Request Demo

Last update 13 Oct 2026

Itepekimab

Last update 13 Oct 2026

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Monoclonal antibody

Synonyms

Anti-IL-33 mAb(Regeneron Pharmaceuticals), Immunoglobulin igg4 (230-proline), anti-(human interleukin 33) (human monoclonal regn3500 .gamma.4-chain), disulfide with human monoclonal regn3500 .kappa.-chain, dimer, 伊塔特珠单抗

+ [2]

Target

IL-33

Action

inhibitors

Mechanism

IL-33 inhibitors(Interleukin-33 inhibitors)

Therapeutic Areas

Respiratory DiseasesInfectious DiseasesOtorhinolaryngologic Diseases

Active Indication

Chronic rhinosinusitis with nasal polypsBronchitis, ChronicModerate chronic obstructive pulmonary disease+ [3]

Inactive Indication

Allergic asthmaAsthmaInflammation+ [4]

Originator Organization

Regeneron Pharmaceuticals, Inc.

Active Organization

Sanofi (China) Investment Co. Ltd.

SanofiSanofi-Aventis Recherche & Développement SA

+ [2]

Inactive Organization-

License Organization

Regeneron Pharmaceuticals, Inc.

Sanofi

Drug Highest PhasePhase 3

First Approval Date-

Regulation-

Structure/Sequence

Sequence Code 17746027H

Source: *****

Sequence Code 17746031L

Source: *****

Clinical Trials associated with Itepekimab

NCT07484230

/ WithdrawnPhase 3

A Randomized, Double-blind, Parallel-group, 52-week Trial to Investigate the Efficacy, Safety, and Tolerability of Itepekimab in Adult Japanese Participants With Inadequately-controlled Chronic Rhinosinusitis With Nasal Polyps

This is a randomized, multicenter, double-blind, Phase 3 study with 2 parallel groups. The purpose of this study is to evaluate the efficacy, safety, and tolerability of 2 different dosing regimens of itepekimab monotherapy in Japanese participants aged 18 years or older with chronic rhinosinusitis with nasal polyp(s) (CRSwNP) who are not adequately controlled despite previous surgery and/or treatment with systemic corticosteroid(s) (SCS).
The total study duration par participant is approximately 76 week, including:
* A screening period for up to 4 weeks.
* A randomized study intervention period for up to 52 weeks
* A post-intervention safety follow-up for up to 20 weeks
* The number of visits will be 9 site visits and 20 phone/home visits

Start Date08 May 2026

Sponsor / Collaborator

Sanofi

[+1]

NCT07424144

/ Active, not recruitingPhase 3

A Double-blinded Extension Study to Evaluate the Long-term Safety and Tolerability of Itepekimab in Adult Participants With Inadequately Controlled Chronic Rhinosinusitis With Nasal Polyps (CRSwNP) Who Participated in Either EFC18418 or EFC18419 Clinical Studies

This is a double-blind, parallel-group, Phase 3, 2-arm study that is designed to provide additional safety information, assess the durability of treatment response, and provide additional PK and immunogenicity assessments.
The primary purpose of this study is to evaluate safety and tolerability of both new or continued treatment with itepekimab 300 mg SC high dose or itepekimab 300 mg SC low dose in participants with CRSwNP having completed the intervention period of the clinical studies EFC18418 or EFC18419. A secondary purpose of this study is to provide efficacy outcomes beyond the intervention period of the parent trials EFC18418 and EFC18419.
Study details include:
* The study duration will be up to 72 weeks.
* The intervention duration will be 52 weeks.
* A follow-up period of 20 weeks will be conducted.
* The number of visits will be 8 and the number of phone contacts will be 4.

Start Date12 Mar 2026

Sponsor / Collaborator

Sanofi

[+1]

NCT06834347

/ TerminatedPhase 3

A Randomized, Double-blind, Placebo-controlled, Parallel-group, 52-week Phase 3 Trial to Investigate the Efficacy, Safety, and Tolerability of Itepekimab in Adult Participants With Inadequately-controlled Chronic Rhinosinusitis With Nasal Polyps

EFC18418 is a multinational, randomized, double-blind, placebo-controlled, parallel-group, Phase 3 study with 3 treatment groups. The purpose of the study is to evaluate the efficacy, safety and tolerability of 2 dosing regimens of itepekimab compared to placebo as add-on therapy to intranasal corticosteroids (INCS) in male and female participants with chronic rhinosinusitis with nasal polyps (CRSwNP) aged 18 years of age and older.
Study details include:
* The study duration per participant (4-week screening, 52-week treatment, 20-week safety follow-up) will be up to 76 weeks. For participants transitioning to the LTS18420 study, the study duration will be 56 weeks.
* The treatment duration will be up to 52 weeks.
* The number of visits will be 9 site visits and 20 phone/home visits.

Start Date12 Feb 2025

Sponsor / Collaborator

Sanofi

[+1]

100 Clinical Results associated with Itepekimab

100 Translational Medicine associated with Itepekimab

100 Patents (Medical) associated with Itepekimab

Literatures (Medical) associated with Itepekimab

31 Dec 2026·mAbs

Structures of clinical antibodies bound to IL-33 uncover two distinct epitopes underlying differential efficacy

Article

Author: Chen, Jing ; Wang, Yue ; Wang, Xinquan

Interleukin-33 (IL-33), an alarmin cytokine of the IL-1 family, drives type 2 inflammation through signaling via the ST2 and IL-1RAcP receptors, making it a critical therapeutic target for inflammatory diseases such as asthma and chronic obstructive pulmonary disease. Current therapeutic strategies have primarily focused on antibodies that target IL-33 or ST2 to disrupt their specific interaction. However, the structural mechanisms underlying antibody-mediated neutralization of IL-33 remain poorly understood. Here, we report the structures of three antibodies in clinical trial - etokimab, itepekimab, and tozorakimab - complexed with IL-33, determined by X-ray crystallography and cryo-electron microscopy. Structural analysis reveals two distinct neutralizing epitopes on IL-33, termed Epitope 1 at IL-33/ST2 binding Site 1 and Epitope 2 at IL-33/ST2 binding Site 2. Tozorakimab, which targets Epitope 1, completely blocks ST2 engagement by sterically occluding the ST2 D1-D2 domain-binding interface. In contrast, etokimab and itepekimab, which recognize Epitope 2, interfere with IL-33 recognition of the ST2 D3 domain and thereby only partially inhibit ST2 binding. These structural and biochemical findings provide a molecular explanation for the differential efficacy of the three antibodies in inhibiting IL-33 signaling in cellular assays. Collectively, our results provide valuable insights into the molecular determinants of efficacy for existing IL-33 therapeutics and offer a structural framework for the rational design of next-generation IL-33 targeted inhibitors.

01 Dec 2026·MOLECULAR BIOLOGY REPORTS

Epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis: mechanistic roles and therapeutic implications

Review

Author: Nelson Kumar, Sadhu ; Siva Ganesh, Vakkalagadda ; Rajaram, Cuddapah ; H R, Sneha ; Dhanush, Yarava

BACKGROUND:

Asthma is a heterogeneous chronic inflammatory airway disease affecting over 300 million people worldwide. The airway epithelium serves as the primary interface with environmental stimuli and responds by releasing epithelial-derived alarmins, thymic stromal lymphopoietin (TSLP), interleukin-33 (IL-33), and interleukin-25 (IL-25), which act as upstream regulators of both innate and adaptive immune responses. Current therapies targeting downstream inflammatory mediators demonstrate limited efficacy in severe and refractory asthma, necessitating novel approaches targeting upstream pathways.

OBJECTIVE:

This narrative review examines the mechanistic roles of epithelial alarmins TSLP, IL-33, and IL-25 in asthma pathogenesis, covering their regulation, receptor signalling, downstream immune activation, and contributions to airway remodelling. Current and emerging biologic therapies targeting these alarmins are summarised, with key clinical trials tabulated.

METHODS:

A comprehensive narrative literature review was conducted. Electronic databases searched included PubMed/MEDLINE, Scopus, Web of Science, and ClinicalTrials.gov, covering publications from January 2015 to March 2025, with seminal earlier studies included where relevant. Search terms used included: "TSLP asthma," "IL-33 asthma," "IL-25 asthma," "epithelial alarmins," "thymic stromal lymphopoietin," "tezepelumab," "itepekimab," "astegolimab," "airway inflammation," "ILC2," "airway remodelling," and "biologic therapy severe asthma." Priority was given to original research articles, randomised controlled trials, and systematic reviews; review articles were included to provide mechanistic context. Studies were selected based on relevance to alarmin biology, immunological pathways, and clinical evidence in asthma.

RESULTS:

TSLP: Functions as a central amplifier of type-2 and mixed inflammatory responses through transcriptional regulation following epithelial stimulation. Activates dendritic cells, group 2 innate lymphoid cells (ILC2s), and granulocytes via the TSLPR/IL-7Rα complex, driving both eosinophilic and non-eosinophilic inflammation. Tezepelumab, an anti-TSLP monoclonal antibody, has achieved regulatory approval (FDA/EMA) for severe asthma with demonstrated exacerbation reduction across multiple endotypes (40-60% reduction in clinical trials). IL-33: Constitutively stored in epithelial cell nuclei, acts as an immediate danger signal upon cellular injury, triggering rapid innate immune activation through the ST2/IL-1RAcP receptor complex. Mediates acute exacerbations, airway hyperresponsiveness, and steroid-refractory inflammation. Anti-IL-33 agents including itepekimab, astegolimab, and tozorakimab are in Phase 2-3 clinical development with promising early efficacy data. IL-25: Predominantly produced by epithelial tuft cells, sustains chronic type-2 immunity, mucus hypersecretion, and corticosteroid-insensitive disease phenotypes through IL-17RA/IL-17RB receptor engagement. IL-25-targeted approaches demonstrate preclinical efficacy and are advancing toward clinical evaluation.

CONCLUSION:

Epithelial alarmins represent critical upstream drivers of asthma pathogenesis, orchestrating diverse inflammatory pathways that determine disease endotypes and severity. Therapeutic targeting of TSLP, IL-33, and IL-25 offers a paradigm shift from downstream cytokine inhibition to source-directed intervention, with potential to reduce exacerbations, prevent airway remodelling, and improve disease control across different asthma phenotypes. The success of anti-TSLP therapy and ongoing clinical development of IL-33 and IL-25 inhibitors validate epithelial alarmins as essential molecular targets for precision medicine approaches in severe and refractory asthma.

01 Oct 2026·Translational Research

Anti-IL-33 monoclonal antibody attenuates MAILD by suppressing the PI3K/AKT/mTOR signal pathway

Article

Author: Qiu, Liyan ; Guo, Zhen ; Men, Liqiong ; Su, Qiyan ; Zhu, Jiarui ; Yang, Jumei ; Hao, Meng ; Huang, Zhuanhui ; Cui, Xi ; Zhang, Sigong

BACKGROUND:

Interstitial lung disease (ILD) is a serious complication of idiopathic inflammatory myopathies (IIM) for which targeted therapies are lacking. Our previous work identified interleukin‑33 (IL‑33) as playing a key role in the pathogenesis of IIM-ILD.

METHODS:

Using a mouse model of myositis-associated ILD (MAILD), including IL‑33 knockout (IL‑33 KO) mice, together with clinical samples, proteomics and multiple cellular reporter systems (dual luciferase, mTOR nuclear translocation reporter), we assessed the effects of IL‑33 NAb on lung injury repair, macrophage polarisation and endothelial/epithelial protection.

RESULTS:

IL‑33 NAb significantly reduced pulmonary inflammation and collagen deposition, improved body weight, and ameliorated liver and muscle biochemical parameters in MAILD mice. Notably, IL‑33 KO MAILD mice exhibited almost identical phenotypic improvements to the IL‑33 NAb‑treated group, confirming IL‑33 as a core driver of the disease. Mechanistically, IL‑33 NAb blocked aberrant NETs deposition, reduced PI3K/AKT/mTOR phosphorylation, and suppressed NF‑κB and STAT3 activation. Consequently, it inhibited both pro‑inflammatory M1 and pro‑fibrotic M2 macrophage polarisation, alleviated alveolar epithelial‑mesenchymal transition (EMT), preserved endothelial CD31 expression, and enhanced tissue repair via cytoskeletal remodelling.

CONCLUSIONS:

IL‑33 NAb exerts significant anti‑inflammatory and anti‑fibrotic effects through multi‑target interventions. Both genetic (IL‑33 KO) and pharmacological (IL‑33 NAb) evidence demonstrate that IL‑33 is a key driver of IIM-ILD, acting via PI3K/AKT/mTOR‑mediated NF‑κB/STAT3 activation. This provides a novel therapeutic strategy for IIM-ILD.

113

News (Medical) associated with Itepekimab

01 Oct 2026

·www.biospace.com

Sanofi pays Regeneron $1B upfront to continue search for Dupixent successor

iStock, Afry Harvy Sanofi and Regeneron have had a long and “sometimes contentious” partnership, BMO Capital Markets noted, as the companies contend with the looming loss of exclusivity of their blockbuster drug Dupixent. As key patent expiries loom over immunology juggernaut Dupixent, Sanofi and Regeneron have renewed their long-term partnership, with the French pharma fronting $1 billion to advance four long-acting, next-generation antibodies for immune-mediated conditions. Sanofi is offering Regeneron up to $7 billion more in development, regulatory and commercial milestones, according to a Thursday morning announcement . The French pharma will co-develop and co-commercialize four Regeneron-discovered antibodies. “Today’s agreement extends a productive (but at some points contentious) partnership,” BMO Capital Markets wrote on Thursday morning. Just last year, Regeneron sued Sanofi , alleging that the French pharma didn’t provide “full access to material information” about Dupixent’s sales. Sanofi has also resisted efforts by Regeneron to audit records related to the blockbuster drug. The companies have settled this dispute, according to their Thursday announcement. The slate of experimental therapies in the renewed partnership is led by the IL-13-targeting REGN20423, which is currently in Phase 1 development for atopic dermatitis. The three other assets are preclinical and include an IL-4xIL-13 bispecific, an anti-IL-4 therapy and a molecule designed to target IL-4R-alpha. All three are expected to enter human studies next year, according to the companies. Legal Regeneron Sues Sanofi, Alleging Stonewalling in Dupixent Pact According to the lawsuit, Sanofi has failed to provide partner Regeneron adequate information regarding the sales of Dupixent—including agreements with payers and pharmacy benefit managers that determine pricing and rebates for the drug. February 7, 2025 · 2 min read · Tristan Manalac Read more The deal could expand beyond these four therapies, as well. Regeneron has the option to include Sanofi’s TSLPxIL-13 bispecific lunsekimig into the alliance—a right that Regeneron can choose to exercise once the molecule clears Phase 3 testing for chronic obstructive pulmonary disease (COPD). Profits for these assets, if they reach the market, will be split 50-50. Lunsekimig is in a pair of Phase 3 trials for COPD, both of which are expected to have initial readouts in 2029. Sanofi is also developing lunsekimig for asthma and chronic rhinosinusitis with nasal polyps, for which it cleared respective mid-stage studies in April. Lunsekimig was also being studied in atopic dermatitis but missed the primary endpoint of improving disease severity in the exploratory Phase 2b VELVET trial. The renewed deal positions “both companies for continued leadership in the development of the next generation of therapeutics for type 2 inflammation-driven disease,” BMO added. Sanofi and Regeneron are expanding their decades-long alliance amid exclusivity concerns for Dupixent. The drug surged 26% last year to bring in $17.8 billion worldwide. But a key U.S. patent is set to expire in 2031 , which could open the blockbuster up to biosimilar challenge and, in turn, erode revenue. Sanofi general counsel Roy Papatheodorou explained during the company’s first quarter call in April that Dupixent has a web of patents extending as far as 2045. Still, the pharma has been working diligently to find a successor. Earnings Sanofi defends Dupixent patents, but execs insist it has nothing to do with CEO change Sanofi’s interim leadership sought on a Thursday earnings call to quell concerns that its sudden defense of Dupixent’s patents had anything to do with the departure of CEO Paul Hudson. April 23, 2026 · 3 min read · Annalee Armstrong Read more Sanofi had pinned a lot of hopes on the autoimmune asset amlitelimab, which came from the $1.4 billion acquisition of Kymab and had been under development for atopic dermatitis and celiac disease. Sanofi in July ended the asset’s development in atopic dermatitis , noting that “the totality of efficacy and safety evidence generated to date does not support further development” in this indication. Similarly being set up as a potential heir to Dupixent was the investigational IL-33 inhibitor itepekimab. Sanofi decided to axe the asset in July following mixed data in a late-stage study for COPD. Amlitelimab and itepekimab no longer appear on the pharma’s pipeline page . Sanofi and Regeneron split Dupixent’s U.S. earnings 50-50, while international profits are divvied up based on a pre-determined sliding scale that gives a slight edge to Sanofi, according to a 2007 agreement between the companies. Thursday’s agreement will not affect the current profit-sharing arrangement for Dupixent, the partners said.

Phase 1Phase 3AcquisitionPhase 2

08 Sep 2026

·firstwordpharma.com

AstraZeneca's tozorakimab cuts COPD exacerbations by up to 34% in Phase III

AstraZeneca has unveiled detailed results from two Phase III trials of tozorakimab in chronic obstructive pulmonary disease (COPD) showing that the IL-33 antibody reduced moderate-to-severe exacerbations by about 30% in both."Today's…results, from two replicate trials, set a new standard for COPD treatment outcomes in a broad population of patients," stated Sharon Barr, the company's EVP of BioPharmaceuticals R&D.Toplined in March, results from the OBERON and TITANIA trials, published Tuesday in NEJM and presented at the European Respiratory Society (ERS) meeting, showed the antibody worked across current and former smokers and a range of blood eosinophil counts, as well as all stages of lung function severity.The studies, which included over 1700 participants combined, tested tozorakimab in patients with persistent COPD exacerbations despite inhaled standard of care. They were randomised to tozorakimab 300 mg or placebo once every four weeks, on top of background therapy.IL-33's mixed recordIn OBERON, the primary endpoint was met with a 29% reduction in annualised rate of moderate-to-severe exacerbations among former smokers, while the reduction was 34% in TITANIA. In the overall population involving both current and former smokers, the corresponding reductions were 30% and 29% in the two studies, respectively.The detailed readouts stand out against a backdrop of previous mixed findings with other drugs targeting the IL-33 pathway (see – KOL Views Q&A: AstraZeneca's IL-33 could expand the reach of biologics in COPD).Sanofi and Regeneron's IL-33 antibody itepekimab yielded split results in the Phase III AERIFY-1 and AERIFY-2 trials last year, as did Roche's astegolimab — which targets ST2, a receptor for IL-33 — succeeding in the Phase IIb ALIENTO study, but falling short in the Phase III ARNASA trial (see – KOL Views Q&A: Itepekimab setback more instructive than destructive for IL-33 therapies in COPD and Spotlight On: Roche further muddies water with more "mixed" messages about IL-33 in COPD).Meanwhile, eosinophil counts appeared to influence the magnitude of tozorakimab's benefit. In a pooled analysis of OBERON and TITANIA, exacerbations fell by 43% among patients with baseline blood eosinophils of at least 300 cells/µL, compared to 23% among those below 150 cells/µL. Patients at or above 150 achieved a 34% reduction.Additionally, AstraZeneca said a separate integrated analysis of the two studies presented at ERS found that tozorakimab also reduced mucus plugging, an emerging COPD measure associated with worse disease outcomes.'Rare' fatal eventsThe drug was generally well tolerated, with the only adverse drug reaction being injection-site reactions. The safety analysis did show that while fatal serious adverse events were similar in OBERON between the tozorakimab and placebo arms (1.3% vs 1.2%), they were more frequent with tozorakimab in TITANIA (2.5% vs 0.9%, respectively)."Although these events were rare, the incidence was similar among patients who received tozorakimab every 4 weeks and those who received tozorakimab every 8 weeks," the study authors wrote. "No patterns in adjudicated components of major adverse cardiovascular events, adjudicated causes of death, or in preferred terms for serious adverse events with the outcome of death were apparent."In April, AstraZeneca reported that tozorakimab had succeeded in the Phase III MIRANDA trial in COPD as well.The FDA has accepted AstraZeneca's filing of tozorakimab for priority review as an add-on maintenance treatment for adults with COPD. A decision is expected in the first quarter of 2027, while regulatory reviews are also underway in Europe and China.Tozorakimab is also being tested in a Phase II trial for severe asthma and in a Phase III trial in severe viral lower respiratory tract disease.

Clinical ResultPhase 3Phase 2Priority Review

24 Aug 2026

·www.biospace.com

Regeneron ends eye disease study after antibody shows ‘unfavorable’ risk/benefit profile

iStock, Aryo Hadi The discontinuation of the uveitis study adds to Regeneron’s series of clinical setbacks, including the Phase 3 failures of the Dupixent follow-up itepekimab and an investigational combo regimen for melanoma. Regeneron has terminated a Phase 1/2 study of an investigational anti-inflammatory antibody, which was being tested for non-infectious uveitis. The decision to end the trial is due to an “unfavorable benefit-risk assessment” of the candidate, called REGN7041, according to a federal clinical trials database . BioSpace has reached out to Regeneron for more details regarding the discontinuation of the study and the company’s future plans for REGN7041. The asset is no longer listed on the pharma’s pipeline page . REGN7041 is a monoclonal antibody that targets CD3, a marker found on immune cells that drives the inflammatory cascade. Non-infectious uveitis is an eye disease characterized by inflammation of a layer of the eye. Common symptoms include redness, pain, sensitivity to light and compromised eyesight. There hasn’t yet been an anti-CD3 therapy approved for uveitis. The discontinuation of the uveitis study continues somewhat of a losing streak for Regeneron. In May last year, for instance, the pharma announced that itepekimab—an interleukin-33 blocker that many had been eyeing as a follow-up to Dupixent— failed one of two late-stage chronic obstructive pulmonary disease trials. A year later, the pharma’s investigational melanoma combo kneeled to Merck’s Keytruda in a Phase 3 trial. Earnings Regeneron’s ‘aversion’ to M&A questioned as bumper Q2 builds war chest Calls for Regeneron to step up dealmaking have intensified as the company has established an $18 billion cash pile and suffered clinical trial setbacks. July 30, 2026 · 2 min read · Nick Paul Taylor Read more In the face of these setbacks, analysts have been piling on the M&A pressure as a way for Regeneron not just to beef up its pipeline, but also make use of what BMO Capital Markets last month called the pharma’s “financial strength.” The company, for its part, has clarified that it is not “allergic to any external opportunity,” CEO Leonard Schleifer said during a second quarter investor call in July. “We look at them all, but we are pretty disciplined in trying to create value with these transactions.” While it’s true that Regeneron hasn’t signed a mega-deal in a while, the pharma has indeed been looking externally for innovation. Just in the past few months, the pharma has inked a handful of partnerships, including one with Telix in April, putting up to $4.3 billion on the line to advance radiopharmaceutical programs for several cancer indications. Shortly after, Regeneron linked up with Parabilis Medicines in a deal that could potentially reach $2.3 billion, hoping to unlock a new class of medicines called antibody-helicon conjugates to address previously undruggable targets. Deals Regeneron, Parabilis set out to create new drug class in deal worth up to $2.3B Right after reporting a major Phase 3 LAG-3 miss that has rattled analysts, Regeneron Pharmaceuticals revealed a back-loaded partnership with Parabilis Medicines aimed at adding a new drug class to its early-stage pipeline. May 18, 2026 · 2 min read · Gabrielle Masson Read more

Phase 3

100 Deals associated with Itepekimab

External Link

KEGG	Wiki	ATC	Drug Bank
D11999	-	-	DB16206

R&D Status

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Nasal Polyps	Phase 3	-	Sanofi	08 May 2026
Chronic rhinosinusitis without nasal polyps	Phase 3	United States	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Japan	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Argentina	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Austria	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Brazil	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Canada	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Chile	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Finland	Sanofi	12 Feb 2025
Chronic rhinosinusitis without nasal polyps	Phase 3	Germany	Sanofi	12 Feb 2025

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04751487 (AERIFY-2, CTgov)	Phase 3	Pulmonary Disease, Chronic Obstructive \| Bronchitis, Chronic	1,234	placebo+itepekimab (Former Smoker Cohort: Placebo)	ibjzegkzvw = pdtmcaeira zcsrmwrcwh (tzrkrozkpp, cqerlitnam - bmpzgypokq) View more	-	09 Oct 2026
				Itepekimab (Former Smoker Cohort: Itepekimab 300 mg Q4W)	ibjzegkzvw = vtzrmmlkjh zcsrmwrcwh (tzrkrozkpp, zoekegbmpi - aoznxbumts) View more
NCT06280391 (CTgov)	Phase 2	Non-cystic fibrosis bronchiectasis	314	Placebo	ezhfvsofnw = kvmqvjgdkk lcgfucbuop (zzfewbvznr, xzrfepygjp - pnqlypdegz) View more	-	07 Oct 2026
NCT05326412 (AERIFY-3, CTgov)	Phase 2	Pulmonary Disease, Chronic Obstructive \| Bronchitis, Chronic	49	itepekimab (Part A: Former Smokers)	rnyuawjbhv(rssupdwtqf) = eeuodogluq nvmsiotcyu (pyowndgbld, qyojtpcvkd - aapcjbgysx) View more	-	31 Aug 2026
				itepekimab (Part B: Current Smokers)	rnyuawjbhv(rssupdwtqf) = rjhmvcmxrs nvmsiotcyu (pyowndgbld, loahgecjpk - jmggytjfsf) View more
NCT04751487 (AERIFY-2, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	-	itepekimab every two weeks	nplwaofldp(npynkuqdam) = nxzodvyiqp wwgqzxibii (cbspyrvakc )	Negative	30 May 2025
				Itepekimab every four weeks	nplwaofldp(npynkuqdam) = qceeesnqml wwgqzxibii (cbspyrvakc )
NCT04701983 (AERIFY-1, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	1,127	itepekimab every two weeks	agqdtrncer(djwserfxoz) = txcsaqjbay euwnkwjmqq (lktljvbfrf )	Positive	30 May 2025
				Itepekimab every four weeks	agqdtrncer(djwserfxoz) = kvhshjlmeq euwnkwjmqq (lktljvbfrf )
NCT03546907 (CTgov)	Phase 2	Pulmonary Disease, Chronic Obstructive	343	Any short-acting β agonist as prescribed by treating physician as standard of care (Placebo)	hwsiqfmafz = aipvtbdtvf xwucytxffe (dgflausifv, edlwcbxciy - gytudolpao) View more	-	22 Nov 2022
				Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340)	hwsiqfmafz = kflqyidjjv xwucytxffe (dgflausifv, ytrbzzcvub - awdbxasbtx) View more
NCT03738423 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	129	Placebo (Placebo Q2W)	rhlewohodm(xeokxyuobz) = zkktfjaqzg dkkwxqfktp (azpferikxj, 41.81) View more	-	10 Jun 2022
				REGN3500 (REGN3500 30 mg Q8W)	rhlewohodm(xeokxyuobz) = wnzyttwpuh dkkwxqfktp (azpferikxj, 31.65) View more
NCT03387852 (CTgov)	Phase 2	Asthma	296	Placebo for dupilumab+Fluticasone+Fluticasone/salmeterol (Placebo)	mjmjmqhxvs = ipfhjmdoiy ogtbqijfgv (rifrfzvclr, hkvzweizuh - gvzgpncydj) View more	-	29 Mar 2022
				Dupilumab+Fluticasone+SAR440340+Fluticasone/salmeterol (SAR440340 + Dupilumab)	mjmjmqhxvs = byjdcdnffi ogtbqijfgv (rifrfzvclr, eektnrgrsn - kmwqnbqlvx) View more
NCT03736967 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	206	Placebo (Placebo Q2W)	clwtcmwcei(zdgsnmgcdf) = ivcifmwhqn mkrgfckknd (cnrxfkpqrm, 31.86) View more	-	01 Nov 2021
				REGN3500 (REGN3500 300 mg Q2W)	clwtcmwcei(zdgsnmgcdf) = ainvbtfnck mkrgfckknd (cnrxfkpqrm, 22.46) View more
NCT03387852 (Pubmed \| N Engl J Med)	Phase 2	Asthma type 2 biomarkers	296	Itepekimab	xwjcaydpxa(yksmxuiukg) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo cnixtxkwdg (qiexxuavks ) View more	Positive	28 Oct 2021
				Itepekimab plus Dupilumab

Translational Medicine

Boost your research with our translational medicine data.

view full example data

Deal

Boost your decision using our deal data.

view full example data

Core Patent

Boost your research with our Core Patent data.

view full example data

Clinical Trial

Identify the latest clinical trials across global registries.

view full example data

Approval

Accelerate your research with the latest regulatory approval information.

view full example data

Biosimilar

Competitive landscape of biosimilars in different countries/locations. Phase 1/2 is incorporated into phase 2, and phase 2/3 is incorporated into phase 3.

view full example data

Regulation

Understand key drug designations in just a few clicks with Synapse.

view full example data

Hiro LS Researcher

The AI Search Engine Built to Accelerate Biopharma Decisions

Search across billion-scale life sciences data to uncover signals, validate evidence, and act with confidence.

Ask any biopharma research question→

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, Patsnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Discover Synapse Data Servers

Synapse data is now integrated into the PatSnap LS Model Context Protocol (MCP) service. Customize your LLM agent now using our MCP server!

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis