--- title: "Depemokimab | PepTracker Pro" url: https://peptrackerpro.com/peptides/depemokimab description: "Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." lang: en --- Skip to main content **Educational information only.** This site does not provide medical advice. Read full disclaimer (https://peptrackerpro.com/disclaimer) **Research-only content.** This page is for educational purposes and does not constitute medical advice. Read full disclaimer → (https://peptrackerpro.com/research-disclaimer) # Depemokimab High Evidence Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical. Aliases Depemokimab +5 more Evidence High Evidence Last Updated 2026-09-17 Reading Time 7 min ## What It Is Depemokimab (Exdensur, depemokimab-ulaa, GSK3511294) is a next-generation anti-IL-5 antibody defined by one headline feature: it only needs to be injected twice a year. Interleukin-5 (IL-5) is the central cytokine controlling the maturation, survival, activation and recruitment of eosinophils, a type of white blood cell that accumulates in the airways and tissues in 'type 2' inflammatory diseases. In severe eosinophilic asthma, high eosinophil activity drives airway inflammation and the recurrent exacerbations that send patients to the hospital, so blocking IL-5 has become an established treatment strategy - the same target hit by the older antibodies mepolizumab and reslizumab (which bind IL-5) and benralizumab (which binds the IL-5 receptor). Depemokimab is a humanized, affinity-matured IgG1 monoclonal antibody that binds circulating IL-5 with very high affinity and prevents it from engaging the IL-5 receptor alpha (IL-5Ra) complex on eosinophils; in cell-based assays it is roughly 29 times more potent than mepolizumab. What makes it 'ultra-long-acting' is a pair of engineering choices: the affinity maturation that tightens IL-5 binding, and a triple amino-acid substitution (M252Y/S254T/T256E, the 'YTE' mutation) in the antibody's Fc region that increases binding to the neonatal Fc receptor (FcRn) and markedly extends the antibody's elimination half-life. Together these allow a fixed 100 mg subcutaneous dose once every 26 weeks - twice-yearly dosing - versus the every-4-weeks or every-8-weeks schedules of earlier IL-5 biologics. The pivotal evidence comes from the replicate Phase 3 SWIFT-1 (NCT04719832) and SWIFT-2 (NCT04718103) trials in adults and adolescents with severe asthma and an eosinophilic phenotype: added to standard inhaled therapy, twice-yearly depemokimab significantly reduced the annualized rate of asthma exacerbations over 52 weeks - about 58% versus placebo in SWIFT-1 and 48% in SWIFT-2 - and a pooled analysis showed roughly a 72% reduction in exacerbations requiring hospitalization or an emergency-department visit. On that basis the FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype (type 2 inflammation) in patients 12 years and older; it is not a rescue inhaler and does not treat acute bronchospasm. Beyond asthma, depemokimab is being studied in other IL-5-driven, eosinophil-associated diseases - most advanced in chronic rhinosinusitis with nasal polyps (CRSwNP), tested in the ANCHOR-1 (NCT05274750) and ANCHOR-2 (NCT05281523) trials, where it has been approved in China - with additional work in conditions such as eosinophilic granulomatosis with polyangiitis and hypereosinophilic syndrome under exploration. Depemokimab is a prescription biologic used under specialist (pulmonology/allergy) care, not a consumer product. Also known as: Depemokimab, Depemokimab-ulaa, Exdensur, GSK3511294, anti-IL-5 monoclonal antibody, ultra-long-acting anti-IL-5 antibody ## Regulatory Status Approved United States: the FDA approved Exdensur (depemokimab-ulaa) in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype (type 2 inflammation) in adult and adolescent patients aged 12 years and older; it is administered as a fixed 100 mg subcutaneous injection once every 26 weeks (twice yearly) and is not indicated for the relief of acute bronchospasm or status asthmaticus. Depemokimab has additionally been approved in China for chronic rhinosinusitis with nasal polyps (CRSwNP) and is under continued development and regulatory review for CRSwNP and other eosinophil-associated diseases in other regions. Marketed by GSK. ## Why Researchers Study It Depemokimab represents a deliberate attempt to solve one of the biggest practical problems with biologic medicines: adherence. Type 2 inflammatory diseases such as severe eosinophilic asthma are driven by eosinophils, and blocking their master cytokine IL-5 with antibodies like mepolizumab, reslizumab and benralizumab already reduces exacerbations - but those drugs require injections every four or eight weeks, and many patients drift off schedule, losing disease control. By pairing affinity maturation (making the antibody bind IL-5 far more tightly) with a well-characterized Fc engineering trick (the YTE mutation that lengthens antibody half-life through FcRn recycling), GSK created an anti-IL-5 antibody potent and durable enough to work at just two injections a year. That makes depemokimab a proof of concept for 'ultra-long-acting' biologics: if a twice-yearly schedule can match the exacerbation reductions of monthly dosing, the same engineering logic could be applied across type 2 inflammation and beyond. Its pivotal SWIFT trials showed roughly half as many exacerbations and a large drop in the most serious, hospitalization-level events, and its development in chronic rhinosinusitis with nasal polyps and other eosinophilic diseases tests how broadly the ultra-long-acting approach can extend. For the field, depemokimab is both a new option for a common, burdensome disease and a bellwether for whether antibody engineering can turn frequent injections into a twice-a-year routine without sacrificing efficacy. ## Proposed Mechanisms - IL-5 neutralization: depemokimab is a humanized IgG1 monoclonal antibody that binds soluble interleukin-5 (IL-5) with very high affinity and prevents it from engaging the IL-5 receptor alpha (IL-5Ra) complex on eosinophils, blocking the principal signal for eosinophil maturation, survival, activation and recruitment. - Eosinophil reduction and control of type 2 inflammation: by removing IL-5 signaling, the antibody lowers blood and airway eosinophil numbers and dampens the eosinophilic (type 2) inflammation that drives severe asthma exacerbations and nasal-polyp disease. - Affinity maturation for high potency: the antibody has been affinity-matured to bind IL-5 far more tightly than first-generation anti-IL-5 antibodies (roughly 29-fold greater potency than mepolizumab in a cell-based assay), helping maintain target suppression between infrequent doses. - YTE Fc engineering for extended half-life: a triple amino-acid substitution (M252Y/S254T/T256E, the 'YTE' mutation) in the Fc region increases binding to the neonatal Fc receptor (FcRn), enhancing antibody recycling and markedly prolonging elimination half-life - the basis for once-every-26-weeks (twice-yearly) dosing. - Maintenance, not rescue: the mechanism reduces the frequency of exacerbations over time by suppressing underlying eosinophilic inflammation; it does not produce immediate bronchodilation and is not a treatment for acute asthma attacks. ## Evidence Snapshot High Evidence Low Medium High | Study Type | Model | Outcome | Link | | --- | --- | --- | --- | | Phase 3 SWIFT-1 and SWIFT-2 trials (replicate, randomized, double-blind, placebo-controlled) in severe asthma with an eosinophilic phenotype. NCT04719832 (SWIFT-1) and NCT04718103 (SWIFT-2). | Adults and adolescents (aged 12+) with severe asthma and an eosinophilic phenotype, randomized to depemokimab 100 mg subcutaneously once every 26 weeks (weeks 0 and 26) or placebo, added to standard inhaled maintenance therapy, over a 52-week treatment period; primary endpoint the annualized rate of asthma exacerbations. | Twice-yearly depemokimab significantly reduced the annualized rate of asthma exacerbations versus placebo over 52 weeks - approximately a 58% reduction in SWIFT-1 and a 48% reduction in SWIFT-2 - and a pooled analysis showed roughly a 72% reduction in exacerbations requiring hospitalization or emergency care. The safety profile was generally consistent with the anti-IL-5 class (including injection-site reactions, headache and nasopharyngitis). These replicate results supported FDA approval of Exdensur in December 2025. | Source | | Phase 3 ANCHOR-1 and ANCHOR-2 trials (randomized, double-blind, placebo-controlled) in chronic rhinosinusitis with nasal polyps (CRSwNP). NCT05274750 (ANCHOR-1) and NCT05281523 (ANCHOR-2). | Adults with CRSwNP randomized to 100 mg subcutaneous depemokimab once every 26 weeks or placebo over a 52-week treatment period; co-primary endpoints assessing nasal polyp size (endoscopic nasal polyp score) and nasal obstruction/congestion. | Depemokimab reduced nasal polyp burden and nasal obstruction relative to placebo, supporting its development in eosinophilic CRSwNP; on the basis of the ANCHOR program depemokimab (Exdensur) has been approved in China for CRSwNP, with regulatory review continuing in other regions. Full details are reported in the trial disclosures and subsequent publications. | Source | ## Commonly Discussed Benefits anti-inflammatory: https://peptrackerpro.com/benefits/anti-inflammatory respiratory: https://peptrackerpro.com/benefits/respiratory Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation type-2-inflammation: https://peptrackerpro.com/benefits/type-2-inflammation Researching Depemokimab? Track it, set reminders, and keep notes in the free app. Track in App (https://app.peptrackerpro.com/?add=depemokimab) ## Safety & Cautions - Depemokimab (Exdensur) is a prescription biologic that must be prescribed and administered under the care of a qualified clinician, typically a pulmonologist or allergist. It is not a supplement, peptide 'research chemical', or performance product; any product sold as 'depemokimab' or 'GSK3511294' outside a licensed pharmacy is unverified and unsafe. - It is a maintenance (preventive) therapy, NOT a rescue medicine: it does not relieve acute asthma symptoms, acute bronchospasm, or status asthmaticus, and patients must keep their prescribed reliever/rescue inhaler and other maintenance controllers unless a clinician directs otherwise. Corticosteroids should not be stopped abruptly when starting depemokimab. - As with other IL-5-targeted biologics, hypersensitivity reactions (including delayed reactions) can occur, and injection-site reactions, headache and nasopharyngitis are among the more common adverse effects reported; patients should be monitored appropriately. - Pre-existing helminth (parasitic worm) infections should be treated before starting therapy, because eosinophils participate in the immune response to parasites and IL-5 blockade may affect that response; new infection during treatment warrants medical attention. - Because dosing is only twice yearly, the drug persists in the body for a long time, so any adverse effect or change in disease control cannot be quickly reversed by stopping injections; long-term and real-world safety data continue to accumulate, and use in pregnancy and breastfeeding should be discussed with a clinician. - This is background information about an approved medicine and its evidence, not medical advice, and does not describe how any individual should be treated. ## Comparisons See how Depemokimab compares to related peptides: Depemokimab vs Efgartigimod: https://peptrackerpro.com/compare/depemokimab-vs-efgartigimod Depemokimab vs Efzofitimod: https://peptrackerpro.com/compare/depemokimab-vs-efzofitimod Depemokimab vs Icotrokinra (ICOTYDE): https://peptrackerpro.com/compare/depemokimab-vs-icotrokinra Depemokimab vs Pegcetacoplan: https://peptrackerpro.com/compare/depemokimab-vs-pegcetacoplan Depemokimab vs Ziltivekimab: https://peptrackerpro.com/compare/depemokimab-vs-ziltivekimab Depemokimab vs Zilucoplan: https://peptrackerpro.com/compare/depemokimab-vs-zilucoplan Depemokimab vs Barzolvolimab: https://peptrackerpro.com/compare/depemokimab-vs-barzolvolimab Depemokimab vs Amlitelimab: https://peptrackerpro.com/compare/depemokimab-vs-amlitelimab Depemokimab vs Rocatinlimab: https://peptrackerpro.com/compare/depemokimab-vs-rocatinlimab ## Calculator Tools Use our research tools to explore dosing and reconstitution data: Reconstitution Calculator: https://peptrackerpro.com/calculators ## Citations 1. [1] Exdensur (depemokimab-ulaa) FDA Approval History - Drugs.com PubMed (https://www.drugs.com/history/exdensur.html) 2. [2] FDA Approves GSK's Exdensur as Twice-Yearly Add-On Therapy for Severe Asthma - Pharmaceutical Executive PubMed (https://www.pharmexec.com/view/fda-gsk-exdensur-eosinophilic-severe-asthma) 3. [3] FDA Approves Depemokimab as Add-On Maintenance Treatment in Severe Asthma - Pharmacy Times PubMed (https://www.pharmacytimes.com/view/fda-approves-depemokimab-as-add-on-maintenance-treatment-in-severe-asthma) 4. [4] EXDENSUR (depemokimab-ulaa) injection, for subcutaneous use - FDA Prescribing Information (label) PubMed (https://www.accessdata.fda.gov/drugsatfda_docs/label/2026/761458Orig1s000lbl.pdf) 5. [5] Depemokimab, the first ultra-long-acting anti-IL-5 monoclonal antibody for severe eosinophilic asthma - Med (Cell Press) PubMed (https://www.cell.com/med/fulltext/S2666-6340(24)00420-3) 6. [6] Efficacy and Safety of Depemokimab (GSK3511294) in Participants With Chronic Rhinosinusitis With Nasal Polyps (ANCHOR-1; NCT05274750) - ClinicalTrials.gov PubMed (https://clinicaltrials.gov/study/NCT05274750) 7. [7] Exdensur (depemokimab) approved in China for the treatment of chronic rhinosinusitis with nasal polyps (CRSwNP) - GSK PubMed (https://www.gsk.com/en-gb/media/press-releases/exdensur-depemokimab-approved-in-china/) 8. [8] Depemokimab: toward biannual biologic therapy for severe eosinophilic asthma - Respiratory Research PubMed (https://link.springer.com/article/10.1186/s12931-026-03801-4) ### Keep researching in the app - Log Depemokimab to your private tracker - Set a dosing reminder - Compare it side-by-side with your stack Open PepTracker Pro Free: https://app.peptrackerpro.com/?add=depemokimab Browse more peptides: https://peptrackerpro.com/peptides ## Related Peptides ### Efgartigimod High Evidence Efgartigimod (efgartigimod alfa, brand names Vyvgart intravenous and Vyvgart Hytrulo subcutaneous) is a first-in-class antagonist of the neonatal Fc receptor (FcRn) developed by argenx as ARGX-113. It is not a small synthetic peptide but an engineered fragment of the human immunoglobulin G1 (IgG1) antibody - specifically the Fc portion that normally binds FcRn - modified with argenx's ABDEG technology to bind FcRn with much higher affinity than natural IgG at both neutral and acidic pH. FcRn is the salvage receptor that rescues circulating IgG from lysosomal degradation and recycles it back into the blood, giving antibodies their long half-life. By outcompeting endogenous IgG for FcRn, efgartigimod blocks that recycling and drives rapid clearance of IgG - including the pathogenic autoantibodies that cause many autoimmune diseases - typically lowering total IgG by roughly 60-70% within weeks, without reducing IgM, IgA, or albumin. It was the first FcRn blocker ever approved: FDA-approved in December 2021 (Vyvgart IV) for acetylcholine-receptor-antibody-positive generalized myasthenia gravis (gMG) on the strength of the Phase 3 ADAPT trial, followed by a subcutaneous co-formulation with recombinant hyaluronidase (Vyvgart Hytrulo) for gMG in 2023 and for chronic inflammatory demyelinating polyneuropathy (CIDP) in 2024. In May 2026 the FDA expanded the gMG label to all serotypes - including AChR-antibody-negative (seronegative) patients - based on the Phase 3 ADAPT SERON trial, making efgartigimod the first and only therapy approved across every gMG antibody subtype. It is being studied in a broad set of other IgG-driven autoimmune diseases, including primary immune thrombocytopenia, myositis, Sjogren's disease, bullous pemphigoid, and lupus nephritis. Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Neuromuscular Function: https://peptrackerpro.com/benefits/neuromuscular-function Rare Disease Treatment: https://peptrackerpro.com/benefits/rare-disease-treatment Disease Modification: https://peptrackerpro.com/benefits/disease-modification View Details: https://peptrackerpro.com/peptides/efgartigimod \+ Compare: https://peptrackerpro.com/compare?select=efgartigimod Track in App: https://app.peptrackerpro.com/?add=efgartigimod ### Efzofitimod Medium Evidence A first-in-class, intravenous immunomodulatory fusion peptide derived from histidyl-tRNA synthetase that selectively binds neuropilin-2 (NRP2) to dampen inflammation in the lung; in Phase 3 development for pulmonary sarcoidosis, an interstitial lung disease. Inflammation: https://peptrackerpro.com/benefits/inflammation Immune Support: https://peptrackerpro.com/benefits/immune-support View Details: https://peptrackerpro.com/peptides/efzofitimod \+ Compare: https://peptrackerpro.com/compare?select=efzofitimod Track in App: https://app.peptrackerpro.com/?add=efzofitimod ### Icotrokinra (ICOTYDE) High Evidence The first FDA-approved targeted oral macrocyclic peptide — an IL-23 receptor antagonist for moderate-to-severe plaque psoriasis, marking a new era for oral peptide therapeutics. Skin: https://peptrackerpro.com/benefits/skin Inflammation: https://peptrackerpro.com/benefits/inflammation Immune Support: https://peptrackerpro.com/benefits/immune-support View Details: https://peptrackerpro.com/peptides/icotrokinra \+ Compare: https://peptrackerpro.com/compare?select=icotrokinra Track in App: https://app.peptrackerpro.com/?add=icotrokinra ### Pegcetacoplan High Evidence A PEGylated cyclic-peptide inhibitor of complement component 3 (C3) built from two compstatin (Cp05) peptide domains bridged by a 40-kDa PEG chain; marketed as Empaveli/Aspaveli (subcutaneous, for paroxysmal nocturnal hemoglobinuria and, since July 2025, C3 glomerulopathy and primary IC-MPGN) and Syfovre (intravitreal, for geographic atrophy in age-related macular degeneration). It is one of the few complement-targeting therapeutic peptides to reach the market. Immune Support: https://peptrackerpro.com/benefits/immune-support Inflammation: https://peptrackerpro.com/benefits/inflammation View Details: https://peptrackerpro.com/peptides/pegcetacoplan \+ Compare: https://peptrackerpro.com/compare?select=pegcetacoplan Track in App: https://app.peptrackerpro.com/?add=pegcetacoplan ### Ziltivekimab Medium Evidence An investigational, fully human monoclonal antibody that neutralizes the pro-inflammatory cytokine interleukin-6 (IL-6) to test whether lowering vascular inflammation - independently of cholesterol - can prevent heart attacks, strokes and cardiovascular death. Given as a low-volume, once-monthly 15 mg subcutaneous injection (half-life ~57 days), ziltivekimab was originally developed by Corvidia Therapeutics and acquired by Novo Nordisk in 2020 for up to $2.1 billion. It is the flagship clinical test of the 'residual inflammatory risk' hypothesis that grew out of the CANTOS trial of the IL-1 beta antibody canakinumab: the idea that many high-risk patients keep having cardiovascular events because of ongoing inflammation (marked by high-sensitivity C-reactive protein, hsCRP) even when LDL cholesterol is well controlled. In the Phase 2 RESCUE trial ziltivekimab cut hsCRP by up to ~92%, and it advanced into three large Phase 3 cardiovascular outcomes trials - ZEUS, HERMES and ARTEMIS. On July 31, 2026, Novo Nordisk announced that the pivotal ZEUS trial (>6,300 patients with atherosclerotic cardiovascular disease, chronic kidney disease and inflammation) MISSED its primary endpoint: despite clear target engagement (large falls in free IL-6 and hsCRP), ziltivekimab did not reduce major adverse cardiovascular events versus placebo (hazard ratio 0.99, 95% CI 0.88-1.11). The heart-failure trial HERMES and the post-heart-attack trial ARTEMIS continue, with readouts expected in the first half of 2027. Ziltivekimab is a prescription-stage investigational biologic - it is not approved anywhere and is not a supplement or research chemical. Inflammation: https://peptrackerpro.com/benefits/inflammation Cardiovascular: https://peptrackerpro.com/benefits/cardiovascular Kidney Health: https://peptrackerpro.com/benefits/kidney-health Cholesterol Management: https://peptrackerpro.com/benefits/cholesterol-management View Details: https://peptrackerpro.com/peptides/ziltivekimab \+ Compare: https://peptrackerpro.com/compare?select=ziltivekimab Track in App: https://app.peptrackerpro.com/?add=ziltivekimab ### Zilucoplan High Evidence A self-administered, once-daily subcutaneous macrocyclic peptide that inhibits complement component 5 (C5), FDA- and EMA-approved for anti-AChR-positive generalized myasthenia gravis. Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Neuromuscular Function: https://peptrackerpro.com/benefits/neuromuscular-function View Details: https://peptrackerpro.com/peptides/zilucoplan \+ Compare: https://peptrackerpro.com/compare?select=zilucoplan Track in App: https://app.peptrackerpro.com/?add=zilucoplan ### Barzolvolimab Medium Evidence Barzolvolimab (development code CDX-0159) is an investigational humanized IgG1 monoclonal antibody from Celldex Therapeutics that works by a mechanism new to allergy and dermatology: it depletes mast cells. It binds with high specificity to the KIT receptor (CD117), a receptor tyrosine kinase that mast cells depend on for their growth, survival and activation, and blocks KIT from being switched on by its natural ligand, stem cell factor (SCF). Because mast cells cannot survive without KIT signaling, blocking the receptor lowers mast-cell numbers throughout the body - an effect visible as a dose-dependent fall in blood tryptase (a mast-cell marker) and a drop in mast cells in the skin. Mast cells are the central drivers of chronic urticaria (chronic hives): when they release histamine and other mediators they cause the wheals, angioedema and itch that define the disease, so removing the cells themselves is a more upstream approach than blocking a single downstream signal. Barzolvolimab's lead program is chronic spontaneous urticaria (CSU) that no longer responds to antihistamines, where it is being tested in two large replicate Phase 3 trials, EMBARQ-CSU1 and EMBARQ-CSU2, which together enrolled 1,939 patients - the largest Phase 3 program ever run in antihistamine-refractory CSU - with topline results expected in late 2026 and a planned regulatory (BLA) filing in 2027. It has also shown strong Phase 2 results in the chronic inducible urticarias - cold urticaria and symptomatic dermographism - and is being explored in prurigo nodularis, atopic dermatitis and eosinophilic esophagitis. Barzolvolimab is an investigational biologic given by subcutaneous injection under clinical-trial or specialist supervision; it is not approved, and it is not a supplement, nootropic or research chemical. Inflammation: https://peptrackerpro.com/benefits/inflammation Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Skin: https://peptrackerpro.com/benefits/skin View Details: https://peptrackerpro.com/peptides/barzolvolimab \+ Compare: https://peptrackerpro.com/compare?select=barzolvolimab Track in App: https://app.peptrackerpro.com/?add=barzolvolimab ### Amlitelimab High Evidence Amlitelimab (SAR445229, formerly KY1005) is a fully human, non-T-cell-depleting monoclonal antibody from Sanofi that blocks OX40 ligand (OX40L), a costimulatory signal that drives and sustains T-cell-mediated inflammation. Rather than neutralizing a single cytokine like IL-4/IL-13 (dupilumab) or IL-5 (depemokimab), amlitelimab acts upstream at the OX40-OX40L checkpoint to dampen a broad, memory-driven inflammatory program without depleting T cells. Its lead (anchor) indication is moderate-to-severe atopic dermatitis in people aged 12 and older, where a distinctive feature is very infrequent dosing: after a loading dose it is given subcutaneously as little as four times a year (every 12 weeks). In the Phase 3 program - COAST 1, COAST 2 and SHORE - amlitelimab met its primary endpoints with EASI-75 and vIGA-AD 0/1 responses that increased over time, though COAST 2's absolute response rates were more modest and some observers called that readout mixed. Amlitelimab is investigational and not yet approved by any regulator; Sanofi originally gained it through its ~$1.1B acquisition of Kymab in 2021. Inflammation: https://peptrackerpro.com/benefits/inflammation Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Skin: https://peptrackerpro.com/benefits/skin type-2-inflammation: https://peptrackerpro.com/benefits/type-2-inflammation View Details: https://peptrackerpro.com/peptides/amlitelimab \+ Compare: https://peptrackerpro.com/compare?select=amlitelimab Track in App: https://app.peptrackerpro.com/?add=amlitelimab ### Rocatinlimab High Evidence Rocatinlimab (AMG 451 / KHK4083) is an investigational anti-OX40 monoclonal antibody developed by Kyowa Kirin and Amgen for moderate-to-severe atopic dermatitis (eczema). Unlike amlitelimab, which blocks the OX40 ligand (OX40L) on antigen-presenting cells without depleting cells, rocatinlimab binds the OX40 receptor directly on activated pathogenic T cells and reduces (depletes) them - a 'T-cell rebalancing' approach meant to reset the immune drivers of chronic inflammation rather than continuously neutralize a single cytokine. In the large Phase 3 ROCKET program the drug met its co-primary endpoints: in ROCKET-IGNITE (NCT05398445; 769 adults, added to topical therapy) week-24 EASI-75 reached about 42% (higher dose) and 36% (lower dose) versus roughly 13% on placebo, and vIGA-AD 0/1 reached about 24% and 19%; in the ROCKET-HORIZON monotherapy study (NCT05651711) EASI-75 was about 33% versus 14% on placebo, though the drug showed no superiority over dupilumab. The pooled Phase 3 results were published in The Lancet in 2025. Despite hitting its endpoints, the program then unraveled on two fronts: in January 2026 Amgen ended the collaboration on strategic-portfolio grounds and returned global rights to Kyowa Kirin, and on March 3, 2026 Kyowa Kirin discontinued ALL rocatinlimab clinical trials - across atopic dermatitis, prurigo nodularis and uncontrolled asthma - after a safety review identified cases of Kaposi's sarcoma (one newly confirmed and one suspected, in addition to a previously confirmed case) that suggested a possible mechanistic link to OX40-pathway modulation. Rocatinlimab is investigational, was never approved by any regulator, and its clinical development has been halted. View Details: https://peptrackerpro.com/peptides/rocatinlimab \+ Compare: https://peptrackerpro.com/compare?select=rocatinlimab Track in App: https://app.peptrackerpro.com/?add=rocatinlimab ## Structured data ```json [ { "@context": "https://schema.org", "@type": "Organization", "name": "PepTracker Pro", "url": "https://peptrackerpro.com", "logo": "https://peptrackerpro.com/favicon.png", "description": "Evidence-based educational resource dedicated to improving peptide research literacy.", "contactPoint": { "@type": "ContactPoint", "email": "hello@peptrackerpro.com", "contactType": "customer support" }, "sameAs": [] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Depemokimab", "description": "Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical.", "url": "https://peptrackerpro.com/peptides/depemokimab", "lastReviewed": "2026-09-17", "reviewedBy": { "@type": "Organization", "name": "PepTracker Pro Research Team", "url": "https://peptrackerpro.com" }, "isPartOf": { "@type": "WebSite", "name": "PepTracker Pro", "url": "https://peptrackerpro.com" } }, { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://peptrackerpro.com" }, { "@type": "ListItem", "position": 2, "name": "Peptides", "item": "https://peptrackerpro.com/peptides" }, { "@type": "ListItem", "position": 3, "name": "Depemokimab", "item": "https://peptrackerpro.com/peptides/depemokimab" } ] }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "Patients and clinicians interested in the first twice-yearly (every-6-months) IL-5 biologic for severe eosinophilic asthma and how its dosing convenience compares with monthly or bimonthly options?", "acceptedAnswer": { "@type": "Answer", "text": "Depemokimab is a research peptide studied in preclinical models. Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." } }, { "@type": "Question", "name": "Pulmonologists and allergists comparing depemokimab with other type 2 / eosinophil-targeted biologics such as mepolizumab, reslizumab, benralizumab, dupilumab and tezepelumab?", "acceptedAnswer": { "@type": "Answer", "text": "Depemokimab is a research peptide studied in preclinical models. Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." } }, { "@type": "Question", "name": "People with severe asthma, chronic rhinosinusitis with nasal polyps (CRSwNP), or other eosinophil-driven diseases evaluating add-on biologic options?", "acceptedAnswer": { "@type": "Answer", "text": "Depemokimab is a research peptide studied in preclinical models. Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." } }, { "@type": "Question", "name": "Readers interested in antibody engineering - affinity maturation and the 'YTE' Fc modification that extends half-life to enable ultra-long-acting dosing?", "acceptedAnswer": { "@type": "Answer", "text": "Depemokimab is a research peptide studied in preclinical models. Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." } }, { "@type": "Question", "name": "Researchers and industry watchers following GSK's respiratory/immunology franchise and the trend toward less-frequent biologic dosing across type 2 inflammatory diseases?", "acceptedAnswer": { "@type": "Answer", "text": "Depemokimab is a research peptide studied in preclinical models. Depemokimab (brand name Exdensur; nonproprietary name depemokimab-ulaa; development code GSK3511294) is a humanized, affinity-matured IgG1 monoclonal antibody that blocks interleukin-5 (IL-5), the master cytokine for eosinophils - the white blood cells that drive type 2 (eosinophilic) inflammation in severe asthma and related diseases. Developed by GSK, it is the first ultra-long-acting IL-5 biologic, engineered both for very high IL-5 binding affinity (roughly 29-fold more potent than mepolizumab in vitro) and with a triple-amino-acid 'YTE' modification in its Fc region that extends its half-life, enabling a fixed 100 mg subcutaneous injection just twice a year (once every 26 weeks). By neutralizing IL-5 before it can reach the IL-5 receptor on eosinophils, depemokimab lowers blood and airway eosinophils and reduces the flare-ups (exacerbations) that define severe eosinophilic asthma. In the pivotal Phase 3 SWIFT-1 and SWIFT-2 trials, twice-yearly depemokimab cut annualized asthma exacerbations by roughly half versus placebo over 52 weeks (58% in SWIFT-1, 48% in SWIFT-2), with a pooled ~72% reduction in exacerbations requiring hospitalization or emergency care. On the strength of those data, the U.S. FDA approved Exdensur in December 2025 as an add-on maintenance treatment for severe asthma with an eosinophilic phenotype in patients aged 12 and older, and it is also being developed - and, in China, approved - for chronic rhinosinusitis with nasal polyps (CRSwNP). Depemokimab is a prescription biologic given under medical care; it is not a supplement, nootropic, or research chemical." } } ] } ] ```