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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)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

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

PubMedBMC pediatrics2026-07-17

An evaluation of cytokine responses and antiseizure medication levels during mild upper respiratory infections in children with epilepsy.

Arslan Elif Acar EA, Özkaya Aslı Begüm AB, Özkan Esra E, Durgut Betül Diler BD et al.

This study aimed to investigate the effect of upper respiratory tract infections on serum antiseizure medication levels in children with idiopathic epilepsy and the relationship between that condition and inflammation. Forty-nine patients aged 2-18 years presenting to our paediatric neurology clinic who were under follow-up with a diagnosis of idiopathic epilepsy and who were receiving valproate or carbamazepine therapy were included in this study. All patients were using either valproic acid (n = 31) or carbamazepine (n = 18). Patients were evaluated at the time of presentation with symptoms of upper respiratory tract infection and during the control period one month later. Serum antiseizure medication, interleukin-17 A and interleukin-23 levels, complete blood count, alanine transaminase levels, creatinine levels, albumin levels, erythrocyte sedimentation rates, and C-reactive protein levels were measured during infection and during the control period one month later. Simultaneous electroencephalography examinations were also performed. No provoked seizures occurred in any patient during the infection period. Serum valproic acid levels were higher in patients during the infection period than in those same patients during the control period after one month, although this difference was not statistically significant (p = 0.073). There was also no significant difference in carbamazepine levels (p = 0.484). While no difference was observed in the interleukin-23 values between the two periods in patients receiving valproic acid, these values were greater in the patients who received carbamazepine during the infection period (p = 0.039). The findings of this study suggest that mild upper respiratory tract infections do not cause clinically significant alterations in serum valproate or carbamazepine levels.

PMID 42464153
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PubMedFrontiers in endocrinology2026-07-17

Interleukin-1 receptor antagonist and heat shock protein 90alfa are independently associated with fatigue and general health in euthyroid Hashimoto's thyroiditis.

Omdal Roald R, Grimstad Tore T, Jonsson Grete G, Kvaløy Jan Terje JT et al.

Patients with Hashimoto's thyroiditis frequently experience fatigue and impaired health-related quality of life (HRQOL) despite biochemical euthyroidism, suggesting that immune-mediated mechanisms beyond thyroid hormone deficiency contribute to symptom generation. The role of specific inflammatory mediators - including interleukin-1 receptor antagonist (IL-1Ra), heat shock protein 90α (HSP90α), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and anti-TPO antibodies - in relation to patient-reported outcomes (PROMs) has not been systematically examined. In a cross-sectional study of 36 euthyroid patients with confirmed Hashimoto's thyroiditis, serum/plasma levels of IL-1Ra, HSP90α, IL-6, and TNF-α were measured alongside anti-TPO. PROMs included the SF-36 General Health subscale (inverted; iGH), the Fatigue Visual Analog Scale (fVAS), and the Fatigue Severity Scale (FSS). Spearman correlations, univariable and multivariable linear regression, and principal component analysis (PCA) were applied. The cohort displayed severe fatigue at baseline (median fVAS 85, FSS 6.7, SF-36 GH 16). IL-1Ra was the most consistent biomarker correlate of symptom burden, independently associated with poorer general health and more fatigue across all regression models. HSP90α showed an inverse and independent association with fatigue in multivariable models, suggesting a potentially protective role. IL-6 contributed in correlation analysis only, while TNF-α and anti-TPO were not significantly associated with any PROM in any analytical approach. IL-1Ra and HSP90α, but not anti-TPO, are independently associated with fatigue and general health in euthyroid Hashimoto's thyroiditis, pointing to IL-1 pathway activity as associated with symptom burden and potentially playing a key role in this condition.

PMID 42466336
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PubMedSeizure2026-07-17

Time-dependent changes in cerebrospinal fluid cytokines in NORSE and FIRES: A systematic review.

Phong Zhi-Ying ZY, Lim Kheng-Seang KS, Wong Won Fen WF, Abdullah Suhailah S et al.

New-onset refractory status epilepticus (NORSE) describes patients with no prior history of epilepsy who develop refractory status epilepticus. A subtype of NORSE with prior fever is known as febrile infection-related refractory status epilepticus (FIRES). This systematic review summarises the temporal dynamics of cytokine profiles in cerebrospinal fluid (CSF) throughout the course of these conditions. We conducted a comprehensive search of PubMed, Scopus, and Web of Science studies published between 1st January 2006 and 30th March 2025. Studies reporting cytokine profiles before and/or after immunotherapies in NORSE and FIRES were included. We reviewed a total of 42 studies. Interleukin (IL) IL-6, IL-8, and IL-1β were most consistently reported and showed observable temporal changes. Mean CSF levels of IL-1β increased from 1.3 ± 1.9 pg/ml at week 1 to a peak of 2.8 ± 2.5 pg/ml at week 2 and declined to 2.6 ± 2.2 pg/ml at week 3. A similar trend was noted in CSF IL-8 level, which increased from 974.7 ± 1489.7 pg/ml at week 1 to 1336.0 ± 2082.2 pg/ml at week 2, then declined to 391.1 ± 284.4 pg/ml at week 3. In contrast, CSF IL-6 level rose markedly to 349.7 ± 559.5 pg/ml at week 1 and declined substantially to 93.1 ± 182.7 pg/ml at week 2, and 83.2 ± 27.9 pg/ml at week 3. Proinflammatory cytokines in CSF were markedly elevated within the first two weeks after seizure onset, highlighting this as a critical window for cytokine profiling and the importance of interpreting cytokine levels in a time-dependent manner to guide immunotherapy in NORSE and FIRES.

PMID 42462374
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PubMedNature reviews. Immunology2026-07-17

Interleukin-18 armours antitumour immune effectors.

Sharma Akshat A, Bishara Gina G GG, Olejniczak Scott H SH, Ohm Joyce E JE et al.

Interleukin-18 (IL-18) is a pleiotropic cytokine of the IL-1 family that has an important role in antitumour and antiviral immunity. Growing interest in its therapeutic potential has led researchers to explore strategies that harness IL-18 to modulate the tumour microenvironment. For example, engineered T cells are being armoured with IL-18 to enhance adoptive cell therapies and strengthen other immunotherapy approaches. As these strategies move towards clinical application, a key translational challenge is identifying the molecular mechanisms that influence treatment response and resistance, crucial for guiding trial design and patient selection across tumour types. This Review revisits the fundamental biology of IL-18, including its origins, cellular sources and regulatory networks, particularly those involving IL-18 binding protein (IL-18BP) and IL-37. We discuss how IL-18 promotes interferon-γ (IFNγ) production within the tumour microenvironment, supporting M1-like macrophage polarization, CD8+ cytotoxic T cell and CD4+ T helper 1 cell responses, natural killer cell activity and durable T cell memory. We also discuss preclinical models of IL-18 delivery, including dendritic cell platforms and cellular therapies, and highlight emerging strategies such as IL-18BP blockade and IL-18-secreting CAR T cells. Finally, we review results from early clinical studies and outline key challenges for translation, including the dual protumour and antitumour roles of IL-18.

PMID 42463973
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PubMedEuropean journal of case reports in internal medicine2026-07-17

A 24-Year-Old Man with Disseminated Tuberculosis and A Corticosteroid-Refractory Paradoxical Reaction to Anti-Tuberculous Treatment.

Charalampidis Charalampos C, Karantana Valentina V, Kavatha Dimitra D, Tsiodras Sotirios S et al.

Paradoxical reactions during anti-tuberculosis treatment are immune-mediated reactions that complicate treatment even in immunocompetent patients. We present the case of a previously healthy 24-year-old man with disseminated tuberculosis, who experienced persistent fever, weight loss, and radiological deterioration despite appropriate treatment. These findings were consistent with a paradoxical reaction to treatment, after extensive work-up excluded treatment failure, co-infections, and systemic inflammatory conditions. However, high-dose corticosteroids failed to achieve improvement. Ultimately, an interleukin-1 receptor antagonist (anakinra) was initiated as a salvage therapy for this corticosteroid-refractory paradoxical reaction, resulting in rapid defervescence, normalization of inflammatory markers, and radiological improvement. This case underscores the diagnostic and therapeutic challenges when managing severe reactions in tuberculosis patients, while highlighting the importance of biologics like anakinra in corticosteroid-refractory paradoxical reactions. Paradoxical reactions to anti-tuberculosis treatment remain an overlooked cause of non-resolving fever in immunocompetent and immunocompromised patients with tuberculosis and should be considered after ruling out treatment-refractory or complicated infection in persistently febrile patients.Prompt treatment of severe reactions prevents major complications and improves clinical outcomes.Corticosteroid-refractory paradoxical reactions illustrate the potential role of biologics, such as tumour necrosis factor inhibitors and, in our case, interleukin-1 receptor antagonists, in controlling excessive inflammation in tuberculosis.

PMID 42466226
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PubMedFrontiers in immunology2026-07-17

Blomia tropicalis allergens induce lung DNA methylation changes in neuroimmune genes in a mouse model of airway inflammation.

Llinás-Caballero Kevin K, Acevedo Nathalie N, Merid Simon Kebede SK, Donado Karen K et al.

House dust mite (HDM) Blomia tropicalis is a major global inducer of allergic asthma, yet its epigenetic impact on airway tissues remains poorly understood. The aim of this study was to perform an exploratory, hypothesis-generating screening of the DNA methylation changes that occur in lung tissue of mice with robust allergic inflammation compared to saline-exposed controls. We sensitized and challenged BALB/c mice with B. tropicalis extract or purified allergens Blo t 2 and Blo t 13 or saline solution in a model of acute allergic airway inflammation, then assessed lung DNA methylation across over 285.000 CpG sites using the Infinium Mouse Methylation BeadChip (Illumina) (n = 6 mice per group, 24 lung samples). Allergen-exposed mice exhibit distinct lung DNA methylation profiles compared to controls following exposure to Blo t 2, Blo t 13, or B. tropicalis extract. Analysis of differentially methylated regions (DMRs) revealed 137, 179 and 313 DMRs in mice exposed to Blo t 2, Blo t 13, or B. tropicalis extract, respectively. Genes in key differentially methylated regions included protocadherin alpha genes (Pcdha1 to Pcdha6), cadherin 8 (Cdh8) and interleukin 11 receptor alpha (Il11ra). Genes in DMRs were enriched in several biological processes including homophilic cell adhesion via plasma membrane adhesion molecules and nervous system development. Notably, there was also found significant differences in mRNA levels of neuronal growth genes such as (Gdf7), N-acetylated alpha-linked acidic dipeptidase 2 (Naalad2), prune homolog 2 with BCH domain (Prune2), cerebellin 1 precursor (Cbln1) and, in the proapoptotic gene Bcl2l11. Exposure to B. tropicalis allergens is associated with lung DNA methylation changes in genes implicated in allergic asthma and inflammatory responses, offering novel epigenetic insights and key targets of house dust mite-induced airway allergy. This exposure may involve a joint neuro-immune epigenetic reprogramming in the lung, altering the methylation of cell-adhesion and local neural signaling genes, alongside key lipid inflammatory drivers. Our results support the hypothesis that Blomia tropicalis exposure disrupts the airway epithelial barrier and sensitizes the local pulmonary neuroendocrine network, strongly predisposing the tissue to hyperreactivity and allergic inflammation.

PMID 42465740
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