dermatitis.

Nguyen Nathalie N, Bauer Maureen M

We describe a pediatric patient treated with upadacitinib for atopic dermatitis (AD) who subsequently achieved sustained clinical and histologic remission of eosinophilic esophagitis (EoE). Upadacitinib is an oral small molecule selective Janus kinase 1 inhibitor that inhibits janus kinase-signal transduction and activation of transcription (JAK-STAT) pathway with wide inhibitory effects on the immune system, including Th2 signaling pathways. Therefore, it leads to broad suppression of inflammatory cytokines, including interleukin-4 (IL-4), interleukin-13 (IL-13), and thymic stromal lymphopoietin (TSLP), that play a central role in the pathogenesis of EoE. Given the broad signaling pathway, if a patient is started on upadacitinib for other indications, cessation of other therapies, particularly biologics like dupilumab, should be considered on a case-by-case basis.

PMID 42499727
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PubMedInflammopharmacology2026-07-25

Imeglimin confers protection against intestinal ischemia/reperfusion injury in rats through AMPK-dependent inhibition of NF-κB/NLRP3 inflammasome signaling and mitigation of oxidative stress and apoptosis.

Abdelzaher Walaa Yehia WY, Khalaf Hanaa Mohamed HM, Saleh Rabeh Khairy RK, Raouf Nehal Refaat NR et al.

Intestinal ischemia/reperfusion (I/R) injury is a critical condition characterized by oxidative stress, inflammation, and apoptosis, leading to significant tissue damage. Imeglimin (IMEG), a novel antidiabetic agent, has recently shown cytoprotective effects through modulation of mitochondrial function, oxidative stress, and inflammatory pathways. We aimed to investigate the potential protective effects of IMEG against II/R injury and to explore the underlying mechanisms involved. Thirty-two adult male Wistar albino rats were divided into four groups; sham group, IMEG group, intestinal I/R group, IMEG + Intestinal I/R group. Oxidative stress markers [malondialdehyde (MDA), reduced glutathione (GSH)], and histopathological changes were assessed. Biochemical analyses included measurement of phosphorylated AMP-activated protein kinase (p-AMPK), NOD-like receptor protein 3 (NLRP3) and caspase-3. Also, gene expression of interleukin (IL)-1β, caspase-1, apoptotic Bcl-2-associated protein x (BAX) and anti-apoptotic B-cell leukemia/lymphoma 2 protein (Bcl-2) were measured. Nuclear factor-κB (NF-κB) immuno expression was estimated. MDA, NLRP3, caspase-3 levels, IL-1β, caspase-1, Bax gene expression, and NF-κB immunohistochemical expression were all significantly elevated in the intestinal I/R group while GSH, p-AMPK levels and Bcl-2 gene expression were significantly decreased. Every metric indicated a notable improvement with IMEG. IMEG exerts a protective effect against intestinal I/R injury through its antioxidant, anti-inflammatory, and anti-apoptotic properties (Fig. 1).

PMID 42498903
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PubMedCase reports in oncology2026-07-25

Achieving Stable Disease in an Adult with Malignant Gastrointestinal Tumor following Cabozantinib Treatment: Case Report.

Iverson Brianna Jo BJ, Milhem Mohammed M MM, Rieth John Markus JM

Malignant gastrointestinal neuroectodermal tumor (GNET) is a rare and aggressive neoplasm that is characterized by EWSR1 rearrangements. Most patients present with metastatic disease. There are no established treatment guidelines, and systemic therapy options remain poorly defined. A woman in her late 30s presented initially with right upper quadrant pain and bloating. Endoscopic biopsy of a duodenal mass revealed a SOX10-positive malignant neoplasm. Molecular testing identified an EWSR1:CREB1 fusion, confirming GNET. Initial treatment with ipilimumab and nivolumab resulted in disease progression. Subsequent therapies included a selective interleukin-2 agonist clinical trial, nivolumab/relatlimab, and temozolomide, all associated with continued progression. Cabozantinib was initiated after further radiographic progression. Follow-up imaging demonstrated tumor regression, and the patient maintained stable disease for 15 months before mild progression. Metastatic GNET has a poor prognosis and lacks standardized systemic therapy. This case demonstrates durable disease stabilization with cabozantinib after progression on immunotherapy and chemotherapy. Tyrosine kinase inhibition may represent a promising therapeutic strategy in GNET and warrants further investigation.

PMID 42499698
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PubMedThe Journal of allergy and clinical immunology2026-07-25

Dupilumab for patients with allergic fungal rhinosinusitis.

Luong Amber U AU, Levy Joshua M JM, Wise Sarah K SK, Han Joseph K JK et al.

Allergic fungal rhinosinusitis (AFRS) is a severe subtype of chronic rhinosinusitis characterized by fungal hypersensitivity and accentuated type 2 inflammation. Dupilumab-a fully human monoclonal antibody blocking interleukin-4/13, approved for type 2 inflammatory diseases, including chronic rhinosinusitis with nasal polyps-may benefit patients with AFRS. In this phase 3 trial, patients with AFRS aged ≥6 years were randomized to dupilumab or matched placebo for 52 weeks. The primary end point was Lund-Mackay computed tomography (LMK-CT) score, quantifying sinus opacification, at 52 weeks. Secondary end points were multiplicity-controlled and hierarchically tested. At week 52, dupilumab (N=33) improved LMK-CT scores vs placebo (N=29) (LSMD -7.36 [95% CI, -9.38 to -5.35]; P<.001). At week 24, dupilumab improved nasal congestion score (-0.87 [-1.18 to -0.56]), total symptom score (-2.18 [-3.04 to -1.32]), and nasal polyp score (NPS; -2.36 [-3.31 to -1.41]) vs placebo, and further decreased NPS to -2.77 (-3.82 to -1.72) (all P<.001) at week 52. Dupilumab lowered the risk of receiving systemic corticosteroids and/or undergoing sinonasal surgery vs placebo by 92% (risk difference -29.1% [95% CI, -46.42 to -11.79]; P=.0010). In patients with comorbid asthma, dupilumab also benefited asthma measures. The proportion of patients having treatment-emergent adverse events was similar between dupilumab and placebo (69.7% and 78.6%). In patients with AFRS, dupilumab vs placebo demonstrated significant improvement in radiographic, endoscopic, clinical, quality-of-life outcomes, and need for systemic corticosteroids and/or surgery. Dupilumab was well tolerated. (Funded by Sanofi and Regeneron Pharmaceuticals; LIBERTY AFRS AIMS ClinicalTrials.gov number, NCT04684524.).

PMID 42498125
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