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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

PubMedCureus2026-07-27

From Pseudo-Surgical Abdomen to Renal Amyloidosis: Delayed Diagnosis of Familial Mediterranean Fever in an Adolescent.

Azal Hind H, Yahyaoui Sophia S, Kaddouri Said S, Zyani Mohamed M et al.

Familial Mediterranean fever (FMF) is an autosomal recessive autoinflammatory disease characterized by recurrent febrile episodes and serositis. Delayed diagnosis remains a major concern, as it may lead to severe complications, particularly AA amyloidosis. We report the case of a male patient, born to a consanguineous family, with recurrent episodes of fever and abdominal pain since early childhood, initially leading to an unnecessary appendectomy. The diagnosis of FMF was established at the age of 13 following the onset of nephrotic syndrome. Renal biopsy confirmed AA amyloidosis, and genetic testing revealed a homozygous M694V mutation in the MEFV gene. Despite colchicine therapy, persistent disease activity required initiation of anakinra, later switched to canakinumab due to ongoing subclinical inflammation, evidenced by an elevated serum amyloid A level with normal C-reactive protein. This case highlights the consequences of delayed diagnosis in FMF, the importance of early recognition in patients with recurrent abdominal pain, and the role of serum amyloid A in disease monitoring. It also illustrates intrafamilial phenotypic variability and the need for therapeutic escalation in colchicine-resistant disease.

PMID 42504328
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PubMedCurrent opinion in oncology2026-07-25

Haemophagocytic lymphohistiocytosis: a life threatening complication of lymphoma.

Antoine Pierre P

Haemophagocytic lymphohistiocytosis (HLH), a hyperinflammatory syndrome leading to organ damage and death, may arise as a complication of lymphomas (L-HLH). L-HLH diagnosis is challenging and optimal treatment strategies, influenced by factors such as timing of onset, lymphoma subtype and disease severity, remain ill-defined. This narrative review summarises recent evidence to support clinicians in navigating the competing priorities posed by L-HLH, including the urgent need to control inflammation, establish a diagnosis and initiate lymphoma-directed therapy, while minimising toxicity and avoiding unnecessary immunosuppression. While HLH-94 and H-score diagnostic criteria were not specifically designed for L-HLH, the optimised HLH inflammatory index (OHI) was developed in L-HLH patients and predicts the risk of multiorgan failure (MOF) but also benefit from etoposide. Recent evidence also highlights improved survival with early administration of lymphoma targeting drugs while, in critically unwell patients, non-myelosuppressive treatment with anakinra, ruxolitinib and intravenous immunoglobulins (IVIg) might offer a survival advantage. Finally, novel markers such as C-X-C motif chemokine ligand 9 (CXCL-9), recently shown to identify patients responding to interferon γ blockade, might become more widely available in the future. L-HLH encompasses a wide range of clinical presentations that force clinicians to balance competing priorities. Recent evidence improves patients stratification and supports early administration of lymphoma targeting drugs when feasible, etoposide in high risk patients and non-myelosuppressive regimens in critically unwell patients.

PMID 42500863
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PubMedFrontiers in immunology2026-07-25

The cell-mediated adaptive immune response to herpes simplex virus type 1 encephalitis: mechanisms and clinical implications.

Osborne Louise L, Dunai Cordelia C, Huang Yun Y, Egbe Franklyn N FN et al.

Herpes simplex virus (HSV) encephalitis is the most frequent cause of sporadic encephalitis globally. Despite the emergence of the antiviral drug aciclovir curtailing mortality, this disease remains a clinical challenge due to its rapid progression and associated neurological sequelae; indicating the urgent requirement for adjunctive neuroprotective treatment options. Recent studies using both human samples and murine models have highlighted how cell mediated immune cells including CD8+, CD4+ and brain tissue-resident memory T cells have the capacity to act as a 'double-edged sword'; both serving to protect the host against HSV encephalitis, but also increasing neuroglial injury by inflammation. Factors which impair cell-mediated immunity may predispose individuals to herpes simplex encephalitis, including defects in viral immune evasion strategies (infected cell protein 47, UL13 kinase), host genetic pre-disposition (toll-like receptor 3 deficiency, lymphotoxin-α deficiency, Rel mutations) and external factors such as stress. Additionally, there is a particular need for clinical vigilance for patients on immunosuppressive treatments which impair cell-mediated immunity, including azathioprine, hydroxychloroquine and methotrexate. Conversely, understanding these molecular mechanisms may provide new insights into the use of immunomodulatory strategies including anakinra, tocilizumab, and the implementation of targeted vaccination. This review summarises the current state of knowledge of how an impaired cell-mediated immune response could promote herpes simplex virus encephalitis, followed by an exploration of the clinical applications and therapeutic interventions which could viably be implemented to ameliorate immune-mediated tissue injury.

PMID 42500662
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PubMedJournal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia2026-07-25

Cerebrovascular involvement in Erdheim-Chester disease: a case report and systematic literature review.

Delacotte Claire C, Arnaud Charlotte C, de Boysson Hubert H, Aouba Achille A et al.

Intracranial perivascular/vascular infiltrations and stenoses related to Erdheim-Chester disease (ECD), often associated with ischemic events, are rarely documented. This study aims to characterize intracranial perivascular/vascular infiltrations and stenoses. We first report a new case of strokes revealing ECD with intracranial arterial involvement. We then searched all English- and French-language publications from database inception to November 2025 across 12 different search interfaces, including grey literature sources. Vascular involvement was defined by the presence of intracranial perivascular/vascular infiltrations and stenosis on imaging and/or histopathological evidence of small-vessel involvement. Cases with intracranial nodules or masses abutting vessels but without clear longitudinal perivascular infiltration were excluded. We present a case of recurrent strokes with intracranial vertebral and basilar artery wall stenosis, and aortitis. Initially diagnosed as giant cell arteritis, the patient was treated with corticosteroids, cyclophosphamide followed by methotrexate, but relapsed. The identification of tibial osteosclerosis led to the diagnosis of ECD, with a favorable response to anakinra. Twelve relevant articles were retrieved, in addition to our own case. Most patients exhibited focal cerebrovascular signs (11/13) and associated parenchymal involvement (11/13). Intracranial perivascular/vascular infiltrations and stenoses involved the carotid arteries (7/13), the vertebrobasilar arteries (1/13), or both territories (4/13). Aorta was involved in 8/12 cases. Among the nine patients with available follow-up data, five had poor overall or neurovascular outcomes. Intracranial perivascular/vascular infiltrations and stenoses, which leads to recurrent focal ischemic events, represents a likely underdiagnosed CNS pattern in ECD, referred to as "cerebrovascular ECD", which worsens overall prognosis. Vascular imaging should be included in brain MRI protocols for patients with ECD, given the overlap with parenchymal involvement.

PMID 42497572
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PubMedLa Revue de medecine interne2026-07-23

Blocking interleukin-1 in pericarditis: Should we move earlier and stronger?

Michaud Martin M, Jamilloux Yvan Y

Acute pericarditis is generally a benign condition, yet 15-30% of patients will develop recurrent pericarditis. Standard first-line therapy combines non-steroidal anti-inflammatory drugs or aspirin with colchicine, which reduces but does not eliminate the risk of recurrence. Patients presenting with a high inflammatory burden, subacute evolution or large pericardial effusion are particularly prone to recurrence, and corticosteroid exposure - still frequent in clinical practice - further increases this risk. Over the last decade, the central role of interleukin-1 (IL-1) in pericardial inflammation has been demonstrated, and IL-1 inhibitors have emerged as the most effective treatment for colchicine-resistant or corticosteroid-dependent recurrent pericarditis. Anakinra, rilonacept and other IL-1-targeting agents provide rapid symptom resolution and dramatically reduce recurrences, thereby transforming the management of difficult-to-treat forms of the disease. This review summarizes current knowledge on the IL-1 pathway in pericarditis and examines whether earlier, targeted intervention could modify disease trajectory, particularly in patients identified as having a high risk of recurrence at presentation. Drawing parallels with Still's disease, in which early IL-1 inhibition improves long-term outcomes, these data support the need for high-quality trials evaluating IL-1 blockade as a first-line strategy in selected patients with acute pericarditis.

PMID 42486738
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PubMedExpert opinion on biological therapy2026-07-19

Anakinra treatment practices in colchicine-resistant familial Mediterranean fever: a survey of pediatric rheumatologists conducted through the PReS AID-WP and the Turkish pediatric rheumatology associations.

Atamyıldız Uçar Sıla S, Tunce Eray E, Sözeri Betül B

Colchicine-resistant familial Mediterranean fever (cr-FMF) represents a therapeutic challenge, and anakinra, a recombinant interleukin-1 receptor antagonist, is widely used in clinical practice. Our aim was to describe real-world practices of pediatric rheumatologists regarding anakinra use in patients with cr-FMF, with a focus on treatment initiation, tapering strategies, and discontinuation approaches. This survey-based study included pediatric rheumatologists with at least one year of clinical experience in managing cr-FMF. The survey assessed physician characteristics, treatment practices including initiation, tapering, and discontinuation strategies. Data were collected via an online survey platform between September and November 2025. A total of 81 pediatric rheumatologists participated, mostly practicing in Türkiye (92.6%). Most respondents preferred once-daily anakinra at 1-2 mg/kg/day and assessed response within the first month. Among tapering strategies, 90.1% favored interval extension, most commonly every 3 days or weekly. 79.0% considered discontinuation after sustained remission (median 6 months). During tapering-related flares, clinicians preferred interval shortening (43.2%) or dose escalation (37.0%), while 19.8% switched to an alternative biologic. After discontinuation-related relapse, 81.5% restarted anakinra at the previous effective dose. While anakinra initiation and relapse management appear relatively consistent, tapering and discontinuation strategies remain highly variable, underscoring the need for evidence-based guidance.

PMID 42471760
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