--- title: "Rocatinlimab | PepTracker Pro" url: https://peptrackerpro.com/peptides/rocatinlimab description: "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." 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) # 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. Aliases Rocatinlimab +8 more Evidence High Evidence Last Updated 2026-09-26 Reading Time 9 min ## What It Is Rocatinlimab (development codes AMG 451 and KHK4083) is a monoclonal antibody that targets OX40 (CD134/TNFRSF4), a costimulatory receptor expressed on activated T cells. OX40 and its ligand OX40L form a 'second signal' that amplifies and sustains effector and memory T-cell responses; in atopic dermatitis and other chronic inflammatory diseases this axis helps keep pathogenic T cells activated and drives the T2/T1/T17/T22 inflammation behind persistent, relapsing disease. There are two ways to drug the axis, and rocatinlimab sits at the opposite pole from amlitelimab. Amlitelimab targets the ligand (OX40L) on antigen-presenting cells and simply blocks the signal without killing cells. Rocatinlimab targets the OX40 receptor on the T cells themselves and, through an antibody-dependent cellular cytotoxicity (ADCC) mechanism, actually reduces the number of OX40-expressing pathogenic effector and memory T cells - what its developers branded a 'T-cell rebalancing' therapy. The strategic bet behind that depleting design was disease modification: by pruning the pathogenic memory T-cell pool that fuels flares, rocatinlimab was hoped to deliver deep responses and durable, off-drug disease control rather than the continuous suppression offered by cytokine blockers. KHK4083 originated at Kyowa Kirin; in 2021 Amgen entered a large collaboration to co-develop and co-commercialize it as AMG 451, and the drug advanced into an unusually broad Phase 3 program called ROCKET, comprising eight studies in moderate-to-severe atopic dermatitis plus programs in prurigo nodularis and moderate-to-severe uncontrolled asthma. The pivotal atopic-dermatitis data were genuinely positive. In ROCKET-IGNITE (NCT05398445), a 24-week, randomized, double-blind, placebo-controlled trial in 769 adults - including patients previously treated with biologics or JAK inhibitors - rocatinlimab added to background topical therapy met both co-primary endpoints: at week 24, EASI-75 (75% improvement in the Eczema Area and Severity Index) was reached by about 42.3% of the higher-dose group and 36.3% of the lower-dose group versus roughly 13% on placebo, and vIGA-AD 0/1 (clear or almost-clear skin) by about 23.6% and 19.1% versus placebo. In the ROCKET-HORIZON monotherapy study (NCT05651711), EASI-75 reached about 33% on rocatinlimab 300 mg versus 14% on placebo, and vIGA-AD 0/1 about 19% versus 7%. The pooled ROCKET-IGNITE and ROCKET-HORIZON results were published in The Lancet in 2025, and a long-term extension (ROCKET-ASCEND) reported top-line data in September 2025. The most common treatment-emergent adverse events were pyrexia (fever), chills, headache and mouth/aphthous ulcers, reflecting the drug's immune-activating-then-depleting pharmacology. But two problems undid the program. First, commercially: rocatinlimab was efficacious versus placebo but did not show superiority over the market-leading eczema biologic dupilumab, and its response rates were more modest than those of some competing agents, raising doubts about its differentiation. In January 2026 Amgen announced the termination of the collaboration, citing strategic portfolio prioritization, and returned global rights to Kyowa Kirin, which said it would take full control and pursue regulatory submission in the first half of 2026. Second, and decisively, safety: on March 3, 2026 Kyowa Kirin announced the discontinuation of all rocatinlimab clinical trials after a safety review identified cases of Kaposi's sarcoma - one newly confirmed and one suspected, in addition to a previously confirmed case across the program - which the company said suggested a potential mechanistic link to OX40-pathway modulation and could not be excluded even though the cases fell below expected background rates. The discontinuation spanned atopic dermatitis, prurigo nodularis and uncontrolled asthma; participants were allowed to complete safety follow-up before formal study termination. The episode reframed the whole OX40/OX40L field: rocatinlimab's OX40-receptor-depleting mechanism came under scrutiny as a possible driver of the malignancy signal, while the OX40-ligand blocker amlitelimab, which reported only a single Kaposi's sarcoma case, proceeded toward regulatory submission - leaving open the question of whether the risk is specific to depleting the OX40-bearing T cells or a broader class concern. Rocatinlimab is investigational, was never approved by the FDA or any other regulator, and its development program has been halted. Also known as: Rocatinlimab, AMG 451, KHK4083, anti-OX40 monoclonal antibody, anti-OX40 receptor antibody, OX40 antagonist antibody, T-cell rebalancing therapy, ROCKET program antibody, Kyowa Kirin OX40 antibody ## Why Researchers Study It Researchers studied rocatinlimab because it tested one of immunology's most ambitious ideas: not just suppressing inflammation, but resetting its cellular drivers. By binding the OX40 receptor on activated T cells and depleting the pathogenic effector and memory populations that sustain chronic disease, rocatinlimab aimed for disease modification - deep responses and durable, off-drug control - rather than the continuous cytokine suppression offered by drugs like dupilumab. That 'T-cell rebalancing' thesis, and the receptor-depleting design that distinguishes it from the ligand-blocking amlitelimab, made it a landmark test of whether the OX40 axis could be drugged for lasting benefit in atopic dermatitis and beyond (prurigo nodularis, asthma). The story ended as a cautionary tale that is, if anything, more scientifically instructive than a clean success. Rocatinlimab met its Phase 3 endpoints and was published in The Lancet, yet it failed commercially by not beating dupilumab and then failed on safety when a small cluster of Kaposi's sarcoma cases pointed to a possible malignancy risk from OX40-pathway modulation, prompting Kyowa Kirin to halt every trial in 2026. That outcome - especially set against amlitelimab's continued advance with only a single such case - turned rocatinlimab into a defining data point in a live debate: does depleting OX40-bearing T cells carry a distinct cancer-surveillance risk, or is this a class-wide concern for the OX40 axis? For anyone studying costimulation blockade, T-cell-directed biologics, or the risk-benefit of disease-modifying immunotherapy, rocatinlimab is now essential reading. ## Proposed Mechanisms - OX40 receptor (CD134/TNFRSF4) targeting: rocatinlimab binds OX40 on activated T cells, blocking the OX40-OX40L costimulatory 'second signal' that amplifies and sustains effector and memory T-cell responses. - T-cell depletion / rebalancing via ADCC: beyond blocking the signal, the antibody engages antibody-dependent cellular cytotoxicity to reduce the number of OX40-expressing pathogenic effector and memory T cells - the feature that distinguishes it from the non-depleting ligand blocker amlitelimab. - Aim of disease modification: by pruning the pathogenic memory T-cell pool thought to drive relapses, rocatinlimab was designed to produce deep responses and durable, potentially off-drug disease control rather than continuous suppression. - Broad dampening of type-2 and mixed inflammation: reducing OX40-driven T-cell activity is proposed to calm the T2/T1/T17/T22 inflammatory program underlying atopic dermatitis and related diseases, upstream of individual cytokines such as IL-4/IL-13. - Transient immune activation on dosing: engaging OX40 can briefly activate T cells before depletion, consistent with the observed pyrexia, chills and mucosal (aphthous ulcer) adverse events. - Possible OX40-pathway malignancy risk: the Kaposi's sarcoma cases that ended the program raised the hypothesis that depleting or modulating OX40-bearing T cells may impair immune surveillance, a concern now central to interpreting the OX40 versus OX40L therapeutic strategies. ## Evidence Snapshot High Evidence Low Medium High | Study Type | Model | Outcome | Link | | --- | --- | --- | --- | | Phase 3 randomized, double-blind, placebo-controlled trial ROCKET-IGNITE (NCT05398445) in adults with moderate-to-severe atopic dermatitis, on background topical therapy; part of the results published in The Lancet (2025). | 769 adults with moderate-to-severe atopic dermatitis (including patients previously treated with biologics or JAK inhibitors) randomized to higher-dose or lower-dose rocatinlimab (subcutaneous, every 4 weeks) added to topical therapy, or placebo, over 24 weeks. | Both co-primary endpoints were met at week 24: EASI-75 was reached by about 42.3% (higher dose) and 36.3% (lower dose) versus roughly 13% on placebo, and vIGA-AD 0/1 by about 23.6% and 19.1% versus placebo (all statistically significant). The most common adverse events were pyrexia, chills and headache; gastrointestinal ulceration occurred in under 1%. | Source | | Phase 3 randomized, double-blind, placebo-controlled monotherapy trial ROCKET-HORIZON (NCT05651711) in adults with moderate-to-severe atopic dermatitis; pooled with IGNITE in the 2025 Lancet publication. | Adults with moderate-to-severe atopic dermatitis randomized to rocatinlimab monotherapy (300 mg) or placebo, with a dupilumab reference arm for context. | EASI-75 reached about 33% on rocatinlimab versus 14% on placebo, and vIGA-AD 0/1 about 19% versus 7% - statistically superior to placebo but showing NO superiority over dupilumab, with adverse events including pyrexia, chills and aphthous ulcers. This efficacy-but-not-differentiation profile contributed to the drug's commercial deprioritization. | Source | | Phase 3 long-term extension ROCKET-ASCEND (top-line data reported September 2025) and the broader eight-study ROCKET program spanning atopic dermatitis, prurigo nodularis and uncontrolled asthma. | Participants continuing rocatinlimab from the pivotal atopic-dermatitis studies into long-term follow-up, plus parallel programs in other indications; a vaccine-response study (ROCKET-VOYAGER, NCT05899816) assessed immune competence. | Top-line long-term extension data were reported in September 2025 to characterize maintenance of response and safety. The program was designed to test rocatinlimab's disease-modifying, durable-control thesis at scale, but definitive long-term outcomes were never established in an approved setting because the program was subsequently halted. | Source | | Program discontinuation and safety review (announced March 3, 2026 by Kyowa Kirin after Amgen returned global rights in early 2026). | Safety data pooled across the rocatinlimab clinical program (atopic dermatitis, prurigo nodularis, uncontrolled asthma). | A safety review identified Kaposi's sarcoma - one newly confirmed and one suspected case in addition to a previously confirmed case - suggesting a possible mechanistic link to OX40-pathway modulation. Kyowa Kirin discontinued ALL rocatinlimab clinical trials, allowing participants to complete safety follow-up. The signal contrasts with the OX40-ligand blocker amlitelimab, which reported only one such case and continued toward regulatory submission, sharpening the debate over whether OX40-receptor depletion carries a distinct malignancy risk. | Source | ## Commonly Discussed Benefits 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 Researching Rocatinlimab? Track it, set reminders, and keep notes in the free app. Track in App (https://app.peptrackerpro.com/?add=rocatinlimab) ## Safety & Cautions - Rocatinlimab is an investigational biologic that was NEVER approved by the FDA or any regulator, and its clinical development has been DISCONTINUED (all trials halted by Kyowa Kirin on March 3, 2026). Any product sold as 'rocatinlimab', 'AMG 451' or 'KHK4083' outside a legitimate clinical trial is unverified and should not be used. - The reason the program was stopped is a malignancy safety signal: 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 modulating the OX40 pathway. Although the cases were rare and reportedly below expected background rates, the company judged the biological concern could not be excluded. - As an immunomodulatory antibody that depletes OX40-expressing T cells, class-level considerations include a theoretical risk of infection (including viral reactivation) and potentially blunted responses to vaccines - a dedicated vaccine-response study (ROCKET-VOYAGER, NCT05899816) was part of the program. - Injection- and infusion-related adverse events were common in trials: the most frequent treatment-emergent events were pyrexia (fever), chills, headache and mouth/aphthous ulcers (stomatitis), reflecting the antibody's transient immune-activating pharmacology. - Even on efficacy, the drug did not clearly stand out: rocatinlimab beat placebo but did NOT show superiority over the established eczema biologic dupilumab, and its response rates were more modest than some competitors - part of why Amgen deprioritized it before the safety-driven shutdown. Its hoped-for disease-modifying, off-drug durability was never confirmed in an approved setting. ## Comparisons See how Rocatinlimab compares to related peptides: Rocatinlimab vs Icotrokinra (ICOTYDE): https://peptrackerpro.com/compare/rocatinlimab-vs-icotrokinra Rocatinlimab vs Depemokimab: https://peptrackerpro.com/compare/rocatinlimab-vs-depemokimab Rocatinlimab vs Barzolvolimab: https://peptrackerpro.com/compare/rocatinlimab-vs-barzolvolimab Rocatinlimab vs Amlitelimab: https://peptrackerpro.com/compare/rocatinlimab-vs-amlitelimab Rocatinlimab vs Frexalimab: https://peptrackerpro.com/compare/rocatinlimab-vs-frexalimab ## Calculator Tools Use our research tools to explore dosing and reconstitution data: Reconstitution Calculator: https://peptrackerpro.com/calculators ## Citations 1. [1] Efficacy and safety of rocatinlimab for the treatment of moderate-to-severe atopic dermatitis in ROCKET-IGNITE and ROCKET-HORIZON: two global, double-blind, placebo-controlled, randomised phase 3 clinical trials - The Lancet (2025) PubMed (https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(25)01865-3/abstract) 2. [2] Amgen and Kyowa Kirin Provide Top-Line Results From Rocatinlimab Phase 3 IGNITE Study in Adults With Moderate to Severe Atopic Dermatitis (March 2025) - Amgen PubMed (https://www.amgen.com/newsroom/press-releases/2025/03/amgen-and-kyowa-kirin-provide-top-line-results-from-rocatinlimab-phase-3-ignite-study-in-adults-with-moderate-to-severe-atopic-dermatitis) 3. [3] Amgen and Kyowa Kirin Announce Top-Line Results From Rocatinlimab Phase 3 ASCEND Long-Term Extension Study in Adults With Moderate to Severe Atopic Dermatitis (September 2025) - Amgen PubMed (https://www.amgen.com/newsroom/press-releases/2025/09/amgen-and-kyowa-kirin-announce-top-line-results-from-rocatinlimab-phase-3-ascend-long-term-extension-study-in-adults-with-moderate-to-severe-atopic-dermatitis) 4. [4] Kyowa Kirin to Regain Control of Rocatinlimab Development and Commercialization (January 30, 2026) - Kyowa Kirin PubMed (https://www.kyowakirin.com/media_center/news_releases/2026/pdf/e20260130_01.pdf) 5. [5] Kyowa Kirin Announces Discontinuation of Rocatinlimab Clinical Trials (March 3, 2026) - Kyowa Kirin PubMed (https://www.kyowakirin.com/media_center/news_releases/2026/e20260303_01.html) 6. [6] Kyowa Kirin abandons touted eczema drug following safety review (2026) - BioPharma Dive PubMed (https://www.biopharmadive.com/news/kyowa-kirin-discontinue-rocatinlimab-ox40-kaposi-sarcoma/813643/) 7. [7] A Study Evaluating Rocatinlimab in Moderate-to-severe Atopic Dermatitis (ROCKET-IGNITE) - ClinicalTrials.gov NCT05398445 PubMed (https://clinicaltrials.gov/study/NCT05398445) 8. [8] ROCKET: a phase 3 program evaluating the efficacy and safety of rocatinlimab in moderate-to-severe atopic dermatitis - Immunotherapy (2025) PubMed (https://www.tandfonline.com/doi/full/10.1080/1750743X.2025.2464528) ### Keep researching in the app - Log Rocatinlimab 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=rocatinlimab Browse more peptides: https://peptrackerpro.com/peptides ## Related Peptides ### 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 ### 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. 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 View Details: https://peptrackerpro.com/peptides/depemokimab \+ Compare: https://peptrackerpro.com/compare?select=depemokimab Track in App: https://app.peptrackerpro.com/?add=depemokimab ### 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. View Details: https://peptrackerpro.com/peptides/amlitelimab \+ Compare: https://peptrackerpro.com/compare?select=amlitelimab Track in App: https://app.peptrackerpro.com/?add=amlitelimab ### Frexalimab High Evidence Frexalimab (SAR441344) is an investigational second-generation, fully human monoclonal antibody from Sanofi that blocks CD40 ligand (CD40L, also called CD154), a costimulatory 'second signal' that helps activate B cells, T cells and antigen-presenting cells and drives adaptive autoimmunity. Rather than depleting immune cells, frexalimab interrupts the CD40-CD40L checkpoint upstream - a mechanism related to but distinct from the OX40-OX40L blockade of amlitelimab. Its lead indication is relapsing multiple sclerosis (RMS), with a second program in nonrelapsing secondary progressive MS (nrSPMS). In the Phase 2 relapsing-MS trial (NCT04879628, published in the New England Journal of Medicine in 2024), frexalimab cut the number of new gadolinium-enhancing brain lesions at week 12 by 89% (higher-dose IV arm) and 79% (lower-dose subcutaneous arm) versus placebo, and open-label extensions out to two and three years show that disease control and reductions in neurofilament light have been sustained. Crucially, frexalimab is engineered so its Fc region does not activate platelets, which is designed to avoid the thromboembolic complications that halted first-generation anti-CD40L antibodies decades ago. It is now in the Phase 3 FREXALT (relapsing MS, versus teriflunomide) and FREVIVA (nrSPMS, versus placebo) trials, with additional Phase 2 programs in type 1 diabetes (FABULINUS) and systemic lupus erythematosus; a Sjogren's syndrome study was discontinued in 2024 after it fell short on efficacy. Frexalimab is investigational and not approved by any regulator. Immune Modulation: https://peptrackerpro.com/benefits/immune-modulation Inflammation: https://peptrackerpro.com/benefits/inflammation autoimmune: https://peptrackerpro.com/benefits/autoimmune Disease Modification: https://peptrackerpro.com/benefits/disease-modification View Details: https://peptrackerpro.com/peptides/frexalimab \+ Compare: https://peptrackerpro.com/compare?select=frexalimab Track in App: https://app.peptrackerpro.com/?add=frexalimab ## 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": "Rocatinlimab", "description": "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.", "url": "https://peptrackerpro.com/peptides/rocatinlimab", "lastReviewed": "2026-09-26", "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": "Rocatinlimab", "item": "https://peptrackerpro.com/peptides/rocatinlimab" } ] }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "People with moderate-to-severe atopic dermatitis (or their clinicians) who followed rocatinlimab as a promising new option and want to understand why it was discontinued despite positive Phase 3 results?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } }, { "@type": "Question", "name": "Dermatologists and immunologists comparing the two ways to drug the OX40 axis - depleting the OX40 receptor on T cells (rocatinlimab, telazorlimab) versus blocking the OX40 ligand without depletion (amlitelimab) - and what the divergent safety outcomes imply?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } }, { "@type": "Question", "name": "Researchers and clinicians tracking the Kaposi's sarcoma safety signal and whether the malignancy risk is specific to OX40-receptor depletion or a broader class-wide OX40-pathway concern?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } }, { "@type": "Question", "name": "Investors and industry analysts following Amgen's and Kyowa Kirin's pipelines who want the timeline of Amgen's 2026 exit, Kyowa Kirin regaining control, and the subsequent program shutdown?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } }, { "@type": "Question", "name": "Patients and advocates weighing the trade-off between a drug that aimed for durable, disease-modifying, off-treatment control and the safety risk that ended its development?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } }, { "@type": "Question", "name": "Readers researching atopic-dermatitis biologics who are comparing rocatinlimab against approved options such as dupilumab, tralokinumab and lebrikizumab and other investigational agents?", "acceptedAnswer": { "@type": "Answer", "text": "Rocatinlimab is a research peptide studied in preclinical models. 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." } } ] } ] ```