For NOMID | About KINERET® (anakinra)

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

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

Prescribe KINERET
Young girl and her mother

Quinn, KINERET patient since 2009

“After Quinn’s treatment began, some of the symptoms that had plagued her entire little life began to ease. It was a turning point in a year of suffering.” —Colleen, Quinn’s mother

NOMID is a rare autoinflammatory disease.

Belonging to a group of disorders known as cryopyrin-associated periodic syndromes (CAPS), NOMID is the most severe. Early diagnosis and treatment is critical to preventing the long-term, irreversible damage and disability that can occur.2-4

NOMID can be challenging to diagnose.

  • A diagnosis is derived from inflammatory markers, clinical symptoms, severity, and age of onset2,3
  • Symptoms of NOMID include aseptic meningitis, urticaria-like rash, fever, vomiting, joint pain, headache, and conjunctivitis1,3
  • Over time, chronic inflammation can lead to developmental delay, sensorineural hearing loss, physical disability, and intellectual disability2,3
  • Although NOMID is often associated with mutations in the CIAS1/NLRP3 gene, approximately 40% of NOMID patients test negative using conventional genetic analyses5
    • 2016 clinical diagnostic criteria for CAPS do not “mandate evidence of a disease-causing NLRP3 mutation”3
NOMID Diagnostic Criteria
Young girl smiling with other girls out of focus

“No one at the hospital—not even the chief neonatologist—had ever seen anything like Quinn’s constellation of symptoms.” —Colleen, Quinn’s mother

See Case Study

NOMID is driven by interleukin-1.

  • Interluekin-1 (IL-1α and IL-1β) is a prototypic proinflammatory cytokine
    • Secretion of IL-1β has an important role in systemic inflammation and in the signs and symptoms of NOMID1,6,7
  • NOMID is often associated with mutations in the CIAS1/NLRP3 gene, which encodes the protein cryopyrin (NLRP3), an important component of the NLRP3 inflammasome*8,9
    • 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 patients9
  • A mutation in cryopyrin leads to an increased rate of inflammasome assembly without the necessary inflammatory stimuli2,9
  • Increased inflammasome activity results in excessive production of the pro-inflammatory cytokine IL-1β2,8,10

* A multiprotein complex that activates inflammatory responses

KINERET blocks the signal to stop inflammation

KINERET blocks both IL-1α and IL-1β.

  • KINERET, a recombinant IL-1 receptor antagonist (IL-1Ra), blocks the biologic activity of both IL-1α and IL-1β by inhibiting IL-1 binding to the IL-1 type 1 receptor (IL-1R1), which is expressed in a wide variety of tissues and organs1
  • KINERET supplements naturally occurring endogenous IL-1Ra, working in a similar way to block the IL-1 receptor without removing endogenous IL-1 from the circulation6
See the Data