Difficult-to-treat RA

KINERET for difficult-to-treat RA

Why some RA patients don’t respond to conventional therapies

If your patient has tried and failed multiple RA treatments, their disease may be driven by autoinflammation.1,2

Difficult-to-treat RA

An older couple wearing sunglasses holds hands and walks through tall grass in a field on a clear day while looking at each other

RA exists along a spectrum

Though RA is primarily defined as an autoimmune disease, the distinction between autoimmune and autoinflammatory disease isn’t clear. Because there are various interactions and similarities between the innate and adaptive immune systems, they may be viewed as 2 ends of the same spectrum.1,2 Some patients have RA that is closer to the autoinflammatory end of that spectrum.1

A horizontal cylindrical shape represents the spectrum of rheumatoid arthritis. On the left of the shape it says "AUTOIMMUNE" with 13 human-shaped icons above it. On the right side of the shape it says "AUTOINFLAMMATORY" and has only 3 human-shaped icons above it

Where does your patient’s RA fall?

Understanding which end of the spectrum your patient’s disease leans toward can be challenging, but there are key clues to watch for. Along with treatment history, you may want to consider any elevated acute-phase reactants and extraarticular signs of inflammation, including:

  • Fever3,4
  • Rash1
  • Fatigue3,4
  • Muscle weakness4
  • Keratoconjunctivitis sicca (dry eye)4

 

Learn more
Megan, an adult female patient with rheumatoid arthritis, stands outside her house holding a thermos and tote bag. She has a determined look on her face as she looks up at the sky

Steroid resistance can be a telling clue

Since RA is typically considered an autoimmune disease, therapies targeting the adaptive immune system (like steroids) are often prescribed. But autoinflammatory disease isn’t usually well controlled by these types of therapies.3 There may be several factors at play, including:

A group of randomly scattered dots

The overexpression of
cytokines that suppress
steroid sensitivity5

An inverted triangular shape consisting of rows of hexagons. The first 4 rows of hexagons fit perfectly together while the next 3 rows appear jumbled and do not fit together

Dysregulation of
steroid receptors5

Three arrows intertwine and point upward

The signaling of
inflammatory pathways5

A double helix

Genetic
mutations5

KINERET is a very specific treatment for a very specific RA patient

RA that is primarily autoinflammatory may be mediated by interleukin-1 (IL-1), cytokines produced by cells in the innate immune system.6 KINERET is an IL-1 receptor antagonist, blocking an underlying cause of inflammation in difficult-to-treat RA.7

Learn how KINERET works
An illustrated diagram of how the KINERET® (anakinra) molecule blocks the receptor from receiving IL-1 signaling
Learn how KINERET works
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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. Savic S, Mistry A, Wilson AG, et al. Autoimmune-autoinflammatory rheumatoid arthritis overlaps: a rare but potentially important subgroup of diseases. RMD Open. 2017;3(2):e000550. 2. Buch MH, Eyre S, McGonagle D. Persistent inflammatory and non-inflammatory mechanisms in refractory rheumatoid arthritis. Nat Rev Rheumatol. 2021;17(1):17-33. 3. Dinarello CA. Interleukin-1 in the pathogenesis and treatment of inflammatory diseases. Blood. 2011;117(14):3720-3732. 4. Vela P. Extra-articular manifestations of rheumatoid arthritis, now. Eur Med J Rheumatol. 2014;1:103-112. 5. Chikanza IC. Mechanisms of corticosteroid resistance in rheumatoid arthritis. Ann NY Acad Sci. 2002;966:39-48. 6. Dinarello CA, Simon A, van der Meer JWM. Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases. Nat Rev Drug Discov. 2012;11(8):633-652. 7. KINERET [Prescribing Information]. Stockholm, Sweden: Swedish Orphan Biovitrum AB (publ).