Drug Database
IN

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

+10 more indications available with a free account

Sign up free to view all indications →

Related Research Articles

PubMedAutoimmunity reviews2026-05-24

The Interleukin-17-T helper 17 axis in primary sclerosing cholangitis: A narrative review of an emerging pathogenic frontier.

Elzubeir Amera A, Patel Meha M, Rushbrook Simon S

Interleukin-17 (IL-17) and IL-17+ secretory cells, including T helper 17 (Th17) cells play pivotal roles in autoimmune diseases such as psoriasis. Emerging evidence implicates the IL-17 pathway in primary sclerosing cholangitis (PSC), a chronic cholestatic liver disease lacking approved pharmacological therapies, for which liver transplantation remains the only life-extending option. The IL-17 pathway and Th17 biology is increasingly implicated in PSC pathogenesis through its interactions with hepatic parenchymal and non-parenchymal cells, including cholangiocytes, neutrophils and hepatic stellate cells which promote periductal fibro-inflammation, immune cell recruitment and pro-inflammatory cytokine release. Th17 cells and IL-17+ secreting lymphocytes localise to peribiliary regions, exacerbating biliary injury and fibrosis. Preclinical murine models suggest that inhibition of IL-17 signalling mitigates hepatic fibro-inflammatory responses, providing a compelling rationale for its investigation as a potential therapeutic target in PSC. Whilst licensed IL-17 inhibitors have demonstrated efficacy and safety in a number of autoimmune and immune-mediated diseases, IL-17 has context-dependent roles in tissue homeostasis and host defence underscoring the pathway's complexity. This narrative review synthesises the biology of the IL-17 family, integrating preclinical and translational evidence relevant to PSC, and discusses the translational potential of approved anti-IL-17 agents as novel therapeutic candidates in PSC, whilst highlighting key uncertainties and gastrointestinal safety considerations.

PMID 42176828
Read full article →
PubMedJournal of the European Academy of Dermatology and Venereology : JEADV2026-05-24

Durability of response to icotrokinra for high-impact site psoriasis: 1-year ICONIC-TOTAL findings.

Warren Richard B RB, Gooderham Melinda M, Lain Edward E, Bissonnette Robert R et al.

High-impact site plaque psoriasis is difficult to treat. Icotrokinra, an oral peptide with high specificity for the interleukin (IL)-23 receptor, demonstrated significantly higher rates of high-impact site psoriasis clearance, versus placebo, with no safety signals, through Week (W)16. Report clinical response rates and safety through 1 year of icotrokinra treatment in participants with high-impact site plaque psoriasis. Participants (≥12 years of age; psoriasis body surface area ≥1%; Investigator's Global Assessment [IGA] ≥2) with at least moderate scalp, genital or hand/foot psoriasis were randomized (2:1) to once-daily icotrokinra 200 mg (N = 208) or placebo (N = 103), with placebo-to-icotrokinra transition at W16 (N = 92). Rates (using nonresponder imputation) of achieving clear/almost clear (0/1) or clear (0) overall skin (IGA), genital (static Physician's Global Assessment of genitalia [sPGA-G]), hand/foot (hf-PGA) psoriasis and absent/very mild (0/1) or absent (0) scalp psoriasis (scalp-specific-IGA [ss-IGA]), modified Nail Psoriasis Severity Index (mNAPSI) percent improvement and safety were assessed through W52. Eighty-eight per cent (275/311) of participants completed treatment through W52. In icotrokinra-randomized participants, response rates increased through W24 and were durable through W52 for overall psoriasis clearance (IGA 0/1 range: 67%-70%) and across high-impact sites (ss-IGA 0/1: 72%-78%; sPGA-G 0/1: 85%-90%; hf-PGA 0/1: 54%-62%); responses were consistent among placebo-randomized participants after transitioning to icotrokinra. High proportions of icotrokinra-randomized participants achieved complete clearance during W24-52 (IGA 0: 44%-51%; ss-IGA 0: 57%-66%; sPGA-G 0: 73%-84%; hf-PGA 0: 44%-58%). Mean mNAPSI improvement increased from W16 (33%) to W52 (62%). Exposure-adjusted rates of participants with ≥1 adverse event (AE) or serious AE through W16 were similar between icotrokinra and placebo, with no increase in AE rates or occurrence of a safety signal through W52. Icotrokinra demonstrated high and durable rates of psoriasis clearance across high-impact sites, with a favourable safety profile, through 1 year.

PMID 42175814
Read full article →
PubMedBMC nephrology2026-05-24

Risk factors and nomogram prediction model for prognosis in sepsis with acute kidney injury.

Lai Jun-Mei JM, Zheng Yang Y, Liang Tian-Yu TY, Huang Jin J et al.

Sepsis-associated acute kidney injury (AKI) is a frequent and life-threatening complication in critically ill patients, yet early risk stratification remains challenging. This study aimed to identify independent prognostic factors and to develop and internally validate a nomogram for predicting 28-day mortality in patients with sepsis-associated AKI. In this retrospective study, 238 adult patients with sepsis defined by Sepsis-3 criteria and AKI defined according to Kidney Disease: Improving Global Outcomes (KDIGO) guidelines were enrolled between January 2021 and December 2024. Clinical and immunologic variables obtained within 24 h of intensive care unit (ICU) admission were analyzed. Multivariable logistic regression was performed to identify independent predictors of 28-day mortality. Model performance was assessed using receiver operating characteristic (ROC) analysis, calibration plots, bootstrap validation, and decision curve analysis (DCA). Among the 238 enrolled patients, 91 were classified as non-survivors and 147 as survivors. Multivariable analysis identified AKI stage 2 (odds ratio [OR] 3.857, 95% confidence interval [CI] 2.101-7.082), AKI stage 3 (OR 5.585, 95% CI 2.652-11.761), ICU stay (OR 1.802, 95% CI 1.304-2.490), T helper 17 cells (OR 2.881, 95% CI 1.257-6.600), interleukin-17 (OR 1.226, 95% CI 1.073-1.401), and 24-hour fluid balance (OR 1.241 per 100 mL/day, P < 0.001) as independent predictors of poor prognosis. The nomogram showed good discrimination, with an area under the curve of 0.859 and a bootstrap-corrected concordance index of 0.844. Calibration and DCA demonstrated adequate model fit and clinical utility. AKI severity, early fluid accumulation, ICU course, and immune-inflammatory activation are independently associated with 28-day mortality in sepsis-associated AKI. The proposed nomogram provides individualized risk estimation and may assist in early prognostic stratification. Not applicable.

PMID 42177426
Read full article →
PubMedLife sciences2026-05-24

Kynurenine pathway impact on immune evasion and inflammation in acute myeloid leukemia.

Wawrzak-Pienkowska Katarzyna K, Golonko Aleksandra A, Ignatiuk Diana D, Swidnicka-Siergiejko Agnieszka A et al.

Acute myeloid leukemia (AML) involves immune dysregulation and evasion, in which tryptophan catabolism via the kynurenine pathway (KP) is central. Leukemic blasts often overexpress indoleamine 2,3-dioxygenase-1 (IDO1) and tryptophan 2,3-dioxygenase (TDO2), driving excess L-kynurenine (Kyn) production. Kyn activates the aryl hydrocarbon receptor (AhR), inducing interleukin-6 (IL-6) secretion and STAT3 phosphorylation with NF-κB co-activation, sustaining chronic inflammation. Concomitantly, KP activation is immunosuppressive: Kyn biases T cells toward FoxP3+ regulatory phenotypes, drives exhaustion of T and NK cells, and impairs dendritic and B-cell function, yielding an immunosuppressive milieu rich in IL-10 and IL-35. Together, these actions link chronic inflammation to immune tolerance in AML. By contrast, while upstream enzymes (IDO1/TDO2) are well studied, downstream KP metabolites remain poorly characterized in AML. In other systems, kynurenic acid (KYNA) mediates anti-inflammatory GPR35/AhR signaling, whereas 3-hydroxykynurenine (3-HK) and quinolinic acid (QUIN) generate reactive oxygen species, activate NF-κB-dependent cytokine cascades, and induce T-cell apoptosis. Collectively, the extended KP emerges as a nexus linking inflammatory signaling and immunosuppression in AML, with implications for disease progression, immune escape, and resistance, warranting further investigation.

PMID 42176883
Read full article →
PubMedPhytomedicine : international journal of phytotherapy and phytopharmacology2026-05-24

Targeting TNFR1 by salvianolic acid B alleviates sepsis-induced acute lung injury and pulmonary-intestinal epithelial barrier damage.

Ma Luyao L, Liu Fanglin F, Shen Jingjing J, Wu Jianchao J et al.

Sepsis-induced acute lung injury (ALI) and intestinal injury were characterized by dysregulated systemic inflammation and organ dysfunction. Host-directed therapy (HDT) that modulates excessive immune responses is a promising complementary strategy. Salvianolic acid B (Sal B) has been reported to modulate various signaling pathways, yet whether it targets TNFR1 to simultaneously inhibit NF-κB, necroptosis, and p-MLCK/p-MLC2 in septic ALI remains unexplored. This study aimed to investigate the protective effects of Sal B against sepsis-induced lung-intestine injury and to elucidate its underlying molecular mechanisms, with a focus on identifying its potential cellular target. A murine model of sepsis-induced ALI was established via lipopolysaccharide (LPS) challenge. H&E staining, ELISA, immunohistochemistry analyses were performed to assess lung, intestinal injury and their barrier damage. In vitro, models of LPS/zVAD-induced macrophage necroptosis and tumor necrosis factor-α (TNF-α) induced epithelial barrier damage were established in J774A.1, THP-1, A549, and HCT116 cells. Cell death, cytokine secretion, the key proteins of necroptosis and signal molecules related to epithelial barrier integrity were evaluated using LDH/PI assays, ELISA, western blotting, and immunofluorescence. By using gene silencing and overexpression techniques, the role of tumor necrosis factor receptor 1 (TNFR1) in regulating the necrotic apoptosis process of macrophages infected with LPS was elucidated. The Sal B-TNFR1 potential interaction was validated using drug target identification methods such as molecular docking and site-directed mutagenesis. In vivo, Sal B alleviated pulmonary edema, histopathological damage in lung and colon, and reduced systemic and local levels of TNF-α and interleukin-1β (IL-1β). It concurrently suppressed the activation of the phospho myosin light-chain kinase/phospho myosin light chain 2 (p-MLCK/p-MLC2) pathway and restored expression of tight junction proteins, while inhibiting the necroptosis pathway. In vitro, Sal B inhibited TNF-α-induced barrier damage in epithelial cells and LPS/zVAD-induced necroptosis in macrophages. Mechanistically, Sal B exhibits a strong binding potential with TNFR1 and may exert protective effects by targeting TNFR1 to modulate necroptosis and pulmonary and intestinal epithelial barrier damage, ultimately attenuating LPS-induced the lung-intestine injury. By potentially targeting TNFR1, Sal B exerts protective effects on both lung and intestine. These findings underscore the therapeutic potential of Sal B as a novel HDT strategy.

PMID 42176509
Read full article →
PubMedActas dermo-sifiliograficas2026-05-24

Safety Profile of Systemic Therapy for the Management of Psoriasis in Patients With Diabetes Mellitus: Data From the BIOBADADERM Prospective Cohort.

Lluch-Galcerá Juan José JJ, Manuel Carrascosa José J, González-Quesada Alicia A, Sahuquillo Antonio A et al.

Patients with psoriasis and concomitant diabetes mellitus (DM) may be vulnerable to diabetes-related adverse events (DM-AEs). This study aimed to evaluate the incidence of DM-AEs associated with systemic treatments used in patients with psoriasis and DM. We conducted a prospective cohort study using data from the BIOBADADERM registry. We calculated incidence rates (IRs) of DM-AEs for each systemic treatment class, including biologics (tumor necrosis factor [TNF] inhibitors, interleukin [IL]-12/23 inhibitors, IL-17 inhibitors, and IL-23 inhibitors), conventional systemic therapies (methotrexate [MTX], cyclosporine, and acitretin), and apremilast (APR). The primary outcome was the adjusted incidence rate ratio (aIRR) for DM-AEs comparing patients receiving MTX with those receiving other systemic therapies using Poisson regression models adjusted for potential confounders. The study included 732 patients, 1401 treatment cycles, and 2865 person-years (PYs) of follow-up. APR (aIRR, 0.30; 95%CI, 0.10-0.60) was associated with a significantly lower risk of DM-AEs compared with MTX. Cyclosporine (aIRR, 7.50; 95%CI, 3.30-17.30) and acitretin (aIRR, 2.10; 95%CI, 1.20-3.70) were associated with a higher risk compared with MTX. Among patients with psoriasis and DM, APR was associated with a lower incidence of DM-AEs, whereas cyclosporine and acitretin were associated with higher incidences compared with MTX.

PMID 42177023
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about interleukin-2