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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

PubMedCureus2026-10-26

Persistent Type B Hyperlactataemia as a Diagnostic Clue to Occult Diffuse Large B-cell Lymphoma-Associated Haemophagocytic Lymphohistiocytosis.

Hassan Nasiba N, Khatib Kavish K

Haemophagocytic lymphohistiocytosis (HLH) is a rare, life-threatening hyperinflammatory disorder characterised by excessive immune activation. It may be primary or secondary, with secondary HLH associated with a range of triggers; the most common are infections, autoimmune and autoinflammatory conditions, haematological malignancies and other immune‑dysregulatory states. We present a case of a man in his 70s who presented with a two-week history of exertional dyspnoea, profound fatigue and anorexia. Initial investigations demonstrated marked hyperferritinaemia, thrombocytopenia, mild anaemia, cholestatic liver dysfunction and disproportionately elevated lactate without acidosis. Despite intravenous fluids, lactate remained persistently elevated, consistent with type B hyperlactataemia. Computed tomography (CT) of the abdomen and pelvis demonstrated appearances suggestive of hepatitis but no organomegaly, significant lymphadenopathy or biliary obstruction. Despite empirical antibiotics and fluid resuscitation, he developed progressive pancytopenia, worsening liver dysfunction and rising lactate. Further investigations supported secondary HLH, with an HScore of 186, hypertriglyceridaemia and markedly elevated lactate dehydrogenase. Initial treatment with corticosteroids and anakinra resulted in limited response. An autoimmune trigger was initially considered given his Raynaud's phenomenon and ongoing connective tissue disease investigation. However, bone marrow biopsy subsequently confirmed diffuse large B-cell lymphoma (DLBCL). Reduced-dose rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone/prednisolone (R-mini-CHOP) was commenced, resulting in the resolution of hyperlactataemia, normalisation of blood counts and liver function and improvement in performance status. PET-CT after two cycles demonstrated a complete metabolic response. This case highlights the importance of considering secondary HLH in patients with unexplained cytopenias, hyperferritinaemia, liver dysfunction and persistent hyperlactataemia. Persistent hyperlactataemia despite adequate fluid resuscitation should prompt the consideration of systemic causes beyond tissue hypoperfusion. Bone marrow biopsy is crucial for identifying occult malignancy when conventional imaging fails to show overt malignancy. The early recognition of HLH and investigation for an underlying aetiology may facilitate timely definitive treatment.

PMID 42928750
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PubMedInternational journal of rheumatic diseases2026-10-25

Anakinra for the Treatment of Severe Still's Disease Complicated With Macrophage Activation Syndrome.

Guo Jiaxian J, Xu Haojie H, Li Weiwei W, Wang Ying Y et al.

To investigate the efficacy and safety of add-on anakinra for severe Still's disease complicated by macrophage activation syndrome (MAS) in a real-world setting. Consecutive patients aged ≥ 16 years with Still's disease and MAS (HLH-2004 criteria adapted for rheumatic diseases) who received anakinra 100 mg subcutaneously once daily were enrolled. Outcomes were CID, remission, and four EULAR/PReS-aligned targets, assessed at baseline, Day 7, Week 4, Month 3, and Month 6. Glucocorticoid (GC) dose was standardized to prednisone-equivalent mg/kg/day. Eight women (mean age 29.9 ± 12.8 years) were included, and anakinra was initiated at the time of MAS diagnosis in six patients, 2 months after MAS diagnosis in one and 2 months before MAS onset in one. Of the seven patients starting anakinra at or after MAS onset, all achieved Targets 1 and 2 and CID at a median of 1.5 months (range 1-5), and all maintained remission for ≥ 6 months; no severe adverse events were observed. Mean prednisone-equivalent dose fell from 1.63 ± 0.59 to 0.16 ± 0.09 mg/kg/day (p < 0.01). Four patients discontinued anakinra within 6 months for reasons of cost and access rather than disease flare. Add-on therapy with anakinra was associated with rapid achievement of EULAR/PReS targets, sustained remission, and substantial GC sparing in severe Still's disease-associated MAS.

PMID 42924443
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PubMedCureus2026-10-25

Breaking the Storm: Hemophagocytic Lymphohistiocytosis/Macrophage Activation Syndrome as the First Manifestation of Systemic Lupus Erythematosus/Mixed Connective Tissue Disease in an Adolescent Successfully Treated With Anakinra.

Alhasan Ramia R, Alenizi Ahmad T AT, Adly Mahmoud M, Mahmoud Mustafa M et al.

Macrophage activation syndrome (MAS), a form of secondary hemophagocytic lymphohistiocytosis (HLH), is an uncommon but life-threatening complication of autoimmune disease and may occasionally represent the first clinical manifestation of systemic lupus erythematosus (SLE). We describe the case of a previously healthy 15-year-old girl who initially presented with persistent fever, mucocutaneous ulcerations, fatigue, and pancytopenia. Her evaluation revealed low complement levels, elevated lactate dehydrogenase, and splenomegaly, and subsequent serologic testing confirmed new-onset SLE with features of mixed connective tissue disease and Class II lupus nephritis. Although she showed early improvement after receiving corticosteroids and hydroxychloroquine, her condition unexpectedly deteriorated with rising ferritin, hypertriglyceridemia, worsening cytopenias, and progressive liver enzyme elevation, raising concern for an evolving hyperinflammatory syndrome. She ultimately fulfilled five HLH-2004 criteria and had an HScore of 261, indicating a very high probability of HLH/MAS, despite the absence of hemophagocytosis on bone marrow biopsy. Targeted immunomodulatory therapy with anakinra was initiated promptly and resulted in rapid clinical and biochemical improvement. This case highlights the diagnostic challenges of MAS when it emerges in parallel with newly diagnosed SLE, emphasizes the importance of distinguishing MAS from SLE flare or infection, and introduces interleukin-1 blockade as a potential therapeutic option. Early recognition and timely introduction of targeted anti-inflammatory therapy may contribute to rapid stabilization and to be lifesaving when corticosteroids alone are insufficient to halt the cytokine-driven inflammatory cascade.

PMID 42926965
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PubMedSwiss medical weekly2026-10-20

SARS-CoV2-induced Schnitzler syndrome, inflammatory flare and successful treatment by anakinra during pregnancy: a case report.

Weible Louise L, Maurer Britta B, Andina Nicola N, Gilgen Marc Daniel MD

Schnitzler syndrome is a rare acquired autoinflammatory disease characterised by a chronic urticarial rash, recurrent fever, arthralgia or arthritis, bone pain, elevated inflammatory markers, and monoclonal gammopathy. The disease is driven by dysregulated inflammasome activation and excessive interleukin-1 (IL-1) production. Because of its rarity, data on the management of Schnitzler syndrome during pregnancy remain extremely limited. We report the case of a pregnant woman presenting with a SARS-CoV-2-induced inflammatory flare that was successfully treated with anakinra, highlighting both the diagnostic and therapeutic challenges of this uncommon condition in pregnancy. A pregnant woman in her early 40s with previously diagnosed Schnitzler syndrome presented with an acute inflammatory flare triggered by SARS-CoV-2 infection. Clinical manifestations included urticaria and musculoskeletal symptoms consistent with disease reactivation, along with elevated inflammatory markers. The diagnosis of Schnitzler syndrome had previously been established based on clinical criteria, supported by the presence of a chronic urticarial rash and monoclonal gammopathy in accordance with the Strasbourg and Lipsker diagnostic criteria. Due to the severity of the symptoms and the central role of IL-1 in disease pathophysiology, treatment with anakinra, an IL-1 receptor antagonist, was initiated. The patient experienced rapid clinical improvement, with resolution of systemic symptoms and normalisation of inflammatory parameters. Treatment was well tolerated, with favourable maternal and foetal outcomes throughout the pregnancy. This case highlights the importance of recognising Schnitzler syndrome as a rare but potentially severe autoinflammatory condition requiring prompt multidisciplinary management. It also suggests that anakinra may be a potential therapeutic option for inflammatory flares during pregnancy. Early recognition and targeted pharmacological treatment are essential to improving patient outcomes and preventing long-term complications.

PMID 42900176
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PubMedPostepy psychiatrii neurologii2026-10-20

Irreversible paraplegia due to transverse myelitis as a rare complication of CAR T-cell therapy in a patient with B-cell lymphoma.

Lojko-Dankowska Anna A, Dynowski Tomasz T, Machała Michał M, Płotka Anna A et al.

To report a rare case of irreversible paraplegia due to transverse myelitis as a severe neurotoxic complication of chimeric antigen receptor (CAR) T-cell therapy. A 45-year-old woman with primary mediastinal B-cell lymphoma received axicabtagene ciloleucel. She deve-loped Grade 4 neurotoxicity with seizures requiring intubation. Upon regaining consciousness, she presented with flaccid paralysis of the lower limbs, sensory loss, and sphincter dysfunction. Magnetic resonance imaging revealed longitudinally extensive spinal cord lesions. Despite treatment with corticosteroids, anakinra, and intravenous immunoglobulin, no neurological improvement was observed. One year after the therapy, the patient remained in complete remission from lymphoma but was wheelchair-dependent, with persistent paralysis and spinal cord atrophy. This case highlights a rare and severe form of CAR T-cell-related neurotoxicity, manifesting as transverse myelitis in the absence of a marked inflammatory response. The refractory course and lack of standard treatment options underscore the need for greater awareness, reporting, and further research into atypical neurological complications of CAR T-cell therapy.

PMID 42898883
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PubMedCurrent pharmaceutical design2026-10-20

Decoding Pyroptosis in Pulmonary Fibrosis: Molecular Mechanisms and Therapeutic Horizons.

Zheng Shuqi S, Hua Chunlei C, Feng Wanze W, Liu Zengxia Z et al.

Pulmonary fibrosis (PF) is a progressive and fatal interstitial lung disease characterized by the depletion of alveolar epithelial cells (AECs) and the pathological accumulation of extracellular matrix (ECM). Despite its high mortality rate, the molecular drivers of PF progression remain partially understood. Recent evidence suggests that pyroptosis, a pro-inflammatory programmed cell death, plays a pivotal role in orchestrating the inflammatory cascade and fibrotic remodeling in the lung. This study employed bibliometric and visual analysis via CiteSpace 6.2.4 to systematically map the research landscape of pyroptosis in PF using the Web of Science Core Collection (2010-2025). Based on the identified hotspots, a comprehensive review of the molecular activation pathways and cell-specific mechanisms was conducted. Bibliometric analysis (Modularity Q=0.5381, Silhouette S=0.8236) revealed a significant shift in research focus from basic pathological descriptions (2010-2015) to detailed pyroptotic mechanisms (2015- 2020), with immune checkpoint inhibitors emerging as the latest frontier since 2020. Mechanistically, we propose an "Initiation-Amplification-Persistence" model: AEC pyroptosis initiates epithelial barrier disruption; macrophage pyroptosis amplifies the inflammatory storm and polarizes the immune microenvironment; and fibroblast activation sustains ECM deposition. Furthermore, we summarized potential therapeutic interventions, including small molecule synthetic compounds (Nintedanib, Pirfenidone, MCC950, VX-765, etc.), natural products (Lycorine, Tanshinone IIA, etc.) and biologically active substances (Canakinumab, Anakinra) that exhibit multi-pathway synergistic effects. Targeting the pyroptosis signaling axis offers a promising strategy for reversing PF progression. Future research should prioritize the identification of pyroptosis- related biomarkers and the development of lung-targeted delivery systems to facilitate clinical translation and precision intervention.

PMID 42897801
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