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Last update 13 Aug 2026

Itepekimab

Last update 13 Aug 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 without nasal polypsChronic rhinosinusitis with nasal polypsBronchitis, Chronic+ [3]

Inactive Indication

Allergic asthmaAsthmaInflammation+ [4]

Originator Organization

Regeneron Pharmaceuticals, Inc.

Active Organization

Regeneron Pharmaceuticals, Inc.

SanofiGenzyme Ireland Ltd.

+ [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

/ Active, not recruitingPhase 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 Sep 2026·Biochemistry and Biophysics Reports

The IL-33/ST2 pathway to modulate the inflammatory microenvironment: A new therapeutic target in chronic obstructive pulmonary disease

Review

Author: Yang, Lei ; Zhong, Jingjing ; Zheng, Gaofeng ; Shen, Hao ; Chen, Jie ; Wu, Yonghong ; Xie, Xiaoyan

The IL-33/ST2 pathway is critically implicated in the pathogenesis and progression of chronic obstructive pulmonary disease (COPD), orchestrating a complex interplay of oxidative stress, immunity, inflammation, and pulmonary injury. Clinical evidence shows that the expression levels of IL-33 and ST2 are significantly elevated in patients with COPD, which correlates strongly with disease severity, increased frequency of acute exacerbations, and negative clinical outcomes. Therapeutic strategies targeting the IL-33/ST2 pathway, including anti-IL-33 monoclonal antibodies and ST2 inhibitors, have demonstrated considerable potential in preclinical studies. These approaches have shown efficacy in mitigating inflammatory responses, enhancing lung function, and reducing the risk of acute exacerbations. Notably, the precise regulatory mechanisms of the IL-33/ST2 pathway in COPD and its crosstalk with inflammation remain incompletely understood and warrant further investigation. This review mainly elaborates the molecular biological characteristics and mechanism of IL-33/ST2, summarizes the function of IL-33/ST2 in COPD development and treatment, illustrates the application of IL-33/ST2 in patient's immune-inflammatory regulation and drug discovery, and discusses the prospects of targeting IL-33/ST2.

109

News (Medical) associated with Itepekimab

06 Aug 2026

·www.biospace.com

Sanofi pauses mid-stage lung study amid new CEO’s ‘rigorous portfolio prioritization’

iStock, BeritK Since stepping in as Sanofi’s CEO in April, Belén Garijo has launched a deep look at the pharma’s pipeline, reassessing assets based on “scientific merit” and potential for long-term value in the quest for a Dupixent follow-up. Sanofi has suspended a Phase 2 study testing an investigational antibody in non-cystic fibrosis bronchiectasis, as new CEO Belén Garijo reassesses the company’s pipeline. The pause was driven by “strategic business reasons to facilitate internal portfolio review,” and not because of the asset’s safety or benefit/risk profile, according to a federal clinical trials database . The asset in question is called SAR445399, a monoclonal antibody designed to block the interleukin-1 receptor 3 (IL-1R3), a key player in immune-related signaling cascades. The drug came to Sanofi in December 2015 when the pharma inked a research and license collaboration with MAB Discovery. ezstandalone.cmd.push(function () { ezstandalone.showAds(129); }); Sanofi’s pipeline page lists SAR445399 as under mid-stage development for hidradenitis suppurativa. That study remains open and recruiting as of July 1. Sanofi has no pipeline entry for the asset in non-cystic fibrosis bronchiectasis. BioSpace has reached out to the pharma for more color on the matter. Sanofi is amid what Garijo calls a “very rigorous portfolio prioritization process.” Garijo, who took the reins in April succeeding former chief executive Paul Hudson , revealed this effort during the company’s second quarter earnings call last week, noting that “we are going to look very deeply at our current late-stage portfolio.” The decision to push an asset forward, she said, will depend on “scientific merit, potential to create long-term value and, obviously, ensuring the right risk pro our pipeline moving forward.” Earnings Sanofi’s new CEO wants more ‘realistic view’ of Phase 3 go/no-go decisions Sanofi is going to “look very deeply” at its late-stage pipeline as part of a portfolio prioritization initiative, though new CEO Belén Garijo didn’t commit to shelving a specific number of assets. July 30, 2026 · 2 min read · Tristan Manalac Read more That same day, Sanofi revealed that it would shelve the IL-33 inhibitor itepekimab, which was being developed for chronic obstructive pulmonary disease. Phase 3 data released in May last year were mixed: itepekimab significantly reduced exacerbations in former smokers with inadequately controlled disease in only one of two late-stage trials. Sanofi had been positioning itepekimab as a successor to its blockbuster drug Dupixent, which will lose key patent protections in the coming years . Sanofi also axed the oral TNFR blocker balinatunfib last week, after the asset failed to significantly ease psoriasis severity in a mid-stage study. Late last month, the pharma also discontinued all but one of its ongoing studies for the investigational antibody amlitelimab after a disappointing showing in a Phase 3 atopic dermatitis trial. Sanofi has also scrapped plans to amlitelimab’s approval, which the company had originally scheduled for later this year. Only a celiac disease study of amlitelimab will stay online, with data expected later this year. Sanofi obtained amlitelimab in its $1.4 billion acquisition of Kymab in 2021. In conjunction with the trial discontinuations, the pharma absorbed a €952 million ($1.1 billion) impairment loss in the second quarter. Drug Development Sanofi’s $1.4B Kymab bet falters again as atopic dermatitis trials scrapped Sanofi had hoped the acquisition of Kymab would fill a major hole that will be left as autoimmune juggernaut Dupixent heads toward a patent cliff. Now, another therapy has failed to meet expectations. July 24, 2026 · 3 min read · Gabrielle Masson Read more

05 Aug 2026

·www.fiercebiotech.com

Sanofi suspends chronic lung disease phase 2 study, tied to ‘strategic business reasons’

Sanofi halted a phase 2 trial testing a monoclonal antibody, SAR445399, in non-cystic fibrosis bronchiectasis, Fierce Biotech has learned. The trial , which began only back in April, was a randomized, double-blind, placebo-controlled study to measure the reduction in mucus plug score following treatment with SAR445399 compared with placebo in adults aged 18 to 80 years with NCFB, a chronic lung disease. The trial was officially reported as halted on July 29, the day before Sanofi’s second-quarter earnings call. The decision to pause the trial was made “as part of a company-wide portfolio review for strategic business reasons,” and not due to safety concerns, a Sanofi spokesperson told Fierce. The move to pause the NCFB trial comes during a trying time for Sanofi following a year filled with a series of trial fails . In February, the French pharma ousted CEO Paul Hudson and appointed Merck KGaA leader Belén Garijo, M.D., Ph.D., to steer the ship. Since then, Garijo has been doing a deep dive on correcting the company’s strewn R&D and clinical strategies. On July 24, Sanofi scrapped amlitelimab for atopic dermatitis, despite its lore as being a potential $5 billion blockbuster. During its second-quarter report, the company abandoned two more assets, balinatunfib and itepekimab, following failed trial results in psoriasis and chronic obstructive pulmonary disease , respectively. SAR445399 , only first revealed by Sanofi in 2023, is an anti-interleukin-1 receptor 3 monoclonal antibody developed to block the interleukin 1, 33, and 36 cytokine pathways. These pathways can be important in chronic immune-related dermatologic diseases, such as atopic dermatitis and hidradenitis suppurativa, as well as respiratory conditions, such as NCFB. NCFB affects roughly half a million people in the U.S., with a global incidence of greater than one million cases. In August 2025, Insmed received FDA approval for Brinsupri , a DPP1 inhibitor targeting neutrophil activation, for treatment of NCFB in adults and kids ages 12 and older. The British biotech Infex Therapeutics showed promising NCFB phase 2a data using their monoclonal antibody, INFEX702 , which acts by disabling Pseudomonas aeruginosa, a bacteria known to be a major pathogen of NCFB. Sanofi is currently running a separate phase 2 study testing SAR445399 as a potential treatment for the inflammatory skin condition hidradenitis suppurativa.

Phase 2Drug ApprovalPhase 1Executive Change

31 Jul 2026

·www.biopharmadive.com

Sanofi to ‘rebuild trust’ with Regeneron; Apnimed adds to string of ‘upsized’ biotech IPOs

Today, a brief rundown of news involving Sanofi and Apnimed, as well as updates from Bristol Myers Squibb, GSK and Pfizer that you may have missed.New Sanofi CEO BelnGarijotold analysts Thursday that one of her key objectives is to repair the companys relationshipwith longtime development partner Regeneron Pharmaceuticals and potentially expand their alliance. Garijo has completed her initial assessment since coming onboard and, since then, Sanofi has axed multiple programs including the once-prized immune drug prospects amlitelimab and itepekimab. Ahead of the looming patent cliff for top-selling drug Dupixent, Sanofi will intensify its business development and M&A activity, Garijo said during an earnings call. But she also wants to rebuild trust and be more transparent with Regeneron in the hopes of adding assets from both sides to the partnership.“Regeneron is of strategic importance to us,“ Garijo said. “And therefore, we will continue the already initiated conversations to be able to land what is best for both companies.“ Ben FidlerBristol Myers Squibb shares oscillated a bit on Thursday even as the company issued an earnings report that surpassed analyst expectations. The pharmaceutical giant recorded $13 billion in revenue during the second quarter, which was 6% higher than the same period from a year prior and 11% above consensus estimates, according to RBC Capital Markets analyst Trung Huynh. While some of the beat stemmed from Bristol Myers growth portfolio of newer products Reblozyl, Breyanzi and Camzyos were up 29%, 41% and 60%, respectively it was also due in good part to the legacy blood thinner Eliquis, sales of which were up 22% to nearly $4.5 billion. Additionally, Bristol Myers disclosed slight delays to key studies of Cobenfy as well as an experimental blood thinner called milvexian. Though largely anticipated, those add uncertainty around the pipeline and temper what was otherwise viewed as a strong quarter operationally, Huynh wrote in a note to clients. During Thursday trading, Bristol Myers shares were at times down nearly 1.5% and up almost 4%, but ultimately closed at $64.86 apiece, up 2.8%. Jacob BellApnimed, a sleep drug developer backed by Shionogi,beat its projections to raise $192 million in an initial public offering Thursday. According to BioPharma Dive data, the IPO is the biopharmaceutical sectors 15th so far this year, and most were upsized meaning that high demand led companies to either sell more shares than expected or hike their price. Attovia Therapeutics, Braveheart Bio and Vogenx could follow Apnimed shortly. All three set terms for their coming offerings this week. Ben FidlerU.K.-based biotechnology startup Relation said Thursdayit has partnered with GSK in a deal focused on using AI technology to better understand disease biology and uncover new therapeutic targets. Through the partnership, the companies will amass data on the way human cells respond to genetic and drug interventions, and use those insights to point the way to new medicines.Relation stands to receive up to $110 million in upfront as well as milestone payments in the deal. Delilah Alvarado Pfizers immune drugLitfulo hit both its main objectivesin two late-stage studies in people with the skin condition vitiligo. Pfizer already sells the medication for alopecia areata, an autoimmune condition causing hair loss. But the company said Thursday that, when compared to a placebo in two Phase 3 trials in vitiligo, treatment was associated with significantimprovements in the severity of depigmented patches on the face and skin after 52 weeks. Pfizer didnt disclose specifics, but said itll share the results with regulatory authorities.Litfulos safety profile was consistent with what was seen in previous testing. Delilah Alvarado '

Phase 3IPOClinical Result

100 Deals associated with Itepekimab

External Link

KEGG	Wiki	ATC	Drug Bank
-	-	-	DB16206

R&D Status

10 top R&D records.

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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, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	-	itepekimab every two weeks	etjnwzjoca(gqrkkwikzj) = prdphtyzgk gqyptyvchu (nzfhfuajak )	Negative	30 May 2025
				Itepekimab every four weeks	etjnwzjoca(gqrkkwikzj) = ikifhoqrgt gqyptyvchu (nzfhfuajak )
NCT04701983 (AERIFY-1, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	1,127	itepekimab every two weeks	tcwxevayhb(biaunwjuuk) = liuhbpajio wbddtozmyq (uuxwhfbfzg )	Positive	30 May 2025
				Itepekimab every four weeks	tcwxevayhb(biaunwjuuk) = ynaebjvbag wbddtozmyq (uuxwhfbfzg )
NCT03546907 (CTgov)	Phase 2	Pulmonary Disease, Chronic Obstructive	343	Any short-acting β agonist as prescribed by treating physician as standard of care (Placebo)	novpzpiypr = sdktxgdqci zikfmbvqex (djfabgzdnc, vfrurzzvoq - aoxepmsjtj) View more	-	22 Nov 2022
				Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340)	novpzpiypr = rloonhxgbr zikfmbvqex (djfabgzdnc, ypypehlfsd - ennbohrsmy) View more
NCT03738423 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	129	Placebo (Placebo Q2W)	nmncvtpyxj(caztqutocg) = pxescppqaw jxnntrtjff (ngzncndsvd, 41.81) View more	-	10 Jun 2022
				REGN3500 (REGN3500 30 mg Q8W)	nmncvtpyxj(caztqutocg) = ullwlmdrnk jxnntrtjff (ngzncndsvd, 31.65) View more
NCT03387852 (CTgov)	Phase 2	Asthma	296	Placebo for dupilumab+Fluticasone+Fluticasone/salmeterol (Placebo)	tykxmxbffd = kvmxtqtwpm urgjdjwcqm (enjtwsqvpc, lowzyiczrq - tpztkircdi) View more	-	29 Mar 2022
				Dupilumab+Fluticasone+SAR440340+Fluticasone/salmeterol (SAR440340 + Dupilumab)	tykxmxbffd = hfnvaqymzb urgjdjwcqm (enjtwsqvpc, kyhtjeblcm - pdiunxpynk) View more
NCT03736967 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	206	Placebo (Placebo Q2W)	jvueftuazs(hhcjbdwgub) = ietyhwhjrm rcozeblfsd (zqkqmalcrh, 31.86) View more	-	01 Nov 2021
				REGN3500 (REGN3500 300 mg Q2W)	jvueftuazs(hhcjbdwgub) = vihkyolmxc rcozeblfsd (zqkqmalcrh, 22.46) View more
NCT03387852 (Pubmed \| N Engl J Med)	Phase 2	Asthma type 2 biomarkers	296	Itepekimab	vsuaxtqdcn(enkyienghu) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo dloewnwthi (wmrvwmkgau ) View more	Positive	28 Oct 2021
				Itepekimab plus Dupilumab

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