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

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

PubMedMedicine2026-09-19

The NF-κB pathway in inflammatory responses in preeclampsia: A systematic review and meta-analysis.

Zhang Hui H, Nong Yanhua Y, Huang Meiqi M, Wei Riyuan R et al.

Preeclampsia is a pregnancy-specific hypertensive disorder associated with systemic inflammation, endothelial dysfunction, and adverse maternal and fetal outcomes. The nuclear factor kappa B (NF-κB) signaling pathway has been implicated in inflammatory activation, but its role in preeclampsia remains incompletely defined. This systematic review and meta-analysis aimed to evaluate the association between NF-κB pathway activation and inflammatory responses in preeclampsia. This meta-analysis reviewed 15 peer-reviewed articles focusing on the involvement of the NF-κB pathway in preeclampsia. Quantitative assessments included changes in systolic and diastolic blood pressure and levels of key inflammatory mediators, including tumor necrosis factor-alpha (TNF-α), interleukin-1 beta, interleukin-6 (IL-6), and NF-κB. Systolic and diastolic blood pressure were significantly elevated in patients with preeclampsia. TNF-α and NF-κB levels were also significantly increased, indicating enhanced inflammatory activation associated with the disease. In contrast, interleukin-1 beta and IL-6 levels did not differ significantly, although IL-6 showed a nonsignificant trend toward increased levels. This meta-analysis suggests that NF-κB activation, together with increased TNF-α levels, may contribute to the inflammatory pathophysiology of preeclampsia. These findings support further investigation of NF-κB-related pathways, including Sirtuin 1-mediated regulation, as potential biomarkers and therapeutic targets.

PubMedApplied biochemistry and biotechnology2026-09-19

Antiproliferative Effects of Reynoutrin via Modulation of Oxidative Stress, Inflammation, and Apoptosis in Breast Cancer (MCF-7) and Prostate Cancer (PC-3) Cell Lines.

Gökmen Sedat S, Çinar İrfan İ

Reynoutrin, a bioactive flavonoid, exhibits various biological effects. Despite its toxic side effects, cisplatin is widely used to treat malignancies. This study aimed to assess the in vitro antiproliferative activity of reynoutrin in MCF-7 and PC-3 cell lines by evaluating its effects on inflammation, oxidative stress, and apoptosis-related pathways. The cytotoxic effects of reynoutrin on MCF-7 and PC-3 cells were evaluated using an MTT assay after 24 h. Total antioxidant status (TAS) and total oxidant status (TOS) were measured using ELISA kits. The mRNA expression levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, caspase-3, caspase-9, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) were analyzed by RT-qPCR. Apoptotic morphological changes were assessed by Hoechst staining. Reynoutrin inhibited MCF-7 and PC-3 cell viability in a dose-dependent manner, with IC₅₀ values of 220 and 412 µg/mL, respectively. Reynoutrin increased TOS and decreased TAS (p < 0.05), indicating an increase in oxidative stress. RT-qPCR showed that TNF-α, IL-1β, and IL-6 mRNA expression levels decreased in a dose-dependent manner following reynoutrin treatment in MCF-7 and PC-3 cells (p < 0.05), suggesting anti-inflammatory effects. In both cancer cell lines, reynoutrin increased caspase-3 and caspase-9 mRNA expression levels and decreased the Bcl-2/Bax expression ratio in a dose-dependent manner (p < 0.05). These findings suggest that reynoutrin exerts antiproliferative effects that are associated with modulation of inflammatory, oxidative stress, and apoptosis-related pathways in cancer cells, highlighting its potential as a natural candidate for further investigation as an anticancer agent.

PubMedFrontiers in pharmacology2026-09-19

Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury.

Yasar Yesim Kaya YK, Sezgin Esra Tuba ET, Suleyman Bahadir B, Mammadov Renad R et al.

In this study, the potential protective effects of adenosine triphosphate (ATP) and glutathione (GSH) against atezolizumab-induced cardiac injury in rat heart tissue were investigated. A total of 24 male albino Wistar rats were used in the experiment. The animals were divided into four groups: healthy group adenosine triphosphate + atezolizumab (ATAZ), GSH + atezolizumab (GHAZ), and atezolizumab alone (ATZ). ATP was administered intraperitoneally at a dose of 4 mg/kg, while GSH was administered orally at a dose of 200 mg/kg for 7 days. Atezolizumab was administered intraperitoneally to the experimental groups at a dose of 10 mg/kg twice weekly. At the end of the experiment, malondialdehyde total glutathione (tGSH), superoxide dismutase catalase, interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in heart tissues were measured using biochemical methods. In addition, histopathological and immunofluorescence examinations were performed. The results showed that oxidative stress and inflammation markers increased, whereas antioxidant parameters decreased in the atezolizumab-treated group. ATP and GSH administration significantly attenuated these changes and exerted protective effects on cardiac tissue. Overall, ATP and GSH ameliorated the biochemical, histopathological, and immunofluorescence changes associated with atezolizumab-induced cardiac injury in this experimental model.

PubMedFrontiers in immunology2026-09-19

Immunological dysregulation of follicular helper T cells, follicular regulatory T cells, and follicular cytotoxic T cells is associated with disease activity and identifies exploratory immune patterns in rheumatoid arthritis.

Fan Yuxin Y, Li Baochen B, Wu Ruihe R, Liu Xiaoyang X et al.

The onset and progression of rheumatoid arthritis (RA) are linked to autoantibody production driven by dysregulated germinal center (GC) responses. Follicular helper T cells (Tfh), follicular regulatory T cells (Tfr), and follicular cytotoxic T cells (Tfc) are important components of follicular immune regulation. However, the circulating profiles and clinical associations of these three cell subsets in the peripheral blood of RA patients remain underexplored through systematic investigations, and the specific function of Tfc cells in RA remains incompletely understood. In the present study, peripheral blood samples were collected from 41 patients with RA and 16 healthy controls (HCs). Modified flow cytometry was employed to detect circulating Tfh, Tfr, and Tfc cells, with the aim of systematically investigating the clinical and immunological implications of these cell subsets in RA. (1) RA patients exhibited a disrupted Tfh/Tfr ratio in peripheral blood, accompanied by an elevated proportion of Tfc cells, both of which correlated with disease activity and autoantibody levels. (2) The ratio of Tfh/Tfr and the proportion of Tfc cells were significantly increased in patients with high disease activity of RA. (3) The frequency of Tfc cells showed a positive correlation with the frequency of Tfh cells and soluble interleukin-2 receptor (sIL-2R) levels. (4) Based on k-means unsupervised clustering analysis, patients with RA were grouped into three exploratory follicular T-cell-associated immune patterns: Cluster 3 patients displayed the highest disease activity, while Cluster 2 patients presented with the lowest white blood cell count. The dynamic imbalance of the circulating Tfh/Tfr/Tfc cells may reflect immune dysregulation in RA. The expansion of Tfc cells may be associated with systemic immune activation in RA. Exploratory clustering analysis further identified distinct follicular T-cell-associated immune patterns, providing new insights into RA immunological heterogeneity.

PubMedCell death discovery2026-09-19

Immunogenic cell death as a mechanism of synergy between sunitinib and 177Lu-DOTATATE peptide receptor radionuclide therapy in pancreatic neuroendocrine tumors.

Essler Markus M, Veit Nadine N, Müller Aurelia A, Marinova Milka M et al.

Peptide receptor radionuclide therapy (PRRT) with ¹⁷⁷Lu-DOTATATE improves outcomes in neuroendocrine tumors (NETs), yet durable disease control remains limited in progressive pancreatic NET (pNET) and higher-grade disease. Combinations that enhance PRRT efficacy may be advantageous. As sunitinib has radiosensitizing and immunomodulatory effects, we explored the clinical activity and mechanistic basis of combining sunitinib with PRRT. Combination treatment with ¹⁷⁷Lu-DOTATATE (1-3 cycles; 7.4 GBq per cycle) and sunitinib at 37.5 mg/day was well tolerated and effective in a pilot group of heavily pretreated pNET patients with progressive disease. Treatment response was assessed by ⁶⁸Ga-DOTATOC PET/CT and serum tumor markers (CgA, NSE). Mechanistic studies were performed in QGP-1 pNET cells using proliferation and apoptosis assays, cell-cycle analysis, and immunogenic cell death (ICD) markers. Combination therapy was well tolerated and induced marked responses: three patients achieved near-complete responses and two partial responses on post-therapy ⁶⁸Ga-DOTATOC PET/CT. In vitro, ¹⁷⁷Lu-DOTATATE and sunitinib showed bidirectional sensitization: low-dose sunitinib reduced the LD50 of ¹⁷⁷Lu-DOTATATE, and low-activity ¹⁷⁷Lu-DOTATATE reduced the LD50 of sunitinib. ¹⁷⁷Lu-DOTATATE induced dose-dependent PARP cleavage and S/G2-M arrest; however, sunitinib shifted cell death toward late apoptosis/necrosis. The combination produced a more-than-additive increase in calreticulin exposure on the tumor cell surface and enhanced HMGB1 but not interleukin- 1ß- or interleukin-18-release compared with either monotherapy, indicating immunogenic late apoptosis/necrosis, without canonical inflammasome activation. Intermittent sunitinib combined with ¹⁷⁷Lu-DOTATATE PRRT demonstrated encouraging activity in progressive pNET. The mechanism of synergy in vitro was enhanced ICD, suggesting that immune responses contribute to the synergy in vivo.

PubMedTheScientificWorldJournal2026-09-19

Evaluating Safety and Efficacy of Bio-Immune (Andrographolide) in Managing URTI Symptoms: A Randomized, Double-Blinded, Placebo-Controlled, Single-Center, Comparative Study.

Singh Shashi Chandrama SC, Choudhary Muskan M, Choudhary Khushi K, Singh Harsh Pal HP

Bio-Immune is a standardized extract containing andrographolide, a diterpenoid lactone derived from the aerial parts of Andrographis paniculata (commonly known as Kalmegh), and the carrier, 2-hydroxypropyl beta-cyclodextrin. Kalmegh has long been used to treat uncomplicated upper respiratory tract infection (URTI) in complementary and alternative medicine. A randomized, double-blind, placebo-controlled clinical trial was conducted to evaluate the efficacy of Bio-Immune (≥ 17% w/w andrographolide content). Participants were randomized to receive either 100 mg Bio-Immune twice daily or placebo for a 5-day intervention period (Clinical trial registration number: CTRI/2024/12/077632, Registered 4, December 2024). The primary outcome measure was the Wisconsin Upper Respiratory Symptom Survey-21 (WURSS-21) score; secondary outcomes included Visual Analogue Scale (VAS) and Numeric Rating Scale (NRS) scores, nasal mucus weight, C-reactive protein (CRP), Interleukin-8 (IL-8), and Immunoglobulin A (IgA) in nasal wash, along with safety. Of 67 screened participants, 56 were enrolled, and 55 completed the study. The WURSS-21, VAS, and NRS scores in the Bio-Immune group improved, with statistically significant reductions suggesting relief from symptoms associated with uncomplicated URTI and sustained functional improvement owing to Bio-Immune supplementation. Although the placebo group showed gradual improvement over time, the speed and magnitude of recovery were consistently and statistically superior in the Bio-Immune cohort, with significant changes evident by 6 h after supplementation. Furthermore, a significant reduction in nasal mucus weight was observed by Day 5, accompanied by minor downward trends in CRP and IL-8, which lacked adequate statistical support. No adverse events were reported during the intervention period. Clinical findings support the efficacy of Bio-Immune at a lower dose in providing URTI symptom relief compared with placebo in a shorter intervention period. Clinical Trial Registry of India: CTRI/2024/12/077632; ClinicalTrials.gov identifier: NCT06689995.

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about interleukin-2