Request Demo

Last update 04 Jul 2026

Itepekimab

Last update 04 Jul 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

Nasal PolypsChronic rhinosinusitis without nasal polypsChronic rhinosinusitis with nasal polyps+ [4]

Inactive Indication

Allergic asthmaAsthmaInflammation+ [3]

Originator Organization

Regeneron Pharmaceuticals, Inc.

Active Organization

Sanofi-Aventis Recherche & Développement SA

Regeneron Pharmaceuticals, Inc.Genzyme 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

/ Not yet recruitingPhase 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

/ Enrolling by invitationPhase 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.

03 Apr 2026·EXPERT OPINION ON BIOLOGICAL THERAPY

Itepekimab for chronic obstructive pulmonary disease therapy

Review

Author: Rascu, Stefan ; Antoniu, Sabina ; Penisoara, Theodor

INTRODUCTION:

Chronic obstructive pulmonary disease (COPD) is characterized by various inflammation patterns, with type 1 and type 3 being the most prevalent. Type 2, which is similar to that found in asthma and is orchestrated by interleukins such as IL-4, IL-5, IL-13, and IL-33, is not common, but is associated with a higher disease burden, including loss of lung volume and higher exacerbations rates.

AREAS COVERED:

IL-33 has recently been found to play a pathogenic role in COPD development and progression; therefore, its blockade with antibodies such as itepekimab may have therapeutic potential. This review summarizes the scientific rationale for the potential use of itepekimab in COPD and reviews the available clinical data.

EXPERT OPINION:

Based on existing clinical data, itepekimab may be a potential therapy for COPD that can be easily administered at home, with dosing tailored to the disease phase (every 2 weeks during exacerbation and every 4 weeks during stable state).

102

News (Medical) associated with Itepekimab

10 Jun 2026

·www.fiercebiotech.com

Sanofi halts phase 3 autoimmune trial early over insufficient efficacy as pipeline woes continue

The update is a blow for an asset that Sanofi lists among its key mid- and late-stage programs. \n Sanofi has stopped a phase 3 autoimmune clinical trial early after an interim analysis found the therapy was “unlikely to provide sufficient efficacy.” The setback eliminates one opportunity for a key late-phase program and continues the “bumpy ride” for the French pharma.Paris-based Sanofi launched two phase 3 studies of riliprubart, an antibody that blocks C1s in the classical complement pathway, in 2024, based on midphase data suggesting the drug candidate could become a subcutaneous alternative to intravenous immunoglobulin. The trials enrolled two distinct populations of chronic inflammatory demyelinating polyneuropathy (CIDP) patients. The drugmaker had planned to compare riliprubart to placebo over 24 weeks in about 140 patients who had been failed by immunoglobulin or corticosteroid therapy. Instead, Sanofi announced June 10 that it had ended the trial early in response to the independent data monitoring committee’s analysis of interim data.The company said it is assessing whether to continue the other phase 3 trial, which is comparing riliprubart to intravenous immunoglobulin in people who responded to the standard of care and are receiving a stable maintenance dose. At Week 24 of Sanofi’s phase 2 study, 87% of standard-of-care patients improved or remained stable after switching to riliprubart. But the drug appeared similarly effective in patients failed by standard of care in the midphase study, only for the phase 3 trial in that population to fail to generate evidence to support further development. The update is a blow for an asset that Sanofi lists among its key mid- and late-stage programs. Looking past a provisionally quiet 2026 for Sanofi’s pipeline, Guggenheim Securities analysts named riliprubart as one of the assets with readouts that could add value in 2027. The analysts, who made the comment in a note to investors last year, estimated 2033 riliprubart sales of 480 million euros ($555 million).Sanofi’s phase 3 riliprubart trials were initially due to deliver data this year, but the drugmaker pushed back the readouts in response to slow enrollment. Having adapted the screening process, Sanofi saw the enrollment rate pick up and was “optimistic about the impact riliprubart can have on patient outcomes,” Houman Ashrafian, Ph.D., head of R&D at the company, said on a first-quarter earnings call in April.The trouble with riliprubart continues a run of clinical setbacks for Sanofi that ultimately led to CEO Paul Hudson\'s ouster from the pharma in February, weeks after admitting that 2025 had been a “bumpy ride” for the company. That ride included the anti-OX40L-ligand antibody amlitelimab flunking a phase 2 asthma trial, the oral TNF inhibitor balinatunfib missing the goal of a midstage psoriasis study and the Regeneron-partnered IL-33 candidate itepekimab failing one of a pair of phase 3 studies in chronic obstructive pulmonary disease. The implications of the setback to riliprubart extend beyond Sanofi. Immunoglobulin manufacturers such as CSL Behring, Grifols and Pfizer could benefit if riliprubart flops. Argenx, which has already won FDA approval for its FcRn inhibitor Vyvgart Hytrulo in CIDP, is running phase 3 trials of a C2 inhibitor in the indication. Dianthus Therapeutics has a C1 inhibitor, called claseprubart, in phase 3. The biotech has cited Sanofi’s phase 2 data as validation of the potential of C1 inhibitors in CIDP, while also arguing that the response rates seen in an open-label claseprubart trial support the hypothesis that its asset is more efficacious than riliprubart.

Phase 3Phase 2Drug ApprovalClinical Result

18 May 2026

·www.fiercebiotech.com

Analysts ‘shaking heads’ after Regeneron melanoma drug fails to beat Keytruda in phase 3 trial

The failure of Regeneron’s “defining catalyst” of the first half of the year puts fresh pressure on the company, analysts said.\n A phase 3 trial of Regeneron’s LAG-3 inhibitor has missed its primary endpoint, leaving the biopharma reeling from the second failure of a key late-stage program in the past year.The trial assessed fianlimab in combination with Regeneron’s PD-1 inhibitor Libtayo as a first-line treatment for unresectable locally advanced or metastatic melanoma. Progression-free survival (PFS) on the drug combination was statistically no better than on Merck & Co.’s PD-1 inhibitor Keytruda, causing the trial to miss its primary endpoint.Median PFS was numerically longer with the fianlimab combination, at 11.5 months on the high dose, compared with 6.4 months on Keytruda. The statistical miss was driven by a late separation in the PFS curves, BMO Capital Markets analysts said in a note to investors after speaking with Regeneron.“It is clear that while mPFS was improved with high-dose fianlimab combo treatment, separation from monotherapy treatment did not occur until later in the study, leading to the not statistically significant result,” the analysts said. “Somewhat encouragingly, [Regeneron’s investor relations] did note a trend in [overall survival] improvement.” The p value was just the wrong side of statistical significance. But, as the analysts said, “close does not count.” The failure of Regeneron’s “defining catalyst” of the first half of the year puts fresh pressure on the company, according to the analysts, who said they were left “shaking our heads” by the latest flop.Pressure began to ratchet up almost one year ago, when Regeneron and Sanofi reported the failure of one of two phase 3 trials of their IL-33 drug itepekimab in chronic obstructive pulmonary disease. The back-to-back misses for key pipeline projects “amp up the pressure” on the next 12 to 18 months of clinical development at Regeneron, the analysts said.Regeneron has ways to salvage fianlimab. A phase 3 trial comparing the high-dose fianlimab combination to Bristol Myers Squibb’s LAG-3/PD-1 fixed-dose immunotherapy Opdualag is continuing. Regeneron sees showing an overall survival benefit over Opdualag and hitting the primary response rate endpoint of the head-to-head trial as paths back for fianlimab, Evercore ISI analysts said in a note to investors. Yet both BMO and Evercore analysts removed fianlimab from their models in response to the phase 3 flop. It is possible that Regeneron will show fianlimab is noninferior to Opdualag, BMO analysts said, but that is no longer the base-case assumption. BMO and Evercore analysts forecast $1.8 billion and $900 million in risk-adjusted peak sales, respectively, in melanoma before removing fianlimab from their models. With fianlimab now seen as a long shot, BMO analysts said “clean positive readouts” from Regeneron’s Factor XI program will be critical to regaining investor confidence. Regeneron is developing two Factor XI antibodies in a broad program, with initial pivotal data expected in 2027 and a series of readouts in the calendar for the coming years. Phase 3 data on the cemdisiran-pozelimab combination are another catalyst, BMO analysts said. Results from pivotal trials of the combination in geographic atrophy and paroxysmal nocturnal hemoglobinuria are due this year.

18 May 2026

·www.biospace.com

Regeneron misses again as melanoma combo bows to Merck’s Keytruda in Phase 3

iStock, Alberto Barros The late-stage miss shakes analyst confidence in Regeneron’s clinical execution, according to BMO Capital Markets, also noting last year’s Phase 3 failure in chronic obstructive pulmonary disease. Regeneron’s investigational LAG-3 inhibitor, when used with the company’s FDA-approved PD-1 blocker Libtayo, does not offer significant survival benefits as a first-line treatment option for patients with unresectable or metastatic melanoma. “This was to be the defining catalyst of 1H26,” analysts at BMO Capital Markets told investors in a note on Sunday evening, adding that “even more pressure has been placed on the company’s pipeline” because of the miss. Truist Securities agreed, calling the readout a “mishap” and saying that “investors may need to wait longer for a strong pipeline driver to emerge.” Regeneron crashed 10% to $624 before Monday’s opening bell. The pharma ran a Phase 3 melanoma study to test its anti-LAG-3 antibody fianlimab as part of a combination regimen with its PD-1 blocker Libtayo against Merck’s mega-blockbuster therapy Keytruda. Results, disclosed late on Friday , showed median progression-free survival (PFS) of 11.5 months in patients with unresectable or metastatic disease who were given the high-dose combo regimen, and 9.6 months in those treated with the low-dose schedule. Comparators on Keytruda, meanwhile, saw a median PFS of 6.4 months. The treatment difference failed to reach statistical significance for both test arms. Truist said that these data “suggest minimal treatment benefit” of the fianlimab doublet versus Keytruda. After speaking with Regeneron management, BMO was able to add more color on the readout. The miss, according to the pharma, was due to “late-separation in PFS curves,” the analysts wrote on Sunday. Regeneron also detected a trend toward improvement in overall survival. But the analysts were unimpressed. “Regardless of how close fianlimab was to success, close does not count,” they wrote. “Commercial dynamics may be improving, but R&D struggles . . . still hold true and need to be addressed.” Immunology and inflammation Sanofi, Regeneron Shares Tumble as Dupixent Follow-Up Fails Phase III COPD Test Analysts at Truist Securities admitted that the result for itepekimab, which the companies were hoping to follow their blockbuster Dupixent in the I&I space, was “contrary to our expectations—we were wrong.” May 30, 2025 · 3 min read · Annalee Armstrong Read more In particular, BMO pointed to the pharma’s late-stage stumble for the IL-33 itepekimab in May 2025. Itepekimab at the time only aced one of two Phase 3 trials in chronic obstructive pulmonary disease, both of which looked at the asset’s ability to reduce the risk of moderate to severe exacerbations. Regeneron had been positioning itepekimab as the successor of its blockbuster drug Dupixent and the failure triggered an 18% slide in shares. “Confidence shaken; frustration mounting around R&D execution,” BMO wrote on Sunday. “We find it hard to reconcile misstep after misstep,” the firm added, expressing dissatisfaction with the pharma’s clinical execution. “Refocusing R&D efforts, capital deployment, and easing the tension between management and the investment community remain to be improved,” the firm said. “We expect more from Regeneron.”

Phase 3Clinical Result

100 Deals associated with Itepekimab

External Link

KEGG	Wiki	ATC	Drug Bank
-	-	-	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, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	-	itepekimab every two weeks	ehyvwplzuv(niehoeubay) = tjktqfrigp wgohkicmnt (gbufggdxaz )	Negative	30 May 2025
				Itepekimab every four weeks	ehyvwplzuv(niehoeubay) = ljdpqdewrl wgohkicmnt (gbufggdxaz )
NCT04701983 (AERIFY-1, Company_Website) Manual	Phase 3	Pulmonary Disease, Chronic Obstructive	1,127	itepekimab every two weeks	rwlvuxhoqb(xntstlprxu) = uogcglohol fgmvczxtvt (anwopuzvdl )	Positive	30 May 2025
				Itepekimab every four weeks	rwlvuxhoqb(xntstlprxu) = pholbnxjda fgmvczxtvt (anwopuzvdl )
NCT03546907 (CTgov)	Phase 2	Pulmonary Disease, Chronic Obstructive	343	Any short-acting β agonist as prescribed by treating physician as standard of care (Placebo)	okuantvcox = gmzjwcrydf enhrhqzoja (otfhmzzkwr, yhikjpkrsj - xmbhbenfmr) View more	-	22 Nov 2022
				Any short-acting β agonist as prescribed by treating physician as standard of care+SAR440340 (SAR440340)	okuantvcox = kujhywdolo enhrhqzoja (otfhmzzkwr, qqnvfikzok - fkvhpbsnpf) View more
NCT03738423 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	129	Placebo (Placebo Q2W)	juosimikuf(roargydgqw) = fqqvbyybqx ldztwassnk (hvaxazccod, 41.81) View more	-	10 Jun 2022
				REGN3500 (REGN3500 30 mg Q8W)	juosimikuf(roargydgqw) = zuooxkacaj ldztwassnk (hvaxazccod, 31.65) View more
NCT03387852 (CTgov)	Phase 2	Asthma	296	Placebo for dupilumab+Fluticasone+Fluticasone/salmeterol (Placebo)	wvrlsqksvp = nwufgvnzxa ztyurzikvl (ofcqpnkclw, xgtjgfuqtc - zeiwtwrncj) View more	-	29 Mar 2022
				Dupilumab+Fluticasone+SAR440340+Fluticasone/salmeterol (SAR440340 + Dupilumab)	wvrlsqksvp = jglqolpxsx ztyurzikvl (ofcqpnkclw, ckbzlkkaes - pchlnhxflb) View more
NCT03736967 (CTgov)	Phase 2	Moderate Atopic Dermatitis \| Severe Atopic Dermatitis	206	Placebo (Placebo Q2W)	joxorrnjuw(kwzhyicxql) = psqkdoaixi llmeysbayh (rzgszkhfcv, 31.86) View more	-	01 Nov 2021
				REGN3500 (REGN3500 300 mg Q2W)	joxorrnjuw(kwzhyicxql) = ngtfwgeftj llmeysbayh (rzgszkhfcv, 22.46) View more
NCT03387852 (Pubmed \| N Engl J Med)	Phase 2	Asthma type 2 biomarkers	296	Itepekimab	jpnefjsvzd(mztyahxamw) = Itepekimab treatment improved asthma control and quality of life, as compared with placebo yfwtatnqzw (jxcddmbixp ) 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

AI Agents Built for Biopharma Breakthroughs

Accelerate discovery. Empower decisions. Transform outcomes.

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.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis