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KINERET® (anakinra) blocks the interleukin-1 (IL-1) receptor to help protect against autoinflammatory events1

IL-1 is a proinflammatory cytokine that plays a key role in autoinflammation.2 Uncontrolled IL-1 activity can lead to chronic and life-threatening systemic inflammation.1,3,4

Learn more about the role of IL-1 in autoinflammation.

KINERET® (anakinra) blocks the interleukin-1 (IL-1) receptor to help protect against autoinflammatory events1

Learn about how IL-1 impacts RA patients. Learn about how IL-1 impacts NOMID patients. Learn about how IL-1 impacts DIRA patients.

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Indications and Important Safety Information
INDICATIONS
KINERET® (anakinra) is an interleukin-1 receptor antagonist indicated for:
Rheumatoid Arthritis (RA)
  • Reduction in signs and symptoms and slowing the progression of structural damage in moderately to severely active rheumatoid arthritis, in patients 18 years of age or older who have failed 1 or more disease-modifying antirheumatic drugs (DMARDs)
Cryopyrin-Associated Periodic Syndromes (CAPS)
  • Treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID)
Deficiency of Interleukin-1 Receptor Antagonist (DIRA)
  • Treatment of Deficiency of Interleukin-1 Receptor Antagonist (DIRA)
IMPORTANT SAFETY INFORMATION
  • KINERET is contraindicated in patients with known hypersensitivity to E. coli–derived proteins, KINERET, or to any components of the product
  • In RA, discontinue use if serious infection develops. In KINERET-treated NOMID or DIRA patients, the risk of a disease flare when discontinuing KINERET treatment should be weighed against the potential risk of continued treatment. Do not initiate KINERET in patients with active infections
  • Use in combination with Tumor Necrosis Factor (TNF)-blocking agents is not recommended
  • Hypersensitivity reactions, including anaphylactic reactions and angioedema, have been reported. Patients with DIRA may have an increased risk of allergic reactions, particularly in the first several weeks after starting KINERET treatment
  • The impact of treatment with KINERET on active and/or chronic infections and the development of malignancies is not known
  • Live vaccines should not be given concurrently with KINERET
  • Neutrophil counts should be assessed prior to initiating KINERET treatment, and while receiving KINERET, monthly for 3 months, and thereafter quarterly for a period up to 1 year

RA: Most common adverse reactions (incidence ≥ 5%) are injection site reaction, worsening of rheumatoid arthritis, upper respiratory tract infection, headache, nausea, diarrhea, sinusitis, arthralgia, flu-like symptoms, and abdominal pain

NOMID: The most common AEs during the first 6 months of treatment (incidence > 10%) are injection site reaction, headache, vomiting, arthralgia, pyrexia, and nasopharyngitis

DIRA: The most common AEs are upper respiratory tract infections, rash, pyrexia, influenza-like illness, and gastroenteritis

  • A higher rate of serious infections has been observed in RA patients treated with concurrent KINERET and etanercept therapy than in patients treated with etanercept alone. Use of KINERET in combination with TNF-blocking agents is not recommended
  • KINERET is indicated for use in pediatric patients with NOMID and DIRA
  • Because there is a higher incidence of infections in the elderly population in general, caution should be used in treating the elderly
  • KINERET is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function
Please see full Prescribing Information.

References: 1. KINERET [Prescribing Information]. Stockholm, Sweden: Swedish Orphan Biovitrum AB (publ). 2. Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev. 2018;281(1):8-27. 3. Diaz A. Deficiency of the interleukin-1 receptor antagonist (DIRA). In: Efthimiou P (ed). Auto-Inflammatory Syndromes. Springer, Cham; 2019:69-83. 4. Goldbach-Mansky R, Dailey NJ, Canna SW, et al. Neonatal-onset multisystem inflammatory disease responsive to interleukin-1β inhibition. N Engl J Med. 2006;355(6):581-592.