Drug Database
AN

anakinra (PerkinRA)

✓ Approved

PersisGen Par · IL1R1 · Recombinant Proteins

What is anakinra?

anakinra is a recombinant proteins developed by PersisGen Par. It is approved for therapeutic indications via injectable (others) or intravenous (iv) or subcutaneous injection.

Drug Profile

Brand NamesPerkinRA
CompanyPersisGen Par
Drug ClassRecombinant Proteins
Molecular TargetIL1R1
RouteInjectable (Others), Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, PersisGen Par

Mechanism of Action

Molecular Targets

anakinra acts on 1 molecular target:

IL1R1interleukin 1 receptor type 1 (P80, CD121A)
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Therapeutic Indications

anakinra is developed for 11 unique indications across 5 therapeutic areas.

Therapeutic AreaConditionPhase
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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Related Research Articles

PubMedClinical rheumatology2026-11-10

Clinical and laboratory outcomes during sequential anakinra and canakinumab treatment in familial Mediterranean fever: a retrospective within-patient study.

Kaya Mehmet Nur MN, Kılıç Özlem Ö, Tecer Duygu D, Yılmaz Sedat S

To describe clinical, laboratory, disease-severity, and safety outcomes after switching from anakinra to canakinumab in FMF patients who required treatment change because of inadequate response and/or intolerance to anakinra. This retrospective within-patient sequential cohort study included 26 adult FMF patients who received anakinra followed by canakinumab between January 2017 and September 2024. Demographic, clinical, genetic, laboratory, treatment-related data, and reasons for switching were obtained from medical records. Annual attack count, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), 24-h proteinuria, International Severity Score for FMF (ISSF), attack manifestations, and adverse events were evaluated using paired analyses. The median age was 35.0 years, and 13 patients (50.0%) were female. During canakinumab treatment, annual attack count [2.0 (1.0-3.0) vs 4.0 (4.0-4.0), p < 0.001], CRP [5.0 (4.0-6.0) vs 20.0 (16.2-61.2) mg/L, p < 0.001], ESR [8.5 (5.5-12.0) vs 35.5 (27.5-63.8) mm/h, p < 0.001], 24-h proteinuria [125.0 (96.8-217.5) vs 310.0 (204.0-702.2) mg/day, p < 0.001], and ISSF score [1 (1-2) vs 2 (2-3), p = 0.002] were significantly lower than during anakinra treatment. Fever and peritonitis were also less frequent during canakinumab treatment. The primary reasons for switching were inadequate response in 18 patients (69.2%) and intolerance or adverse events leading to treatment discontinuation in 8 patients (30.8%). In this small retrospective switch cohort, canakinumab treatment was associated with lower attack frequency, lower inflammatory markers, and lower retrospectively calculated ISSF scores after switching from anakinra. Proteinuria findings remain exploratory. These findings suggest that canakinumab may be a useful subsequent option in selected difficult-to-treat FMF patients, but prospective controlled studies are needed to confirm these observations.

PMID 43004123
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PubMedEuropean journal of clinical investigation2026-11-09

Clinical-Immunological Phenomapping in Recurrent Pericarditis: Disentangling Biological Traits, Inflammatory State and Treatment Exposure.

Wu M A MA, Kessel C C, Colombo R R, Fuehner S S et al.

Phenotype-oriented management is increasingly advocated in recurrent pericarditis (RP), but it remains unclear whether clinically recognizable phenotypes reflect underlying disease biology or are shaped by current inflammation and treatment exposure. We used multidimensional phenomapping to investigate this heterogeneity. We analysed 101 patients with idiopathic RP from the multicenter PERIPLO cohort. Factor analysis of mixed data followed by hierarchical clustering defined the index solution. Robustness was assessed across alternative specifications and models excluding treatment, inflammatory state or the IL-1Ra axis. Three clinical-immunological patterns emerged: a predominantly remission-state, anakinra-treated group; a predominantly remission-state group largely managed without IL-1 blockade; and an active inflammatory group enriched for anti-IL-1Ra autoantibodies and characterized by markedly reduced measured IL-1Ra. The two antibody-negative groups were extensively reorganized after treatment variables were removed, whereas exclusion of the IL-1Ra axis nearly abolished agreement with the original partition. In contrast, anti-IL-1Ra positivity remained consistently associated with active inflammation and very low measured IL-1Ra. In this cohort, the phenotypic heterogeneity of RP was better represented as a clinical-immunological spectrum shaped by inflammatory state and treatment exposure than as discrete, stable endotypes. The anti-IL-1Ra-associated inflammatory signature was the most internally consistent biological signal. These exploratory findings require external validation, and longitudinal multidimensional phenomapping should test whether this signature can inform patient management.

PMID 43001649
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PubMedDrug design, development and therapy2026-11-06

Corticotropin-Releasing Factor: A Key Player in Intestinal Barrier Dysfunction of Diarrhea-Predominant Irritable Bowel Syndrome-A Narrative Mechanistic Review.

Jin Rijuan R, Lou Yijie Y

Corticotropin-Releasing Factor (CRF) plays a crucial role in the pathophysiology of diarrhea-predominant irritable bowel syndrome (IBS-D) primarily by disrupting intestinal barrier function. In this narrative review of PubMed and Web of Science literature published through January 2026, we summarize the mechanisms by which CRF mediates intestinal barrier dysfunction in IBS-D and discuss potential therapeutic strategies. This review examines the mechanisms by which CRF impairs the intestinal barrier through several signaling pathways, including GC/NR3C1, MAPK/ERK, and Rho/ROCK/MLC. These pathways cause the downregulation of tight junction proteins, increased intestinal permeability, and dysregulated immune responses. Additionally, CRF induces immune inflammation via TLR signaling and promotes the activation of immune cells, further exacerbating barrier dysfunction. The disruption of epithelial barrier integrity is central to IBS-D, leading to visceral hypersensitivity and worsening gastrointestinal symptoms. Current therapeutic approaches for IBS-D often begin with lifestyle interventions. However, preclinical evidence suggests that interventions such as metformin, Eritoran, Puerarin, and anakinra may restore barrier integrity and alleviate symptoms by ameliorating CRF-mediated intestinal barrier dysfunction. Nevertheless, the mechanisms underlying CRF-induced IBS-D and the relevant therapeutic approaches have not been fully elucidated, and the available evidence is predominantly derived from animal and cell models, thus requiring further clinical validation. Future studies should further dissect CRF-related signaling pathways and develop intervention strategies aimed at restoring the intestinal barrier, thereby facilitating clinical translation and improving the prognosis of patients with IBS-D.

PMID 42992095
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PubMedSeminars in respiratory and critical care medicine2026-11-05

Precision Immunotherapy in Sepsis.

Psarrakis Christos C, Netea Mihai G MG, Giamarellos-Bourboulis Evangelos J EJ

Precision immunotherapy is usually used as an adjunctive treatment in patients with sepsis and/or septic shock. Previously reported clinical trials have failed to prove efficacy due to great heterogeneity among sepsis patients. This has led to the need for a different strategic approach. At the first stage, patient stratification has been performed based on transcriptional endotypes, clinical-based phenotypes, or biomarker-enriched endotypes, the latest being the most convenient and commonly used. Biomarker endotypes can be broadly categorized into hyperinflammation, immunoparalysis and endothelial dysfunction endotypes, each with different subclasses. The biomarker used for the diagnosis reflects a specific dysregulated immune pathway that is being targeted for treatment. The SAVE-MORE and the ImmunoSep clinical trials are examples of a biomarker-enriched classification system that guided precision immunotherapy. In the SAVE-MORE randomized controlled clinical trial, patients with COVID-19 pneumonia who were at risk for developing severe respiratory failure and who were defined by soluble urokinase plasminogen activator receptor levels ≥ 6 ng/mL were treated with either anakinra or placebo. The study met the primary endpoint and a lower 28-day mortality in favor of anakinra was also found. Based on these findings, anakinra received approval by the European Medicines Agency for this indication. In the ImmunoSep clinical trial, patients with macrophage activation-like syndrome, defined as those with ferritin levels > 4,420 ng/mL, were treated with anakinra or placebo, and patients with immunoparalysis, defined as those with the combination of ferritin ≤ 4,420 ng/mL and < 5,000 HLA-DR receptors on CD45 +/CD14 + monocytes, were treated with rhIFNγ or placebo. The study met its primary endpoint. Several clinical trials of precision immunotherapy are actively recruiting patients using biomarker classification systems. There are still unanswered questions regarding the stability of endotypes over the course of illness and whether time can affect the efficacy of precision immunotherapy.

PMID 42987870
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PubMedCell & bioscience2026-11-05

Macrophage-derived IL-1β drives endothelial-mesenchymal transition in diabetes mellitus erectile dysfunction.

Zhang Yijun Y, Liu Siyu S, Wang Wenhao W, Li Shufeng S et al.

Diabetes mellitus erectile dysfunction (DMED) is frequently accompanied by corpus cavernosum (CC) fibrosis and endothelial dysfunction; however, the cellular drivers and molecular mechanisms underlying these pathological changes remain incompletely understood. Endothelial-to-mesenchymal transition (EndMT), a phenotypic conversion in which endothelial cells lose endothelial characteristics and acquire mesenchymal features, has emerged as a key contributor to tissue fibrosis under inflammatory and metabolic stress conditions. Macrophages (Mφ), the predominant immune cell population in CC tissue in diabetes, are major sources of pro-inflammatory cytokines and may promote fibrosis by driving EndMT. This study investigated the role and mechanisms of Mφ in CC fibrosis during DMED and explored potential therapeutic targets. In a streptozotocin-induced DMED rat model, erectile function was significantly impaired, as evidenced by a marked reduction in the maximum intracavernous pressure-to-mean arterial pressure (ICP-to-MAP) ratio. This functional deterioration resulted from pronounced Mφ infiltration and enhanced fibrotic remodeling in CC. Pharmacological depletion of Mφ using clodronate liposomes significantly restored erectile function and increased the smooth muscle-to-collagen ratio. In vitro, co-culture of corpus cavernosum endothelial cells (CCEC) with Mφ under high-glucose (HG) conditions impaired endothelial tube formation and sprouting capacity, accelerated wound closure, and induced EndMT, characterized by downregulation of endothelial markers (CD34 and VE-cadherin) and upregulation of mesenchymal markers (Vimentin and α-SMA). RNA sequencing identified enrichment of interleukin-1 (IL-1)-related responses and Nuclear factor kappa B (NF-κB) signaling during EndMT. Further analyses demonstrated that HG stimulated Mφ to upregulate and secrete interleukin-1 beta (IL-1β), which in turn induced EndMT in CCEC accompanied by activation of NF-κB signaling, as evidenced by increased phosphorylation of p65 and IκBα. Pharmacological inhibition of the IL-1 receptor or NF-κB signaling effectively attenuated EndMT in vitro. Notably, in vivo administration of the IL-1 receptor antagonist Anakinra significantly improved erectile function and suppressed EndMT-associated molecular changes in DMED rats. Mφ-derived IL-1β promotes cavernosal fibrosis and erectile dysfunction in diabetes by inducing EndMT through activation of the NF-κB pathway. Targeting the IL-1β/NF-κB/EndMT axis represents a promising therapeutic strategy for the treatment of DMED.

PMID 42983767
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PubMedFrontiers in immunology2026-11-04

Dressler syndrome and post-cardiac injury syndrome: an autoinflammatory framework for reappraising a seventy-year-old diagnosis: a state-of-the-art review.

Sethi Yashendra Y, Moinuddin Arsalan A, Mahajan Kunal K, Sharma Amit A et al.

Dressler syndrome, the delayed pericarditis after myocardial infarction remains firmly established in cardiological teaching, yet contemporary direct evidence specific to it is sparse. Its reported incidence has fallen markedly in the reperfusion era, while post-cardiac injury syndrome (PCIS) is now encountered chiefly after cardiac surgery and catheter-based procedures. These trends reflect a change in the clinical settings in which delayed post-injury pericardial inflammation is recognised, rather than evidence of a transfer of the same biological disease burden; incidence estimates across eras and procedures are not directly comparable. The historical anti-heart antibody framework does not, on its own, account for current observations. Randomised trials in predominantly idiopathic recurrent pericarditis show that colchicine and interleukin-1 (IL-1)-directed agents (anakinra, rilonacept, goflikicept) reduce recurrence, and experimental and human pericardial tissue data implicate the NLRP3 inflammasome. These data support an important role for innate immune signalling in pericarditis, but they do not establish IL-1 dependency in late post-infarction Dressler syndrome, and they do not exclude a contribution of adaptive immunity to amplification, persistence or recurrence. We grade the evidence at three levels-direct human PCIS data, data from other human pericarditis phenotypes, and experimental data-and stratify therapeutic evidence by phenotype and drug class, distinguishing colchicine, for which randomised prevention data exist in post-pericardiotomy syndrome, from IL-1 blockade, for which no PCIS-specific trial exists. We propose a pericardial injury-threshold model as a testable hypothesis in which clinical expression reflects the interaction of damage-associated molecular pattern load, the directness of pericardial and mesothelial exposure, and host inflammatory susceptibility, with adaptive responses acting as potential amplifiers. The model yields falsifiable predictions and identifies a key unanswered question: whether IL-1 inhibition during infarct healing is safe and effective. We outline a staged research programme, including a candidate two-tier research case definition requiring prospective validation, registry-based ascertainment, pericardial fluid immunophenotyping, inflammasome genetics, and phenotype-specific trials, including of emerging direct NLRP3 inhibitors.

PMID 42978947
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