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anakinra (PerkinRA)

✓ Approved

PersisGen Par · IL1R1 · 重组蛋白

什么是 anakinra？

anakinra 是一种重组蛋白，由PersisGen Par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PerkinRA
公司PersisGen Par
药物类别重组蛋白
分子靶点IL1R1
给药途径Injectable (Others), Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, PersisGen Par

作用机制

分子靶点

anakinra 作用于 1 个分子靶点：

IL1R1interleukin 1 receptor type 1 (P80, CD121A)
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

anakinra 针对 11 个适应症，涉及 5 个治疗领域。

治疗领域疾病/病症分期
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Musculoskeletal and connective tissue disordersStill's disease✓ Approved
Musculoskeletal and connective tissue disordersJuvenile idiopathic arthritis✓ Approved
Congenital, familial and genetic disordersChronic infantile neurological cutaneous and articular syndrome✓ Approved
Congenital, familial and genetic disordersMuckle-Wells syndrome✓ Approved

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相关研究文献

PubMedCancers2026-06-12

Prophylactic Anakinra to Prevent Neurotoxicity After CAR T-Cell Therapy in Aggressive B-Cell Lymphomas: A Single-Center Real-World Experience.

Schmid Tina T, Shaforostova Inna I, Bacher Ulrike U, Seipel Katja K et al.

Background/Objectives: Chimeric antigen receptor T-cell (CAR T) therapy is an effective treatment for relapsed/refractory (r/r) aggressive B-cell lymphomas; however, acute toxicities, such as immune effector cell-associated neurotoxicity syndrome (ICANS), remain common. Interleukin-1 (IL-1) has been implicated in the pathogenesis of ICANS, suggesting that prophylactic anakinra, an IL-1 receptor antagonist, might reduce its incidence or severity. Methods: We retrospectively analyzed 80 patients with B-cell lymphomas who received CD19-directed CAR T-cell therapy (tisagenlecleucel, axicabtagene ciloleucel, or lisocabtagene maraleucel) at the Bern University Hospital between April 2019 and June 2022. One cohort received prophylactic anakinra (100 mg subcutaneously on days 0 to +6 post-infusion), while the comparison cohort did not. Results: The incidence of ICANS was similar between groups (14 patients, 35%) with anakinra vs. 10 (25%) in the standard cohort (p = 0.464). Rates of grade 3 ICANS were also comparable (eight (20%) vs. seven (18%), p > 0.999). Among patients who developed ICANS, median hospitalization was numerically shorter with anakinra (27 vs. 40 days, p = 0.077). Anakinra did not impair CAR T-cell expansion and was well tolerated, with no treatment-related adverse events. Survival outcomes, including overall survival (OS) and progression-free survival (PFS), were similar between cohorts. Conclusions: In summary, prophylactic anakinra did not reduce the incidence or severity of ICANS in our analysis; however, it may be associated with shorter hospitalization in affected patients. Whether this reflects a direct therapeutic effect or improved overall toxicity management remains uncertain. Larger prospective studies are warranted to further clarify the role of anakinra for prophylactic treatment of ICANS following CAR T-cell therapy.

PMID 42279369
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PubMedJoint bone spine2026-06-12

Club Rhumatismes et Inflammation guidelines for anti-interleukin-1 therapy: 2026 update.

Mitrovic Stéphane S, Delplanque Marion M, Ea Hang-Korng HK, Frémond Marie-Louise ML et al.

Interleukin-1 inhibitors (anti-IL-1 agents) are an essential therapeutic class in the management of autoinflammatory diseases (AIDs). The latest version of the Club Rhumatismes et Inflammations (CRI) guidelines for anti-IL-1 therapy dates from 2014. The present work aimed to update the CRI guidelines. A group of 13 writers (6 rheumatologists, 3 internists, and 4 paediatricians) who are experts in AIDs conducted a rigorous review of the literature up to November 2025 in their respective fields of expertise to write each guideline area. All guidelines were reviewed by the two scientific coordinators. The update concerned only the two anti-IL-1 molecules available in France and most European countries: anakinra and canakinumab. A total of 20 sets of guidelines were written on pre-treatment assessment and follow-up of patients on anti-IL-1 therapy as well as the course of action to be taken in the event of bacterial or viral infections, solid or haematological neoplasia, haematologic biological abnormalities, cardiovascular conditions, skin or systemic intolerance, autoimmune or demyelinating conditions, biological hepatitis, macrophage activation syndrome, renal failure or dialysis, drug combinations, surgery, dental care, burns or trauma, pregnancy, use of anti-IL-1 agents in low-weight children, vaccination, travel, Kawasaki disease, recurrent pericarditis, acute gout attacks and Schnitzler syndrome. These guidelines are a practical tool for clinicians, summarizing the course of action to be taken in clinical situations they may encounter, based on the latest scientific data on efficacy and tolerance.

PMID 42276158
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PubMedFrontiers in immunology2026-06-08

Dynamic hyperinflammatory response assessment using HIC scores in COVID-19: application to a large series of patients receiving anakinra.

Amikishiyev Shirkhan S, Deniz Rabia R, Gunver Mehmet Guven MG, Aghamuradov Sarvan S et al.

Hyperinflammatory responses substantially contribute to morbidity and mortality in severe COVID-19 and share features with secondary hemophagocytic lymphohistiocytosis and macrophage activation syndrome. The Hyperinflammation in COVID-19 (HIC) criteria allow early diagnosis and may provide a framework for dynamic treatment monitoring. We retrospectively analyzed 218 hospitalized patients with hyperinflammation (HIC ≥35) who received anakinra at a tertiary referral center. The daily anakinra dose (100-800 mg/day, administered intravenously or subcutaneously) was adjusted according to clinical and laboratory parameters. The primary outcome was in-hospital mortality. Secondary outcomes included time to ≥50% CRP reduction, ICU admission, mechanical ventilation, and dynamic changes in ΔHIC and inflammatory biomarkers. Overall mortality was 12.8%. Survivors achieved earlier CRP reduction than non-survivors (3.1 vs. 4.7 days) and showed a progressive decline in HIC, whereas non-survivors had persistently elevated or rising scores. Divergence in ΔHIC and other parameters, including neutrophil count, D-dimer, LDH, procalcitonin, and creatine kinase, emerged within 3-4 days. ROC analysis demonstrated that HIC on the day of anakinra initiation and at the final assessment discriminated survivors from non-survivors (AUC 0.75, p < 0.001; cut-offs 70.8 and 66.5, with high sensitivity but moderate specificity), whereas baseline and first-response-day HIC had limited predictive value (AUC approximately 0.50-0.55) . These findings support the HIC score as both a diagnostic and dynamic monitoring tool during IL-1 blockade. Initiating anakinra when HIC is ≥35 but <70, and reassessing treatment response after 3-4 days using ΔHIC together with CRP kinetics, may help optimize outcomes.

PMID 42253999
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PubMedPediatric rheumatology online journal2026-06-05

Breaking the storm: canakinumab as salvage therapy for refractory macrophage activation syndrome in pediatric systemic lupus erythematosus-a case report.

Selvarajan Tarun T, Kannekanti Lavanya L, Green Ashlyn A, Smith Alexandra Zamora AZ et al.

Macrophage activation syndrome (MAS) complicating pediatric systemic lupus erythematosus (cSLE) is a life-threatening hyperinflammatory state driven by dysregulated cytokine release. A recent systematic literature review identified only a limited number of cSLE-MAS cases treated with IL-1 inhibitors, with variable efficacy, underscoring the need for evidence-based salvage strategies when first-line biologic therapy fails. We report a 17-year-old female with cSLE who developed secondary hemophagocytic lymphohistiocytosis/MAS fulfilling HLH-2004 criteria approximately 17 months after initial diagnosis, in the setting of medication nonadherence and nutritional failure. The MAS course was refractory to intravenous immunoglobulin, pulse methylprednisolone, dexamethasone, cyclosporine, and intravenous anakinra, and was further complicated by a secondary Clostridioides difficile superinfection precipitating a MAS flare with ferritin peaking at > 10,000 ng/mL. Following transfer to our institution, subcutaneous canakinumab at standard weight-based dosing produced prompt defervescence, sustained ferritin normalization, and clinical stabilization permitting transition to outpatient immunomodulation. This case highlights canakinumab as a viable salvage therapeutic option for patients with biologic-refractory cSLE-MAS. Emerging evidence supports an expanding role for selective IL-1β blockade in pediatric lupus-associated hyperinflammatory syndromes; prospective studies are needed to define optimal dosing, sequencing, and treatment duration.

PMID 42243916
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PubMedExpert review of hematology2026-06-03

Managing cytokine release syndrome in hematological malignancies being treated with CAR-T cell therapy.

Alarcon Tomas Ana A, Segura Alicia A, Chavez Julio J

Cytokine release syndrome (CRS) is a potentially life-threatening toxicity associated with chimeric antigen receptor (CAR)-T cell therapy, particularly in hematological malignancies. As CAR-T therapies are increasingly integrated into clinical practice, managing CRS effectively is critical to maximizing therapeutic benefit while minimizing harm. This review provides a comprehensive overview of CRS in the context of CAR-T therapy for hematologic cancers. It outlines the current definitions and grading systems, highlights key aspects of CRS pathophysiology, and analyzes the incidence and severity of CRS across pivotal clinical trials in large B-cell lymphoma, acute lymphoblastic leukemia, and multiple myeloma. Standard management approaches, including anti-cytokine therapies and corticosteroids, are discussed alongside emerging strategies such as early intervention and prophylaxis using anakinra and corticosteroids. The review is informed by a structured evaluation of clinical studies and real-world data, reflecting evolving treatment paradigms. CRS remains a major challenge, therefore early recognition, standardized grading, and targeted intervention will improve outcomes. Future efforts should focus on predictive biomarkers, personalized prophylaxis, and next-generation CAR constructs to reduce toxicity. The real-world experience mirrors trial data, reinforcing the reproducibility and scalability of these evolving management strategies.

PMID 42233607
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PubMedScience China. Life sciences2026-06-02

Immune interventions in stroke: current progress and perspectives.

Guo Cunle C, Guan Di D, Liu Qiang Q, Han Zhaoli Z

Acute ischemic stroke (AIS) is a devastating cerebrovascular disorder associated with high morbidity, mortality, and long-term disability, where neuroinflammation serves as a central pathogenic driver mediating secondary brain injury and functional impairment. This comprehensive review synthesizes the latest advances in neuroimmune interventions for AIS over the past decade, drawing on systematic literature retrieval from PubMed, Web of Science, Embase, and Ovid Medicine. We first delineate the dual pro-inflammatory and anti-inflammatory mechanisms of key immune cells-including microglia, astrocytes, T cells, B cells, natural killer (NK) cells, monocytes, and neutrophils-in the ischemic brain. Specifically, we highlight their dynamic phenotypic polarization, intercellular crosstalk, and regulatory roles in shaping the post-ischemic immune microenvironment, which provides a theoretical basis for targeted immune interventions. Subsequently, we systematically summarize the clinical research progress on promising therapeutic strategies, encompassing traditional and novel agents such as tirofiban, methylprednisolone, natalizumab, fingolimod combined with alteplase, edaravone dexborneol, butylphthalide, JAK/STAT pathway inhibitors, ApTOLL, anakinra, and tocilizumab, as well as cell transplantation therapies. For each intervention, we analyze its efficacy, safety, underlying immune-modulatory mechanisms, and current clinical trial status. Finally, we discuss the existing challenges in clinical translation-such as suboptimal targeting efficiency, individual variability in treatment response, and unresolved safety concerns-and prospect future directions for precision immune therapy in AIS. This review offers a comprehensive and up-to-date overview of the neuroimmune landscape in AIS, providing valuable insights for researchers and clinicians engaged in stroke treatment and drug development.

PMID 42228253
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