anifrolumab
Anifrolumab is a fully human IgG1κ monoclonal antibody that binds to subunit 1 of the type I interferon receptor (IFNAR1), blocking signaling of all type I interferons (IFN-α, IFN-β, IFN-ω). It is approved for moderately to severely active systemic lupus erythematosus (SLE) in adults receiving standard therapy. It is the first type I IFN receptor antagonist approved for SLE and addresses the interferon signature that drives SLE pathogenesis.
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Quick Reference

Anifrolumab is a fully human IgG1κ monoclonal antibody that binds to subunit 1 of the type I interferon receptor (IFNAR1), blocking signaling of all type I interferons (IFN-α, IFN-β, IFN-ω). It is approved for moderately to severely active systemic lupus erythematosus (SLE) in adults receiving standard therapy. It is the first type I IFN receptor antagonist approved for SLE and addresses the interferon signature that drives SLE pathogenesis.
Anifrolumab (anifrolumab) belongs to the Type I interferon receptor antagonist / Biologic class of medications. It was first approved by the FDA in 2021. This medication requires a prescription from a licensed healthcare provider.
This is a summary only. Always read the full prescribing information and consult your healthcare provider for personalized medical advice.
Anifrolumab is prescribed for the following conditions. Some uses are FDA-approved indications; others may be evidence-based off-label uses. Consult your healthcare provider for personalized guidance.

The following are general dosing guidelines only. Your actual dose should be determined by your healthcare provider based on your condition, renal/hepatic function, and other medications.
300 mg intravenous infusion over 30 minutes once every 4 weeks. Premedication with antihistamine recommended to reduce infusion reactions.
Not approved for patients under 18 years.
No dose adjustment required for renal impairment based on available PK data.
No dose adjustment required; monoclonal antibody not hepatically metabolized.
Available Forms
Available Strengths


Always inform your healthcare provider and pharmacist about ALL medications you take, including prescriptions, OTC medicines, vitamins, and supplements.
Live attenuated vaccines
Avoid live vaccines during anifrolumab therapy. Complete all live vaccinations before starting treatment.
Other immunosuppressants (belimumab, mycophenolate, azathioprine, cyclophosphamide)
Additive immunosuppression. Anifrolumab was studied on background standard of care (antimalarials, steroids, mycophenolate/azathioprine). Co-administration with other biologics (belimumab) has not been studied and is generally not recommended.
Infections: type I IFN blockade may impair immune response to infections, particularly viral infections. Screen for TB before initiation. Monitor closely for infections during therapy.
Herpes zoster: higher incidence in anifrolumab-treated patients (6% vs. 2% placebo in TULIP trials). Ensure VZV vaccination (Shingrix — recombinant, not live) before initiation in appropriate patients.
Anaphylaxis: infusion reactions possible. Pre-medicate with antihistamine; have resuscitative equipment available.
Malignancy: as with other immunosuppressants, monitor for signs of malignancy.
Live vaccines: avoid during therapy and discuss timing with all vaccinations.
Interferon signature: anifrolumab is most effective in patients with high type I IFN gene signature activity (pharmacodynamic biomarker), but was approved based on pooled TULIP-1 and TULIP-2 data regardless of IFN signature status.

Anifrolumab binds with high affinity and selectivity to subunit 1 of the type I interferon receptor (IFNAR1). This blocks the binding and signaling of all type I interferons — IFN-α (13 subtypes), IFN-β, and IFN-ω — to the IFNAR1/IFNAR2 receptor complex on target cells. Type I interferons are central to SLE pathogenesis: they are produced in excess due to defective clearance of apoptotic cells and immune complexes, which activate plasmacytoid dendritic cells (pDCs) via Toll-like receptors (TLR7, TLR9). Type I IFN signaling drives maturation of dendritic cells, B cell activation and autoantibody production, T cell activation, innate immune amplification, and upregulation of autoimmune-related gene programs — collectively the 'interferon signature' detectable in blood of ~75–80% of SLE patients. By blocking IFNAR1, anifrolumab suppresses this central pathogenic amplification loop.
Absorption
Administered intravenously; 100% systemic bioavailability.
Half-Life
Approximately 17–19 days (terminal elimination half-life).
Metabolism
Proteolytic catabolism to amino acids and small peptides; not metabolized by CYP450.
Excretion
Eliminated through protein catabolism; no significant renal or biliary excretion of intact antibody.

Consult your healthcare provider.
Full Pregnancy InformationMany medications pass into breast milk in varying amounts. Before using Anifrolumabwhile breastfeeding, discuss the benefits and risks with your healthcare provider or pharmacist — they can weigh your dose, your infant's age, and available lactation safety data to find the safest option for you and your baby.

Refrigerate at 36°F–46°F (2°C–8°C). Protect from light. Do not freeze or shake. Diluted solution should be used within 4 hours at room temperature or 24 hours refrigerated.
Anifrolumab and belimumab both target SLE but through entirely different mechanisms. Belimumab blocks BLyS/BAFF, reducing B cell survival and autoantibody-producing plasma cell differentiation — primarily an anti-B cell approach. Anifrolumab blocks the type I interferon receptor (IFNAR1), suppressing the interferon gene signature that amplifies innate and adaptive autoimmunity — a more upstream, innate immunity-focused mechanism. In the TULIP trials, anifrolumab showed stronger effects on mucocutaneous SLE and permitted greater steroid tapering. The two agents have not been compared head-to-head, and whether they can be combined is unknown — combination is generally not recommended outside clinical trials.
The 'interferon signature' refers to overexpression of interferon-stimulated genes (ISGs) in blood cells, detected in approximately 75–80% of SLE patients. It reflects excess type I IFN production driven by immune complex activation of TLR7/9 in plasmacytoid dendritic cells. In the TULIP-1 and TULIP-2 trials, patients with high IFN gene signature activity tended to show greater BICLA response rates with anifrolumab vs. placebo. However, anifrolumab received FDA approval for all SLE patients on standard therapy regardless of IFN signature status, as some patients with low signature also responded. An approved companion diagnostic test for IFN signature is not currently required for prescribing.
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Anifrolumab (Saphnelo) is a fully human IgG1κ monoclonal antibody that blocks subunit 1 of the type I interferon receptor (IFNAR1), preventing signaling by all type I interferons (IFN-α, IFN-β, IFN-ω). Approved by the FDA in August 2021 for moderately to severely active systemic lupus erythematosus (SLE) in adults receiving standard therapy, it represents the first approved therapy targeting the type I interferon axis in SLE — and only the second new mechanism approved for SLE in over 60 years, after belimumab (2011). The pivotal TULIP-2 trial demonstrated that anifrolumab 300 mg IV every 4 weeks achieved a BICLA (BILAG-based Composite Lupus Assessment) response rate of 47.8% vs. 31.5% for placebo at 52 weeks, with meaningful reductions in steroid dose and improvements in skin and joint manifestations. The TULIP-1 trial, which used a different primary endpoint (SRI-4), missed statistical significance, but its BICLA data were consistent with TULIP-2, leading to regulatory approval based on pooled data. Anifrolumab is particularly effective for mucocutaneous SLE manifestations and offers a novel option for patients with inadequate response to antimalarials and conventional immunosuppressants.
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The information on this page is for educational purposes only and is not intended as medical advice, diagnosis, or treatment. Always consult your doctor, pharmacist, or qualified healthcare provider before starting, stopping, or changing any medication.