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interleukin-2 (Interking)

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Shenzhen Neptunus · IL2RA · 重组蛋白

什么是 interleukin-2？

interleukin-2 是一种重组蛋白，由Shenzhen Neptunus研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名Interking
公司Shenzhen Neptunus
药物类别重组蛋白
分子靶点IL2RA
给药途径Injectable (Others), Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Shenzhen Neptunus

作用机制

分子靶点

interleukin-2 作用于 1 个分子靶点：

IL2RAinterleukin 2 receptor subunit alpha (IL2R, TCGFR)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

interleukin-2 针对 15 个适应症，涉及 4 个治疗领域。

治疗领域疾病/病症分期
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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相关研究文献

PubMedThe Journal of biological chemistry2026-08-06

Peptides containing SARS-CoV-2 spike-protein residues are antagonists of α7 and α9α10 nAChRs and modulate interleukin-1β release from human monocytes.

Hone Arik J AJ, Richter Katrin K, Riaz Zoha Z, Wakkuri Joseph J et al.

Immune system dysregulation during COVID-19 illness remains an area of intense investigation. Excessive release of proinflammatory cytokines and multi-organ injury suggest aberrant control of the immune system. Given the established role of nicotinic acetylcholine receptors (nAChRs) in modulating inflammatory responses, we explored the possibility that the SARS-CoV-2 spike-protein may directly perturb this regulatory pathway. The spike protein contains a furin cleavage-site with sequence similarities to α-neurotoxins known to antagonize α7, α9, and α10 nAChR subtypes. To test whether this region of the spike protein can influence nAChR function, we synthesized short peptides corresponding to putative nAChR-interacting domains from several SARS-CoV-2 variants. Electrophysiological recordings from Xenopus laevis oocytes expressing human nAChRs revealed potent, virus-variant dependent inhibition of nAChR activity. In human monocytic THP-1 cells, these peptides reversed acetylcholine-mediated suppression of interleukin-1β release. Our findings identify a potential molecular mechanism by which SARS-CoV-2 may directly suppress nAChR signaling on immune cells thereby amplifying inflammatory cytokine release. This work supports the broader concept that structural motifs present in the SARS-CoV-2 spike-protein can disrupt cholinergic anti-inflammatory pathways and elucidates a mechanism that may contribute to the pathophysiology and immune system dysregulation that can occur in severe COVID-19.

PMID 42556725
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PubMedComputational and structural biotechnology journal2026-08-06

Computational Modeling of Pro-inflammatory Cytokine-Enhanced Blood Coagulation.

Li Geli G, Zhao Chen C, Frydman Galit H GH, Li He H

The interplay between inflammation and coagulation is a central driver of thrombotic risk across various diseases. While mathematical models of blood coagulation are well established, there remains a critical gap in quantitative frameworks that capture inflammation-induced hypercoagulability. In this study, we develop a mathematical model that explicitly simulates the interaction between pro-inflammatory cytokines and the coagulation cascade. The model incorporates key mechanisms, including: (a) up-regulation of tissue factor by interleukin-1𝛽, interleukin-6, and tumor necrosis factor-α; (b) suppression of natural anticoagulants, namely, antithrombin III and tissue factor pathway inhibitor, by interleukin-6 and tumor necrosis factor-α; and (c) feedback amplification of pro-inflammatory cytokines by thrombin. By encoding the bidirectional feedback between inflammatory and coagulation pathways, the model captures essential features of inflammation-driven hypercoagulability and enables systematic quantification of how variability in inflammatory extent and duration result in heterogeneous thrombin generation (TG) dynamics. To evaluate its effectiveness, we integrate the model with TG assays and apply it to virtual patient cohorts representing 4 clinically distinct conditions: COVID-19, sickle cell disease, type 2 diabetes mellitus and hemophilia A. Model simulations predict that disease-specific inflammatory environments induce distinct shifts in TG dynamics. In COVID-19 and type 2 diabetes mellitus, elevated cytokine levels lead to shortened lag times and increased thrombin peak, whereas in sickle cell disease, shortened lag times are accompanied by a reduced thrombin peak. These effects are strongly modulated by both cytokine concentration and duration of exposure. These results demonstrate that the proposed computational model augments conventional TG assays by mechanistically linking inflammatory signaling to disease-specific coagulation responses. Collectively, the proposed computational framework extends conventional TG assays by considering the interplay between inflammation and coagulation, thereby providing a mechanistic exploratory platform for generating testable hypotheses regarding disease-specific thromboinflammatory regulation. This framework lays a foundation to support future clinical prediction or individualized therapeutic decision-making after validation using prospective patient-level longitudinal datasets.

PMID 42558747
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PubMedDiseases of the colon and rectum2026-08-06

Electroacupuncture for Postoperative Gastrointestinal Recovery After Laparoscopic Colorectal Cancer Resection: A Randomized Controlled Trial Electroacupuncture Fastens Recovery.

Li Haoyang H, Cai Yuling Y, Wang Ye Y, Yi Chen C et al.

Globally, the disease burden of colorectal cancer has been gradually increasing. Radical resection is the cornerstone treatment for colorectal cancer, but postoperative gastrointestinal dysfunction has been a potential complication. Current therapies are unsatisfactory. Acupuncture has the merits of inexpensive and easy-operative and has the potential to be a promising strategy. This study aimed to observe the effect and safety of electroacupuncture in facilitating the postoperative recovery of colorectal cancer patients. Randomized controlled study. Prospective, single-center study. Patients over 18 years old who undergone radical resection of colorectal cancer. Electroacupuncture or sham electroacupuncture at 2h after surgery and on the morning of the first 2 days after surgery, with 30 minutes each session. The primary outcome was first flatus time. Secondary outcomes included first oral feeding time, bowel sound recovery time, length of postoperative hospitalization, adverse events, serum inflammatory cytokine indicators and heart rate variability indicators. One hundred fifteen patients met the inclusion criteria and 101 patients completed the treatment and were enrolled into statistical analysis. There was no statistically significant difference (p > 0.05) in baselines. First flatus time, first oral feeding time, bowel sound recovery time were improved in electroacupuncture group (p < 0.05). Length of postoperative hospitalization was not significantly different. On postoperative day 1, interleukin-1β was lower in electroacupuncture group (p < 0.05); On postoperative day 3, interleukin -1 β, and interleukin -6 were lower in electroacupuncture group (p < 0.05). Percentage of difference between adjacent normal RR intervals exceeding 50ms and high frequency were higher in electroacupuncture group (p < 0.05). Kaplan-Meier curve analysis, multiple linear regression and correlation analysis secured the stability of the main results. This is a single-center trial with a small sample size and long-term follow-up was absent. No blank control group was set. EA facilitated postoperative recovery without increasing the incidence of complications. This effect was hypothesized to be related to lower IL-1β/IL-6 levels and the rebalance of autonomic nervous system. See Video Abstract.Clinical trial registration: The trial has been registered at chictr.org.cn (ChiCTR2100050660 https://www.chictr.org.cn/hvshowproject.html?id=167502&v=1.9).

PMID 42559736
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PubMedThe Annals of pharmacotherapy2026-08-06

Depemokimab-ulaa: A Long-Acting Interleukin-5 Inhibitor.

Linenfelser Lauren L, Lipari Melissa M, Kale-Pradhan Pramodini P

To review the pharmacology, efficacy, and safety of subcutaneous depemokimab-ulaa as add-on therapy in the treatment of severe eosinophilic asthma. PubMed database, Embase, and ClinicalTrials.gov were searched using the following terms: depemokimab, depemokimab-ulaa, Exdensur, and GSK3511294. Articles published in English between January 2020 and March 2026, related to pharmacology, safety, efficacy, and clinical trials, were reviewed. Four studies met inclusion criteria. In phase 3 trials, SWIFT-1 and SWIFT-2, depemokimab-ulaa demonstrated comparable reductions in elevated blood eosinophil (EOS) counts when compared to other interleukin-5 (IL-5) targeting therapies in patients with severe eosinophilic asthma. The annualized exacerbation rates were 0.46 and 0.56 with depemokimab-ulaa vs 1.11 and 1.08 with placebo (P < .001), respectively. There were no differences in other outcomes that were studied. In the phase 3 NIMBLE trial, depemokimab-ulaa did not meet the noninferiority margin when patients were switched from other anti-IL-5 therapies. Depemokimab-ulaa maintained a favorable safety profile, with no serious adverse events or deaths considered to be related to the drug.Relevance to Patient Care and Clinical Practice in Comparison to Existing Drugs:When compared with other anti-IL-5 agents, depemokimab-ulaa might serve as an effective alternative option with its twice-yearly dosing offering a significant advantage potentially improving patient adherence and clinical outcomes. Depemokimab-ulaa's twice-yearly dosing offers a convenient alternative to other anti-IL-5 therapies as add-on treatment for severe eosinophilic asthma.

PMID 42557941
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PubMedCell reports. Medicine2026-08-06

Phase 1 study of intracranial T cell therapy with pemetrexed for refractory brain metastases and glioblastomas.

Li Congcong C, Wang Shuang S, Rong Xiumei X, Zeng Chuxiong C et al.

Therapeutic options remain limited for advanced intracranial malignancies, including brain metastases and glioblastomas, particularly in patients ineligible for surgery, radiotherapy, or systemic therapies. This phase 1 study evaluates the safety and feasibility of intracranial administration of low-dose pemetrexed followed by RetroNectin-activated killer cells (RAKs) and interleukin 2 via an Ommaya reservoir (collectively referred to as SCOPE-T) in 25 patients with refractory intracranial malignancies. Nineteen patients completed at least one treatment cycle, and 17 received the maximum tested RAK dose (5 × 108 cells). Treatment is well tolerated, with no treatment-related adverse events greater than grade 2; transient fever and headache are the most common toxicities. Exploratory radiographic and clinical assessments suggest disease stabilization in evaluable patients. These findings support the feasibility and safety of intracranial SCOPE-T and indicate preliminary signals of therapeutic activity. Given the small sample size and non-randomized design, the results should be interpreted as exploratory (ClinicalTrials.gov: NCT05459441).

PMID 42556340
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PubMedNagoya journal of medical science2026-08-06

Keratotic macules and plaques with mild erythema in deficiency of interleukin 36 receptor antagonist cases with monoallelic pathogenic variants of IL36RN.

Omi Michiya M, Takeichi Takuya T, Tanahashi Kana K, Adachi Hidesada H et al.

Classic deficiency of interleukin-36 (IL-36) receptor antagonist (DITRA) is characterized by severe, recurrent generalized pustular psoriasis (GPP) with systemic inflammation and is typically caused by biallelic IL36RN variants. However, monoallelic c.115+6T>C and c.28C>T variants of IL36RN have also been reported to underlie DITRA. To the best of our knowledge, no cases of a heterozygous IL36RN c.28C>T variant presenting with the unilateral localization of symptoms have been reported. Our present case emphasize that IL36RN-related disease should be considered even with the atypical skin symptoms, thereby broadening the spectrum of DITRA.

PMID 42558832
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