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~ 88% reduction in median Annualized Bleeding Rate (ABR) for all bleeds and 94% reduction in median ABR for spontaneous joint bleeds in highest dose tested ~ ~ SerpinPC observed to be well-tolerated ~ ~ Company has initiated planning for global registrational program ~ ~ Conference call and webcast scheduled for today at 8:30 a.m. EDT ~ CAMBRIDGE, Mass. and LONDON, Sept. 09, 2021 (GLOBE NEWSWIRE) -- Centessa Pharmaceuticals plc (“Company”) (Nasdaq: CNTA), together with subsidiary ApcinteX Limited (“ApcinteX”), today announced positive topline results from the Phase 2a part of AP-0101, the six-month repeat dose portion of its ongoing first-in-human proof-of-concept study evaluating SerpinPC in severe hemophilia A and B patients. AP-0101 is a Phase 1/2a proof-of-concept study evaluating SerpinPC, an inhibitor of activated protein C (“APC”), in 23 male subjects with either severe hemophilia A or B who were not on prophylaxis.1 The Phase 2a part of the study assessed the safety, tolerability and pharmacokinetics across three dose cohorts (0.3 mg/kg, 0.6 mg/kg and 1.2 mg/kg) of SerpinPC administered as a subcutaneous (SC) injection every 4 weeks over a 24-week period (6 total doses). Reduction in the annualized bleeding rates (ABRs) were exploratory outcomes. Although eligible, none of the patients in the study had inhibitors. SerpinPC was well-tolerated. As previously disclosed, one subject with a history of a skin disorder discontinued treatment on SerpinPC due to an injection site reaction. No other SerpinPC-related adverse events have been recorded. There was no reported sustained elevation in D-dimer, a sensitive measure of excess thrombin generation, throughout the 24-week study. Two subjects had anti-drug antibodies and remained on treatment without apparent impact on ABRs. In the highest dose cohort, SerpinPC reduced the self-reported all bleeds ABR by 88% during the last 12 weeks of treatment (pre-specified primary assessment period) as compared to the all bleeds ABR prospectively measured during the pre-exposure observation period. In the highest dose cohort, five out of eight subjects had zero or one bleed during the 12-week pre-specified primary assessment period. Self-reported spontaneous joint bleeds ABR was reduced by 94% in the highest dose cohort. ABR reductions were similar between patients with either hemophilia A or hemophilia B. Dose Tested Exploratory Efficacy Endpoints 0.3 mg/kg n=7 0.6 mg/kg n=7 1.2 mg/kg n=8 All Bleeds ABR (median percent change) -80% p=0.016 -70% p=0.031 -88% p=0.016 Spontaneous Joint Bleeds ABR (median percent change) -76% p=0.016 -69% p=0.031 -94% p=0.023 Above analyses compared last 12 weeks of treatment (pre-specified primary assessment period) to pre-exposure baseline measures. Bleeding events were self-reported. p-values presented are based on small numbers and are exploratory in nature. The median number of target joints (joint with >3 bleeds in any 6-month period) was reduced to zero at the end of the study from a pre-exposure baseline of 2.5. All subjects had target joints at the start of the study and 15 subjects had zero target joints at the end of the study. All 22 patients who completed the Phase 2a portion of the study have elected to enroll into the 48-week open label extension (“OLE”) portion of the study in which a single flat 60 mg subcutaneous dose of SerpinPC will be administered every 4 weeks over a period of 48 weeks (13 doses total). Centessa expects to report results from the OLE portion of this study in the second half of 2022. “The compelling reduction in bleeds and continued tolerability that we observed in both hemophilia A and hemophilia B patients in this proof-of-concept study are very encouraging, and we are eager to move SerpinPC into a global development plan aimed at pursuing one or more registrations. We see broad utility of SerpinPC across the hemophilia landscape and will seek the most rapid path to bring this potential subcutaneous therapy to hemophilia patients,” said Antoine Yver, M.D., M.Sc., Chief Medical Officer of Centessa Pharmaceuticals. “The results of this Phase 2a study of SerpinPC continue to show an excellent tolerability pro this molecule, and the exploratory efficacy results seen in this study of severe hemophilia A and B patients are also very promising. A safe, subcutaneous, prophylaxis option for both hemophilia A and B patients would be an important addition to our treatment choices,” said David Lillicrap, M.D., Professor of Pathology and Molecular Medicine at Queen's University, Kingston, Ontario, Canada and previously a World Federation of Hemophilia Advisory Board member. ¹ Clinicaltrials.gov identifier: NCT04073498 ( ) Conference Call and Webcast Centessa Pharmaceuticals will host a webcast and conference call today, September 9, 2021, at 8:30 a.m. EDT to discuss topline data from the proof-of-concept trial. To access the audio webcast with slides, please visit the "Events & Publications" page in the Investors & Media section of the Company's website at . The call can also be accessed by dialing (855) 493-3565 (domestic) or (929) 517-9002 (international) with conference ID 8459296. An archive of today's webcast will be available on the Company’s website. About Centessa Pharmaceuticals Centessa Pharmaceuticals plc aims to bring impactful new medicines to patients by combining the strengths of an asset-centric model with the benefits of scale and diversification typical of larger R&D organizations. The asset-centric model refers to a highly specialized, singular-focused company that is led by a team of well-recognized subject matter experts. Centessa’s asset-centric companies’ programs range from discovery-stage to late-stage development and include diverse therapeutic areas such as oncology, hematology, immunology/inflammation, neuroscience, hepatology, pulmonology and nephrology. For more information, visit . About ApcinteX Limited ApcinteX Limited is focused on developing SerpinPC for the treatment of hemophilia A and hemophilia B. Hemophilia is a rare bleeding disorder that is caused by a deficiency of thrombin generation upon vascular damage. About SerpinPC SerpinPC, a biologic based on the serpin family of proteins, is designed to allow more thrombin to be generated by inhibiting activated protein C (APC) thus rebalancing coagulation in hemophilia patients. SerpinPC has the potential to treat all types of hemophilia regardless of severity or inhibitor status, and may also prevent bleeding associated with other bleeding disorders. About AP-0101 AP-0101 is an ongoing Phase 1/2a open-label clinical trial to investigate the safety, tolerability and pharmacokinetics of intravenous and subcutaneous doses of SerpinPC in healthy male volunteers and male persons with severe hemophilia ( ). About Hemophilia A (HA) and Hemophilia B (HB) HA and HB are X-linked genetic disorders affecting one in 5,000 and one in 20,000 live male births, respectively, resulting in spontaneous internal bleeding that can be life-threatening. More than 70% of bleeds occur into joints (hemarthrosis) causing chronic joint damage (arthropathy) with musculoskeletal destruction. The bleeding associated with these disorders is the result of a defect or deficiency in factor VIII (in the case of HA) or factor IX (in the case of HB), the two components of the intrinsic tenase complex. Normal blood coagulation (hemostasis) is a crucial part of the physiological response to tissue damage. When blood components come into contact with extravascular cells and proteins, platelets accumulate and ultimately lead to the formation of thrombin, the effector enzyme of blood coagulation. Prothrombinase activity is required for the rapid, localized production of thrombin needed for adequate blood clotting. Prothrombinase is continuously degraded by APC, which is present in the circulation at low concentrations. In the setting of deficient intrinsic tenase activity (hemophilia), the natural anticoagulant activity of the circulating APC results in insufficient prothrombinase activity for normal blood clotting. Forward Looking Statements This press release contains forward-looking statements. These statements may be identified by words such as "believe," "anticipate," "plan," "expect," "intend," "will," "may," "goal," "project," "estimate," "potential," and variations of these words or similar expressions that are intended to identify forward-looking statements. Any such statements in this press release that are not statements of historical fact may be deemed to be forward-looking statements. These statements include discussions of the open label extension study of SerpinPC and its design and conduct; plans for continued development of SerpinPC, including our global development plan and registrational path for this candidate; our expectations with respect to the treatment paradigm for hemophilia A and B; our ability to deliver impactful medicines to patients; the ability of our key executives to drive execution of our portfolio of programs; our asset-centric business model and the intended advantages and benefits thereof; research and clinical development plans; the scope, progress, results and costs of developing our product candidates or any other future product candidates; strategy; regulatory matters, including the timing and likelihood of success of obtaining approvals to initiate or continue clinical trials or market any products; market size and opportunity; and our ability to complete certain milestones. Any forward-looking statements in this press release are based on our current expectations, estimates and projections only as of the date of this release and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements. These risks and uncertainties include, but are not limited to, the safety, tolerability and efficacy pro SerpinPC observed to date may change adversely in future clinical trials, ongoing analyses of trial data or subsequent to commercialization; foreign regulatory agencies may not agree with our regulatory approval strategies, components of our filings, such as clinical trial designs, conduct and methodologies, or the sufficiency of data submitted; risks inherent in developing products and technologies; risks related to our ability to protect and maintain our intellectual property position; business, regulatory, economic and competitive risks, uncertainties, contingencies and assumptions about the Company; our ability to obtain adequate financing to fund our planned clinical trials and other expenses; trends in the industry; the legal and regulatory framework for the industry; future expenditures risks related to our asset-centric corporate model; the risk that any one or more of our product candidates will not be successfully developed and commercialized; the risk that the results of preclinical studies or clinical studies will not be predictive of future results in connection with future studies; and risks related to the COVID-19 pandemic including the effects of the Delta variant. These and other risks concerning our programs and operations are described in additional detail in our most recent Form 10-Q, which is on the SEC and available on the SEC’s website at . We operate in a very competitive environment in which new risks emerge from time to time. These forward-looking statements are based on our current expectations, and speak only as of the date hereof. We explicitly disclaim any obligation to update any forward-looking statements except to the extent required by law. Contacts: Investor Contact: Media Contacts: Jennifer Porcelli, Head of Investor Relations US Centessa Pharmaceuticals Dan Budwick, 1AB jennifer.porcelli@centessa.com dan@1abmedia.com UK/Greater Europe Mary Clark, Optimum Strategic Communications centessa@optimumcomms.com Switzerland Marcus Veith, VEITHing Spirit marcus@vspirit.ch M: +41 79 20 75 111

After 20 years of toiling and dreaming, the field of genome editing has arrived. Since the 1990s, it has been arriving slowly, out of the limelight. That all changed in 2012 when Jennifer Doudna and Emmanuelle Charpentier pioneered CRISPR/Cas9 – the molecular toolkit that allows scientists to change the genetic code of living organisms. Since then, companies like Editas Medicine, CRISPR Therapeutics, Intellia Therapeutics, and Vertex Pharmaceuticals, have been working to turn the technology into actionable therapeutics. “I thought gene therapy was going to be fabulous and groundbreaking, and then there was hiccup after hiccup after hiccup. Every meeting for years was: ‘this is what's going to happen in gene therapy,’ and I finally got to the point where I was like ‘just call me when it starts working’. Well, guess what? About five years ago, it started working,” said Dr. Lisa Michaels, EVP and chief medical officer at Editas. When Doudna and Charpentier won the Nobel Prize in 2020, the discovery was hailed as “rewriting the code of life.” CRISPR, which stands for Clustered, Regularly Interspaced, Short Palindromic Repeats, has reenergized the gene editing space as a faster, cheaper, and more accurate approach. Gene therapy has the potential to change the lives of people with severe and life-threatening genetic ailments, including Duchenne muscular dystrophy, Hemophilia A, and Sickle cell disease (SCD) by correcting “spelling mistakes” inside the human genome. Hopes have soared many times over the past five years. In 2016, scientists at Temple University successfully eliminated the HIV-1 virus from the genome of human T-cells, rendering them invulnerable to HIV infection. Unfortunately, the excitement was short-lived as the virus survived the treatment and began to infect the T-cells just two weeks later. This was due to mutations that occurred when CRISPR cut the DNA. But the industry kept on trying, and today, hopes have never been higher. In December, CRISPR Therapeutics and Vertex reported success using CRISPR/Cas9 in two genetic blood diseases, sickle cell disease (SCD) and β-thalassemia (TDT). The experimental therapy, CTX001, was effective in raising fetal hemoglobin ( hemoglobin F) levels. According to data presented at the 2020 ASH conference, 10 patients - three with SCD and seven with beta-thalassemia – have all had relief from bouts of pain and had gone several months without a transfusion. “We know that in children with sickle cell disease, when their hemoglobin F remains very high, they don't have sickle cell disease, they don't sickle until those levels drop off. So we know that by raising the hemoglobin F level, we can ameliorate the disease,” Michaels said. In the U.S. alone, there are nearly 100,000 people living with SCD, which causes fatigue, pain, and infections. Current treatments, such as blood transfusions, only manage symptoms and can have lasting complications. Editas is developing EDIT-301, which edits the beta-globin locus to directly increase the level of fetal hemoglobin using CRISPR nuclease, Cas12a. Michaels explained how Cas12a, which makes use of a shorter guide RNA than Cas9, can be used for a more targeted approach that limits potential long-term problems. “It allows a little more precision so we can get to a more complex part of the gene,” she said. “The result is that we induce a mutation, the peremptory persistence fetal hemoglobin mutation. That mutation is known to result in relatively high levels of hemoglobin F, it's not associated with any disease, and we've got a very clear human proof of concept.” In the gene editing space, which maybe more than any other, relies on fine-tuning, Michaels believes that Cas12a could be a game-changer. “I don't think I fully appreciated this before I came into the field, that every one of the enzymes being used by us and the editors is a little bit different,” she said. “Even the base editing techniques are still somewhat dependent upon the use of Cas9, and Cas12a, which we have complete proprietary ownership of, is a uniquely different approach.” On June 26, Intellia and Regeneron Pharmaceuticals, Inc. took CRISPR yet another step further, announcing the first-ever clinical data supporting the safety and efficacy of in vivo CRISPR gene editing in human patients. The landmark data, presented at the Peripheral Nerve Society (PNS) Annual Meeting, demonstrated that Intellia’s lead in vivo candidate, NTLA-2001, greatly reduced the disease-causing protein after a single infusion. The drug is being developed for the treatment of hereditary transthyretin amyloidosis (ATTR) amyloidosis, a rare, life-threatening protein misfolding disorder caused by a specific mutation in the transthyretin (TTR) gene. With this milestone, the field is now wide open for the next in vivo CRISPR success, and Editas is hoping that it will be in the ocular disease space. The company’s lead in vivo candidate, EDIT-101, is being developed for Leber congenital amaurosis type 10 (LCA10), an early onset retinal degenerative disease that leads to significant vision loss and blindness. EDIT-101 targets a disease-causing mutation in the CEP290 gene that causes degeneration in ocular photoreceptor cells, which are critical for normal vision. Editas aims to knock this gene out. Speaking of setbacks to overcome in gene therapy, the Editas’s BRILLIANCE trial had the misfortune of launching in February 2020 – right before the COVID-19 pandemic hit. “This trial was up and running in February a full year ago, and then we couldn't get patients into the treatment centers because things just locked down. So, we've been focusing an awful lot on trying to move this thing forward at a much more aggressive pace to try to make up lost time,” Michaels said. And moving forward they are. On June 23, the company announced that it had received Independent Data Monitoring Committee (IDMC) clearance to begin enrolling the first of two planned pediatric cohorts in the trial. The endorsement was given based on positive safety data from the adult low and mid-dose cohorts. Editas is also now enrolling an adult high-dose cohort. Michaels explained that LCA10 is a great illustration of gene editing’s sweet spot. “We've really progressed. We don't only knock out genes. We're often knocking in genes or doing rearrangements, but LCA10 is a classic example of where knocking out a gene can actually be very helpful,” Michaels said. “The CEP290 gene is huge, and it cannot be fit inside a vector. So this is not a disease that can be treated by gene therapy. We remove the splice mutation, and as a consequence, the cell is able to make the normal protein.” The next phase of the journey is where Michaels believes Editas may begin to see positive efficacy signals. “We're really just now getting into that window of time where I'm really hoping that we will demonstrate not only a physiological measurement showing that productive editing has happened in the eye, but maybe now with the patient population being enrolled, we will also be able to demonstrate changes in vision,” she said. Editas expects to report initial clinical data from the EDIT-101 program in September. As gene therapies such as these get closer to being realized for patients, Michaels is excited to witness the next phase. “Most of the focus has been on inherited genetic diseases, but there are also inherited predispositions to diseases. We note that the turning on of certain genes, or episomal changes that take place within genes, may also result in late disease. Can you prevent the onset of late disease?” she said. “As we begin to make this space safer, the number of different diseases that we can move into starts to become incredibly broad.”

Basel, 02 July 2021 - Roche (SIX: RO, ROG; OTCQX: RHHBY) today announced that new data from its haemophilia A clinical programme will be presented at the virtual International Society on Thrombosis and Haemostasis (ISTH) 2021 Congress, from 17-21 July 2021. Data will include the final analysis from the phase IIIb STASEY study of Hemlibra® (emicizumab) and updated data from the phase I/II study of SPK-8011, an AAV-based gene therapy in development by Spark Therapeutics (a member of the Roche Group).1,2 “We’re excited to present new data from our haemophilia A programme at the ISTH 2021 Congress,” said Levi Garraway, M.D., Ph.D., Roche’s Chief Medical Officer and Head of Global Product Development. “These data reinforce our continued commitment to developing transformational therapies for the haemophilia A community and advancing understanding of the long-term efficacy and safety profile of Hemlibra.” Haemophilia A is a serious, inherited bleeding disorder in which a person’s blood doesn't clot properly, as they either lack or do not have enough of a clotting protein called factor VIII. This can lead to uncontrolled bleeding, either spontaneously or after minor trauma. These bleeds can present a significant health concern as they often cause pain and can lead to chronic swelling, deformity, reduced mobility, and long-term joint damage.3 The development of factor VIII inhibitors can be a significant challenge in the treatment of people with haemophilia A as they bind to and block the efficacy of replacement factor VIII.4 The STASEY study is one of the largest open-label studies primarily assessing the safety and tolerability of a medicine for adults and adolescents with haemophilia A with factor VIII inhibitors. Final data from the STASEY study, evaluating the safety and tolerability of Hemlibra prophylaxis in adults and adolescents with haemophilia A with factor VIII inhibitors, will be presented at the congress.1 These results confirm the favourable safety profile of Hemlibra, as previously demonstrated in the phase III HAVEN clinical trials.1,5,6,7 Spark Therapeutics will share updated data from the ongoing phase I/II clinical trial of SPK-8011, an investigational AAV-based gene therapy developed for the treatment of haemophilia A. These data demonstrate that hepatocyte expression of factor VIII can be stable and durable for up to four years following vector administration, with an acceptable safety profile.2 “We are looking forward to sharing data on our investigational gene therapy, SPK-8011, which is being evaluated in the largest phase I/II gene therapy trial in haemophilia A to date, and which reinforces Spark’s mission to bring a novel gene therapy option to persons with haemophilia A,” said Gallia Levy, M.D., Ph.D., Chief Medical Officer, Spark Therapeutics. SPK-8011 data presentationUpdated results from Spark’s ongoing phase I/II study of investigational SPK-8011 will be shared as an oral presentation during the meeting. These data highlight the safety profile and durability of SPK-8011 in 18 participants, up to four years following vector administration with SPK-8011 in four dose cohorts, ranging from 5x1011 vg/kg to 2×1012 vg/kg, with results showing a 93% reduction in annualised bleed rate (ABR) and a 97% reduction in annualised infusion rate.2 Key Hemlibra and haemophilia data presentationsFinal data from the STASEY study presented at the congress demonstrate that Hemlibra is effective, with ABRs consistent with observations reported from the pivotal HAVEN studies.1,5,6,7 Additionally, no new safety signals were identified in adults and adolescents with haemophilia A with factor VIII inhibitors, consistent with previous safety observations.1 Roche will also present a retrospective analysis comparing ABR and Hemlibra concentrations among obese and non-obese adults with haemophilia A from pooled data from the HAVEN 1, 3, and 4 studies.8 These data suggest that body weight does not significantly impact the efficacy of Hemlibra, regardless of dosing regimen, demonstrating that Hemlibra offers an effective, well tolerated treatment, with flexible dosing options, in obese and non-obese people with haemophilia A. Additionally, an analysis of data from the 2017 CHESS PAEDs (Cost of Haemophilia across Europe: a Socioeconomic Survey in the Paediatric Population) study, examining the association between physical activity levels and bleed rates in children with haemophilia A, will be presented.9 Results from this analysis demonstrate the potential treatment needs and clinical burden in physically active children with moderate and severe haemophilia A receiving factor VIII replacement therapy. Key abstracts from Roche and Spark that will be presented at ISTH can be found in the table below. Follow Roche and Spark on Twitter via @Roche and @Spark_tx respectively, and keep up to date with ISTH 2021 Congress news and updates by using the hashtag #ISTH2021. About Hemlibra® (emicizumab)Hemlibra is approved for routine prophylaxis of bleeding episodes in people with haemophilia A with and without factor VIII inhibitors in over 100 countries worldwide for those with inhibitors and over 80 countries for those without inhibitors, in adults and children, ages newborn and older. Hemlibra is a bispecific factor IXa- and factor X-directed antibody. It is designed to bring together factor IXa and factor X, proteins involved in the natural coagulation cascade, and restore the blood clotting process for people with haemophilia A. Hemlibra is a prophylactic (preventative) treatment that can be administered by an injection of a ready-to-use solution under the skin (subcutaneously) once-weekly, every two weeks or every four weeks (after an initial once-weekly dose for the first four weeks). Hemlibra was created by Chugai Pharmaceutical Co., Ltd. and is being co-developed globally by Chugai, Roche and Genentech. It is marketed in the United States by Genentech as Hemlibra (emicizumab-kxwh), with kxwh as the suffix designated in accordance with Nonproprietary Naming of Biological Products Guidance for Industry issued by the US Food and Drug Administration. About SPK-8011 for haemophilia AInvestigational SPK-8011, a novel bio-engineered adeno-associated viral (AAV) vector utilizing the AAV-LK03 capsid, also referred to as Spark200, contains a codon-optimized human factor VIII gene under the control of a liver-specific promoter. The Food and Drug Administration (FDA) granted orphan-disease designation and breakthrough therapy designation in the U.S., while the European Commission has granted orphan designation to SPK-8011. About haemophilia AHaemophilia A is an inherited, serious disorder in which a person’s blood does not clot properly, leading to uncontrolled and often spontaneous bleeding. Haemophilia A affects around 900,000 people worldwide,10,11 approximately 35-39% of whom have a severe form of the disorder.11 People with haemophilia A either lack or do not have enough of a clotting protein called factor VIII. In a healthy person, when a bleed occurs, factor VIII brings together the clotting factors IXa and X, which is a critical step in the formation of a blood clot to help stop bleeding. Depending on the severity of their disorder, people with haemophilia A can bleed frequently, especially into their joints or muscles.10 These bleeds can present a significant health concern as they often cause pain and can lead to chronic swelling, deformity, reduced mobility, and long-term joint damage.3 A serious complication of treatment is the development of inhibitors to factor VIII replacement therapies.12 Inhibitors are antibodies developed by the body’s immune system that bind to and block the efficacy of replacement factor VIII,13 making it difficult, if not impossible, to obtain a level of factor VIII sufficient to control bleeding. About Roche and Spark Therapeutics gene therapy research in haemophilia AWe believe gene therapy has the potential to revolutionise medicine and improve the lives of patients with genetic and other serious diseases. Pairing Roche’s long-standing commitment to developing medicines in haemophilia with Spark Therapeutics’ proven gene therapy expertise brings together the best team of collaborators researching gene therapies in haemophilia A. It is our aligned objective to develop gene therapies for haemophilia A that, with the lowest effective dose and the optimal immunomodulatory regimen, demonstrate safety, predictability, efficacy, and durability for patients. About Spark TherapeuticsAt Spark Therapeutics, a fully integrated, commercial company committed to discovering, developing and delivering gene therapies, we challenge the inevitability of genetic diseases, including blindness, haemophilia, lysosomal storage disorders and neurodegenerative diseases. We currently have four programs in clinical trials. At Spark, a member of the Roche Group, we see the path to a world where no life is limited by genetic disease. For more information, visit , and follow us on Twitter and LinkedIn. About Roche in haematologyRoche has been developing medicines for people with malignant and non-malignant blood diseases for over 20 years; our experience and knowledge in this therapeutic area runs deep. Today, we are investing more than ever in our effort to bring innovative treatment options to patients across a wide range of haematologic diseases. Our approved medicines include MabThera®/Rituxan® (rituximab), Gazyva®/Gazyvaro® (obinutuzumab), Polivy® (polatuzumab vedotin), Venclexta®/Venclyxto® (venetoclax) in collaboration with AbbVie, and Hemlibra® (emicizumab). Our pipeline of investigational haematology medicines includes T-cell engaging bispecific antibodies, glofitamab and mosunetuzumab, targeting both CD20 and CD3, and cevostamab, targeting FcRH5 and CD3; Tecentriq® (atezolizumab), a monoclonal antibody designed to bind with PD-L1; and crovalimab, an anti-C5 antibody engineered to optimise complement inhibition. Our scientific expertise, combined with the breadth of our portfolio and pipeline, also provides a unique opportunity to develop combination regimens that aim to improve the lives of patients even further.About RocheRoche is a global pioneer in pharmaceuticals and diagnostics focused on advancing science to improve people’s lives. The combined strengths of pharmaceuticals and diagnostics, as well as growing capabilities in the area of data-driven medical insights help Roche deliver truly personalised healthcare. Roche is working with partners across the healthcare sector to provide the best care for each person. Roche is the world’s largest biotech company, with truly differentiated medicines in oncology, immunology, infectious diseases, ophthalmology and diseases of the central nervous system. Roche is also the world leader in in vitro diagnostics and tissue-based cancer diagnostics, and a frontrunner in diabetes management. In recent years, Roche has invested in genomic profiling and real-world data partnerships and has become an industry-leading partner for medical insights. Founded in 1896, Roche continues to search for better ways to prevent, diagnose and treat diseases and make a sustainable contribution to society. The company also aims to improve patient access to medical innovations by working with all relevant stakeholders. More than thirty medicines developed by Roche are included in the World Health Organization Model Lists of Essential Medicines, among them life-saving antibiotics, antimalarials and cancer medicines. Moreover, for the twelfth consecutive year, Roche has been recognised as one of the most sustainable companies in the Pharmaceuticals Industry by the Dow Jones Sustainability Indices (DJSI). The Roche Group, headquartered in Basel, Switzerland, is active in over 100 countries and in 2020 employed more than 100,000 people worldwide. In 2020, Roche invested CHF 12.2 billion in R&D and posted sales of CHF 58.3 billion. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit trademarks used or mentioned in this release are protected by law.References[1] Jiménez-Yuste J, et al. Final Analysis of the STASEY Trial: A Single-arm, Multicenter, Open-label, Phase III Clinical Trial Evaluating the Safety and Tolerability of Emicizumab Prophylaxis in Persons with Hemophilia A (PwHA) with factor (F)VIII Inhibitors. Presented at: International Society on Thrombosis and Haemostasis (ISTH) Congress; 2021 Jul 17-21; Philadelphia, PA, USA. Abstract PB0521.[2] George LA, et al. Phase I/II trial of SPK-8011: Stable and Durable FVIII Expression After AAV Gene Transfer for Hemophilia A. Presented at: International Society on Thrombosis and Haemostasis (ISTH) Congress; 2021 Jul 17-21; Philadelphia, PA, USA. Abstract OC 67.2.[3] Franchini M, et al. Haemophilia A in the third millennium. Blood Rev. 2013; 179-84.[4] Shannon L. Meeks at al. Hemophilia and inhibitors: current treatment options and potential new therapeutic approaches. Hematology Am Soc Hematol Educ Program 2016 (1): 657–662. [5] Oldenburg J, et al. Emicizumab Prophylaxis in Hemophilia A with Inhibitors. N Engl J Med. 2017; 377:809-818.[6] Young G, et al. Emicizumab prophylaxis provides flexible and effective bleed control in children with hemophilia A with inhibitors: results from the HAVEN 2 study. Blood. 2018; 132 (Supplement 1): 632.[7] Pipe S, et al. Emicizumab subcutaneous dosing every 4 weeks is safe and efficacious in the control of bleeding in persons with haemophilia A with and without inhibitors: Results from the phase 3 HAVEN 4 study. Presented at: WFH World Congress; 2018 May 20-24; Glasgow, Scotland, UK. Abstract M-LBMED01-005 (854).[8] Recht M, et al. Emicizumab in Obese Adults with Hemophilia A – Pooled Data from Three Phase III Studies (HAVEN 1, 3 and 4). Presented at: International Society on Thrombosis and Haemostasis (ISTH) Congress; 2021 Jul 17-21 Philadelphia, PA, USA. Abstract PB0495.[9] Ofori-Asenso et al. Association of Physical Activity with Bleeding Frequency in Children with Hemophilia A: a CHESS PAEDs Study Analysis. Presented at: International Society on Thrombosis and Haemostasis (ISTH) Congress; 2021 Jul 17-21; Philadelphia, PA, USA. Abstract PB0512.[10] Srivastava, A, Santagostino, E, Dougall, A, et al. WFH Guidelines for the Management of Hemophilia, 3rd edition. Haemophilia. 2020: 26 (Suppl 6): 1‐158.[11] Iorio A et al. Establishing the Prevalence and Prevalence at Birth of Hemophilia in Males. Ann Intern Med. 2019 Oct 15;171(8):540-546.[12] Gomez K, et al. Key issues in inhibitor management in patients with haemophilia. Blood Transfus. 2014; 12:s319-s329.[13] Whelan SF, et al. Distinct characteristics of antibody responses against factor VIII in healthy individuals and in different cohorts of haemophilia A patients. Blood. 2013; 121:1039-48.Roche Group Media RelationsPhone: +41 61 688 8888 / e-mail: media.relations@roche.com Attachment