This is a multicenter prospective and retrospective observational clinical study in patients with primary or post polycythemia vera or post essential thrombocythemia myelofibrosis to test the efficacy of fedratinib in the rea world. Participants will be managed according to the clinical practice of the participating Center. All Centers will be Italian Hematology Units belonging to the GIMEMA Organization in Italy.

Start Date29 Jan 2024

Sponsor / Collaborator

Gruppo Italiano Malattie EMatologiche dell'Adulto

NCT06073847 / RecruitingNot Applicable

Inrebic® (Fedratinib) Post-Marketing Surveillance in Korean Patients With Myelofibrosis

The purpose of this study is to assess the real-world safety of fedratinib for the treatment of adult participants with primary myelofibrosis (PMF), post polycythemia vera myelofibrosis (post-PV MF), or post essential thrombocythemia myelofibrosis (post-ET MF) who were previously treated with ruxolitinib. Participants will represent the overall patient population with PMF, post-PV MF or post-ET MF who lost adequate response to and/or are intolerant to ruxolitinib. Inadequate response definitions will follow Ministry of Food and Drug Safety-approved label and reimbursement criteria of the Health Insurance Review & Assessment Service.

Start Date13 Jul 2023

Sponsor / Collaborator

Bristol Myers Squibb Co.

ISRCTN88102629 / RecruitingPhase 2IIT

A phase II study to evaluate the tolerability, safety and activity of fedratinib combined with ropeginterferon alfa-2b in patients with myelofibrosis

Start Date12 Sep 2022

Sponsor / Collaborator

University of Birmingham

100 Clinical Results associated with Fedratinib Hydrochloride

100 Translational Medicine associated with Fedratinib Hydrochloride

100 Patents (Medical) associated with Fedratinib Hydrochloride

264

Literatures (Medical) associated with Fedratinib Hydrochloride

01 Sep 2024·Lancet Haematology

Efficacy and safety of fedratinib in patients with myelofibrosis previously treated with ruxolitinib (FREEDOM2): results from a multicentre, open-label, randomised, controlled, phase 3 trial

Article

Author: Brown, Patrick ; Vannucchi, Alessandro Maria ; Hernandez, Christopher ; Rose, Shelonitda ; Passamonti, Francesco ; Talpaz, Moshe ; Al-Ali, Haifa Kathrin ; Wang, Jia ; Benevolo, Giulia ; Kim, InHo ; Xicoy, Blanca ; Mesa, Ruben ; Palandri, Francesca ; Iurlo, Alessandra ; Harrison, Claire N ; Kiladjian, Jean-Jacques ; Mediavilla, Clemence

BACKGROUND:

Most patients with myelofibrosis develop ruxolitinib intolerance or disease that is relapsed or refractory, and survival rates after ruxolitinib discontinuation are poor. We aimed to evaluate the safety and efficacy of fedratinib versus best available therapy (BAT) in patients with myelofibrosis previously treated with ruxolitinib.

METHODS:

FREEDOM2 was a multicentre, open-label, randomised, controlled, phase 3 trial in 86 clinics in 16 countries, in which patients aged at least 18 years with intermediate-2 or high-risk myelofibrosis that was relapsed or refractory or intolerant to ruxolitinib with Eastern Cooperative Oncology Group performance status 0-2 were stratified by spleen size by palpation, platelet count, and previous ruxolitinib treatment, and randomly assigned 2:1 by interactive response technology to receive fedratinib 400 mg per day (4 × 100 mg capsules orally once daily, open-label) or BAT. Patients received prophylactic antiemetics and thiamine supplementation, and symptomatic antidiarrhoeals as required. Primary endpoint was proportion of patients reaching spleen volume reduction (SVR) of at least 35% (SVR35) at end of cycle 6 in the intention-to-treat population. This manuscript reports the primary analysis of the trial; follow-up is ongoing. This trial is registered at clinicaltrials.gov, NCT03952039.

FINDINGS:

Between Sept 9, 2019 and June 24, 2022, of 316 patients screened, 201 were randomly assigned and treated (134 to fedratinib, 67 to BAT [including 52 receiving ruxolitinib]); 46 patients from the BAT group crossed over to fedratinib. Approximately half of enrolled patients were male (fedratinib 75 [56%] of 134; BAT 30 [45%] of 67) and most were White (fedratinib 106 [79%] of 134; BAT 58 [87%] of 67). At data cutoff (Dec 27, 2022), median survival follow-up was 64·5 weeks (IQR 37·9-104·9). SVR35 at end of cycle 6 was seen in 48 (36%) of 134 patients receiving fedratinib versus four (6%) of 67 patients receiving BAT (30% difference; 95% CI 20-39; one-sided p-value <0·0001). During the first six cycles 53 (40%) of 134 patients in the fedratinib group and 8 (12%) of 67 patients in the BAT group had grade 3 or greater treatment-related adverse events, most frequently anaemia (fedratinib 12 [9%] of 134; BAT 6 [9%] of 67) and thrombocytopenia (fedratinib 16 [12%] of 134; BAT 2 [3%] of 67); one patient in the fedratinib group died from acute kidney injury suspected to be related to study drug (no treatment-related deaths in the BAT group). Gastrointestinal adverse events occurred more frequently in the fedratinib group compared with the BAT group, but were mostly grade 1-2 in severity and more frequent in early cycles, and were less frequent than in prior clinical trials. A total of 28 (21%) of 134 patients in the fedratinib group and 3 (4%) of 67 patients in the BAT group had thiamine levels below lower limit of normal per central laboratory assessment, with only one case of low thiamine in the fedratinib arm after the introduction of prophylactic thiamine supplementation.

INTERPRETATION:

Findings from FREEDOM2 support fedratinib as a second-line Janus kinase inhibitor option to reduce spleen size after ruxolitinib failure or intolerance in patients with myelofibrosis, and shows effective strategies for management of gastrointestinal adverse events and low thiamine concentrations through prophylaxis, monitoring, and treatment.

FUNDING:

Bristol Myers Squibb.

01 Sep 2024·ADVANCES IN THERAPY

Momelotinib versus Continued Ruxolitinib or Best Available Therapy in JAK Inhibitor-Experienced Patients with Myelofibrosis and Anemia: Subgroup Analysis of SIMPLIFY-2

Article

Author: Yacoub, Abdulraheem ; Platzbecker, Uwe ; Sirhan, Shireen ; Ellis, Catherine ; Gerds, Aaron T ; Hernandez-Boluda, Juan Carlos ; Passamonti, Francesco ; Vannucchi, Alessandro M ; Harrison, Claire N ; Recher, Christian ; Strouse, Bryan ; Patel, Bharat

Abstract:

Introduction:

Some Janus kinase (JAK) inhibitors such as ruxolitinib and fedratinib do not address and may worsen anemia in patients with myelofibrosis. In these cases, the JAK inhibitor may be continued at a reduced dose in an effort to maintain splenic and symptom control, with supportive therapy and/or red blood cell (RBC) transfusions added to manage anemia. This post hoc descriptive analysis of the phase 3 SIMPLIFY-2 trial evaluated the relative benefits of this approach versus switching to the JAK1/JAK2/activin A receptor type 1 inhibitor momelotinib in patients for whom anemia management is a key consideration.

Methods:

SIMPLIFY-2 was a randomized (2:1), open-label, phase 3 trial of momelotinib versus best available therapy (BAT; 88.5% continued ruxolitinib) in JAK inhibitor-experienced patients with myelofibrosis (n = 156). Patient subgroups (n = 105 each) were defined by either baseline (1) hemoglobin (Hb) of < 100 g/L or (2) non-transfusion independence (not meeting the criteria of no transfusions and no Hb of < 80 g/L for the previous 12 weeks); outcomes have been summarized descriptively.

Results:

In both subgroups of interest, week 24 transfusion independence rates were higher with momelotinib versus BAT/ruxolitinib: baseline Hb of < 100 g/L, 22 (33.3%) versus 5 (12.8%); baseline non-transfusion independent, 25 (34.7%) versus 1 (3.0%). Mean Hb levels over time were also generally higher in both subgroups with momelotinib, despite median transfusion rates through week 24 with momelotinib being comparable to or lower than with BAT/ruxolitinib. Spleen and symptom response rates with momelotinib in these subgroups were comparable to the intent-to-treat population, while rates with BAT/ruxolitinib were lower.

Conclusion:

In patients with moderate-to-severe anemia and/or in need of RBC transfusions, outcomes were improved by switching to momelotinib rather than continuing ruxolitinib and using anemia supportive therapies.

Trial Registration:

ClinicalTrials.gov: NCT02101268.

01 Aug 2024·ANNALS OF HEMATOLOGY

FRACTION: protocol of a phase II study of Fedratinib and Nivolumab combination in patients with myelofibrosis and resistance or suboptimal response to JAK-inhibitor treatment of the German MPN study group (GSG-MPN)

Article

Author: Heidel, Florian H ; Becker, Heiko ; Isfort, Susanne ; Hochhaus, Andreas ; Al-Ali, Haifa Kathrin ; Griesshammer, Martin ; Wohn, Luisa ; le Coutre, Philipp ; Götze, Thorsten ; Manz, Kirsi ; Moskwa, Claudia ; Palandri, Francesca ; Riedel, Johanna ; Döhner, Konstanze ; von Bubnoff, Nikolas

Abstract:

Development of Janus-kinase (JAK) inhibitors has revolutionized the therapeutic landscape for patients with myeloproliferative neoplasia (MPN). Following approval of the first JAK1/2-inhibitor Ruxolitinib, symptoms of this inflammatory disease, characterized by splenomegaly, release of inflammatory cytokines and appearance of thrombosis, could be effectively reduced for the first time. However, JAK-inhibitor treatment is limited in several aspects: 1) duration of response: 3 years after initiation of therapy more than 50% of patients have discontinued JAK-inhibitor treatment due to lack of efficacy or resistance; 2) reduction of disease burden: while effective in reducing inflammation and constitutional symptoms, JAK-inhibitors fail to reduce the malignant clone in the majority of patients and therefore lack long-term efficacy. Early clinical trials for patients with myelofibrosis (MF) have tried to address these issues for patients with suboptimal response to Ruxolitinib therapy while combination therapies with Fedratinib are rare. Recent reports provided first evidence on how the JAK2-V617F mutated myeloid cells may influence T-cell responses. JAK2-V617F promoted the synthesis of PD-L1 in MPN cells leading to limited anti-neoplastic T-cell responses, metabolic changes in T-cells and eventually JAK2-V617F-driven immune-escape of MPN cells. These findings may facilitate the use of immunotherapeutic approaches for JAK-mutated clones. Immune checkpoints refer to a variety of inhibitory pathways that are crucial for maintaining self-tolerance and modulating the duration and amplitude of physiological immune responses in peripheral tissues in order to minimize collateral tissue damage. The FRACTION study is a single arm, open label Phase II trial investigating the combination of Fedratinib with the PD-1 inhibitor Nivolumab in patients with myelofibrosis and suboptimal or lack of response to JAK-inhibitor therapy. Over a 12 months period the trial assesses longer term outcomes, particularly the effects on clinical outcomes, such as induction of clinical remissions, quality of life and improvement of anemia. No prospective clinical trial data exist for combinations of JAK- and immune-checkpoint-inhibitors in the planned MF study population and this study will provide new findings that may contribute to advancing the treatment landscape for MF patients with suboptimal responses and limited alternatives.

News (Medical) associated with Fedratinib Hydrochloride

13 May 2024

·firstwordpharma.com

Ajax raises $95 million to launch a ‘JAK attack’

More than a decade after the FDA approved the first JAK inhibitor to treat myelofibrosis, Ajax Therapeutics thinks it has improved on the formula by targeting a less-well-known, inactive conformation of the kinase to boost efficacy and tolerability. The biotech raised $95 million in an oversubscribed series C, led by Goldman Sachs Alternatives, to bring its potentially first-in-class inhibitor, AJ1-11095, to the clinic next half. Monday’s round – which also saw participation from new investors Eli Lilly, Vivo Capital, RA Capital Management, Point72, as well as existing investors EcoR1 Capital, Boxer Capital, Schrödinger, and Inning One Ventures – adds to $40 million raised in 2021.Scientific originsAround 2017, five experts on the biology of the JAK pathway got together with one goal in mind – creating an improved kinase inhibitor that elicits a deeper and more durable response in patients with myelofibrosis. One of the scientists was Ross Levine, an oncologist at Memorial Sloan Kettering Cancer Center who helped discover the mutations in JAK2 associated with myelofibrosis.“We all were excited when the discoveries were made, and then hopeful that the drugs that were developed – ruxolitinib, pacritinib, momelotinib, fedratinib – would really be game changers for patients. And they brought real, meaningful benefits to patients, but they don't lead to molecular or clinical regressions,” Levine told FirstWord.Additionally, patient response isn’t durable, with most patients discontinuing treatment within a few years due to a loss of efficacy. And once a myelofibrosis patient fails on a JAK inhibitor, their life expectancy is around a year or two.“There's quite a lot of room between where these molecules are… and what would be optimal engagement,” Levine said.Out of the scientific consortium, an idea arose to design pleiotropic molecules that engage the inactive, Type II conformation of JAK2, rather than the active, Type 1 conformation, which the four myelofibrosis-approved JAK inhibitors target. Thus, Ajax – an abbreviation of “attack JAK” – was born in 2019, with Levine as a co-founder and serving as chair of the scientific advisory board.Preclinical potency The researchers had developed early chemical matter and structures that showed better efficacy than approved molecules, which gave the newco a foothold to begin designing a completely different kind of JAK inhibitor.But for the Type II conformation, “it’s not as easy as just screening the kinase domain and finding an inhibitor,” Ajax co-founder and CEO Martin Vogelbaum told FirstWord.So the team turned to digital chemistry company Schrödinger, which, along with serving as a co-founding investor, signed an exclusive collaboration with Ajax to apply its computational molecular discovery methods and expertise in structure based drug design to transform the biotech’s early work into a potent, specific and clinically tractable Type II JAK2 inhibitor. Now, after five years of work optimising a highly selective compound, Ajax thinks AJ1-11095 is a safer molecule that produces a deeper, more durable response – and is ready to enter the clinic. A Phase I study in myelofibrosis is expected to begin in the second half.Vogelbaum said that repeated mice experiments suggest Ajax’s lead candidate has similar, if not better, efficacy than ruxolitinib alone or in combination with another approved agent.“Our preclinical data suggest that we can achieve greater target engagement at doses with a wide range that are efficacious – well beyond the current drugs – and are very well tolerated,” Ross said, adding that the team feels “very confident” that AJ1-11095 won’t have the off-target toxicities of others in the JAK class.

Phase 1Drug Approval

01 Apr 2024

·www.prnewswire.com

Cellenkos® enters into Sponsored Research Agreement with Icahn School of Medicine at Mount Sinai, New York.

Research exploring CK0804 (CXCR4-enriched, allogeneic, cord blood-derived T-regulatory cells) for treatment of myelofibrosis patients. HOUSTON and NEW YORK, April 1, 2024 /PRNewswire/ -- Cellenkos®, a clinical stage biotech cell therapy company focused on treating autoimmune diseases and inflammatory disorders, today announced that it has entered into a sponsored research agreement with the Icahn School of Medicine at Mount Sinai, New York, to explore the application of CK0804, CXCR4 enriched, allogeneic, cord blood T regulatory (Treg) cells, for treatment of myelofibrosis. This research will be conducted under the guidance of Ronald Hoffman, MD, Albert A. and Vera G. List Professor of Medicine and Director of the Myeloproliferative Disorders Research Program at The Tisch Cancer Institute- Mount Sinai. "We are very excited by our collaboration with Mount Sinai and eagerly anticipate gaining a deeper understanding of mechanisms of CK0804 Tregs work in myelofibrosis, especially to decrease inflammation," said Tara Sadeghi, Chief Operating Officer, Cellenkos Inc. "CK0804 is already in phase 1 clinical trial to examine its safety and efficacy in patients with myelofibrosis who have suboptimal response to the JAK2 inhibitor, ruxolitinib. We are particularly intrigued by the possibility of using CK0804 in treatment naïve myelofibrosis patients as well as in combination with other approved therapies including ruxolitinib, momelotinib, pacritinib and fedratinib." "We are eager to find out if this novel cell therapy product has the potential to transform the care of myelofibrosis patients," said Dr. Ronald Hoffman, principal investigator, "We will investigate the role of Treg cells in the pathogenesis of the myeloproliferative neoplasms and examine the effectiveness of CK0804, especially in patients with low blood counts." CK0804 is a novel allogeneic, CXCR4 enriched, Treg cell therapy product that utilizes Cellenkos' proprietary CRANE® technology to generate disease specific products. CK0804 engage with CXCL12 ligand and preferentially home to the inflamed bone marrow. When compared to control, CK0804 significantly decrease TGFβ1 and TGFβ2, in vivo. The ongoing, multicenter, first-in-human, Phase 1b trial, shows safety of multiple doses of CK0804 in myelofibrosis patients in the ambulatory setting as well as improvement in their blood transfusion requirements, spleen volume reduction and symptom burden. The ability to administer CK0804 cells in ambulatory setting without requiring lymphodepletion or immune suppression, positions this potentially lifesaving treatment to be made available to patients in the community setting. The trial is open for accrual at Albert Einstein Hospital, Bronx, NY, MD Anderson Cancer Center, Houston, TX and University of California Davis, Sacramento, CA. ClinicalTrials.gov ID NCT05423691. Dr. Ronald Hoffman serves as a paid consultant for Cellenkos. About Cellenkos®, Inc. Cellenkos is a clinical-stage biotechnology company located in Houston, Texas, USA, dedicated to the development and commercialization of the allogeneic, "off-the-shelf" cell-based products for the treatment of rare inflammatory diseases and autoimmune disorders. Cellenkos' T regulatory cells (Tregs) are derived from umbilical cord blood and as such are naïve, bonafide suppressor cells that do not require HLA or ABO matching and resolve inflammation through multiple direct and indirect mechanisms. Cellenkos' proprietary CRANE® technology platform tailors Tregs to home to target tissue. Cellenkos' current clinical portfolio includes CK0801 (bone marrow failure); CK0802 (COVID associated acute respiratory distress syndrome); CK0803 (Amyotrophic Lateral Sclerosis) and CK0804 (myelofibrosis). For more information, please visit . Contact: Stacy Minor [email protected]. SOURCE Cellenkos, Inc.

Cell TherapyPhase 1

18 Mar 2024

·www.globenewswire.com

Arvinas Appoints Noah Berkowitz, M.D., Ph.D., as Chief Medical Officer

- Awards Dr. Berkowitz an Inducement Grant in accordance with Nasdaq Listing Rule 5635(c)(4) -NEW HAVEN, Conn., March 18, 2024 (GLOBE NEWSWIRE) -- Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company creating a new class of drugs based on targeted protein degradation, today announced the appointment of Noah Berkowitz, M.D., Ph.D., to the role of Chief Medical Officer and a member of the Executive Committee reporting to President and Chief Executive Officer John Houston, Ph.D. Effective today, Dr. Berkowitz will lead the ongoing clinical development of Arvinas’ PROTAC® protein degrader programs in oncology and neuroscience. “We are thrilled to have Dr. Berkowitz join Arvinas as we continue advancing multiple programs with the goal of improving the lives of patients with serious diseases,” said John Houston, Ph.D., Chairperson, President and Chief Executive Officer at Arvinas. “Noah’s vision, expertise, and proven track record in designing and launching successful clinical programs across all stages of clinical development complement our rapidly advancing portfolio of novel PROTAC protein degraders. His leadership and experience will be invaluable as we approach our first Phase 3 data readout and continue progressing multiple ongoing and planned clinical-stage programs.” Dr. Berkowitz has more than 20 years of experience in advancing programs through early and late stages of development, with proven ability in leading clinical development, regulatory, and medical affairs. He has led multidisciplinary teams and has extensive knowledge of clinical trial design and execution. Dr. Berkowitz joins Arvinas from Bristol-Myers Squibb (BMS), where he was Senior Vice President, Development Unit Head, Hematology. While at BMS, Dr. Berkowitz’s teams achieved initial or subsequent global indications for Abecma®, Breyanzi®, Reblozyl®, Onureg®, and Inrebic®, managed development life cycles for Revlimid®, Pomalyst®, and Sprycel®, and initiated and/or designed registration trials for iberdomide, mezigdomide, and alnuctamab. Prior to BMS, Dr. Berkowitz held roles of increasing responsibility in the areas of oncology, rare diseases, and hematology at Novartis, most recently as Vice President and Clinical Development Head for Hematology. Dr. Berkowitz earned his M.D. and Ph.D. from Columbia University and trained in medical oncology at the National Cancer Institute. “Arvinas is the leader in targeted protein degradation and is on the cusp of its first pivotal data, an important step in potentially bringing an innovative therapeutic approach to patients with serious diseases,” said Dr. Berkowitz. “Arvinas’ progress over the last several years is impressive and I look forward to working with my colleagues, including the strong leadership team at Arvinas, as we prepare for many important upcoming clinical milestones ahead.” The Company also announced that Ron Peck, M.D., who was Chief Medical Officer since joining Arvinas in mid-2019, will be leaving to pursue other opportunities. “In less than five years, Ron built robust clinical development and medical affairs organizations, enabling the planning and initiation of multiple clinical trials across our oncology and neuroscience portfolios,” continued Dr. Houston. “Under Ron’s leadership and in partnership with Pfizer, vepdegestrant has advanced from the start of Phase 1 to multiple ongoing and planned Phase 3 studies in advanced breast cancer. Ron’s teams also progressed our androgen receptor programs, with ARV-766 moving towards Phase 3 initiation, and initiated human dosing of ARV-102, our neuroscience program targeting LRRK2,” said Dr. Houston. “We thank Ron for his tremendous efforts and take confidence in knowing that Dr. Berkowitz is inheriting a high-performing organization.” In connection with the commencement of Dr. Berkowitz’s employment, Arvinas granted Dr. Berkowitz an option to purchase 93,879 shares of common stock and a restricted stock unit award with respect to 63,452 shares of common stock on March 18, 2024, as an inducement material to entering into employment with Arvinas. The option and restricted stock units were granted in accordance with Nasdaq Listing Rule 5635(c)(4) and not pursuant to Arvinas’ stock incentive plan. The option has a 10-year term and an exercise price of $42.60 per share, which is equal to the closing price per share of Arvinas’ common stock on the grant date. The option vests over four years, with 25% of the original number of shares underlying the option vesting on the one-year anniversary of the date of grant and 1/48th of the original number of shares vesting monthly thereafter, and the restricted stock unit award vests in four equal installments on each one-year anniversary of Dr. Berkowitz’s employment start date until the fourth anniversary of Dr. Berkowitz’s start date, subject to his continued service with Arvinas through the applicable vesting dates.  About ArvinasArvinas is a clinical-stage biotechnology company dedicated to improving the lives of patients suffering from debilitating and life-threatening diseases through the discovery, development, and commercialization of therapies that degrade disease-causing proteins. Arvinas uses its proprietary PROTAC® Discovery Engine platform to engineer proteolysis targeting chimeras, or PROTAC® targeted protein degraders, that are designed to harness the body’s own natural protein disposal system to selectively and efficiently degrade and remove disease-causing proteins. In addition to its robust preclinical pipeline of PROTAC protein degraders against validated and “undruggable” targets, the company has four investigational clinical-stage programs: vepdegestrant (ARV-471) for the treatment of patients with locally advanced or metastatic ER+/HER2- breast cancer; ARV-766 and bavdegalutamide for the treatment of men with metastatic castration-resistant prostate cancer; and ARV-102 for the treatment of patients with neurodegenerative disorders. For more information, visit www.arvinas.com. Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements with respect to Arvinas’ development plans; the anticipated data readout for Arvinas’ first Phase 3 clinical trial with vepdegestrant (ARV-471); the potential, pending regulatory approval, for vepdegestrant to address an area of significant unmet need and offer patients an innovative therapeutic approach; and the potential advantages and therapeutic benefits of vepdegestrant (ARV-471). All statements, other than statements of historical facts, contained in this press release, including statements regarding Arvinas’ strategy, future operations, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “might,” “plan,” “predict,” “project,” “target,” “potential,” “will,” “would,” “could,” “should,” “continue,” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Arvinas may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on such forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements Arvinas makes as a result of various risks and uncertainties, including but not limited to: Arvinas’ and Pfizer, Inc.’s (“Pfizer”) performance of the respective obligations with respect to Arvinas’ collaboration with Pfizer; whether Arvinas and Pfizer will be able to successfully conduct and complete clinical development for vepdegestrant (ARV-471); whether Arvinas will be able to successfully conduct and complete development for its other product candidates, including ARV-766, and including whether Arvinas initiates and completes clinical trials for its product candidates and receive results from its clinical trials on its expected timelines or at all; whether Arvinas and Pfizer, as appropriate, will be able to obtain marketing approval for and commercialize vepdegestrant (ARV-471), ARV-766 and other product candidates on current timelines or at all; Arvinas’ ability to protect its intellectual property portfolio; whether Arvinas’ cash and cash equivalent resources will be sufficient to fund its foreseeable and unforeseeable operating expenses and capital expenditure requirements; and other important factors discussed in the “Risk Factors” section of Arvinas’ Annual Report on Form 10-K for the year ended December 31, 2023 and subsequent other reports on file with the U.S. Securities and Exchange Commission. The forward-looking statements contained in this press release reflect Arvinas’ current views with respect to future events, and Arvinas assumes no obligation to update any forward-looking statements, except as required by applicable law. These forward-looking statements should not be relied upon as representing Arvinas’ views as of any date subsequent to the date of this release. Contacts Investors:Jeff Boyle+1 (347) 247-5089Jeff.Boyle@arvinas.com Media:Maurissa Messier+1 (908) 208-9254Maurissa.messier-c@arvinas.com

Executive ChangePhase 3PROTACsPhase 1

100 Deals associated with Fedratinib Hydrochloride

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KEGG	Wiki	ATC	Drug Bank
-	Fedratinib Hydrochloride	L01XE57	DB12500

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Post-essential thrombocythemia myelofibrosis	EU	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	IS	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	LI	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	NO	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	EU	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	IS	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	LI	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	NO	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	EU	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	IS	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	LI	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	NO	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	EU	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	IS	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	LI	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	NO	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Myelofibrosis	US	Bristol Myers Squibb Co.	16 Aug 2019
Polycythemia Vera	US	Bristol Myers Squibb Co.	16 Aug 2019
Thrombocythemia, Essential	US	Bristol Myers Squibb Co.	16 Aug 2019

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Hematologic Neoplasms	Phase 3	US	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	AU	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	AT	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	BE	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	BR	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	CA	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	FR	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	DE	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	HU	Sanofi	01 Dec 2011
Hematologic Neoplasms	Phase 3	IE	Sanofi	01 Dec 2011

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


Pubmed \| Lancet Haematol	Not Applicable	-	-	Fedratinib 400 mg per day	hpyzqundnv(ydpniubsum) = one patient in the fedratinib group died from acute kidney injury suspected to be related to study drug (no treatment-related deaths in the BAT group) qcalsmtgpd (psaeauzuvc )	-	01 Sep 2024
				Best Available Therapy (BAT)
NCT03952039 (FREEDOM2, EHA2024) Manual	Phase 3	Myelofibrosis Second line	201	Fedratinib 400mg daily	skvrvnqtrb(zpokhjnase) = vpkeqxlthj ikorxjipgp (nozvoyoogj ) View more	Positive	14 May 2024
				Best Available Therapy	skvrvnqtrb(zpokhjnase) = owvaqkkuaa ikorxjipgp (nozvoyoogj ) View more
Tandem Meetings ASTCT and CIBMTR2024	Not Applicable	Myelofibrosis	18	Fedratinib 400 mg once daily	figqmkxbdr(aruogkuaxu) = n=4 (22.2%) deaths were recorded as of May 2023. Two of the 4 deaths were related to MF and both patients had disease transformation to blast phase MPN before HSCT. A median duration of 14.5 months elapsed between FEDR initiation and death among these 4 patients fnfkaufgon (asyrsdxizo ) View more	Positive	01 Feb 2024
NCT03952039 (FREEDOM2, CTgov)	Phase 3	Post-essential thrombocythemia myelofibrosis \| Post-polycythemia vera myelofibrosis \| Primary Myelofibrosis	202	Best Available Therapy (BAT)	llqbktbvqw(afchgbcbvm) = mwhaljgomh xqooobtuts (vqnmnwrtsw, ixwnrzrwzu - oavjcaabci) View more	-	30 Jan 2024
NCT04817007 (CA011-023, ASH2023)	Phase 1/2	Primary Myelofibrosis	40	BMS-986158+Ruxolitinib	cpxmpkyemi(kcmdqydnay) = auztnoiznx jwtxuoyyzm (lcgfcvuovu )	-	10 Dec 2023
				BMS-986158+Fedratinib	cpxmpkyemi(kcmdqydnay) = yhghrsottv jwtxuoyyzm (lcgfcvuovu )
ASH2023	Not Applicable	Second line	-	Ruxolitinib	urglnkhkyd(pgjzsyzoor) = gpfsjuense tytziefuaz (zpntemegxn ) View more	-	09 Dec 2023
				Fedratinib	urglnkhkyd(pgjzsyzoor) = qegpykfuqr tytziefuaz (zpntemegxn )
ASH2023	Not Applicable	Primary Myelofibrosis	58	Fedratinib	aqjrcvchjj(dxxgvduvml) = uudwaxmype poxojalzrm (euilvnneht )	-	09 Dec 2023
NCT05177211 (ASH2023)	Phase 2	Leukemia, Neutrophilic, Chronic \| Myeloproliferative Disorders	10	Fedratinib	gcxcqimppg(occmtrnsuz) = uetarwcvkj uqbvlzlkzl (bifqvkrcoa ) View more	-	09 Dec 2023
NCT03755518 (FREEDOM, CTgov)	Phase 3	Post-essential thrombocythemia myelofibrosis \| Post-polycythemia vera myelofibrosis \| Primary Myelofibrosis	38	Fedratimib (Fedratimib)	lfmcxvdyfj(nqukopzaea) = csgbcxpnjt gejnspltor (syqwcrzsti, xitxgophim - unyxngfkmr) View more	-	09 Mar 2023
				Fedratinib (Fedratinib)	wwiojoakps(acepdrkmmn) = iyvqfereca xjrjnsjeta (pyfbynxczn, zppntwztbm - jvnklhbneg) View more
NCT03755518 (FREEDOM, ASH2022) Manual	Phase 3	Polycythemia Vera \| Post-essential thrombocythemia myelofibrosis \| Primary Myelofibrosis	38	Fedratinib	alnszhufxu(bwwltsbyfv) = yvfpaqbexp cbodqsvwot (dhkuuhlthk ) View more	Positive	15 Nov 2022

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