{"success":true,"data":{"pressRelease":{"id":"38283","rtpr_id":"nGNX6t6Pr7","ticker":"SASY","exchange":"Euronext Paris","all_tickers":["SASY"],"title":"Press Release: ATS: phase 2 data demonstrate the superiority of efdoralprin alfa over a standard-of-care augmentation therapy in achieving higher fAAT levels in AATD  ","author":"Globe Newswire","published_at":"2026-05-18T19:30:00.562Z","article_body":"ATS: phase 2 data demonstrate the superiority of efdoralprin alfa over a\nstandard-of-care augmentation therapy in achieving higher fAAT levels in AATD\n* Data from the head-to-head study show efdoralprin alfa normalized and\nmaintained functional AAT levels in people living with alpha-1 antitrypsin\ndeficiency\n* Efdoralprin alfa is a recombinant protein distinct from plasma-derived\ntherapy, which has been the standard-of-care for nearly 40 years\nParis, May 18, 2026. Data from the global ElevAATe phase 2 study (clinical\nstudy identifier: NCT05856331\n(https://clinicaltrials.gov/study/NCT05856331?term=NCT05856331&rank=1))\ndemonstrated superiority of investigational efdoralprin alfa over\nstandard-of-care therapy in achieving and maintaining normalized functional\nalpha-1 antitrypsin (fAAT) levels in adult patients with alpha-1 antitrypsin\ndeficiency (AATD)-related emphysema. These results are being presented today\nat the 2026 American Thoracic Society (ATS) International Conference in\nOrlando, FL, US.\n\nEfdoralprin alfa, dosed every three weeks (Q3W), achieved mean increases in\nfAAT trough levels more than three times greater than plasma-derived protein\n(pdAAT) dosed weekly (Q1W), meeting the primary endpoint (p<0.0001). All key\nsecondary endpoints in the study were also met (p<0.0001), highlighting the\npotential for efdoralprin alfa to be the first therapy to sustain normal fAAT\nlevels for patients and do so with less frequent dosing. In patients dosed\nQ3W, fAAT levels remained above the normal threshold (23.8 μM) for 100% of\ndays during the 32-week study compared to 41% of days in patients on a\nstandard-of-care augmentation therapy.\n\nAATD is an underdiagnosed, rare genetic condition that can cause considerable\nrespiratory illness and is characterized by low levels or absence of AAT, a\nprotein designed to protect the lungs from damaging inflammation. Without\nadequate fAAT levels, patients often experience progressive deterioration of\nthe lung tissue and may develop emphysema, the most common form of chronic\nobstructive pulmonary disease (COPD), accounting for up to 72% of deaths in\npeople with AATD. An estimated 90% of individuals with AATD are believed to be\nundiagnosed.\n\n“AATD presents a persistent clinical challenge. Widespread lack of awareness\nof the condition as a genetic cause of some forms of COPD leaves many patients\nunder-served. Without treatment to address the underlying AAT protein\ndeficiency, these patients are unable to maintain protective protein levels\nand become vulnerable to progressive lung disease,” said Igor Barjaktarevic,\nMD, PhD, Associate Professor, David Geffen School of Medicine at UCLA, Los\nAngeles, CA, US and principal investigator on the ElevAATe phase 2 study.\n“The ElevAATE data suggest efdoralprin alfa, through its mechanism of\naction, may be able to restore normal AAT levels and keep patients in that\nrange for longer than the standard-of-care therapy, helping to address an\nunmet need of this disease with a restorative recombinant approach.”\n\nThe ElevAATe phase 2 study \nThe ElevAATe phase 2 study was a double-blind, randomized study evaluating\nefdoralprin alfa versus a standard-of-care augmentation therapy in patients\nwith AATD-related emphysema. Ninety-seven patients were randomized 2:2:1 to\nreceive efdoralprin alfa every three or four weeks, or plasma-derived\naugmentation therapy once weekly.\n\nThe following results are being shared today:\n\n                                                                                                               Efdoralprin alfa Q3W                 Efdoralprin alfa Q4W                 Plasma-derived augmentation therapy Q1W  \n Primary endpoint                                                                                                                                                                                                                 \n Mean change in average serum fAAT trough concentrations from baseline to steady state at week 32*             24.1μM [22.8μM, 25.3μM] p<0.0001     16.8μM [15.5μM, 18.1μM] p<0.0001     7.6μM [6.0μM, 9.3μM]                     \n Key secondary endpoints                                                                                                                                                                                                          \n Mean change in serum fAAT average concentrations from baseline to steady state at week 32*                    32.9μM [31.7μM, 34.2μM] p<0.0001     26.0μM [24.6μM, 27.3μM] p<0.0001     17.9μM [16.2μM, 19.6μM]                  \n Percentage of days that steady state fAAT levels were above the lower limit of the normal range at week 32**  100% p<0.0001                        89.3% p<0.0001                       40.8%                                    \n\n*Least square mean change; [95% confidence interval].\n** Normal range for functional AAT = 23.8-42.4 uM.\nQ4W: every four weeks.\n\nEfdoralprin alfa was well tolerated with a safety profile comparable to pdAAT,\nwith no participants experiencing treatment-emergent adverse events (TEAEs)\nleading to permanent discontinuation of study intervention. The most common\nTEAEs in the efdoralprin alfa Q3W, efdoralprin alfa Q4W and pdAAT therapy arms\nwere COPD exacerbations (34.1%, 42.1% and 44.4%, respectively), headache\n(19.5%, 13.2% and 11.1%, respectively), and COVID-19 infection (17.1%, 2.6%\nand 16.7%, respectively). Notably, the incidence of grade ≥2 COPD\nexacerbations, which were captured as an adverse event of special interest in\nthe ElevAATe study, were numerically lower for the efdoralprin alfa Q3W arm\n(26.8%) versus the efdoralprin alfa Q4W (42.1%) and pdAAT (44.4%) arms.\nEfdoralprin alfa anti-drug antibodies were detected in two participants and\nwere transient and non-neutralizing.\n\n“The data demonstrate efdoralprin alfa, a restorative recombinant therapy\ndesigned to achieve a longer half-life than standard of care augmentation\ntherapy, has the potential to raise and sustain fAAT levels within normal\nrange with less frequent dosing. This could represent an important advancement\nin the treatment of AATD-related emphysema, offering patients new hope in a\ndisease state where innovation has been limited over the past 40 years,”\nsaid Christopher Corsico, Global Head of Development at Sanofi.\n\nSanofi is engaging with global regulatory authorities on the appropriate next\nsteps for efdoralprin alfa. Efdoralprin alfa was granted fast track\ndesignation and orphan drug designation in the US and orphan designation in\nthe EU. Additional long-term safety and efficacy outcomes are being evaluated\nin the ElevAATe OLE phase 2 study (clinical study identifier: NCT05897424\n(https://www.clinicaltrials.gov/study/NCT05897424)).\n\nEfdoralprin alfa is currently in clinical development, and its safety and\nefficacy have not been evaluated by any regulatory authority.\n\nAbout efdoralprin alfa\nEfdoralprin alfa is a recombinant human AAT-Fc fusion protein being\ninvestigated as a restorative therapy in adults with AATD emphysema, with Q3W\nor Q4W dosing. This investigational treatment, designed to achieve a longer\nhalf-life than plasma-derived augmentation therapy, is being studied to\nrestore and maintain fAAT levels to the normal range and inhibit neutrophil\nelastase and other proteases that can cause lung tissue damage in patients\nwith AATD.\n\nAbout AATD\nAATD is a rare, inherited disorder characterized by low levels or absence of\nAAT, a protein produced by the liver that protects the lungs from inflammation\nand damage. The disease causes progressive deterioration of the tissue of the\nlungs and liver. Without adequate AAT levels, affected individuals often\nexperience lung damage and develop COPD, including emphysema, and in severe\nforms of the disease patients can sometimes require lung transplantation.\nPlasma-derived therapies were introduced in 1987 to treat the condition but\nsince then, no new treatment approaches have become available to patients.\nAbout 235,000 people worldwide live with AATD, with nearly 100,000 people in\nthe US, but about 90% of individuals with AATD are likely undiagnosed.\n\nAbout Sanofi \nSanofi is an R&D driven, AI-powered biopharma company committed to improving\npeople’s lives and delivering compelling growth. We apply our deep\nunderstanding of the immune system to invent medicines and vaccines that treat\nand protect millions of people around the world, with an innovative pipeline\nthat could benefit millions more. Our team is guided by one purpose: we chase\nthe miracles of science to improve people’s lives; this inspires us to drive\nprogress and deliver positive impact for our people and the communities we\nserve, by addressing the most urgent healthcare, environmental, and societal\nchallenges of our time.\nSanofi is listed on EURONEXT: SAN and NASDAQ: SNY\n\nMedia Relations\nSandrine Guendoul | +33 6 25 09 14 25 | sandrine.guendoul@sanofi.com \nEvan Berland | +1 215 432 0234 | evan.berland@sanofi.com\nLéo Le Bourhis | +33 6 75 06 43 81 | leo.lebourhis@sanofi.com\nVictor Rouault | +1 617 356 4751 | victor.rouault@sanofi.com \nTimothy Gilbert | +1 516 521 2929 | timothy.gilbert@sanofi.com \nLéa Ubaldi | +33 6 30 19 66 46 | lea.ubaldi@sanofi.com\nEkaterina Pesheva | +1 410 926 6780 | ekaterina.pesheva@sanofi.com\n\nInvestor Relations\nThomas Kudsk Larsen |+ 44 7545 513 693 | thomas.larsen@sanofi.com\nAlizé Kaisserian | + 33 6 47 04 12 11 | alize.kaisserian@sanofi.com \nKeita Browne | + 1 781 249 1766 | keita.browne@sanofi.com \nNathalie Pham | + 33 7 85 93 30 17 | nathalie.pham@sanofi.com \nNina Goworek | +1 908 569 7086 | nina.goworek@sanofi.com \nThibaud Châtelet | + 33 6 80 80 89 90 | thibaud.chatelet@sanofi.com \nYun Li | +33 6 84 00 90 72 | yun.li3@sanofi.com\n\nSanofi forward-looking statements\nThis press release contains forward-looking statements within the meaning of\napplicable securities laws, including the Private Securities Litigation Reform\nAct of 1995, as amended. Forward-looking statements are statements that are\nnot historical facts. These statements include projections and estimates and\ntheir underlying assumptions, statements regarding plans, objectives,\nintentions, and expectations with respect to future financial results, events,\noperations, services, product development and potential, and statements\nregarding future events and economic performance. Words such as “expect,”\n“anticipate,” “believe,” “intend,” “estimate,” “plan,”\n“can,” “contemplate,” “could,” “is designed to,” “may,”\n“might,” “potential,” “objective,” \"attempt,\" “target,”\n“project,” \"strategy,\" \"strive,\" \"desire,\" “predict,” “forecast,”\n“ambition,” “guideline,” \"seek,\" “should,” “will,” \"goal,\" or\nthe negative of these, and similar expressions are intended to identify\nforward-looking statements. Although Sanofi’s management believes that the\nexpectations reflected in such forward-looking statements are reasonable,\ninvestors are cautioned that forward-looking information and statements are\nsubject to various risks and uncertainties, many of which are difficult to\npredict and generally beyond the control of Sanofi, that could cause actual\nresults and developments to differ materially from those expressed in, or\nimplied or projected by, the forward-looking information and statements. These\nrisks and uncertainties include among other things, the uncertainties inherent\nin research and development, future clinical data and analysis, including post\nmarketing, decisions by regulatory authorities, such as the U.S Food and Drug\nAdministration or the European Medicines Agency, regarding whether and when to\napprove any drug, device or biological application that may be filed for any\nsuch product candidates as well as their decisions regarding labelling and\nother matters that could affect the availability or commercial potential of\nsuch product candidates; the fact that product candidates if approved may not\nbe commercially successful; unexpected regulatory actions or delays, or\ngovernment regulation generally; authorities’ decisions regarding whether\nand when to approve a product candidate; political pressure in the United\nStates to mandate lower drug prices including “most favored nation”\npricing for State Medicaid programs; the future approval and commercial\nsuccess of therapeutic alternatives; Sanofi’s ability to benefit from\nexternal growth opportunities, to complete related transactions and/or obtain\nregulatory clearances, including future clinical data and analysis of existing\nclinical data relating to the product, including post marketing, unexpected\nsafety, quality or manufacturing issues, competition in general; risks\nassociated with intellectual property and any related pending or future\nlitigation and the ultimate outcome of such litigation;  trends in exchange\nrates and prevailing interest rates, volatile economic and market conditions,\ncost containment initiatives and subsequent changes thereto, and the impact\nthat global crises may have on us, our customers, suppliers, vendors, and\nother business partners, and the financial condition of any one of them, as\nwell as on our employees and on the global economy as a whole. The risks and\nuncertainties also include the uncertainties discussed or identified in the\npublic filings with the SEC and the French Markets Authority (AMF) made by\nSanofi, including those listed under “Risk Factors” and “Cautionary\nStatement Regarding Forward-Looking Statements” in Sanofi’s annual report\non Form 20-F for the year ended December 31, 2025 or contained in our periodic\nreports on Form 6-K. Other than as required by applicable law, Sanofi does not\nundertake any obligation to update or revise any forward-looking information\nor statements. In light of these risks, uncertainties and assumptions, you\nshould not place undue reliance on any forward-looking statements contained\nherein.\n\nAll trademarks mentioned in this press release are the property of the Sanofi\ngroup.\n\nAttachment\n*     Press Release\n(https://ml-eu.globenewswire.com/Resource/Download/3781c969-bb6e-4038-9ebc-f04b7d541a2e)\n(https://www.globenewswire.com/NewsRoom/AttachmentNg/06da731a-67a1-4258-939f-6ef0531ee3bf)\n\n\n\nGlobeNewswire, Inc. 2026","article_body_html":"","raw_payload":{"data":{"id":"nGNX6t6Pr7","title":"Press Release: ATS: phase 2 data demonstrate the superiority of efdoralprin alfa over a standard-of-care augmentation therapy in achieving higher fAAT levels in AATD  ","author":"Globe Newswire","ticker":"SASY","created":"2026-05-18T19:30:00.562Z","tickers":["SASY"],"exchange":"Euronext Paris","article_body":"ATS: phase 2 data demonstrate the superiority of efdoralprin alfa over a\nstandard-of-care augmentation therapy in achieving higher fAAT levels in AATD\n* Data from the head-to-head study show efdoralprin alfa normalized and\nmaintained functional AAT levels in people living with alpha-1 antitrypsin\ndeficiency\n* Efdoralprin alfa is a recombinant protein distinct from plasma-derived\ntherapy, which has been the standard-of-care for nearly 40 years\nParis, May 18, 2026. Data from the global ElevAATe phase 2 study (clinical\nstudy identifier: NCT05856331\n(https://clinicaltrials.gov/study/NCT05856331?term=NCT05856331&rank=1))\ndemonstrated superiority of investigational efdoralprin alfa over\nstandard-of-care therapy in achieving and maintaining normalized functional\nalpha-1 antitrypsin (fAAT) levels in adult patients with alpha-1 antitrypsin\ndeficiency (AATD)-related emphysema. These results are being presented today\nat the 2026 American Thoracic Society (ATS) International Conference in\nOrlando, FL, US.\n\nEfdoralprin alfa, dosed every three weeks (Q3W), achieved mean increases in\nfAAT trough levels more than three times greater than plasma-derived protein\n(pdAAT) dosed weekly (Q1W), meeting the primary endpoint (p<0.0001). All key\nsecondary endpoints in the study were also met (p<0.0001), highlighting the\npotential for efdoralprin alfa to be the first therapy to sustain normal fAAT\nlevels for patients and do so with less frequent dosing. In patients dosed\nQ3W, fAAT levels remained above the normal threshold (23.8 μM) for 100% of\ndays during the 32-week study compared to 41% of days in patients on a\nstandard-of-care augmentation therapy.\n\nAATD is an underdiagnosed, rare genetic condition that can cause considerable\nrespiratory illness and is characterized by low levels or absence of AAT, a\nprotein designed to protect the lungs from damaging inflammation. Without\nadequate fAAT levels, patients often experience progressive deterioration of\nthe lung tissue and may develop emphysema, the most common form of chronic\nobstructive pulmonary disease (COPD), accounting for up to 72% of deaths in\npeople with AATD. An estimated 90% of individuals with AATD are believed to be\nundiagnosed.\n\n“AATD presents a persistent clinical challenge. Widespread lack of awareness\nof the condition as a genetic cause of some forms of COPD leaves many patients\nunder-served. Without treatment to address the underlying AAT protein\ndeficiency, these patients are unable to maintain protective protein levels\nand become vulnerable to progressive lung disease,” said Igor Barjaktarevic,\nMD, PhD, Associate Professor, David Geffen School of Medicine at UCLA, Los\nAngeles, CA, US and principal investigator on the ElevAATe phase 2 study.\n“The ElevAATE data suggest efdoralprin alfa, through its mechanism of\naction, may be able to restore normal AAT levels and keep patients in that\nrange for longer than the standard-of-care therapy, helping to address an\nunmet need of this disease with a restorative recombinant approach.”\n\nThe ElevAATe phase 2 study \nThe ElevAATe phase 2 study was a double-blind, randomized study evaluating\nefdoralprin alfa versus a standard-of-care augmentation therapy in patients\nwith AATD-related emphysema. Ninety-seven patients were randomized 2:2:1 to\nreceive efdoralprin alfa every three or four weeks, or plasma-derived\naugmentation therapy once weekly.\n\nThe following results are being shared today:\n\n                                                                                                               Efdoralprin alfa Q3W                 Efdoralprin alfa Q4W                 Plasma-derived augmentation therapy Q1W  \n Primary endpoint                                                                                                                                                                                                                 \n Mean change in average serum fAAT trough concentrations from baseline to steady state at week 32*             24.1μM [22.8μM, 25.3μM] p<0.0001     16.8μM [15.5μM, 18.1μM] p<0.0001     7.6μM [6.0μM, 9.3μM]                     \n Key secondary endpoints                                                                                                                                                                                                          \n Mean change in serum fAAT average concentrations from baseline to steady state at week 32*                    32.9μM [31.7μM, 34.2μM] p<0.0001     26.0μM [24.6μM, 27.3μM] p<0.0001     17.9μM [16.2μM, 19.6μM]                  \n Percentage of days that steady state fAAT levels were above the lower limit of the normal range at week 32**  100% p<0.0001                        89.3% p<0.0001                       40.8%                                    \n\n*Least square mean change; [95% confidence interval].\n** Normal range for functional AAT = 23.8-42.4 uM.\nQ4W: every four weeks.\n\nEfdoralprin alfa was well tolerated with a safety profile comparable to pdAAT,\nwith no participants experiencing treatment-emergent adverse events (TEAEs)\nleading to permanent discontinuation of study intervention. The most common\nTEAEs in the efdoralprin alfa Q3W, efdoralprin alfa Q4W and pdAAT therapy arms\nwere COPD exacerbations (34.1%, 42.1% and 44.4%, respectively), headache\n(19.5%, 13.2% and 11.1%, respectively), and COVID-19 infection (17.1%, 2.6%\nand 16.7%, respectively). Notably, the incidence of grade ≥2 COPD\nexacerbations, which were captured as an adverse event of special interest in\nthe ElevAATe study, were numerically lower for the efdoralprin alfa Q3W arm\n(26.8%) versus the efdoralprin alfa Q4W (42.1%) and pdAAT (44.4%) arms.\nEfdoralprin alfa anti-drug antibodies were detected in two participants and\nwere transient and non-neutralizing.\n\n“The data demonstrate efdoralprin alfa, a restorative recombinant therapy\ndesigned to achieve a longer half-life than standard of care augmentation\ntherapy, has the potential to raise and sustain fAAT levels within normal\nrange with less frequent dosing. This could represent an important advancement\nin the treatment of AATD-related emphysema, offering patients new hope in a\ndisease state where innovation has been limited over the past 40 years,”\nsaid Christopher Corsico, Global Head of Development at Sanofi.\n\nSanofi is engaging with global regulatory authorities on the appropriate next\nsteps for efdoralprin alfa. Efdoralprin alfa was granted fast track\ndesignation and orphan drug designation in the US and orphan designation in\nthe EU. Additional long-term safety and efficacy outcomes are being evaluated\nin the ElevAATe OLE phase 2 study (clinical study identifier: NCT05897424\n(https://www.clinicaltrials.gov/study/NCT05897424)).\n\nEfdoralprin alfa is currently in clinical development, and its safety and\nefficacy have not been evaluated by any regulatory authority.\n\nAbout efdoralprin alfa\nEfdoralprin alfa is a recombinant human AAT-Fc fusion protein being\ninvestigated as a restorative therapy in adults with AATD emphysema, with Q3W\nor Q4W dosing. This investigational treatment, designed to achieve a longer\nhalf-life than plasma-derived augmentation therapy, is being studied to\nrestore and maintain fAAT levels to the normal range and inhibit neutrophil\nelastase and other proteases that can cause lung tissue damage in patients\nwith AATD.\n\nAbout AATD\nAATD is a rare, inherited disorder characterized by low levels or absence of\nAAT, a protein produced by the liver that protects the lungs from inflammation\nand damage. The disease causes progressive deterioration of the tissue of the\nlungs and liver. Without adequate AAT levels, affected individuals often\nexperience lung damage and develop COPD, including emphysema, and in severe\nforms of the disease patients can sometimes require lung transplantation.\nPlasma-derived therapies were introduced in 1987 to treat the condition but\nsince then, no new treatment approaches have become available to patients.\nAbout 235,000 people worldwide live with AATD, with nearly 100,000 people in\nthe US, but about 90% of individuals with AATD are likely undiagnosed.\n\nAbout Sanofi \nSanofi is an R&D driven, AI-powered biopharma company committed to improving\npeople’s lives and delivering compelling growth. We apply our deep\nunderstanding of the immune system to invent medicines and vaccines that treat\nand protect millions of people around the world, with an innovative pipeline\nthat could benefit millions more. Our team is guided by one purpose: we chase\nthe miracles of science to improve people’s lives; this inspires us to drive\nprogress and deliver positive impact for our people and the communities we\nserve, by addressing the most urgent healthcare, environmental, and societal\nchallenges of our time.\nSanofi is listed on EURONEXT: SAN and NASDAQ: SNY\n\nMedia Relations\nSandrine Guendoul | +33 6 25 09 14 25 | sandrine.guendoul@sanofi.com \nEvan Berland | +1 215 432 0234 | evan.berland@sanofi.com\nLéo Le Bourhis | +33 6 75 06 43 81 | leo.lebourhis@sanofi.com\nVictor Rouault | +1 617 356 4751 | victor.rouault@sanofi.com \nTimothy Gilbert | +1 516 521 2929 | timothy.gilbert@sanofi.com \nLéa Ubaldi | +33 6 30 19 66 46 | lea.ubaldi@sanofi.com\nEkaterina Pesheva | +1 410 926 6780 | ekaterina.pesheva@sanofi.com\n\nInvestor Relations\nThomas Kudsk Larsen |+ 44 7545 513 693 | thomas.larsen@sanofi.com\nAlizé Kaisserian | + 33 6 47 04 12 11 | alize.kaisserian@sanofi.com \nKeita Browne | + 1 781 249 1766 | keita.browne@sanofi.com \nNathalie Pham | + 33 7 85 93 30 17 | nathalie.pham@sanofi.com \nNina Goworek | +1 908 569 7086 | nina.goworek@sanofi.com \nThibaud Châtelet | + 33 6 80 80 89 90 | thibaud.chatelet@sanofi.com \nYun Li | +33 6 84 00 90 72 | yun.li3@sanofi.com\n\nSanofi forward-looking statements\nThis press release contains forward-looking statements within the meaning of\napplicable securities laws, including the Private Securities Litigation Reform\nAct of 1995, as amended. Forward-looking statements are statements that are\nnot historical facts. These statements include projections and estimates and\ntheir underlying assumptions, statements regarding plans, objectives,\nintentions, and expectations with respect to future financial results, events,\noperations, services, product development and potential, and statements\nregarding future events and economic performance. Words such as “expect,”\n“anticipate,” “believe,” “intend,” “estimate,” “plan,”\n“can,” “contemplate,” “could,” “is designed to,” “may,”\n“might,” “potential,” “objective,” \"attempt,\" “target,”\n“project,” \"strategy,\" \"strive,\" \"desire,\" “predict,” “forecast,”\n“ambition,” “guideline,” \"seek,\" “should,” “will,” \"goal,\" or\nthe negative of these, and similar expressions are intended to identify\nforward-looking statements. Although Sanofi’s management believes that the\nexpectations reflected in such forward-looking statements are reasonable,\ninvestors are cautioned that forward-looking information and statements are\nsubject to various risks and uncertainties, many of which are difficult to\npredict and generally beyond the control of Sanofi, that could cause actual\nresults and developments to differ materially from those expressed in, or\nimplied or projected by, the forward-looking information and statements. These\nrisks and uncertainties include among other things, the uncertainties inherent\nin research and development, future clinical data and analysis, including post\nmarketing, decisions by regulatory authorities, such as the U.S Food and Drug\nAdministration or the European Medicines Agency, regarding whether and when to\napprove any drug, device or biological application that may be filed for any\nsuch product candidates as well as their decisions regarding labelling and\nother matters that could affect the availability or commercial potential of\nsuch product candidates; the fact that product candidates if approved may not\nbe commercially successful; unexpected regulatory actions or delays, or\ngovernment regulation generally; authorities’ decisions regarding whether\nand when to approve a product candidate; political pressure in the United\nStates to mandate lower drug prices including “most favored nation”\npricing for State Medicaid programs; the future approval and commercial\nsuccess of therapeutic alternatives; Sanofi’s ability to benefit from\nexternal growth opportunities, to complete related transactions and/or obtain\nregulatory clearances, including future clinical data and analysis of existing\nclinical data relating to the product, including post marketing, unexpected\nsafety, quality or manufacturing issues, competition in general; risks\nassociated with intellectual property and any related pending or future\nlitigation and the ultimate outcome of such litigation;  trends in exchange\nrates and prevailing interest rates, volatile economic and market conditions,\ncost containment initiatives and subsequent changes thereto, and the impact\nthat global crises may have on us, our customers, suppliers, vendors, and\nother business partners, and the financial condition of any one of them, as\nwell as on our employees and on the global economy as a whole. The risks and\nuncertainties also include the uncertainties discussed or identified in the\npublic filings with the SEC and the French Markets Authority (AMF) made by\nSanofi, including those listed under “Risk Factors” and “Cautionary\nStatement Regarding Forward-Looking Statements” in Sanofi’s annual report\non Form 20-F for the year ended December 31, 2025 or contained in our periodic\nreports on Form 6-K. Other than as required by applicable law, Sanofi does not\nundertake any obligation to update or revise any forward-looking information\nor statements. In light of these risks, uncertainties and assumptions, you\nshould not place undue reliance on any forward-looking statements contained\nherein.\n\nAll trademarks mentioned in this press release are the property of the Sanofi\ngroup.\n\nAttachment\n*     Press Release\n(https://ml-eu.globenewswire.com/Resource/Download/3781c969-bb6e-4038-9ebc-f04b7d541a2e)\n(https://www.globenewswire.com/NewsRoom/AttachmentNg/06da731a-67a1-4258-939f-6ef0531ee3bf)\n\n\n\nGlobeNewswire, Inc. 2026"},"type":"article","timestamp":"2026-05-18T19:30:00.622761379Z","server_sent_at_ms":1779132600622},"received_at":"2026-05-18T19:30:00.678Z","source_url":null},"analysis":{"id":"27725","press_release_id":"38283","analysis_json":{"industry":{"label":"Pharmaceuticals, Biotechnology & Life Sciences","sector":"Health Care"},"redFlags":[],"eventType":"clinical_trial","narrative":"Sanofi reported positive Phase 2 data for efdoralprin alfa, demonstrating superiority over standard-of-care plasma-derived therapy in raising functional AAT levels in patients with AATD-related emphysema.\n\nThe investigational drug, dosed every three weeks, increased mean fAAT trough levels by 24.1 μM compared to 7.6 μM for the standard therapy, with 100% of days above the normal threshold versus 41% for the control.\n\nAll key secondary endpoints were met with high statistical significance (p<0.0001), and the drug showed a comparable safety profile with no permanent discontinuations due to adverse events.","sentiment":"bullish","agentHooks":{"shouldPost":true,"suggestedAngle":"Sanofi's efdoralprin alfa shows clear superiority over standard of care in Phase 2 AATD data, offering a potential first-in-class restorative therapy in 40 years."},"keyFigures":{"drugName":"efdoralprin alfa","phaseOfTrial":"Phase 2","customDimensions":{"patient_count":97,"fAAT_increase_q3w":"24.1 μM","fAAT_increase_q4w":"16.8 μM","fAAT_increase_soc":"7.6 μM","study_duration_weeks":32,"days_above_normal_q3w":"100%","days_above_normal_soc":"41%","primary_endpoint_p_value":"<0.0001"}},"quotedText":"The data demonstrate efdoralprin alfa, a restorative recombinant therapy designed to achieve a longer half-life than standard of care augmentation therapy, has the potential to raise and sustain fAAT levels within normal range with less frequent dosing.","namedEntities":{"people":[{"name":"Igor Barjaktarevic","role":"Principal Investigator"},{"name":"Christopher Corsico","role":"Global Head of Development"}],"products":["efdoralprin alfa","ElevAATe"],"companies":[{"name":"Sanofi","ticker":"SNY","relationship":"developer"},{"name":"David Geffen School of Medicine at UCLA","relationship":"research institution"}],"dollarAmounts":[]},"materialImpact":{"score":4,"reasoning":"Positive Phase 2 head-to-head data showing superiority over standard-of-care in a rare disease with no new treatments in 40 years. The drug met primary and key secondary endpoints with a favorable safety profile, de-risking the path to Phase 3."},"tickerRelevance":{"others":[{"ticker":"SNY","relevance":"developer"}],"primary":"SASY"},"globalImportance":65,"audienceRelevance":45,"eventTypeSecondary":[],"importanceComponents":{"tickerTier":"mega-cap","eventGravity":"positive_phase_2_data","sectorWeight":"high","rareDiseaseContext":true,"householdBrandBoost":true}},"event_type":"clinical_trial","event_type_secondary":null,"sentiment":"bullish","material_impact_score":4,"narrative":"Sanofi reported positive Phase 2 data for efdoralprin alfa, demonstrating superiority over standard-of-care plasma-derived therapy in raising functional AAT levels in patients with AATD-related emphysema.\n\nThe investigational drug, dosed every three weeks, increased mean fAAT trough levels by 24.1 μM compared to 7.6 μM for the standard therapy, with 100% of days above the normal threshold versus 41% for the control.\n\nAll key secondary endpoints were met with high statistical significance (p<0.0001), and the drug showed a comparable safety profile with no permanent discontinuations due to adverse events.","key_figures":{"drugName":"efdoralprin alfa","phaseOfTrial":"Phase 2","customDimensions":{"patient_count":97,"fAAT_increase_q3w":"24.1 μM","fAAT_increase_q4w":"16.8 μM","fAAT_increase_soc":"7.6 μM","study_duration_weeks":32,"days_above_normal_q3w":"100%","days_above_normal_soc":"41%","primary_endpoint_p_value":"<0.0001"}},"named_entities":{"people":[{"name":"Igor Barjaktarevic","role":"Principal Investigator"},{"name":"Christopher Corsico","role":"Global Head of Development"}],"products":["efdoralprin alfa","ElevAATe"],"companies":[{"name":"Sanofi","ticker":"SNY","relationship":"developer"},{"name":"David Geffen School of Medicine at UCLA","relationship":"research institution"}],"dollarAmounts":[]},"model_name":"qwen3_6_27b_awq","prompt_hash":"sha256:727b4b9429a443af","schema_hash":"sha256:05005c02d9cffac9","created_at":"2026-05-18T19:30:24.781Z","global_importance":65,"audience_relevance":45,"importance_components":{"tickerTier":"mega-cap","eventGravity":"positive_phase_2_data","sectorWeight":"high","rareDiseaseContext":true,"householdBrandBoost":true}},"durationMs":24152,"modelName":"george-droid-qwen-72b"}}