Anakinra 100mg/0.67ml solution for injection pre-filled syringes
Prescription only
Requires a prescription from a doctor or prescriber
Anakinra is a recombinant human interleukin-1 (IL-1) receptor antagonist (IL-1Ra) composed of 153 amino acid residues.
Active ingredients:
Anakinra
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Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Anakinra
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Kineret 100mg/0.67ml solution for injection pre-filled syringes
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WHO defined daily dose (DDD)
100 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
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Clinical guidelines and formulary information
British National Formulary
Anakinra
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(4)
Anakinra for treating Still's disease (TA685)
TA685
Technology appraisal
Updated Mar 2021Tocilizumab for the treatment of systemic juvenile idiopathic arthritis (TA238)
TA238
Technology appraisal
Updated Dec 2011Rheumatoid arthritis in adults: management (NG100)
NG100
NICE guideline
Updated Oct 2020TNF-alpha inhibitors for treating active ankylosing spondylitis and non-radiographic axial spondyloarthritis (TA383)
TA383
Technology appraisal
Updated Feb 2016Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
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Codes for healthcare professionals and prescribing systems
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NHS UK identifiers
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
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Searching UK clinical trials...
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
4 to 6 hours
Mechanism
Interleukin-1 (IL-1) plays an important role in inflammation and immunological responses.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
95%
The bioavailability of anakinra is 95% in healthy subjects administered a 70 mg subcutaneous bolus injection.…
Half-life
4 to 6 hours
In patients with rheumatoid arthritis (RA), the terminal half-life of anakinra ranged from 4 to 6 hours.…
Protein binding
Not Available
Volume of distribution
18.5 L
In adult subjects with rheumatoid arthritis (RA) treated with anakinra (n=35), the volume of distribution averaged 18.5 L.
[L41628]
[L41628]
Metabolism
As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body.
Elimination
Anakinra is mostly excreted by the kidney; therefore, the risk of toxic reactions may increase in patients with impaired renal function.
[L35415]
[L35415]
Clearance
50-80 mL/min
In patients with rheumatoid arthritis (RA), the clearance of anakinra was relatively consistent for different dose levels.
[L41628]…
[L41628]…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Biologic
About this compound
Anakinra is a recombinant human interleukin-1 (IL-1) receptor antagonist (IL-1Ra) composed of 153 amino acid residues. Unlike native human IL-1Ra, anakinra has an additional methionine residue at the amino terminus. This drug binds to the IL-1 receptor, competing with and inhibiting the activity of IL-1 alpha and beta.[L35415] Anakinra is indicated for the management of rheumatoid arthritis (RA) in patients 18 years of age or older who have failed one or more disease-modifying antirheumatic drugs (DMARDs), as well as the treatment of neonatal-onset multisystem inflammatory disease (NOMID) and deficiency of interleukin-1 receptor antagonist (DIRA).[L35415] Since IL-1 has an important role in inflammation and immunological responses, anakinra is also used for the off-label treatment of inflammatory diseases.[A247000]
Anakinra is produced using the E. Coli bacterial expression system. On November 14, 2001, it was approved by the FDA for the treatment of rheumatoid arthritis. It was later approved for the treatment of NOMID and DIRA on December 21, 2012, and December 18, 2020, respectively. A few studies have evaluated the use of anakinra for the treatment of coronavirus disease 2019 (COVID-19).[A247265] On November 8, 2022, the FDA issued an emergency use authorization (EUA) of anakinra for the treatment of COVID-19 in hospitalized patients who are at risk of progressing to severe respiratory failure.[L43932]
Anakinra is produced using the E. Coli bacterial expression system. On November 14, 2001, it was approved by the FDA for the treatment of rheumatoid arthritis. It was later approved for the treatment of NOMID and DIRA on December 21, 2012, and December 18, 2020, respectively. A few studies have evaluated the use of anakinra for the treatment of coronavirus disease 2019 (COVID-19).[A247265] On November 8, 2022, the FDA issued an emergency use authorization (EUA) of anakinra for the treatment of COVID-19 in hospitalized patients who are at risk of progressing to severe respiratory failure.[L43932]
Properties:
View FDA drug labelliquid
DrugBank indication
Anakinra is an interleukin-1 receptor antagonist indicated for the reduction in signs and symptoms and slowing the progression of structural damage in moderately to severely active rheumatoid arthritis (RA), in patients 18 years of age or older who have failed one or more disease-modifying antirheumatic drugs (DMARDs). Anakinra can be used alone or in combination with DMARDs other than Tumor Necrosis Factor (TNF) blocking agents.
[L35415]
Anakinra is also indicated for the treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID) and the treatment of Deficiency of Interleukin-1 Receptor Antagonist (DIRA).
[L35415]
Anakinra is also used off-label for the treatment of several inflammatory diseases.
[A247000]
The FDA has issued an emergency use authorization (EUA) for the emergency use of anakinra for the treatment of coronavirus disease 2019 (COVID-19) in hospitalized adults with positive results of direct SARS-CoV-2 viral testing with pneumonia requiring supplemental oxygen (low- or high-flow oxygen) who are at risk of progressing to severe respiratory failure and likely to have an elevated plasma soluble urokinase plasminogen activator receptor (suPAR). Since anakinra is approved for this condition under EUA, the drug should only be used when there are no alternative treatment available.
[L43927]
[L35415]
Anakinra is also indicated for the treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID) and the treatment of Deficiency of Interleukin-1 Receptor Antagonist (DIRA).
[L35415]
Anakinra is also used off-label for the treatment of several inflammatory diseases.
[A247000]
The FDA has issued an emergency use authorization (EUA) for the emergency use of anakinra for the treatment of coronavirus disease 2019 (COVID-19) in hospitalized adults with positive results of direct SARS-CoV-2 viral testing with pneumonia requiring supplemental oxygen (low- or high-flow oxygen) who are at risk of progressing to severe respiratory failure and likely to have an elevated plasma soluble urokinase plasminogen activator receptor (suPAR). Since anakinra is approved for this condition under EUA, the drug should only be used when there are no alternative treatment available.
[L43927]
Also known as(15)
Anakinra
IL-1RA
Interleukin-1 receptor antagonist anakinra
3.2.2.6
CD121 antigen-like family member A
IL-1R-1
IL-1R-alpha
IL-1RT-1
Dosage forms(6)
(Subcutaneous) — 100 mg/0.67ml
(Subcutaneous) — 100 mg
Injection, solution (Parenteral; Subcutaneous) — 100 MG/0.67ML
Injection, solution (Subcutaneous) — 100 mg/0.67mL
Solution (Subcutaneous) — 150 mg / mL
Injection, solution (Parenteral) — 100 mg/0.67ml
Drug interactions(1041)
Known interactions with other medications. Always consult a healthcare professional.
The risk or severity of adverse effects can be increased when Denosumab is combined with Anakinra.
Peginterferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2a is combined with Anakinra.
Interferon alfa-n1
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n1 is combined with Anakinra.
Interferon alfa-n3
Unknown severity
The risk or severity of adverse effects can be increased when Interferon alfa-n3 is combined with Anakinra.
Peginterferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Peginterferon alfa-2b is combined with Anakinra.
Interferon gamma-1b
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Interferon gamma-1b.
Interferon alfa-2a
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Interferon alfa-2a.
Aldesleukin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Aldesleukin.
Gemtuzumab ozogamicin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Gemtuzumab ozogamicin.
Pegaspargase
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Pegaspargase.
Interferon beta-1b
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Interferon beta-1b.
Interferon alfacon-1
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Interferon alfacon-1.
The risk or severity of adverse effects can be increased when Anakinra is combined with Rituximab.
Basiliximab
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Basiliximab.
The risk or severity of adverse effects can be increased when Anakinra is combined with Muromonab.
Ibritumomab tiuxetan
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Ibritumomab tiuxetan.
Tositumomab
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Tositumomab.
Alemtuzumab
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Alemtuzumab.
The risk or severity of adverse effects can be increased when Anakinra is combined with Alefacept.
Efalizumab
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Efalizumab.
Antithymocyte immunoglobulin (rabbit)
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Antithymocyte immunoglobulin (rabbit).
Interferon alfa-2b
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Interferon alfa-2b.
Daclizumab
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Daclizumab.
Phenylalanine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Phenylalanine.
Cladribine
Moderate
Anakinra may increase the immunosuppressive activities of Cladribine.
The risk or severity of adverse effects can be increased when Anakinra is combined with Amsacrine.
The risk or severity of adverse effects can be increased when Anakinra is combined with Bleomycin.
Chlorambucil
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Chlorambucil.
Raltitrexed
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Raltitrexed.
The risk or severity of adverse effects can be increased when Anakinra is combined with Mitomycin.
Floxuridine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Floxuridine.
Tioguanine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Tioguanine.
Dexrazoxane
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Dexrazoxane.
Streptozocin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Streptozocin.
Trifluridine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Trifluridine.
Gemcitabine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Gemcitabine.
Epirubicin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Epirubicin.
Chloramphenicol
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Chloramphenicol.
Lenalidomide
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Lenalidomide.
Altretamine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Altretamine.
The risk or severity of adverse effects can be increased when Anakinra is combined with Cisplatin.
Oxaliplatin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Oxaliplatin.
Propylthiouracil
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Propylthiouracil.
Pentostatin
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Pentostatin.
The risk or severity of adverse effects can be increased when Anakinra is combined with Linezolid.
Clofarabine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Clofarabine.
Methimazole
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Methimazole.
Sulfasalazine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Sulfasalazine.
Temozolomide
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Temozolomide.
Penicillamine
Unknown severity
The risk or severity of adverse effects can be increased when Anakinra is combined with Penicillamine.
Showing 50 of 1041 interactions
Toxicity & overdose
In clinical trials done in patients with rheumatoid arthritis (RA) and neonatal-onset multisystem inflammatory disease (NOMID) treated with anakinra, no cases of overdose were reported.
[L35415]
Sepsis trials were performed using mean calculated doses up to 35 times the ones given to patients with RA over 72 hours. Anakinra did not produce any serious toxicities at this dose range.
[L35415]
In preclinical studies done in rats, where up to 100 mg/kg/day were administered either intravenously or subcutaneously over 14 days, and given at doses of 2, 20 or 200 mg/kg/day subcutaneously for 6 months, anakinra was well tolerated. Toxicity ranged from mild to moderate, and dose-related inflammation, hemorrhage and fibrosis at the injection site were detected in both rats and monkeys.
[L41634]
The no observable adverse effect level (NOAEL) in rats receiving a daily subcutaneous dose of anakinra for 6 months was 2 mg/kg/day.
In rats receiving a daily intravenous injection of anakinra for 14 or 28 days, the NOAEL was 30 mg/kg/day. The NOAEL in Rhesus monkeys was 150 mg/kg/day when anakinra was administered via intravenous infusion for 7 days, 10-30 mg/kg/day when administered via intravenous bolus injection for 14 days and 5 mg/kg/day when administered subcutaneously for 14 days.
[L41634]
Anakinra had no effects on fertility and reproductive capacity in both male and female rats given the maximum recommended human dose.
[L35415]
[L35415]
Sepsis trials were performed using mean calculated doses up to 35 times the ones given to patients with RA over 72 hours. Anakinra did not produce any serious toxicities at this dose range.
[L35415]
In preclinical studies done in rats, where up to 100 mg/kg/day were administered either intravenously or subcutaneously over 14 days, and given at doses of 2, 20 or 200 mg/kg/day subcutaneously for 6 months, anakinra was well tolerated. Toxicity ranged from mild to moderate, and dose-related inflammation, hemorrhage and fibrosis at the injection site were detected in both rats and monkeys.
[L41634]
The no observable adverse effect level (NOAEL) in rats receiving a daily subcutaneous dose of anakinra for 6 months was 2 mg/kg/day.
In rats receiving a daily intravenous injection of anakinra for 14 or 28 days, the NOAEL was 30 mg/kg/day. The NOAEL in Rhesus monkeys was 150 mg/kg/day when anakinra was administered via intravenous infusion for 7 days, 10-30 mg/kg/day when administered via intravenous bolus injection for 14 days and 5 mg/kg/day when administered subcutaneously for 14 days.
[L41634]
Anakinra had no effects on fertility and reproductive capacity in both male and female rats given the maximum recommended human dose.
[L35415]
How it works
Mechanism of action
Interleukin-1 (IL-1) plays an important role in inflammation and immunological responses. Inflammatory stimuli trigger its production, and it binds to the IL-1 receptor to activate a wide variety of mechanisms. The activity of the IL-1 receptor is also regulated by a naturally occurring IL-1 receptor antagonist (IL-1Ra) that competes for the binding sites of the IL-1 receptor.[L35415] In rheumatoid arthritis (RA) patients, IL-1 levels are elevated, inducing cartilage degradation and the stimulation of bone resorption, and the amount of IL-1Ra in the synovium and synovial fluid of RA patients cannot compete with the high level of IL-1 present.[L35415] Anakinra is a recombinant, non-glycosylated form of IL-1Ra that competes with and inhibits IL-1 by binding to the IL-1 receptor; therefore, the administration of this drug reduces the inflammatory response in RA patients.[A246908][L35415]
Anakinra can also be used in the treatment of neonatal-onset multisystem inflammatory disease (NOMID) and deficiency of interleukin-1 receptor antagonist (DIRA).[L35415] Patients with NOMID have spontaneous mutations in CIAS1/NLRP3, a gene that encodes cryopyrin, an inflammasome component. When activated, the inflammasome enhances and promotes the production of IL-1β, an isoform of IL-1.[A246898][L35415] DIRA is an autoinflammatory disease caused by mutations in the IL1RN gene. These mutations reduce the amount of IL-1Ra that is secreted, leading to the unopposed action of IL-1.[L35415] Anakinra controls NOMID and DIRA symptoms by inhibiting IL-1 activity.[L35415]
Anakinra can also be used in the treatment of neonatal-onset multisystem inflammatory disease (NOMID) and deficiency of interleukin-1 receptor antagonist (DIRA).[L35415] Patients with NOMID have spontaneous mutations in CIAS1/NLRP3, a gene that encodes cryopyrin, an inflammasome component. When activated, the inflammasome enhances and promotes the production of IL-1β, an isoform of IL-1.[A246898][L35415] DIRA is an autoinflammatory disease caused by mutations in the IL1RN gene. These mutations reduce the amount of IL-1Ra that is secreted, leading to the unopposed action of IL-1.[L35415] Anakinra controls NOMID and DIRA symptoms by inhibiting IL-1 activity.[L35415]
Pharmacodynamics
Anakinra is a recombinant human interleukin-1 receptor antagonist (IL-1Ra) that blocks the biologic activity of interleukin-1 (IL-1) by competitively inhibiting its ability to bind to the IL-1 type I receptor (IL-1RI). IL-1 production is higher in inflammatory diseases such as rheumatoid arthritis, where the amount of naturally occurring IL-1Ra cannot compete with the high level of IL-1 present.[L35415]
Anakinra has been associated with a higher probability of developing a severe infection, and the use of TNF blocking agents can increase this incidence.[L35415] Hypersensitivity reactions have been reported in patients using anakinra. The prevalence of allergic reactions may be higher in patients with deficiency of interleukin-1 receptor antagonist (DIRA), since they lack the naturally occurring IL-1Ra.[L35415] Anakinra can also decrease neutrophil counts in patients. Therefore, neutrophil counts should be assessed before initiating anakinra.[L35415]
Anakinra has been associated with a higher probability of developing a severe infection, and the use of TNF blocking agents can increase this incidence.[L35415] Hypersensitivity reactions have been reported in patients using anakinra. The prevalence of allergic reactions may be higher in patients with deficiency of interleukin-1 receptor antagonist (DIRA), since they lack the naturally occurring IL-1Ra.[L35415] Anakinra can also decrease neutrophil counts in patients. Therefore, neutrophil counts should be assessed before initiating anakinra.[L35415]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
The bioavailability of anakinra is 95% in healthy subjects administered a 70 mg subcutaneous bolus injection. In patients with rheumatoid arthritis (RA) administered a subcutaneous dose of anakinra, the maximum plasma concentration was detected 3 to 7 hours later. No unexpected accumulation was observed in RA patients receiving this drug for up to 24 weeks.
[L35415]
In a phase 1, single-center, randomized, sequential single-dose escalation PK study done in patients with stable RA, AUC increased in a relatively dose-proportional manner.
While the tmax and Cmax fluctuated across the different doses provided to these patients (range from 0.5 to 6 mg/kg), clearance appeared to be consistent.
[L41628]
In patients with neonatal-onset multisystem inflammatory disease (NOMID) treated with a subcutaneous dose of 3 mg/kg of anakinra for an average of 3.5 years (n=16), Cmax was 3628 ng/mL and C24h was 203 ng/mL.
[L35415]
[L35415]
In a phase 1, single-center, randomized, sequential single-dose escalation PK study done in patients with stable RA, AUC increased in a relatively dose-proportional manner.
While the tmax and Cmax fluctuated across the different doses provided to these patients (range from 0.5 to 6 mg/kg), clearance appeared to be consistent.
[L41628]
In patients with neonatal-onset multisystem inflammatory disease (NOMID) treated with a subcutaneous dose of 3 mg/kg of anakinra for an average of 3.5 years (n=16), Cmax was 3628 ng/mL and C24h was 203 ng/mL.
[L35415]
Half-life
In patients with rheumatoid arthritis (RA), the terminal half-life of anakinra ranged from 4 to 6 hours. In patients with neonatal-onset multisystem inflammatory disease (NOMID), the median half-life of anakinra was 5.7 h (range=3.1-28.2, n=12).
[L35415]
[L35415]
Protein binding
Not Available
Volume of distribution
In adult subjects with rheumatoid arthritis (RA) treated with anakinra (n=35), the volume of distribution averaged 18.5 L.
[L41628]
[L41628]
Metabolism
As a protein-based therapy, anakinra is expected to be metabolized by proteases throughout the body.
Route of elimination
Anakinra is mostly excreted by the kidney; therefore, the risk of toxic reactions may increase in patients with impaired renal function.
[L35415]
[L35415]
Clearance
In patients with rheumatoid arthritis (RA), the clearance of anakinra was relatively consistent for different dose levels.
[L41628]
Clearance is variable and increases with increasing creatinine clearance and body weight. However, gender and age were not significant factors.
[L35415]
In patients with mild (creatinine clearance 50-80 mL/min) and moderate (creatinine clearance 30-49 mL/min) renal impairment, the mean plasma clearance of anakinra was 16% and 50% lower, respectively. In patients with severe renal insufficiency and end-stage renal disease (creatinine clearance < 30 mL/min), the mean plasma clearance of anakinra was 70% and 75% lower, respectively.
[L35415]
[L41628]
Clearance is variable and increases with increasing creatinine clearance and body weight. However, gender and age were not significant factors.
[L35415]
In patients with mild (creatinine clearance 50-80 mL/min) and moderate (creatinine clearance 30-49 mL/min) renal impairment, the mean plasma clearance of anakinra was 16% and 50% lower, respectively. In patients with severe renal insufficiency and end-stage renal disease (creatinine clearance < 30 mL/min), the mean plasma clearance of anakinra was 70% and 75% lower, respectively.
[L35415]
Drug targets(1)
Proteins and enzymes this drug interacts with in the body
Interleukin-1 receptor type 1
IL1R1
antagonist
Specific functioninterleukin-1 binding
Cellular location
Membrane
General function & pharmacology
Receptor for IL1A, IL1B and IL1RN .
PMID:2950091 PMID:37315560
After binding to interleukin-1 associates with the coreceptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves the recruitment of adapter molecules such as TOLLIP, MYD88, and IRAK1 or IRAK2 via the respective TIR domains of the receptor/coreceptor subunits. Binds ligands with comparable affinity and binding of antagonist IL1RN prevents association with IL1RAP to form a signaling complex.
Involved in IL1B-mediated costimulation of IFNG production from T-helper 1 (Th1) cells PMID:10653850
PMID:2950091 PMID:37315560
After binding to interleukin-1 associates with the coreceptor IL1RAP to form the high affinity interleukin-1 receptor complex which mediates interleukin-1-dependent activation of NF-kappa-B, MAPK and other pathways. Signaling involves the recruitment of adapter molecules such as TOLLIP, MYD88, and IRAK1 or IRAK2 via the respective TIR domains of the receptor/coreceptor subunits. Binds ligands with comparable affinity and binding of antagonist IL1RN prevents association with IL1RAP to form a signaling complex.
Involved in IL1B-mediated costimulation of IFNG production from T-helper 1 (Th1) cells PMID:10653850
Scientific references(6)
Chen X., Ji Z.L., Chen Y.Z.
TTD: Therapeutic Target Database.
Nucleic Acids Research
200230(1):412-415. doi: 10.1093/nar/30.1.412
Lequerre T., Quartier P., Rosellini D., Alaoui F., De Bandt M., Mejjad O., Kone-Paut I., Michel M., Dernis E., Khellaf M., Limal N., Job-Deslandre C., Fautrel B., Le Loet X., Sibilia J.
Interleukin-1 receptor antagonist (anakinra) treatment in patients with systemic-onset juvenile idiopathic arthritis or adult onset Still disease: preliminary experience in France.
Annals of the Rheumatic Diseases
200867(3):302-308. doi: 10.1136/ard.2007.076034
Fleischmann R.M., Schechtman J., Bennett R., Handel M.L., Burmester G.R., Tesser J., Modafferi D., Poulakos J., Sun G.
Anakinra, a recombinant human interleukin-1 receptor antagonist (r-metHuIL-1ra), in patients with rheumatoid arthritis: A large, international, multicenter, placebo-controlled trial.
Arthritis Rheum
2003 Apr48(4):927-34. doi: 10.1002/art.10870
Bachove I., Chang C.
Anakinra and related drugs targeting interleukin-1 in the treatment of cryopyrin-associated periodic syndromes.
Open Access Rheumatol
2014 Mar 36:15-25. doi: 10.2147/OARRR.S46017. eCollection 2014
Cavalli G., Dinarello C.A.
Anakinra Therapy for Non-cancer Inflammatory Diseases.
Front Pharmacology
2018 Nov 69:1157. doi: 10.3389/fphar.2018.01157. eCollection 2018
Kim J.S., Lee J.Y., Yang J.W., Lee K.H., Effenberger M., Szpirt W., Kronbichler A., Shin J.I.
Immunopathogenesis and treatment of cytokine storm in COVID-19.
Theranostics
2021 Jan 111(1):316-329. doi: 10.7150/thno.49713. eCollection 2021
ATC classification(1 code)
ATC L04AC03
Affected organisms(1)
Humans and other mammals
Experimental properties(4)
Commercial products(8)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Anakinra
Additional database identifiers
Drugs Product Database (DPD)
12604
HUGO Gene Nomenclature Committee (HGNC)
HGNC:5993
GenAtlas
IL1R1
GeneCards
IL1R1
GenBank Gene Database
X16896
GenBank Protein Database
33801
Guide to Pharmacology
1734
UniProt Accession
IL1R1_HUMAN
International reference pricing
2 formulations
Reference pricing from DrugBank. Prices are indicative and may not reflect current UK costs.
From $61.80/syringe
To $449.90/box
Kineret 100 mg/0.67 ml syr
$61.80/syringe
Kineret 1 Box = 7 Syringes, 4.69ml Box
$449.90/box
Source: DrugBank. Used under CC BY-NC 4.0 academic licence for non-commercial purposes.
Patent information
All patents expired, 2 expired
1341322
Canada
Approved 27 Nov 2001 · Expires 27 Nov 2018
Expired
2141953
Canada
Approved 8 Apr 2008 · Expires 17 Sept 2013
Expired
Patent protection has expired — generic versions may be available.
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 26 days ago(8 Mar 2026)