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TRIALISTMD · DRUG INTELLIGENCE
DERMATOLOGY
IL-4Rα Antagonist · Monoclonal Antibody · BLA 761055
dupilumab
DUPIXENT®
Recombinant fully human IgG4 monoclonal antibody targeting the IL-4Rα subunit, blocking both IL-4 and IL-13 signaling via Type I and Type II receptor complexes. First systemic biologic approved for moderate-to-severe atopic dermatitis, establishing a new paradigm in type 2 inflammatory disease.
01
Drug Overview
Molecule Class
IgG4 mAb
Human monoclonal antibody
Target
IL-4Rα
Blocks IL-4 & IL-13 signaling
Molecular Weight
~147 kDa
Recombinant CHO cell production
Phase 3 Trials
3 RCTs
SOLO 1, SOLO 2, CHRONOS
Mechanism of Action
Dual IL-4 / IL-13 Blockade: Dupilumab binds the IL-4Rα subunit shared by the Type I receptor (IL-4Rα / γc) and the Type II receptor (IL-4Rα / IL-13Rα1). This single binding event simultaneously blocks IL-4 signaling via Type I and both IL-4 and IL-13 signaling via Type II, thereby suppressing multiple arms of type 2 (Th2) inflammation — including IgE synthesis, eotaxin-3 production, and epithelial barrier gene dysregulation — without systemic immunosuppression.
Indication (Initial Approval — March 2017)
Treatment of adult patients with moderate-to-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable. May be used with or without topical corticosteroids.
Pivotal Trial Program Summary
| Study | Design | N | Duration | Key Intervention |
|---|---|---|---|---|
| SOLO 1 (1334) | R, DB, PC, MC | 671 | 16 weeks | Dupilumab 300 mg Q2W vs Placebo — monotherapy |
| SOLO 2 (1416) | R, DB, PC, MC | 708 | 16 weeks | Dupilumab 300 mg Q2W vs Placebo — monotherapy |
| CHRONOS (1224) | R, DB, PC, MC | 740 | 52 weeks | Dupilumab 300 mg Q2W + TCS vs Placebo + TCS |
R=randomized; DB=double-blind; PC=placebo-controlled; MC=multicenter; TCS=topical corticosteroids. All studies enrolled adults (≥18 years) with IGA ≥3, EASI ≥16, and BSA ≥10%. Source: BLA 761055, Clinical Review, Brenda Carr MD.
Clinical Context
Atopic dermatitis affects approximately 3% of adults globally, with 10–30% of childhood-onset cases persisting into adulthood. The AD population is characterised by heightened Th2 immune polarisation with elevated IL-4, IL-13, IgE, and peripheral eosinophilia. At the time of dupilumab’s approval, the only FDA-approved systemic option was systemic corticosteroids, which are generally not recommended for long-term use. Dupilumab was the first targeted biologic approved for AD, and its approval represented a paradigm shift enabling cytokine-directed therapy in this indication.
The Phase 3 development program enrolled 2,119 subjects across the three pivotal trials. The primary endpoint — IGA 0/1 with ≥2-point improvement at Week 16 — was met with high statistical significance (p<0.0001) in all three trials. Dupilumab also substantially reduced pruritus (≥4-point NRS improvement) and EASI scores, and the safety profile was favourable, with conjunctivitis being the most notable drug-related adverse event signal.
02
Baseline Characteristics
SOLO 1 (Trial 1334) — Monotherapy
Randomized
671
224 / 224 / 223
Mean Age
~39 yr
Range 18–85
Male
58%
Q2W arm: 58%
White / Asian
69% / 24%
Q2W arm
| Characteristic | Dupilumab 300 mg Q2W | Placebo |
|---|---|---|
| Randomized (FAS) | 224 | 224 |
| Mean Age (yr) | 39.8 ± 14.7 | 39.5 ± 13.9 |
| Male | 130 (58%) | 118 (53%) |
| White / Asian / Black | 69% / 24% / 5% | 65% / 25% / 7% |
| IGA Moderate (3) / Severe (4) | 52% / 48% | 50% / 50% |
| Mean EASI score | 33.0 ± 13.6 | 34.5 ± 14.5 |
| Mean BSA involved (%) | 54.7 ± 23.2 | 57.5 ± 23.4 |
| Weekly Average Peak Pruritus NRS | 7.2 ± 1.9 | 7.4 ± 1.8 |
| Baseline NRS ≥4 | 213 (95%) | 212 (95%) |
SOLO 2 (Trial 1416) — Monotherapy
| Characteristic | Dupilumab 300 mg Q2W | Placebo |
|---|---|---|
| Randomized (FAS) | 233 | 236 |
| Mean Age (yr) | 36.9 ± 14.0 | 37.4 ± 14.1 |
| Male | 137 (59%) | 132 (56%) |
| White / Asian / Black | 71% / 19% / 6% | 66% / 21% / 9% |
| IGA Moderate (3) / Severe (4) | 51% / 49% | 51% / 49% |
| Mean EASI score | 31.8 ± 13.1 | 33.6 ± 14.3 |
| Mean BSA involved (%) | 52.7 ± 21.2 | 54.3 ± 23.1 |
| Weekly Average Peak Pruritus NRS | 7.6 ± 1.6 | 7.5 ± 1.9 |
| Baseline NRS ≥4 | 225 (97%) | 221 (94%) |
CHRONOS (Trial 1224) — Dupilumab + TCS
| Characteristic | Dupilumab 300 mg Q2W + TCS | Placebo + TCS |
|---|---|---|
| Randomized (FAS) | 106 | 315 |
| Mean Age (yr) | 39.6 ± 14.0 | 36.6 ± 13.0 |
| Male | 62 (59%) | 193 (61%) |
| White / Asian / Black | 70% / 27% / 2% | 66% / 26% / 6% |
| IGA Moderate (3) / Severe (4) | 50% / 50% | 53% / 47% |
| Mean EASI score | 33.6 ± 13.3 | 32.6 ± 12.9 |
| Mean BSA involved (%) | 59.5 ± 20.8 | 56.9 ± 21.7 |
| Weekly Average Peak Pruritus NRS | 7.4 ± 1.7 | 7.3 ± 1.8 |
| Baseline NRS ≥4 | 102 (96%) | 299 (95%) |
Comorbid Atopic Disease (Combined SOLO Studies)
High atopic burden across all trials: ~48% asthma, ~49% allergic rhinitis, ~37% food allergy, ~27% allergic conjunctivitis (prior history). These comorbidities reflect the systemic Th2-skewed immune phenotype of the AD population and were consistent across treatment arms.
Source: BLA 761055 Clinical Review, Tables 9, 10, 22, 23, 38, 39. Demographic and baseline disease characteristics were well-balanced across treatment arms in all three trials. The AD diagnosis required ≥3 years of chronic disease and was made using AAD Consensus Criteria (Eichenfield 2014).
03
Efficacy
Primary Endpoint: Proportion of subjects achieving IGA 0 (clear) or 1 (almost clear) with ≥2-point improvement from baseline at Week 16. Dupilumab was statistically superior to placebo (p<0.0001) in all three pivotal trials using dupilumab 300 mg Q2W (following 600 mg loading dose at Week 0).
IGA 0 or 1 at Week 16 — Primary Endpoint
SOLO 1 (Trial 1334) — Monotherapy · N=224 vs 224
p<0.0001
SOLO 2 (Trial 1416) — Monotherapy · N=233 vs 236
p<0.0001
CHRONOS (Trial 1224) — + TCS · N=106 vs 315
p<0.0001
EASI-75 at Week 16 (≥75% improvement from baseline)
SOLO 1 — Monotherapy
p<0.0001
SOLO 2 — Monotherapy
p<0.0001
CHRONOS — + TCS
p<0.0001
Peak Pruritus NRS ≥4-point Improvement at Week 16
SOLO 1 — Monotherapy (NRS baseline ≥4: 213 vs 212)
p<0.0001
SOLO 2 — Monotherapy (NRS baseline ≥4: 225 vs 221)
p<0.0001
CHRONOS — + TCS (NRS baseline ≥4: 102 vs 299)
p<0.0001
EASI-90 at Week 16 (≥90% improvement)
Across Trials (dupilumab Q2W vs placebo)
p<0.0001
Durability of Response — CHRONOS at Week 52 (IGA 0/1)
| Response Pattern | Dupilumab Q2W + TCS (n=89) | Placebo + TCS (n=264) |
|---|---|---|
| Responder at Week 16 and Week 52 | 22% | 7% |
| Responder Week 16, Non-responder Week 52 | 20% | 7% |
| Non-responder Week 16, Responder Week 52 | 13% | 6% |
| Non-responder at both Week 16 and 52 | 44% | 80% |
| Overall Responder Rate at Week 52 | 36% | 13% |
IGA Response by Baseline Severity
Moderate vs Severe Disease: Subjects with IGA=3 (moderate) at baseline consistently achieved higher IGA 0/1 response rates than those with IGA=4 (severe): SOLO 1 — Q2W moderate 52% vs severe 21%; SOLO 2 — Q2W moderate 45% vs severe 26%. The Q2W regimen was not inferior to QW in overall efficacy and showed higher responses in moderate disease.
Source: BLA 761055 Clinical Review (Brenda Carr, MD) and FDA-approved prescribing information. All percentages are FAS (all randomized). Subjects receiving rescue treatment or with missing data considered non-responders. CMH test stratified by baseline IGA severity and geographic region.
04
Safety & Adverse Drug Reactions
Safety Database: 1,472 subjects treated with dupilumab across 4 trials (Trials 1–4); 739 subjects treated for ≥1 year. Discontinuation due to AEs was 1.9% in dupilumab groups vs 1.9% in placebo (monotherapy through Week 16) and 1.8% vs 7.6% (CHRONOS through Week 52). The overall safety profile was favourable, with conjunctivitis/eye disorders and injection site reactions as the most notable drug-related signals.
Warnings & Precautions
- Hypersensitivity: Generalized urticaria, serum sickness and serum sickness-like reactions reported in <1% of subjects. Two subjects developed high-titer anti-drug antibodies with serum sickness-like reactions. Discontinue immediately if clinically significant hypersensitivity occurs.
- Conjunctivitis and Keratitis: Conjunctivitis was the most frequently reported eye disorder (10% dupilumab vs 2% placebo in monotherapy; 16% vs 9% over 52 weeks). Keratitis reported in 4% dupilumab+TCS vs 0% placebo+TCS at Week 52. Most cases mild-to-moderate and resolved during treatment. Advise patients to report new or worsening eye symptoms.
- Comorbid Asthma: Efficacy and safety not established for treatment of asthma. Advise patients not to adjust or stop asthma therapy without physician guidance.
- Parasitic (Helminth) Infections: Patients with known helminth infections were excluded. Effect on helminthic immunity is unknown.
Adverse Reactions Occurring ≥1% — Week 16 (Table 1, PI)
| Adverse Reaction | Dupi Mono Q2W N=529 | Placebo Mono N=517 | Dupi+TCS Q2W N=110 | Placebo+TCS N=315 |
|---|---|---|---|---|
| Injection site reactions | 10% | 5% | 10% | 6% |
| Conjunctivitis (cluster)† | 10% | 2% | 9% | 5% |
| Oral herpes | 4% | 2% | 3% | 2% |
| Other herpes simplex virus‡ | 2% | 1% | 1% | <1% |
| Eye pruritus | 1% | <1% | 2% | 1% |
| Blepharitis | <1% | <1% | 5% | 1% |
| Keratitis (cluster)§ | <1% | 0% | 4% | 0% |
| Dry eye | <1% | 0% | 2% | <1% |
† Conjunctivitis cluster includes allergic, bacterial, viral, giant papillary conjunctivitis, eye irritation, and eye inflammation.
‡ Herpes simplex cluster excludes eczema herpeticum.
§ Keratitis cluster includes keratitis, ulcerative, allergic, atopic keratoconjunctivitis, and ophthalmic herpes simplex.
Monotherapy data pooled from Trials 1334, 1416 (AD-1021). Source: FDA-approved prescribing information, March 2017.
Specific Safety Signals
Eosinophilia
Initial transient increase in eosinophil count observed in monotherapy trials (not in TCS trial). Counts declined to near-baseline by Week 16. Treatment-emergent eosinophilia ≥500 cells/µL was similar between groups; <1% dupilumab-treated had ≥5,000 cells/µL.
Eczema Herpeticum & Herpes Zoster
Rate of eczema herpeticum similar between placebo and dupilumab groups. Herpes zoster <0.1% dupilumab vs <1% placebo (16-week trials). In CHRONOS, herpes zoster 1% dupilumab+TCS vs 2% placebo+TCS.
Eye Disorders (AESI)
Conjunctivitis the primary ocular safety signal; most events mild-to-moderate. Over 52 weeks (CHRONOS): 16% dupilumab vs 9% placebo. Keratitis in 4% dupilumab+TCS vs 0% placebo+TCS at 52 weeks (12 vs 0 per 100 subject-years). Most resolved during treatment. Mechanism not fully elucidated; may relate to altered IL-4/IL-13 signalling at ocular surface.
Serious Adverse Events
More SAEs reported in placebo group than dupilumab group during 16-week period (placebo 5%, dupilumab Q2W 2.5%). Pattern consistent at 52 weeks. Three deaths in the AD program (asthma exacerbation, completed suicide, road traffic accident) — none considered related to dupilumab.
Immunogenicity
| Parameter | 16-Week Monotherapy | 52-Week + TCS |
|---|---|---|
| Anti-drug antibody (ADA) development | ~7% (dupilumab) | ~7% (dupilumab+TCS) |
| Neutralizing ADA | ~30% of ADA+ ≈ 2% overall | ~14% of ADA+ ≈ 1% overall |
| Persistent antibody response | Not characterized | ~2% (≥2 consecutive positive samples) |
| Clinical impact | ADA associated with lower serum dupilumab concentrations; some high-titer ADA+ subjects had no detectable drug | Same pattern |
| Placebo ADA | ~2% | ~8% (placebo+TCS) |
Drug Interactions
Live Vaccines: Avoid. Immune response to live vaccines not evaluated with dupilumab.
Non-Live Vaccines: Antibody responses to tetanus toxoid (Adacel) and meningococcal polysaccharide (Menomune) were similar in dupilumab-treated and placebo-treated subjects at 12 weeks of treatment. No dose adjustment required.
CYP450 Substrates: IL-4 and IL-13 can alter CYP450 enzyme formation during chronic inflammation. Monitor effect or concentrations of narrow therapeutic index CYP450 substrates (e.g., warfarin, cyclosporine) on initiation or discontinuation of dupilumab. No formal drug interaction studies conducted.
Source: BLA 761055, FDA-approved prescribing information March 2017, Clinical Review Brenda Carr MD.
05
Pharmacology & Pharmacokinetics
Mechanism of Action
Dupilumab is a fully human IgG4 monoclonal antibody that specifically binds the IL-4Rα subunit. The IL-4Rα chain is shared between two distinct receptor complexes: the Type I receptor (IL-4Rα + γc, expressed on T cells, mast cells, basophils) which is the primary signalling complex for IL-4, and the Type II receptor (IL-4Rα + IL-13Rα1, expressed on non-haematopoietic cells including keratinocytes and fibroblasts) which mediates both IL-4 and IL-13 signalling. By blocking IL-4Rα with a single agent, dupilumab prevents both pathways simultaneously.
Downstream effects of IL-4Rα blockade: Inhibition of STAT6 phosphorylation → reduced TARC/CCL17, eotaxin-3, IgE class switching (B cells), Th2 polarisation, and epithelial barrier disruption. Consistent with this, serum IL-4 and IL-13 levels are elevated following dupilumab treatment (ligand accumulation due to receptor blockade), while clinical markers of type 2 inflammation improve.
Pharmacokinetic Parameters
Cmax (after 600 mg SC load)
70.1 ± 24.1 µg/mL
Reached ~1 week post-initial dose
Steady-State Trough (300 mg Q2W)
73.3–79.9 µg/mL
Achieved by Week 16 (mean ± SD ~40 µg/mL SD)
Steady-State Trough (300 mg QW)
173–193 µg/mL
Twice recommended dosing frequency
Bioavailability (SC)
~64%
Estimated from SC vs IV data
Volume of Distribution
4.8 ± 1.3 L
Central compartment (small Vd, limited tissue distribution)
Time to Non-detectable (<78 ng/mL)
10–13 wk
After last steady-state dose (Q2W/QW, respectively)
Pharmacokinetic Characteristics
| Parameter | Details |
|---|---|
| Absorption | Slow subcutaneous absorption; Tmax ~1 week after single 600 mg load |
| Distribution | Low volume of distribution (~4.8 L); minimal tissue penetration as expected for large IgG molecule |
| Metabolism | Not formally characterized. Expected to undergo catabolism to small peptides and amino acids via standard IgG catabolic pathways |
| Elimination | Nonlinear (target-mediated drug disposition, TMDD). Exposure increases >dose-proportionally: 30-fold AUC increase for 8-fold dose increase (75→600 mg) |
| Dose linearity | Non-linear TMDD. At higher doses/steady-state, target saturation predominates and PK approaches linearity |
| Body weight effect | Higher body weight → lower trough concentrations. No dose adjustment required based on available data |
| Geriatric (≥65 yr) | Steady-state trough 69.4±31.4 µg/mL (Q2W). No dose adjustment required |
| Renal/Hepatic impairment | No formal studies conducted |
| Drug interaction studies | Not conducted with DUPIXENT |
Pharmacodynamics
Receptor blockade with dupilumab leads to predictable pharmacodynamic changes: serum IL-4 and IL-13 levels increase following treatment (consistent with ligand accumulation), while markers of type 2 inflammation — including TARC/CCL17, total IgE, and peripheral eosinophil count — decrease over the treatment period. In monotherapy trials, a transient initial rise in eosinophil counts was observed (not seen in TCS combination trial), with levels returning to near-baseline by Week 16.
PD–Efficacy Relationship: The exact pharmacodynamic mechanism(s) by which dupilumab exerts its clinical effects on AD lesions has not been fully defined. The relationship between pharmacodynamic biomarker changes (e.g., TARC, IgE) and clinical endpoints remains an active area of investigation.
Description
| Property | Value |
|---|---|
| Class | Recombinant human IgG4 monoclonal antibody |
| Molecular target | IL-4Rα (interleukin-4 receptor alpha subunit) |
| Molecular weight | ~147 kDa |
| Production | Chinese Hamster Ovary (CHO) cell suspension culture, recombinant DNA technology |
| Formulation | Sterile, preservative-free, clear to slightly opalescent, colorless to pale yellow solution |
| Excipients | L-arginine hydrochloride (10.5 mg), L-histidine (6.2 mg), polysorbate 80 (4 mg), sodium acetate (2 mg), sucrose (100 mg), water for injection; pH 5.9 |
| Presentation | 300 mg/2 mL single-dose pre-filled syringe (with or without needle shield); 2.25 mL siliconized Type-1 clear glass; non-latex needle cap |
Source: BLA 761055 prescribing information Section 12, Clinical Pharmacology. No formal drug interaction studies have been conducted. CYP450 monitoring warranted for narrow-TI substrates.
06
Dosing & Contraindications
Recommended Dosing Regimen
Moderate-to-Severe Atopic Dermatitis (Adults)
- Loading dose: 600 mg SC (two 300 mg injections at different sites) at Week 0
- Maintenance: 300 mg SC every other week (Q2W)
- Administer into thigh, abdomen (except 5 cm around navel), or upper arm (caregiver only)
- Rotate injection sites; do not inject into tender, damaged, bruised, or scarred skin
- Allow syringe to reach room temperature for ≥45 minutes before injection
Missed Dose Instructions
- If missed dose is identified within 7 days: administer immediately and resume original schedule
- If >7 days since missed dose: skip and administer next dose on the original schedule
- May be used with or without topical corticosteroids (TCS)
- Topical calcineurin inhibitors may be added for problem areas (face, neck, intertriginous, genital)
Note on Q2W vs QW dosing: A third arm (300 mg QW) was included in all three pivotal trials. This regimen did not demonstrate additional treatment benefit over 300 mg Q2W and was not approved. The approved regimen is 600 mg loading → 300 mg Q2W.
Dosage Forms & Strengths
| Form | Strength | NDC |
|---|---|---|
| Single-dose pre-filled syringe with needle shield | 300 mg/2 mL | 0024-5914-01 (pack of 2) |
| Single-dose pre-filled syringe (without needle shield) | 300 mg/2 mL | 0024-5916-01 (pack of 2) |
Storage & Handling
| Condition | Specification |
|---|---|
| Refrigerated storage | 36–46°F (2–8°C); store in original carton, protected from light |
| Room temperature storage | ≤77°F (25°C) for maximum 14 days; discard if >14 days at room temperature |
| Prohibited conditions | Do NOT freeze. Do NOT expose to heat. Do NOT shake. Do NOT expose to direct sunlight. |
| Pre-injection | Allow to reach room temperature (≥45 minutes before injection; do not use external heat source) |
| Preservative | None — discard any unused portion |
Contraindications
Known Hypersensitivity: Dupilumab is contraindicated in patients with known hypersensitivity to dupilumab or any excipient in DUPIXENT. Hypersensitivity reactions including generalized urticaria, serum sickness, and serum sickness-like reactions have been reported in <1% of subjects.
Special Populations
| Population | Guidance |
|---|---|
| Pregnancy | No human data available. Human IgG4 crosses the placental barrier; fetal exposure possible. No adverse developmental effects in cynomolgus monkeys at doses up to 10× MRHD through organogenesis to parturition. Benefits vs risks must be assessed individually. |
| Lactation | No data on dupilumab presence in human milk. Human IgG present in breast milk. Consider benefits of breastfeeding alongside maternal clinical need. |
| Pediatric (<18 yr) | Safety and efficacy not established at initial approval (2017). [Note: subsequent label updates expanded indication to adolescents and children.] |
| Geriatric (≥65 yr) | 67/1472 subjects ≥65 years in pivotal program. No differences in safety or efficacy observed; however, sample size insufficient for definitive conclusions. No dose adjustment required. |
| Renal impairment | No formal studies; no dose adjustment recommended based on population PK. |
| Hepatic impairment | No formal studies; no dose adjustment recommended. |
| Body weight | Higher body weight associated with lower trough concentrations; clinical significance not established; no weight-based dose adjustment recommended. |
Key Drug Interactions
- Live Vaccines: Avoid use of live (attenuated) vaccines in patients treated with dupilumab. Immune response to live vaccines not formally studied.
- CYP450 Narrow Therapeutic Index Substrates (e.g., warfarin, cyclosporine): IL-4 and IL-13 can alter CYP450 enzyme expression. Upon initiation or discontinuation of dupilumab, monitor for pharmacodynamic effects or drug concentrations of CYP450 substrates with narrow therapeutic windows.
Source: BLA 761055 FDA-approved prescribing information (March 2017). This profile reflects the original approval label; subsequent label supplements have expanded the indication to additional populations and indications (asthma, CRSwNP, EoE, prurigo nodularis, CSU).
07
Regulatory History
Application Type
BLA
Biologics License Application
Application Number
761055
Orig1s000
Review Classification
Priority
PDUFA goal: March 29, 2017
Regulatory Timeline (U.S.)
JULY 29, 2016
BLA 761055 Received by FDA
Submitted July 28, 2016; received July 29, 2016. Division of Dermatology and Dental Products (DDDP) / ODE III.
MARCH 15, 2017
Clinical Review Completed
Review by Brenda Carr, MD; recommendation: Approval for moderate-to-severe AD in adults inadequately controlled by topical therapies.
MARCH 28, 2017
Initial FDA Approval
Approved for moderate-to-severe atopic dermatitis in adult patients (≥18 years) inadequately controlled by topical prescription therapies. First systemic biologic approved for AD. BLA 761055 Orig1s000.
OCTOBER 2018
Supplemental Approval — Asthma (≥12 yr)
Expanded indication for moderate-to-severe asthma as add-on maintenance therapy.
JUNE 2019
Supplemental Approval — AD Adolescents (12–17 yr)
Expanded to adolescents 12–17 years with moderate-to-severe AD.
JUNE 2022
Supplemental Approval — AD Children (6–11 yr)
Further expansion to children 6–11 years.
JUNE 2022
Approval — Eosinophilic Esophagitis (≥12 yr)
First FDA approval for EoE in adolescents and adults.
SEPTEMBER 2022
Approval — Prurigo Nodularis (Adults)
First FDA approval for prurigo nodularis.
MARCH 2024
Approval — Chronic Spontaneous Urticaria (≥12 yr)
For patients ≥12 years who remain symptomatic on H1 antihistamines.
Regulatory Context
First-in-Class Milestone: Dupilumab’s March 2017 approval represented the first systemic biologic approved for atopic dermatitis and the first FDA approval for a targeted therapy specifically designed for type 2 inflammatory disease in dermatology. The clinical reviewer concluded that dupilumab would “considerably advance the state of the treatment armamentarium” and would be “the first systemic product approved for AD since corticosteroids.” Priority Review was granted reflecting the unmet medical need in this population.
Regulatory Review Team
| Role | Detail |
|---|---|
| Clinical Reviewer | Brenda Carr, MD |
| Division | Division of Dermatology and Dental Products (DDDP) |
| Office | ODE III (Office of Drug Evaluation III) |
| Applicant | Regeneron Pharmaceuticals, Inc. (BLA holder) / sanofi-aventis U.S. LLC (co-marketer) |
| Reference ID | 4075125 (Clinical Review); 4075926 (Label) |
| Manufacturing | Regeneron Pharmaceuticals, Inc., Tarrytown, NY 10591 (U.S. License No. 1760) |
Postmarketing Requirements & Commitments
Postmarketing commitments included: (1) ophthalmological assessments incorporated into an ongoing open-label extension (OLE) study to further evaluate the eye disorder signal; (2) ongoing pharmacovigilance for conjunctivitis, keratitis, and herpes virus infections. The eye disorder signal was considered the primary identified risk, offset by the significant unmet need and favourable benefit-risk profile.
Regulatory timeline based on BLA 761055 clinical review and FDA Drugs@FDA records. Subsequent supplemental approvals are listed for contextual completeness and reflect post-2017 label expansions not covered by the original BLA documents uploaded. For the most current prescribing information visit: https://www.fda.gov/drugsatfda (BLA 761055).