NOMID

KINERET for NOMID

She’s one of a kind. So is her treatment

KINERET is the first and only FDA-approved treatment for neonatal-onset multisystem inflammatory disease (NOMID).1

Prescribe KINERET

NOMID

Young girl and her mother

NOMID is a rare, predominantly
pediatric autoinflammatory disease2

NOMID can be challenging to diagnose and can cause long-term disability without treatment.2

  • A diagnosis is derived from inflammatory markers, clinical symptoms, severity, and age of onset3,4
  • Symptoms of NOMID include chronic aseptic meningitis, urticaria-like rash, fever, vomiting, joint pain, headache, and conjunctivitis4
  • Over time, chronic inflammation can lead to developmental delay, sensorineural hearing loss, physical disability, and intellectual disability5
  • Although NOMID is often associated with mutations in the CIAS1/NLRP3 gene, approximately 40% of NOMID patients test negative using conventional genetic analyses6
    • 2016 clinical diagnostic criteria for CAPS do not “mandate evidence of a disease-causing NLRP3 mutation”4
A chart showing the diagnostic criteria for NOMID
A chart showing the diagnostic criteria for NOMID
Two overlapping squares that are transparent

The degenerative, autoinflammatory nature of NOMID can cause irreversible damage, so early identification is vital.3

Young girl smiling with other girls out of focus

Autoinflammation in NOMID is driven by IL-12

  • IL-1 (IL-1α and IL-1β) is a prototypic proinflammatory cytokine7
    • Secretion of IL-1β has an important role in systemic inflammation and in the signs and symptoms of NOMID1
  • NOMID is often associated with mutations in the CIAS1/NLRP3 gene, which encodes the protein cryopyrin (NLRP3), an important component of the NLRP3 inflammasome8,9,*
    • Although approximately 40% of patients test negative for CIAS1/NLRP3 using conventional genetic analyses, advanced testing techniques have identified somatic NLRP3 mosaicism in ~70% of these patients6
  • A mutation in cryopyrin leads to an increased rate of inflammasome assembly without the necessary inflammatory stimuli3
  • Increased inflammasome activity results in excessive production of the proinflammatory cytokine IL-1β3,8

*A multiprotein complex that activates inflammatory responses.

KINERET blocks the signal to stop inflammation
Learn how KINERET works
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Indications and Important Safety Information
INDICATION

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.kineretrx.com/hcp/
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 [Prescribing Information]. Stockholm, Sweden: Swedish Orphan Biovitrum AB (publ). 2. Neonatal-onset multisystem inflammatory disease. National Organization for Rare Disorders. Accessed December 17, 2021. https://rarediseases.org/rare-diseases/neonatal-onset-multisystem-inflammatory-disease/ 3. Hashkes PJ, Toker O. Autoinflammatory syndromes. Pediatr Clin North Am. 2012;59(2):447-470. 4. Kuemmerle-Deschner JB, Ozen S, Tyrell PN, et al. Diagnostic criteria for cryopyrin-associated periodic syndrome (CAPS). Ann Rheum Dis. 2017;76:942-947. 5. 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. 6. Tanaka N, lzawa K, Saito MK, et al. High incidence of NLRP3 somatic mosaicism in patients with chronic infantile, neurologic, cutaneous, articular syndrome: results of an international multicenter collaborative study. Arthritis Rheum. 2011;63(11):3625-3632. 7. Dinarello CA. Overview of the IL-1 family in innate inflammation and acquired immunity. Immunol Rev. 2018;281(1):8-27. 8. Hoffman HM, Wanderer AA. lnflammasome and IL-1β-mediated disorders. Curr Allergy Asthma Rep. 2010;10(4):229-235. 9. Dinarello CA, Simon A, van der Meer JW. Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases. Nat Rev Drug Discov. 2012;11(8):633-652.