Delving into the Latest Updates on Fedratinib Hydrochloride with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

FEDR, Fedratinib, INREBIC

+ [4]

Target

FLT3 x JAK2

Action

inhibitors

Mechanism

FLT3 inhibitors(Tyrosine-protein kinase receptor FLT3 inhibitors), JAK2 inhibitors(Tyrosine-protein kinase JAK2 inhibitors)

Therapeutic Areas

NeoplasmsHemic and Lymphatic DiseasesOther Diseases+ [1]

Active Indication

Post-essential thrombocythemia myelofibrosisPost-polycythemia vera myelofibrosisPrimary Myelofibrosis+ [10]

Inactive Indication

Advanced Malignant Solid NeoplasmBlast Phase Chronic Granulocytic LeukemiaMycosis Fungoides+ [2]

Originator Organization

TargeGen, Inc.

Active Organization

Bristol Myers Squibb Co.

Celgene Corp.Bristol-Myers Squibb Pharma EEIG

+ [2]

Inactive Organization

TargeGen, Inc.

Drug Highest PhaseApproved

First Approval Date

United States (16 Aug 2019),

MyelofibrosisPolycythemia VeraThrombocythemia, Essential

RegulationOrphan Drug (United States)

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Structure/Sequence

Molecular FormulaC27H36N6O3S

InChIKeyJOOXLOJCABQBSG-UHFFFAOYSA-N

CAS Registry936091-26-8

View All Structures (2)

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 Jun 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

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100 Translational Medicine associated with Fedratinib Hydrochloride

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100 Patents (Medical) associated with Fedratinib Hydrochloride

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546

Literatures (Medical) associated with Fedratinib Hydrochloride

01 Apr 2025·Molecular Diversity

Targeting AFP-RARβ complex formation: a potential strategy for treating AFP-positive hepatocellular carcinoma

Article

Author: Raju, Rajesh ; Abhinand, Chandran S ; Kumar, Pankaj ; Ramakrishnan, Krishnapriya ; Soman, Sowmya ; Kalath, Haritha ; Vishwakarma, Riya ; Revikumar, Amjesh ; Banjan, Bhavya ; Rehman, Niyas ; Dev, Radul R

Alpha-fetoprotein (AFP) is a glycoprotein primarily expressed during embryogenesis, with declining levels postnatally. Elevated AFP levels correlate with pathological conditions such as liver fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Recent investigations underscore AFP's intracellular role in HCC progression, wherein it forms complexes with proteins like Phosphatase and tensin homolog (PTEN), Caspase 3 (CASP3), and Retinoic acid receptors and Retinoid X receptors (RAR/RXR). RAR and RXR regulate gene expression linked to cell death and tumorigenesis in normal physiology. AFP impedes RAR/RXR dimerization, nuclear translocation, and function, promoting gene expression favoring cancer progression in HCC that provoked us to target AFP as a drug candidate. Despite extensive studies, inhibitors targeting AFP to disrupt complex formation and activities remain scarce. In this study, employing protein-protein docking, amino acid residues involved in AFP-RARβ interaction were identified, guiding the definition of AFP's active site for potential inhibitor screening. Currently, kinase inhibitors play a significant role in cancer treatment and, the present study explores the potential of repurposing FDA-approved protein kinase inhibitors to target AFP. Molecular docking with kinase inhibitors revealed Lapatinib as a candidate drug of the AFP-RARβ complex. Molecular dynamics simulations and binding energy calculations, employing Mechanic/Poisson-Boltzmann Surface Area (MM-PBSA), confirmed Lapatinib's stability with AFP. The study suggests Lapatinib's potential in disrupting the AFP-RARβ complex, providing a promising avenue for treating molecularly stratified AFP-positive HCC or its early stages.

19 Feb 2025·Future Oncology

Real-world treatment patterns and health outcomes for patients with myelofibrosis treated with fedratinib

Article

Author: Yucel, Aylin ; Zissler, Dorothy ; Rombi, Julien ; Chevli, Manoj ; Korgaonkar, Siddhi ; Davis, Keith L ; Passamonti, Francesco ; Slaff, Samantha ; Parikh, Rohan C ; Jones, Shalon

AIMAssess real-world fedratinib (FEDR) treatment patterns and clinical outcomes in patients with primary or secondary myelofibrosis following discontinuation of ruxolitinib (RUX).PATIENTS & METHODSThis study was a retrospective, noninterventional medical record review of patients in Canada, Germany, and the United Kingdom (UK). A total of 70 physicians (primarily hematologist-oncologists [78.6%]) provided data for 196 eligible patients.RESULTSPatients were mostly male (62.8%) with primary myelofibrosis (76.5%) and initiated FEDR at a mean age of 67.7 years. Median treatment duration was 11.5 months (median follow-up, 13.8 months), and nearly half (49.5%) of patients initiated FEDR at the label-indicated dose of 400 mg daily. Six months post-initiation, 77.7% and 66.8% of patients experienced symptom and spleen response, respectively. Kaplan-Meier estimates of median progression-free and overall survival from initiation were 23.8 months (95% CI, 21.1-27.6) and 29.8 months (95% CI, 23.9-NE), respectively.CONCLUSIONThese findings demonstrate real-world FEDR effectiveness among patients with myelofibrosis who discontinued RUX.

01 Feb 2025·Bone Marrow Transplantation

Fedratinib as an alternative to splenectomy for refractory splenomegaly prior to transplant for myelofibrosis

Letter

Author: Urbach, David R ; Urbach, David R. ; Cheung, Verna ; England, James T ; Nye, Taylor ; Sibai, Hassan ; England, James T. ; Gupta, Vikas ; Viswabandya, Auro

25

News (Medical) associated with Fedratinib Hydrochloride

20 Dec 2024

·www.prnewswire.com

Vanda Pharmaceuticals Announces Orphan Drug Designation Granted for VGT-1849A, a Novel and Selective Antisense Oligonucleotide Candidate for the Treatment of Polycythemia Vera

WASHINGTON, Dec. 20, 2024 /PRNewswire/ -- Vanda Pharmaceuticals Inc. (Vanda) (Nasdaq: VNDA) today announced the U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation for VGT-1849A, a selective antisense oligonucleotide (ASO)-based JAK2 inhibitor for the treatment of polycythemia vera (PV), a form of a rare hematologic malignancy that is estimated to affect 1 in 2000 Americans.1 PV is a chronic myeloproliferative disorder characterized by aberrant hematopoiesis of myeloid lineage with exuberant red cell production and increased release of pro-inflammatory cytokines. More than 95% of PV patients harbor the JAK2 V617F gain-of-function mutation leading to aberrant JAK2 production.2 Inhibiting JAK2 acts to suppress hematopoiesis, consequently reducing red blood cell, neutrophil, platelet, and lymphocyte production. JAK2 inhibitors have been shown to be efficacious in treating various JAK-dependent hematologic malignancies, including the treatment of PV. By selective reduction of JAK2 levels, the ASO VGT-1849A has the potential to reduce JAK2V617F-driven pathogenic signaling, ultimately suppressing the malignant proliferation and survival of hematopoietic cells. Currently available small molecule inhibitors targeting the JAK2 protein kinase, such as Jakafi®, Inrebic®, Ojjaara®, and Vonjo®, lack sole selectivity for the target protein, which can result in off target effects. The adverse side effects that may occur from JAK inhibition emphasize the importance of selectively targeting JAK2 while avoiding inhibition of other JAK family members. By specifically targeting JAK2, Vanda seeks to reduce the risk of infection and toxic effects that are seen with inhibitors also blocking JAK1, JAK3, TYK2, or other kinases outside of the JAK family. If approved, VGT-1849A could offer targeted efficacy with an improved safety profile and convenient dosing. "This orphan designation for VGT-1849A is an important milestone in precision medicine-based therapeutics in the space of hematological malignancies. This milestone marks the second precision medicine therapeutic for Vanda following the development of VCA-894A for Charcot-Marie-Tooth3 that is expected to begin clinical testing in the coming months," said Mihael H. Polymeropoulos, M.D., Vanda's President, CEO and Chairman of the Board. VGT-1849A is a novel ASO treatment candidate for PV and other JAK2-driven hematologic malignancies. By selectively targeting JAK2, VGT-1849A reduces downstream signaling and JAK2V617F-driven autonomous cell proliferation, without any off-target kinase effects. The ability of VGT-1849A to reduce JAK2 activity may alleviate the disease burden that patients with PV face with a favorable safety profile, resulting in a higher quality of life for patients. Orphan Drug Designation is granted by the FDA to investigational therapies addressing rare medical conditions and provides benefits to drug developers. References: Grunwald, M. R.; Stein, B. L.; Boccia, R. V.; Oh, S. T.; Paranagama, D.; Parasuraman, S.; Colucci, P.; Mesa, R. Clinical and Disease Characteristics From REVEAL at Time of Enrollment (Baseline): Prospective Observational Study of Patients With Polycythemia Vera in the United States. Clin Lymphoma Myeloma Leuk 2018, 18 (12), 788-795.e2. . P. Gou, W. Zhang, and S. Giraudier, "Insights into the Potential Mechanisms of JAK2V617F Somatic Mutation Contributing Distinct Phenotypes in Myeloproliferative Neoplasms," Myeloproliferative Neoplasms. Int. J. Mol. Sci, vol. 2022, p. 1013, 2022, S. Smieszek, C. Tyner, A. Kaden, C. Johnson, C. Polymeropoulos, G. Birznieks, M. Polymeropoulos. Potential treatment for CMT2S caused by IGHMBP2 cryptic splice variant, with ASO based therapeutic [abstract]. Mov Disord. 2023; 38 (suppl 1). . About Vanda Pharmaceuticals Inc. Vanda is a leading global biopharmaceutical company focused on the development and commercialization of innovative therapies to address high unmet medical needs and improve the lives of patients. For more on Vanda Pharmaceuticals Inc., please visit and follow us on X @vandapharma. About VGT-1849A VGT-1849A is an antisense oligonucleotide (ASO) that selectively targets JAK2, reducing increased activity of JAK2 that may cause hematologic malignancies. ASOs have broad applicability in addressing a number of disorders caused by genetic variants. CAUTIONARY NOTE REGARDING FORWARD-LOOKING STATEMENTS Various statements in this press release, including, but not limited to statements regarding the estimated prevalence of PV, the potential therapeutic effects of VGT-1849A, the timing of the initiation of clinical testing of VCA-894A and the potential benefits of VGT-1849A, are "forward-looking statements" under the securities laws. Forward-looking statements are based upon current expectations that involve risks, changes in circumstances, assumptions and uncertainties. Important factors that could cause actual results to differ materially from those reflected in Vanda's forward-looking statements include, among others, the accuracy of the reporting and diagnosis of PV cases, the ability of VGT-1849A to safely and effectively treat PV, Vanda's ability to begin clinical testing of VCA-894A during the specified timeframe and Vanda's ability to successfully complete the clinical development of, and obtain regulatory approval for, VGT-1849A in the treatment of PV. There can be no assurance that the actual results or developments anticipated by Vanda will be realized or, even if substantially realized, that they will have the expected consequences to, or effects on, Vanda. Therefore, no assurance can be given that the outcomes stated in such forward-looking statements and estimates will be achieved. Forward-looking statements in this press release should be evaluated together with the various risks and uncertainties that affect Vanda's business and market, particularly those identified in the "Cautionary Note Regarding Forward-Looking Statements", "Risk Factors" and "Management's Discussion and Analysis of Financial Condition and Results of Operations" sections of Vanda's Annual Report on Form 10-K for the fiscal year ended December 31, 2023, as updated by Vanda's subsequent Quarterly Reports on Form 10-Q, Current Reports on Form 8-K and other filings with the U.S. Securities and Exchange Commission, which are available at . All written and verbal forward-looking statements attributable to Vanda or any person acting on its behalf are expressly qualified in their entirety by the cautionary statements contained or referred to herein. Vanda cautions investors not to rely too heavily on the forward-looking statements Vanda makes or that are made on its behalf. The information in this press release is provided only as of the date of this press release, and Vanda undertakes no obligation, and specifically declines any obligation, to update or revise publicly any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law. Corporate Contact: Kevin Moran Senior Vice President, Chief Financial Officer and Treasurer Vanda Pharmaceuticals Inc. 202-734-3400 [email protected] Jim Golden / Jack Kelleher / Dan Moore Collected Strategies [email protected] SOURCE Vanda Pharmaceuticals Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Orphan DrugOligonucleotide

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

100 Deals associated with Fedratinib Hydrochloride

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External Link

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	European Union	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	Iceland	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-essential thrombocythemia myelofibrosis	Norway	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	Norway	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	European Union	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	Iceland	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Post-polycythemia vera myelofibrosis	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	Norway	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	European Union	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Primary Myelofibrosis	Iceland	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	Norway	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	Liechtenstein	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	Iceland	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Splenomegaly	European Union	Bristol-Myers Squibb Pharma EEIG	08 Feb 2021
Myelofibrosis	United States	Bristol Myers Squibb Co.	16 Aug 2019
Polycythemia Vera	United States	Bristol Myers Squibb Co.	16 Aug 2019
Thrombocythemia, Essential	United States	Bristol Myers Squibb Co.	16 Aug 2019

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Mycosis Fungoides	Phase 2	Israel	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Singapore	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Italy	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Sweden	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Poland	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Ireland	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Russia	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Hungary	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	Austria	Bristol Myers Squibb Co.	01 Dec 2011
Mycosis Fungoides	Phase 2	United States	Bristol Myers Squibb Co.	01 Dec 2011

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03952039 (FREEDOM2, Pubmed \| Lancet Haematol) Manual	Phase 3	Myelofibrosis Second line	201	Fedratinib 400 mg per day	(uifqsxxwwr) = abvbgfxvtv lotrruptrp (ixpgtzuyfu ) View more	Positive	01 Sep 2024
				Best Available Therapy (BAT)	(uifqsxxwwr) = vppydghycp lotrruptrp (ixpgtzuyfu ) View more
NCT03755518 (FREEDOM, Pubmed \| Leuk Lymphoma)	Phase 3	Myelofibrosis	38	Fedratinib	(qitalxagak) = yewcyyxedp ypwzozgroq (rmtulrplda, 12.5 - 43.3) View more	Positive	28 Jul 2024
NCT03952039 (FREEDOM2, EHA2024) Manual	Phase 3	Myelofibrosis Second line	201	Fedratinib 400mg daily	(yqywraanhi) = dpumilbldq vdxpplmzuk (ipbodngsjk ) View more	Positive	14 May 2024
				Best Available Therapy (BAT)	(yqywraanhi) = jqtrygpiyx vdxpplmzuk (ipbodngsjk ) View more
NCT03952039 (FREEDOM2, CTgov)	Phase 3	Post-essential thrombocythemia myelofibrosis \| Post-polycythemia vera myelofibrosis \| Primary Myelofibrosis	202	Best Available Therapy (BAT)	ekgwngkuwu(crjjynsswu) = qeeqvoexye eatuoezmzm (efmhtowwqf, aieozdtnvf - laajlkppds) View more	-	30 Jan 2024
NCT04817007 (CA011-023, ASH2023)	Phase 1/2	Primary Myelofibrosis	40	BMS-986158+Ruxolitinib	(tjjhufccas) = amqarqmksa wafcadqglv (imdjpxpofr )	-	10 Dec 2023
				BMS-986158+Fedratinib	(tjjhufccas) = vjygudkuju wafcadqglv (imdjpxpofr )
ASH2023	Not Applicable	Second line	-	Ruxolitinib	yjyvzdnxzm(otmqxyvjkk) = qydjhskzkv fraefeeoam (exiqioyfli ) View more	-	09 Dec 2023
				Fedratinib	yjyvzdnxzm(otmqxyvjkk) = laemklettr fraefeeoam (exiqioyfli )
ASH2023	Not Applicable	Primary Myelofibrosis	58	Fedratinib	(jxlikpiyrh) = vdmhsuenql rbiddeeerf (vjsseguueo )	-	09 Dec 2023
NCT05177211 (ASH2023)	Phase 2	Leukemia, Neutrophilic, Chronic \| Myeloproliferative Disorders	10	Fedratinib	egzzbmqzpj(kkwmrqaeiy) = yivcwlmoct tbpurmpwtb (banhxamsah ) View more	-	09 Dec 2023
NCT03755518 (FREEDOM, CTgov)	Phase 3	Post-essential thrombocythemia myelofibrosis \| Post-polycythemia vera myelofibrosis \| Primary Myelofibrosis	38	Fedratimib (Fedratimib)	yarkejqhbk(txdbefdkzd) = rldkvgzwfm niszbqpvqx (ocevnofifk, ursxlaejpd - mxoxmzlrea) View more	-	09 Mar 2023
				Fedratinib (Fedratinib)	zejcuygypb(wdljexhcjf) = rfgpirbrcg hbqjrnuoln (jnihrsyqsb, azgiseihkw - wgxjxipyps) View more
NCT03755518 (FREEDOM, ASH 12022 \| ASH 22022) Manual	Phase 3	Polycythemia Vera \| Post-essential thrombocythemia myelofibrosis \| Primary Myelofibrosis	38	Fedratinib	iucotoctuh(njllprznbw) = wohawwqvtz wczwmkjezn (yurcdqwzvn ) View more	Positive	15 Nov 2022