Drug Monograph

Saphnelo (Anifrolumab)

anifrolumab-fnia

Type I Interferon Receptor Antagonist (Anti-IFNAR1 Monoclonal Antibody) · Intravenous Infusion
Pharmacokinetic Profile
Elimination
Non-linear (TMDD); undetectable ~16 wk after last dose at steady state
Metabolism
Proteolytic degradation (not CYP-mediated)
Protein Binding
Not applicable (monoclonal antibody)
Bioavailability
100% (IV); ~87% (SC, Phase 1 data)
Volume of Distribution
6.23 L (Vss)
Clinical Information
Drug Class
Type I IFN receptor antagonist (human IgG1κ mAb)
Available Doses
300 mg/2 mL (150 mg/mL) single-dose vial
Route
Intravenous infusion (30 min)
Renal Adjustment
None required (mild-moderate impairment studied)
Hepatic Adjustment
None expected (not hepatically metabolised)
Pregnancy
Insufficient data; pregnancy registry available
Lactation
Unknown; weigh benefits vs risks
Schedule
Prescription only (not controlled)
Generic Available
No
Rx

Indications

IndicationApproved PopulationTherapy TypeStatus
Moderate to severe systemic lupus erythematosus (SLE)Adults (≥18 years) receiving standard therapyAdd-on to standard therapyFDA Approved

Anifrolumab is the first type I interferon receptor antagonist approved for SLE. It was approved on July 30, 2021 based on efficacy data from the MUSE, TULIP-1, and TULIP-2 trials. Approximately 60–80% of adult patients with active SLE have elevated type I interferon-inducible gene expression, which is the pharmacological target of anifrolumab. Efficacy has not been evaluated in severe active lupus nephritis or severe active CNS lupus, and anifrolumab is not recommended for those settings. The 2023 EULAR recommendations and 2025 ACR guidelines both position anifrolumab alongside belimumab as a biologic option for patients with inadequate response to standard therapy.

Off-Label Uses

Cutaneous lupus erythematosus (refractory): Post hoc analyses of TULIP trials showed significant improvements in cutaneous disease activity (CLASI scores). EULAR 2023 lists anifrolumab as an option for refractory cutaneous lupus. Evidence quality: Moderate (post hoc of RCTs).

Lupus nephritis: Phase 2 data (TULIP-LN) are exploratory; not FDA-approved for this indication. Evidence quality: Low.

Myositis / dermatomyositis: Case reports and small series suggest potential benefit given the role of type I IFN; clinical trials underway. Evidence quality: Very low.

Dose

Anifrolumab Dosing

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Moderate-to-severe SLE — standard regimen300 mg IV q4wk300 mg IV q4wk300 mg q4wkInfuse over 30 minutes through 0.2–15 μm in-line filter
No loading dose required; steady state reached by Day 85
Missed dose management300 mg IV as soon as possible300 mg IV q4wk300 mgMaintain minimum 14-day interval between infusions
Resume regular q4wk schedule thereafter
Patients with history of infusion reactions300 mg IV q4wk300 mg IV q4wk300 mg q4wkConsider premedication (e.g., antihistamine) before infusion
No dose reduction; same dose for all adult patients regardless of weight
Clinical Pearl: Preparation & Administration

Withdraw 2 mL from a 50 mL or 100 mL bag of 0.9% sodium chloride, then add 2 mL (300 mg) of anifrolumab. Mix by gentle inversion — do not shake. Administer through an in-line or add-on filter (0.2–15 μm). Flush the line with 25 mL normal saline after infusion to ensure full dose delivery. Do not co-administer other medications through the same IV line. Unlike belimumab, anifrolumab is a fixed flat dose (300 mg) regardless of body weight, simplifying preparation and reducing waste.

PK

Pharmacology

Mechanism of Action

Anifrolumab is a fully human IgG1κ monoclonal antibody that binds with high affinity and specificity to subunit 1 of the type I interferon receptor (IFNAR1). By occupying this receptor subunit, anifrolumab blocks signalling by all type I interferons (including IFN-α, IFN-β, and IFN-κ), which are key drivers of inflammation in SLE. Beyond simple competitive inhibition, anifrolumab induces internalisation and downregulation of surface IFNAR1, further reducing the cell’s capacity to respond to type I IFN stimulation. Downstream effects include suppression of IFN-responsive gene expression, inhibition of plasma cell differentiation, and normalisation of peripheral T-cell subsets. In clinical trials, the 300 mg dose achieved sustained neutralisation (≥80%) of a 21-gene type I IFN gene signature from Week 4 through Week 52, which returned to baseline within 8–12 weeks after treatment cessation.

ADME Profile

ParameterValueClinical Implication
AbsorptionIV infusion (100% bioavailability); non-linear PK with more-than-dose-proportional AUC increases across 100–1000 mg range; steady state by Day 85; accumulation ratio 1.36 (Cmax), 2.49 (Ctrough)Fixed flat dose (300 mg) regardless of body weight; no loading dose needed. SC formulation (Phase 1: ~87% relative bioavailability) is under FDA review
DistributionVss = 6.23 L (typical 69.1 kg patient)Small Vd consistent with a monoclonal antibody confined primarily to the intravascular and interstitial compartments
MetabolismProteolytic degradation into peptides and amino acids; dual elimination via reticuloendothelial system and IFNAR1-mediated target-mediated drug disposition (TMDD)No CYP involvement; no dose adjustment for hepatic impairment. Non-linear clearance means higher doses produce disproportionately greater exposure
EliminationCL = 0.193 L/day (at 300 mg IV q4wk); serum concentrations undetectable in 95% of patients ~16 weeks after last dose at steady state, ~10 weeks after a single dosePharmacodynamic effects (IFN gene signature suppression) reverse within 8–12 weeks of stopping therapy; longer washout than conventional immunosuppressants
SE

Side Effects

≥10%Very Common
Adverse EffectIncidenceClinical Note
Upper respiratory tract infections (includes nasopharyngitis, pharyngitis)34% (vs 23% placebo)Most common adverse reaction; significant excess over placebo reflecting type I IFN blockade and impaired mucosal antiviral defence
Bronchitis (includes viral bronchitis, tracheobronchitis)11% (vs 5.2% placebo)More than double the placebo rate; monitor for lower respiratory tract progression
2–10%Common
Adverse EffectIncidenceClinical Note
Infusion-related reactions9.4% (vs 7.1% placebo)Mild-moderate; most common symptoms: headache, nausea, vomiting, fatigue, dizziness
Herpes zoster6.1% (vs 1.3% placebo)Nearly 5-fold increase over placebo; 2 cases of disseminated disease with hospitalisation. Multidermatomal involvement reported
Cough5.0% (vs 3.2% placebo)May be part of respiratory infection spectrum; evaluate for lower tract involvement
Respiratory tract infection (includes viral, bacterial)3.3% (vs 1.5% placebo)Distinguish from URTI; consider chest imaging if symptoms persistent
Hypersensitivity reactions2.8% (vs 0.6% placebo)Predominantly mild-moderate; includes angioedema (n=2 serious). Rarely led to discontinuation
SeriousSerious Adverse Effects
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Serious infections (pneumonia most frequent)4.8% (vs 5.6% placebo)Any time during treatmentConsider interrupting anifrolumab; treat aggressively. COVID-19 and pneumonia were most common in LTE
Fatal infections (including COVID-19)0.4% (vs 0.2% placebo)Any timeEvaluate infection risk prior to initiation; remain vigilant throughout therapy
Disseminated herpes zoster0.4% (2/459)Variable; weeks to monthsHospitalisation required; initiate IV antiviral therapy; consider treatment interruption
AnaphylaxisVery rare (1 case in development programme at 150 mg dose)During or shortly after infusionDiscontinue permanently; administer emergency treatment. Contraindicated after anaphylaxis
AngioedemaRare (4 reports at 300 mg; 2 serious)During or after infusionManage per hypersensitivity protocol; consider premedication for future doses if mild
Malignancy (excluding NMSC)0.7% (vs 0.6% placebo)Any timeAssess individual risk before prescribing; monitor for malignancy; consider risk-benefit if malignancy develops
DiscontinuationDiscontinuation Rates
Overall AE-Related Discontinuation
Not specifically reported as a headline rate
The PI notes that hypersensitivity reactions were predominantly mild-moderate and generally did not lead to treatment discontinuation
Long-Term Extension Completion
68.9% completed 4 years (vs 46.4% placebo)
Higher completion rate on anifrolumab vs placebo in LTE; safety profile consistent with 52-week trials
Managing Herpes Zoster Risk

Herpes zoster is the most notable safety signal distinguishing anifrolumab from placebo, with an EAIR of 6.9 vs 1.5 per 100 patient-years. The risk reflects impaired type I IFN-mediated antiviral defence. Before initiating therapy, verify varicella immunity and consider recombinant zoster vaccine (Shingrix) in eligible patients aged ≥50 years or those on immunosuppressants. Advise patients to report any new painful, blistering rashes immediately. Early antiviral therapy (valaciclovir or aciclovir) should be initiated promptly for suspected zoster.

Int

Drug Interactions

No formal drug interaction studies have been conducted with anifrolumab. As a monoclonal antibody eliminated through proteolytic degradation and IFNAR1-mediated target-mediated drug disposition, anifrolumab does not interact with CYP450 enzymes. Population pharmacokinetic analyses confirmed no clinically meaningful effect of concomitant corticosteroids, antimalarials, immunosuppressants, NSAIDs, ACE inhibitors, or statins on anifrolumab pharmacokinetics. The primary interaction concerns relate to additive immunosuppression and vaccine interference.

MajorLive / Live-Attenuated Vaccines
MechanismType I IFN receptor blockade impairs antiviral immune responses
EffectRisk of vaccine-strain infection; potentially inadequate immune response
ManagementAvoid concurrent use. Update all immunisations per current guidelines before starting therapy
FDA PI
MajorOther Biologic Therapies (e.g., belimumab, rituximab)
MechanismOverlapping immunosuppressive mechanisms; not studied in combination
EffectUnknown but potentially additive immunosuppression and infection risk
ManagementNot recommended for concomitant use. If switching from another biologic, complete a washout of at least 5 half-lives
FDA PI
ModerateImmunosuppressants (azathioprine, mycophenolate, methotrexate)
MechanismAdditive immunosuppression when combined with standard SLE therapies
EffectThese were co-administered in pivotal trials without clinically meaningful PK interactions; overall infections elevated (69.7% vs 55.4% placebo)
ManagementStandard practice to continue standard SLE therapy; maintain vigilance for infections, especially respiratory and herpes zoster
FDA PI — PopPK analysis
MinorCorticosteroids & NSAIDs
MechanismNo significant effect on anifrolumab PK per population analyses
EffectAnifrolumab allows steroid tapering — 52% of patients on ≥10 mg/day achieved sustained reduction to ≤7.5 mg/day in TULIP-2 (vs 30% placebo)
ManagementNo dose adjustment needed; target OCS tapering to ≤7.5 mg/day during treatment
FDA PI — TULIP-2
MinorInactivated Vaccines
MechanismIFN receptor blockade may reduce immune response to new immunisations
EffectPotentially diminished antibody response
ManagementComplete vaccinations before starting therapy when feasible; inactivated vaccines are not contraindicated during treatment
FDA PI
Mon

Monitoring

  • Infection surveillanceEvery visit
    Routine
    Overall infections occurred in 69.7% (vs 55.4% placebo). Screen for URI, bronchitis, pneumonia, and herpes zoster at each encounter. Consider treatment interruption for new serious infections.
  • Herpes zoster vigilanceEvery visit
    Routine
    Incidence 6.1% vs 1.3% placebo (EAIR 6.9 vs 1.5/100 PY). Ask about new rashes or pain in dermatomal distribution. Verify vaccination status before initiation. Early antiviral treatment critical for suspected cases.
  • Infusion monitoringDuring and after each infusion
    Trigger-based
    Infusion-related reactions in 9.4% (vs 7.1% placebo). Administer in settings prepared for anaphylaxis management. Monitor for headache, nausea, vomiting, dizziness. Serious hypersensitivity occurred in 0.6%.
  • SLE disease activityEvery 3–6 months
    Routine
    Track SLEDAI-2K, BILAG, PGA, anti-dsDNA, complement C3/C4. Treatment led to numerical anti-dsDNA reductions and complement normalisation through Week 52. BICLA and SRI-4 as clinical response metrics.
  • Steroid taperingWeeks 8–40 per protocol
    Routine
    Patients on baseline OCS ≥10 mg/day should attempt tapering to ≤7.5 mg/day between Weeks 8 and 40, as demonstrated in TULIP-2 and -3. Monitor for flare during taper.
  • Malignancy screeningPer standard guidelines
    Routine
    Malignancies (including NMSC) reported in 1.3% vs 0.6% placebo. Rodent IFNAR1 blockade models showed increased carcinogenic potential. Maintain age-appropriate cancer screening.
CI

Contraindications & Cautions

Absolute Contraindications

  • History of anaphylaxis with anifrolumab-fnia: The sole absolute contraindication per the FDA label.

Relative Contraindications (Specialist Input Recommended)

  • Clinically significant active infection: Avoid initiating treatment until the infection resolves or is adequately treated. Particular caution with chronic or recurrent infections given the elevated overall infection rate.
  • Severe active lupus nephritis or severe active CNS lupus: Efficacy has not been evaluated; use is not recommended.
  • Concomitant biologic therapy: Not studied in combination with other biologics including B-cell-targeted agents. A wash-out period of at least 5 half-lives of the prior biologic is required before starting anifrolumab.
  • Known malignancy or high malignancy risk: Increased carcinogenic potential observed in rodent models of IFNAR1 blockade. Assess individual risk-benefit before prescribing.

Use with Caution

  • History of recurrent infections or herpes zoster: Consider varicella immunity status and recombinant zoster vaccination before initiation.
  • Geriatric patients: Only 3% (n=20) of clinical trial patients were ≥65 years; insufficient data to determine differential responses.
  • Pregnancy: Monoclonal IgG antibodies cross the placenta, particularly during the third trimester. Animal studies showed no fetal harm at 28x MRHD. No adequate human data; pregnancy registry available (1-877-693-9268).
FDA Label Warnings Serious Infections, Hypersensitivity Reactions, Malignancy, Immunisations

The anifrolumab prescribing information highlights warnings for serious and sometimes fatal infections (including COVID-19), increased risk of respiratory infections and herpes zoster, hypersensitivity reactions including anaphylaxis and angioedema, potential increased malignancy risk, and interference with live vaccine responses. While there is no traditional boxed warning, these warnings and precautions carry significant weight for clinical decision-making and require pre-treatment risk assessment and ongoing surveillance.

Pt

Patient Counselling

Purpose of Therapy

Anifrolumab is a biologic medicine that works by blocking type I interferon, a group of proteins that drive inflammation in lupus. It is given as an intravenous infusion every 4 weeks alongside your other lupus medications. The goal is to reduce disease activity, improve skin and joint symptoms, and potentially allow your doctors to lower your steroid dose over time. Meaningful improvements are typically assessed at 6–12 months of therapy.

How to Take

Anifrolumab is administered as a 30-minute intravenous infusion by a healthcare provider every 4 weeks. Unlike some other lupus biologics, it is a fixed dose (not based on your weight). You will be monitored during the infusion. If you miss a scheduled infusion, it should be rescheduled as soon as possible, maintaining at least 14 days between doses.

Infection Risk & Respiratory Infections
Tell patientAnifrolumab affects your immune system and may increase your risk of infections, particularly upper respiratory infections and bronchitis. Practice good hygiene and avoid close contact with people who are ill. Ensure vaccinations are up to date before starting treatment. Live vaccines cannot be given during therapy.
Call prescriberIf you develop fever, chills, persistent cough, shortness of breath, burning urination, diarrhoea, or any new or worsening signs of infection.
Shingles (Herpes Zoster)
Tell patientPatients taking anifrolumab have a higher risk of developing shingles compared to placebo. Shingles appears as a painful, blistering rash, usually in a band on one side of the body. If eligible, your doctor may recommend you receive the shingles vaccine (Shingrix) before starting treatment.
Call prescriberContact your prescriber immediately if you notice a new painful rash with blisters, especially if it appears on your trunk or face. Early treatment with antiviral medication is important.
Allergic & Infusion Reactions
Tell patientSome patients experience reactions during or after the infusion, including headache, nausea, and dizziness. Rarely, serious allergic reactions (swelling, breathing difficulty) can occur. You will be monitored during the infusion.
Call prescriberSeek immediate medical attention for swelling of face, tongue, or throat, difficulty breathing, severe rash, or fainting/lightheadedness during or after an infusion.
Pregnancy & Family Planning
Tell patientIt is not known whether anifrolumab can harm an unborn baby. Monoclonal antibodies cross the placenta, especially in the third trimester. If you are planning pregnancy, discuss the timing of stopping treatment with your rheumatologist. A pregnancy exposure registry is available (1-877-693-9268).
Call prescriberInform your prescriber immediately if you become pregnant or suspect pregnancy while on anifrolumab.
Steroid Tapering
Tell patientOne goal of anifrolumab treatment is to enable reduction of your steroid dose. Your doctor will guide a gradual taper. Do not change your steroid dose on your own, as sudden changes can cause disease flares or adrenal insufficiency.
Call prescriberIf you experience new joint pain, rash, fatigue, or any worsening lupus symptoms during steroid tapering, contact your prescriber before the next scheduled visit.
Ref

Sources

Regulatory (PI / SmPC)
  1. AstraZeneca Pharmaceuticals LP. SAPHNELO (anifrolumab-fnia) prescribing information. Revised August 2024. FDA Label Primary source for all dosing, safety, pharmacokinetic, and clinical trial data in this monograph.
  2. European Medicines Agency. Saphnelo (anifrolumab) Summary of Product Characteristics. EMA SmPC European regulatory label including SC bioavailability data and additional PK parameters.
Key Clinical Trials
  1. Morand EF, Furie R, Tanaka Y, et al. Trial of anifrolumab in active systemic lupus erythematosus (TULIP-2). N Engl J Med. 2020;382(3):211-221. doi:10.1056/NEJMoa1912196 Pivotal Phase 3 trial establishing BICLA response (47.8% vs 31.5% placebo at Week 52) and steroid reduction benefit.
  2. Furie RA, Morand EF, Bruce IN, et al. Type I interferon inhibitor anifrolumab in active systemic lupus erythematosus (TULIP-1). Lancet Rheumatol. 2019;1(4):e208-e219. doi:10.1016/S2665-9913(19)30076-1 Phase 3 trial; SRI-4 primary endpoint not met (49.0% vs 43.0%), but BICLA response was 47.1% vs 30.2%.
  3. Furie R, Khamashta M, Merrill JT, et al. Anifrolumab, an anti-interferon-α receptor monoclonal antibody, in moderate-to-severe systemic lupus erythematosus (MUSE). Arthritis Rheumatol. 2017;69(2):376-386. doi:10.1002/art.39962 Phase 2b trial demonstrating dose-response and selecting 300 mg as optimal dose; 1000 mg offered no additional efficacy but increased herpes zoster.
  4. Vital EM, Merrill JT, Morand EF, et al. Anifrolumab efficacy and safety by type I interferon gene signature and target engagement: post hoc analysis of TULIP-1 and TULIP-2. Ann Rheum Dis. 2022;81(7):951-961. doi:10.1136/annrheumdis-2021-221973 Post hoc analysis showing enhanced efficacy in patients with high type I IFN gene signature and correlation between IFN neutralisation and clinical response.
Guidelines
  1. Fanouriakis A, Kostopoulou M, Andersen J, et al. EULAR recommendations for the management of systemic lupus erythematosus: 2023 update. Ann Rheum Dis. 2024;83(1):15-29. doi:10.1136/ard-2023-224762 EULAR guideline positioning anifrolumab alongside belimumab as a biologic option for patients with inadequate response to standard therapy.
  2. Sammaritano LR, Askanase A, Bermas BL, et al. 2025 American College of Rheumatology (ACR) guideline for the treatment of systemic lupus erythematosus. Arthritis Care Res. 2025. doi:10.1002/acr.25690 2025 ACR guideline conditionally recommending anifrolumab for moderate-to-severe cutaneous and musculoskeletal SLE refractory to standard treatment.
Mechanistic / Basic Science
  1. Crow MK. Type I interferon in the pathogenesis of lupus. J Immunol. 2014;192(12):5459-5468. doi:10.4049/jimmunol.1002795 Seminal review of the role of type I interferons in SLE pathogenesis, providing mechanistic rationale for IFNAR blockade.
  2. Peng L, Oganesyan V, Wu H, et al. Molecular basis for antagonistic activity of anifrolumab, an anti-interferon-α receptor 1 antibody. MAbs. 2015;7(2):428-439. doi:10.1080/19420862.2015.1007810 Structural and functional characterisation of anifrolumab binding to IFNAR1 and receptor internalisation mechanism.
Pharmacokinetics / Special Populations
  1. Almquist J, Kuruvilla D, Engel S, et al. Nonlinear population pharmacokinetics of anifrolumab in healthy volunteers and patients with systemic lupus erythematosus. J Clin Pharmacol. 2022;62(9):1163-1176. doi:10.1002/jcph.2055 Population PK analysis across 5 studies establishing clearance (0.193 L/day), Vss (6.23 L), and washout predictions (~16 weeks post-discontinuation).
  2. Tummala R, Rouse T, Engel S, et al. Safety, tolerability and pharmacokinetics of subcutaneous and intravenous anifrolumab in healthy volunteers. Lupus Sci Med. 2018;5(1):e000252. doi:10.1136/lupus-2017-000252 Phase 1 healthy volunteer study establishing SC bioavailability (~87% of IV AUC), Tmax 4–7 days, and dose-proportional SC PK.
  3. Kuruvilla D, Engel S, Engel L, et al. Clinical pharmacokinetics, pharmacodynamics, and immunogenicity of anifrolumab. Clin Pharmacokinet. 2023;62(5):655-671. doi:10.1007/s40262-023-01240-8 Comprehensive review of anifrolumab PK/PD across clinical development including exposure-response relationships and immunogenicity (ADA incidence 2.6%).