KINERET® (anakinra) blocks the interleukin-1 (IL-1) receptor to help protect against autoinflammatory events1
Support for your patients and practice.
References
- Kineret [Prescribing Information]. Stockholm, Sweden: Swedish Orphan Biovitrum AB (publ); 2018.
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)
CONTRAINDICATION
KINERET is contraindicated in patients with known hypersensitivity to E. coli–derived proteins, KINERET, or to any components of the product
IMPORTANT SAFETY INFORMATION
Serious Infections. 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
Immunosuppression. The impact of treatment with KINERET on active and/or chronic infections and the development of malignancies is not known
Immunizations. 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
Serious Adverse Reactions
RA: The most serious adverse reactions were: Serious Infections and Neutropenia, particularly when used in combination with TNF blocking agents.
NOMID and DIRA: The most serious adverse events were infections.
Most Common Adverse Reactions
RA: The 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
Post-marketing Experience
Hepato-biliary disorders (elevations of transaminases; non-infectious hepatitis) and thrombocytopenia, including severe thrombocytopenia have been identified during postapproval use of KINERET. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure.
These are not all the possible risks associated with KINERET. Please see Full Prescribing Information for KINERET at https://www.KineretRxHCP.com/home.php
To report suspected adverse reactions, contact Sobi North America at 1-866-773-5274 or FDA at 1-800-FDA-1088
Click here for full Prescribing Information for KINERET.
References: 1. KINERET (anakinra) prescribing information. Stockholm, Sweden: Sobi, Inc. 2020. 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.