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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

PubMedFrontiers in immunology2026-11-11

Juvenile idiopathic arthritis and rheumatoid arthritis: a narrative review of age-dependent, subtype-specific immune mechanisms, biomarkers, and treatment strategies.

Sheng Wenwen W, Yang Xinyue X, Yu Zhenzhe Z, Yang Yongqi Y et al.

Juvenile idiopathic arthritis (JIA) and adult rheumatoid arthritis (RA) share chronic inflammatory arthritis, but their biological drivers and implications vary by developmental stage and phenotype. JIA arises during immune and skeletal maturation and encompasses heterogeneous conditions, whereas adult RA develops after skeletal maturity. Existing reviews have considered the diseases separately or focused on polyarticular JIA, leaving uncertain which adult RA-derived mechanisms, biomarkers, and treatment principles transfer to JIA phenotypes. A targeted search of PubMed/MEDLINE and Web of Science through 25 September 2026 informed an age-by-endotype framework comparing JIA phenotypes with adult RA across immune and tissue mechanisms, structural consequences, biomarker function and evidence maturity, and treatment mechanism, exposure, and safety. Systemic JIA, conceptualized within the Still's disease spectrum, diverges most from adult RA because of myeloid-cell activation, macrophage activation syndrome risk, and inflammation associated with interleukin-1, interleukin-6, and interleukin-18. Rheumatoid factor (RF)-positive polyarticular JIA shows partial convergence with adult seropositive RA through autoantibody-associated adaptive immunity, chronic synovitis, and erosive potential, but development and pediatric safety preclude equivalence. Oligoarticular JIA is distinguished by synovitis and uveitis, whereas enthesitis-related arthritis and juvenile psoriatic arthritis align more closely with entheseal and psoriatic-spectrum biology than with RA. Biomarker interpretation and treatment are phenotype-specific: ferritin, interleukin-18, and S100 proteins inform systemic hyperinflammation; RF and anti-citrullinated protein antibodies characterize RA-like polyarthritis; antinuclear antibodies inform uveitis surveillance; and human leukocyte antigen B27 supports classification in enthesitis-related arthritis. Treatment ranges from early interleukin-1 or interleukin-6 inhibition in systemic JIA to methotrexate, biologic disease-modifying antirheumatic drugs, and selected Janus kinase inhibitor use in RA-like polyarthritis after consideration of regulatory approval and individualized risk, and therapy directed at tumor necrosis factor or interleukin-17 in entheseal or psoriatic disease. Tissue, imaging, multi-omic, microbiome, and treatment-response biomarkers remain investigational. The relationship between JIA and adult RA is phenotype- and domain-specific rather than universal. This framework identifies where adult-derived evidence can inform pediatric interpretation and where direct pediatric validation is required. Longitudinal, subtype-defined pediatric cohorts integrating tissue, imaging, and multi-omic data are needed to support mechanism-based, developmentally appropriate care.

PMID 43011779
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PubMedAllergologie select2026-11-11

Epithelial alarmins at the crossroads of type 2 immunity: Experimental insights from skin and airway models.

Liao Kexin K, Khani Maghanaki Jamal Maurice JM, Schotters Leonie Friederike LF, Zou Yulin Y et al.

Epithelial alarmins such as thymic stromal lymphopoietin (TSLP), interleukin-33 (IL-33) and IL-25 orchestrate the initiation of type 2 immune responses at barrier surfaces. Dysregulated release of these cytokines links environmental cues to chronic allergic inflammation in the skin and airways. Recent experimental work using human keratinocytes, organotypic 3D skin equivalents, airway epithelial models, and murine challenge systems shows that barrier disruption, allergens, microbial components, and environmental irritants or pollutants induce strong alarmin expression. These mediators condition dendritic cells (DCs) and group 2 innate lymphoid cells (ILC2s), generating the cytokine milieu that drives Th2 polarization and neuro-immune crosstalk. This mini review summarizes molecular principles, highlights recent mechanistic findings from experimental systems, and discusses translational implications for allergic diseases such as atopic dermatitis, asthma, and chronic rhinosinusitis with nasal polyps (CRSwNP). Understanding the epithelial-alarmin axis offers opportunities for targeted prevention and therapy across barrier organs.

PMID 43011479
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PubMedMedicine2026-11-11

Intravascular large B-cell lymphoma presenting as unilateral lymphedema in a patient with rheumatoid arthritis and sarcoidosis: A case report.

Kimura Masatoshi M, Sasaki Haruka H, Kudo Risa R, Murai Masayuki M et al.

Intravascular large B-cell lymphoma (IVLBCL) is an uncommon subtype of diffuse large B-cell lymphoma, typically presenting with nonspecific symptoms and lacking lymphadenopathy or visible tumor lesions, which makes early diagnosis challenging. A 66-year-old female developed progressive unilateral lymphedema despite ongoing treatment for rheumatoid arthritis and sarcoidosis. Sarcoidosis-related lymph node lesions were also considered as a potential cause, and the prednisolone dose was increased. Despite these measures, the edema worsened, and a fever of around 38°C developed. At the initial evaluation, the serum soluble interleukin-2 receptor level was already elevated at 9985 U/mL. Initial investigations, including imaging, bone marrow aspiration, and random skin biopsies, failed to reveal malignancy. Subsequent monitoring revealed that the serum level of serum soluble interleukin-2 receptor had risen further to 19,835 U/mL and that thrombocytopenia was present, prompting a repeat random skin biopsy that ultimately confirmed IVLBCL through the identification of intravascular cluster of differentiation 20-positive lymphoma cells. Chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone was initiated. However, the patient developed peripheral neuropathy, suspected to be an adverse drug reaction. Consequently, the regimen was switched to polatuzumab vedotin, rituximab, cyclophosphamide, doxorubicin, and prednisolone. After completing 8 courses, the patient achieved remission. The left lower-limb lymphedema improved significantly. This case highlights several clinically significant points: first, IVLBCL can present solely as unilateral lymphedema without detectable lymph node enlargement or tumorous lesions, underscoring the diagnostic difficulty. Second, repeated random skin biopsies, including adipose-rich vascular tissue, are crucial in establishing a definitive diagnosis when initial biopsies are inconclusive. Third, patients with underlying autoimmune conditions such as rheumatoid arthritis and sarcoidosis, particularly those receiving immunosuppressive therapies, may have an increased susceptibility to lymphoma, suggesting that systemic immune dysregulation could contribute to disease onset.

PMID 43012796
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PubMedJournal of agricultural and food chemistry2026-11-11

Structural Characterization of LDP-1, a Polysaccharide from Lyophyllum decastes, and Its Protective Effects against PEDV-Induced Intestinal Inflammation In Vitro and In Vivo.

Zhao Wen W, Wei Yuheng Y, Lin Changhua C, Zhao Shuo S et al.

Porcine epidemic diarrhea virus (PEDV) infection causes severe intestinal inflammation and barrier injury in piglets. In this study, a purified polysaccharide fraction, Lyophyllum decastes polysaccharide-1 (LDP-1), was isolated and structurally characterized, and its protective effects against PEDV-induced intestinal injury were evaluated in IPEC-J2 cells and piglets. LDP-1 predominantly comprised glucose and exhibited a peak molecular weight of 30.56 kDa, with an α-(1→4)-glucan backbone. In vitro, LDP-1, particularly under pretreatment and whole-process treatment, attenuated PEDV-induced inflammatory cytokine expression. In vivo, LDP-1 pretreatment reduced diarrhea, alleviated intestinal pathological injury, and partially restored villus-crypt morphology. LDP-1 also decreased intestinal interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) expression and restored zonula occludens-1 (ZO-1), Claudin-1, and Occludin expression. These findings indicate that LDP-1 protects against PEDV-induced intestinal inflammation and barrier injury and may serve as a potential natural protective agent.

PMID 43012683
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PubMedAnalytical chemistry2026-11-11

One-step immunoassay for Interleukin-4 (IL4) Detection Using IL4-Receptor Mimotopes Screened from Fv-Antibody Library.

Kwon Soonil S, Jung Jaeyong J, Sung Jeong Soo JS, Bae Hyung Eun HE et al.

One-step immunoassay for IL4 was developed using a hypervariable part of immunoglobulin G (Fv-antibody) and switching-peptides. Conventional immunoassays require multistep procedures, whereas one-step immunoassays do not require additional steps. Fv-antibodies comprise three complementarity-determining regions (CDRs) and three frame regions (FRs). An Fv-antibody library was constructed using site-directed mutagenesis of the CDR3 region (with 11 amino acid residues) and expressed on the outer membrane of Escherichia coliusing autodisplay technology. Two IL4 receptor (IL4r) mimotopes, designated Fv-1 and Fv-2, were screened from the Fv-antibody library using the anti-IL4r antibody. These mimotopes were expressed as soluble proteins with three CDRs and four FRs. Using the surface plasmon resonance (SPR) biosensor, the binding affinities of the mimotopes Fv-1 and Fv-2 to the anti-IL4r antibody were 39.5 and 48.8 nM, respectively. Using HEK-Blue IL4 cells, the expressed IL4r mimotopes were analyzed to determine whether they compete with IL4r for the binding of IL4. The inhibition constants of mimotopes were 2.3 and 1.9 μM for Fv-1 and Fv-2, respectively. The interaction between mimotopes and IL4r (binding affinity and amino acids) was analyzed and compared with that of IL4 using a docking simulation. The interaction between mimotopes and IL4 occurred at binding sites on IL4r. A complex of expressed mimotopes and switching-peptides (fluorescence-labeled) was used for detecting IL4. The binding of IL4 to the complex resulted in the quantitative release of switching-peptides. IL4 detection was within the clinically required IL4 concentration range.

PMID 43010545
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PubMedInternational journal of immunopathology and pharmacology2026-11-11

Ayanin attenuates thioacetamide-induced liver toxicity in vivo: Modulation of oxidative stress, inflammation, and apoptosis.

Ibrahim Alsharif Hanan H, Jabbar Ahmed A J AAJ

BackgroundAyanin is an O-methylated flavonol isolated from many plant species recognized for its in vitro antioxidant and anti-inflammatory properties. However, studies on its toxicity profile and hepatoprotective effects are scarce.ObjectiveTherefore, this study investigates the acute toxicity and hepatoprotective effects of ayanin in thioacetamide (TAA)-induced hepatotoxicity in rats, along with its association with the regulation of cellular processes.DesignAcute toxicity evaluation included a single oral delivery of 250 and 500 mg/kg Ayanin to rats, which were observed regularly for 14 days. In a hepatoprotective experiment, rats were treated (p.o.) with 50 mg/kg silymarin, 20 mg/kg Ayanin, or 40mg/kg Ayanin p. o. daily, along with 200 mg/kg TAA (2 injections/week, i.p.) for two months.ResultsThe results indicated non-toxic effect of up to 500 mg/kg Ayanin, and a noticeable hepatoprotective effect of Ayanin (20 and 40 mg/kg), preserving body weight/liver weight index and liver histoarchitecture (lowering liver fibrosis phenotypes, including hemorrhage, reduced splenic congestion/necrosis, and collagen generation). These effects aligned with its antioxidant(up-regulating superoxide dismutase, catalase, and reducing malondialdehyde levels) and anti-inflammatory effects (reducing tumour necrosis factor-α and interleukin-6). The anti-apoptotic effects of Ayanin (20 and 40 mg/kg) were confirmed by significant (p<0.001) lowering of Bax by 10.20% and 34.04%; lessening caspase-3 by 26.02 and 47.74%; while increasing Bcl-2 concentration by 107.51 and 122.55%, respectively, which ultimately improved the liver's function.ConclusionThe results suggest that Ayanin exhibits anti-fibrotic action, attributable to orchestrated pathways associated with oxidative stress, inflammation, and apoptosis.

PMID 43010865
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