ALK2 inhibitors(Activin receptor type-1 inhibitors), CSF-1R antagonists(Colony stimulating factor 1 receptor antagonists), FLT3 inhibitors(Tyrosine-protein kinase receptor FLT3 inhibitors)

Therapeutic Areas

Hemic and Lymphatic DiseasesOther DiseasesNeoplasms+ [2]

Active Indication

Primary MyelofibrosisThrombocytopeniaPost-essential thrombocythemia myelofibrosis+ [9]

Inactive Indication

Adult Acute Myeloblastic LeukemiaAdvanced LymphomaBCR-ABL Negative Atypical Chronic Myeloid Leukemia+ [9]

Originator Organization

CTI BioPharma Corp.

Active Organization

CTI BioPharma Corp.

University of Washington

University of Kansas

+ [2]

Inactive Organization

S*BIO Pte Ltd.

Washington University School of Medicine

Drug Highest PhaseApproved

First Approval Date

US (28 Feb 2022),

Primary MyelofibrosisThrombocytopenia

RegulationPriority Review (US), Fast Track (US), Accelerated Approval (US), Orphan Drug (US)

Structure

Molecular FormulaC28H32N4O3

InChIKeyHWXVIOGONBBTBY-ONEGZZNKSA-N

CAS Registry937272-79-2

Clinical Trials associated with Pacritinib

NCT06303193 / Not yet recruitingPhase 1/2IIT

Phase I/II Trial of Pacritinib, a Kinase Inhibitor of CSF1R, IRAK1, JAK2, and FLT3, in Adults and Pediatric Participants 12 Years of Age or Older With Myelodysplastic Syndromes or Myelodysplastic/Myeloproliferative Neoplasms

Background:
Myelodysplastic syndrome (MDS) and myelodysplastic/myeloproliferative neoplasm (MDS/MPN) are blood disorders that can cause serious complications in children and adults. MDS and MDS/MPN can also progress to acute myeloid leukemia. Treatments for these disorders are risky and not always effective. Better treatments are needed.
Objective:
To test a study drug (pacritinib) in adults and children with MDS or MDS/MPN.
Eligibility:
Children (aged 12 to 17 years) and adults (aged 18 years and older) with MDS or MDS/MPN.
Design:
Participants will be screened. They will have a physical exam with blood tests. They will have tests of their heart function. They may have a bone marrow biopsy: An area over the hip will be numbed; a needle will be inserted to remove a sample of soft tissue from inside the hipbone.
Pacritinib is a capsule taken by mouth. All participants will take the study drug 2 times a day, every day, in 28-day cycles. They will write down the date and time they take each capsule. Doctors will assign varying dosages of the drug to different participants.
Participants will have clinic visits each week during cycle 1; every 2 weeks during cycle 2; and gradually increasing to every 3 months after cycle 13. Treatment will continue for up to 8 years.
Bone marrow biopsies, heart tests, and other tests will be repeated at intervals throughout the study. Participants will also fill out questionnaires about their quality of life, the symptoms of their disease, and other topics.

Start Date21 May 2024

Sponsor / Collaborator

National Cancer Institute

NCT06052618 / Not yet recruitingPhase 2IIT

Phase II Study of Pacritinib in Kaposi Sarcoma Herpesvirus (KSHV)-Associated Multicentric Castleman Disease and KSHV-Associated Inflammatory Cytokine Syndrome (KICS)

Background:
Kaposi sarcoma herpesvirus (KSHV)-associated inflammatory cytokine syndrome (KICS) and KSHV-multicentric Castleman disease (MCD) occur in people living with HIV. These diseases cause severe inflammation that can be fatal if not treated.
Objective:
To test a drug (pacritinib) in people with KSHV-associated KICS or MCD.
Eligibility:
People aged 18 years and older with KSHV-associated KICS or MCD. They must have at least one symptom.
Design:
Participants will be screened. They will have a physical exam with blood tests and tests of their heart function. They will have imaging scans. Their ability to perform everyday tasks will be reviewed. In some participants who have Kaposi sarcoma (KS) with KICS or MCD, these individuals may need a bronchoscopy and/or endoscopy of the upper or lower intestine: A flexible tube with a camera and a light source will be inserted through the mouth or anus to see these structures and assess any KS.
Pacritinib is a capsule taken by mouth. Participants will take the drug twice a day, every day, for up to 24 weeks. They will write down each dose in a diary.
Participants will visit the clinic 3 times in the first 4 weeks. Their visits will taper to once every 4 weeks. Imaging scans, blood tests, and other tests will be repeated during these visits. Participants will give samples of saliva. They may opt to allow tissues samples to be taken from their skin and lymph nodes.
Participants will have follow-up visits 7 days and 30 days after their last dose of pacritinib. After that, they will visit the clinic every 3 months for up to 1 year. The physical exam and blood, heart, and imaging tests will be repeated at these visits.

Start Date21 May 2024

Sponsor / Collaborator

National Cancer Institute

NCT06414681 / Not yet recruitingEarly Phase 1IIT

An Open Label Pilot Trial of the Combination of Tagraxofusp With Pacritinib in Patients With Intermediate-1 or Higher Myelofibrosis, Who Have Had Prior Therapy With the Approved JAK Inhibitors or in Which Therapy With the Approved JAK Inhibitors is Not Appropriate, Contraindicated or Declined

The goal of this open-label, single-center, pilot trial is to test the combination of Tagraxofusp (TAG) with Pacritinib (PAC) in patients with intermediate-II or higher myelofibrosis (MF), who have had prior therapy with the approved JAK1/2 inhibitor or in which therapy with the approved JAK1/2 inhibitors is not appropriate, contraindicated or declined by the subjects.
The Primary Objective is to:
1. Characterized efficacy of the combination of Tagraxofusp and Pacritinib.
The Secondary Objective is to:
1. characterize the safety profile of the combination Tagraxofusp and Pacritinib.
2, Characterize the feasibility of the combination Tagraxofusp and Pacritinib. 3. Characterize hematologic improvement with the combination Tagraxofusp and Pacritinib.
4. Evaluate and compare the effect of Tagraxofusp and Pacritinib on participant reports of MF symptoms.
Exploratory:
Pharmacokinetic (PK) testing of Tagraxofusp and Pacritinib to assess clinical predictors of response.
Next Generation Sequencing (NGS) Testing to define the number and the allele burden of pathological mutations, as well as the changes over the course of therapy, both in regard to progression and response.
Blood will be collected and stored at KU BRCF for future study related PK analysis

Start Date01 May 2024

Sponsor / Collaborator

University of Kansas

100 Clinical Results associated with Pacritinib

100 Translational Medicine associated with Pacritinib

100 Patents (Medical) associated with Pacritinib

153

Literatures (Medical) associated with Pacritinib

01 Feb 2024·American Journal of Hematology

Momelotinib expands the therapeutic armamentarium for myelofibrosis: Impact on hierarchy of treatment choices

Review

Author: Tefferi, Ayalew ; Gangat, Naseema ; Pardanani, Animesh

Abstract:

The primary objective of treatment in myelofibrosis (MF) is prolongation of life, which is currently accomplished only by allogeneic hematopoietic stem cell transplantation (AHSCT). Determination of optimal timing for AHSCT is facilitated by molecular risk stratification. Non‐transplant treatment options in MF are palliative in scope and include Janus kinase 2 (JAK2) inhibitors (JAKi): momelotinib (FDA approved on September 15, 2023), ruxolitinib (November 16, 2011), fedratinib (August 16, 2019), and pacritinib (February 28, 2022); all four JAKi are effective in reducing spleen size and alleviating symptoms, considered a drug class effect and attributed to their canonical JAK–STAT inhibitory mechanism of action. In addition, momelotinib exhibits erythropoietic effect, attributed to alleviation of ineffective erythropoiesis through inhibition of activin A receptor type‐I (ACVR1). In transplant‐ineligible or deferred patients, the order of treatment preference is based on specific symptoms and individual assessment of risk tolerance. Because of drug‐induced immunosuppression and other toxicities attributed to JAKi, we prefer non‐JAKi drugs as initial treatment for MF‐associated anemia that is not accompanied by treatment‐requiring splenomegaly or constitutional symptoms. Otherwise, it is reasonable to consider momelotinib as the first‐line JAKi treatment of choice, in order to target the triad of quality‐of‐life offenders in MF: anemia, splenomegaly, and constitutional symptoms/cachexia. For second‐line therapy, we favor ruxolitinib, over fedratinib, based on toxicity profile. Pacritinib and fedratinib provide alternative options in the presence of severe thrombocytopenia or ruxolitinib‐resistance/intolerance, respectively. Splenectomy remains a viable option for drug‐resistant symptomatic splenomegaly and cytopenia.

01 Feb 2024·JCO Precision Oncology

Discontinuation Syndrome With JAK2 Selective Agents: Case Presentation and Mechanistic Insights

Article

Author: Yu, Ashley ; Becker, Michelle ; Handa, Shivani ; Tremblay, Douglas ; Salib, Christian ; Marcellino, Bridget K ; Feld, Jonathan ; Farina, Kyle A ; Kelly, Brianna ; Shih, Alan H ; Mascarenhas, John

We report the first case of pacritinib-withdrawal syndrome with in vitro elucidation of underlying mechanisms.

07 Nov 2023·American Journal of Health-System Pharmacy

Current therapies for classic myeloproliferative neoplasms: A focus on pathophysiology and supportive care

Article

Author: Chung, Clement

Abstract:

Purpose:

This article concisely evaluates current therapies that have received regulatory approval for the treatment of classic myeloproliferative neoplasms (MPNs). Pertinent pathophysiology and supportive care are discussed. Emerging therapies are also briefly described.

Summary:

MPNs are a heterogeneous group of diseases characterized by acquired abnormalities of hematopoietic stem cells (HSCs), resulting in the generation of transformed myeloid progenitor cells that overproduce mature and immature cells within the myeloid lineage. Mutations in JAK2 and other driver oncogenes are central to the genetic variability of these diseases. Cytoreductive therapies such as hydroxyurea, anagrelide, interferon, and therapeutic phlebotomy aim to lower the risk of thrombotic events without exposing patients to an increased risk of leukemic transformation. However, no comparisons can be made between these therapies, as reduction of thrombotic risk has not been used as an endpoint. On the other hand, Janus kinase (JAK) inhibitors such as ruxolitinib, fedratinib, pacritinib, and momelotinib (an investigational agent at the time of writing) directly target the constitutively activated JAK–signal transducer and activator of transcription (JAK-STAT) pathway of HSCs in the bone marrow. Mutations of genes in the JAK-STAT signaling pathway provide a unifying understanding of MPNs, spur therapeutic innovations, and represent opportunities for pharmacists to optimize mitigation strategies for both disease-related and treatment-related adverse effects.

Conclusion:

Treatment options for MPNs span a wide range of disease mechanisms. The growth of targeted therapies holds promise for expanding the treatment arsenal for these rare, yet complex diseases and creates opportunities to optimize supportive care for affected patients.

News (Medical) associated with Pacritinib

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

25 Apr 2024

·www.prnewswire.com

Sobi Q1 2024 report: Strong sales reflecting the strength of the portfolio

STOCKHOLM, April 25, 2024 /PRNewswire/ -- Swedish Orphan Biovitrum AB (publ) (Sobi®) today announced its report for the first quarter 2024 First Quarter 2024 Total revenue increased 19 per cent, 20 per cent at constant exchange rates, (CER)1, to SEK 6,256 M (5,239) Haematology revenue increased 46 per cent at CER to SEK 4,075 M (2,815), reflecting growth in all medicines, mainly driven by strong sales of Doptelet® of SEK 756 M (475), sales of Vonjo® of SEK 320 M (—), and sales of Aspaveli®/Empaveli® of SEK 240 M (95) Immunology revenue decreased 11 per cent at CER to SEK 1,908 M (2,151), mainly reflecting a significant drop in Synagis® sales to SEK 520 M (1,398), partly compensated by strong sales of Gamifant® of SEK 438 M (219), and royalty on Beyfortus™ of SEK 318 M (—) Revenue from medicines in the strategic portfolio more than doubled in the quarter, to SEK 2,193 M (794), driving the majority of the growth. The strategic portfolio grew by 177 per cent at CER and helped to further transform the company The adjusted EBITA margin1,2 was 37 per cent (40), excluding items affecting comparability (IAC)2. EBITA was SEK 2,177 M (2,121), corresponding to a margin of 35 per cent (40). EBIT was SEK 1,313 M (1,495) Earnings per share (EPS) before dilution was SEK 2.35 (3.44)3. Adjusted EPS before dilution1 was SEK 2.70 (3.44)3. Cash flow from operating activities was SEK 2,256 M (1,983) Outlook 2024 - unchanged Revenue is anticipated to grow by a high single-digit percentage at CER The adjusted EBITA margin is anticipated to be in the mid-30s percentage of revenue The strategic portfolio includes Sobi's medicines Aspaveli/Empaveli, Doptelet excluding China, Gamifant, Vonjo and Zynlonta®, and royalty on Sanofi's sales on Altuviiio™ and Beyfortus. Investors, analysts and media are invited to participate in a conference call, which will include a presentation of the results and a Q&A session on the same day at 16:00 CEST. The presentation can be followed live here or afterwards on sobi.com. The slides will be made available on sobi.com prior to the conference call. To participate in the conference call, please use the following dial-in details: Sweden: +46 8 5051 0031 United Kingdom: +44 207 107 06 13 United States: +1 631 570 56 13 For other countries, please find the details here. Sobi Sobi® is a specialised international biopharmaceutical company transforming the lives of people with rare and debilitating diseases. Providing reliable access to innovative medicines in the areas of haematology, immunology and specialty care, Sobi has approximately 1,800 employees across Europe, North America, the Middle East, Asia and Australia. In 2023, revenue amounted to SEK 22.1 billion. Sobi's share (STO: SOBI) is listed on Nasdaq Stockholm. More about Sobi at sobi.com and LinkedIn. Contacts For details on how to contact the Sobi Investor Relations Team, please click here. For Sobi Media contacts, click here. This information is information that Sobi is obliged to make public pursuant to the EU Market Abuse Regulation. The information was submitted for publication, through the agency of the contact person set out below, on 25 April 2024 at 08:00 CEST. Gerard Tobin Head of Investor Relations This information was brought to you by Cision The following files are available for download:

Financial StatementBiosimilar

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 Pacritinib

External Link

KEGG	Wiki	ATC	Drug Bank
D11768	-	-	DB11697

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Primary Myelofibrosis	US	CTI BioPharma Corp.	28 Feb 2022
Thrombocytopenia	US	CTI BioPharma Corp.	28 Feb 2022

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Post-essential thrombocythemia myelofibrosis	Phase 3	US	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	AU	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	BE	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	CZ	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	FR	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	DE	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	HU	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	IT	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	NL	CTI BioPharma Corp.	01 Jan 2013
Post-essential thrombocythemia myelofibrosis	Phase 3	NZ	CTI BioPharma Corp.	01 Jan 2013

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


PERSIST-2 and PAC203 (ASH2023)	Phase 3	Primary Myelofibrosis	117	Pacritinib 200 mg BID	suukuxndau(ynddknoyes) = dtiuvnqinu xfrkggmdpl (oacpipjxra ) View more	-	11 Dec 2023
				Best Available Therapy (BAT)	gtgtxivrho(tfrsfsdhrk) = ngrhvqywvj baubshksog (xouyhbivfm ) View more
NCT02891603 (CTgov)	Phase 1/2	Graft vs Host Disease	40	Allogenic hematopoietic cell transplant (alloHCT)+Pacritinib+Tacrolimus+Sirolimus (Phase 1, Level 1: Pacritinib With Sirolimus and Tacrolimus)	tiziswmvdr(qfciodvflq) = lwbnttcfan qfbkdairpl (adljmnwpwp, ahqxrgmcae - tmboznjbts) View more	-	25 Oct 2023
				Allogenic hematopoietic cell transplant (alloHCT)+Pacritinib+Tacrolimus+Sirolimus (Phase 1, Level 2: Pacritinib With Sirolimus and Tacrolimus)	tiziswmvdr(qfciodvflq) = nywdhcremz qfbkdairpl (adljmnwpwp, uwmhcfcesb - gkqnqcqkbz) View more
EHA2023	Not Applicable	Myelofibrosis	276	Pacritinib 200 mg twice daily	nntyxawwtk(rzztwxveue) = lxsxvcelno prsbhzxlff (dmhjacqryr )	-	08 Jun 2023
				Pacritinib 400 mg daily	nntyxawwtk(rzztwxveue) = ahnsudofzm prsbhzxlff (dmhjacqryr )
PERSIST-2 (EHA2023)	Not Applicable	Myelofibrosis	-	Pacritinib 200 mg BID	efhvdbtmob(kaogmjyons) = yaftkzwyla mrkenrqdvj (mqcrottlqy )	-	08 Jun 2023
HOVON-134 (EHA2023)	Phase 2	Myelofibrosis	61	Pacritinib	ltkfswwneo(wiepjakydi) = pragsmgaup spsmfmcoil (tgjzbxfeiq )	-	08 Jun 2023
NCT01773187 (PERSIST-1 and PERSIST-2, ASCO2023)	Phase 3	Primary Myelofibrosis	276	Pacritinib	rpqducneth(yqudjjazrg) = dnwszbhaue nxpdusmmkb (znvsrrvrvl ) View more	-	31 May 2023
NCT04404361 (Pubmed)	Phase 2	COVID-19	200	Pacritinib	rgzuefvuii(gcetgbxztk) = kmtthjqpqo jrcifanvff (avytkxyefr ) View more	Negative	01 Dec 2022
				Placebo	rgzuefvuii(gcetgbxztk) = hpemgpgtkx jrcifanvff (avytkxyefr ) View more
NCT02055781 \| NCT04884191 (PERSIST-2 and PAC203, ASCO2022)	Phase 2/3	Myelofibrosis	-	Pacritinib 200 mg BID	xggzhpjbla(fugxwviqvc) = haotujhfzy ohfkewxzui (yctuvgjpld )	Positive	02 Jun 2022
				Best Available Therapy (including Ruxolitinib)	vpqfwjpgns(gexlbwatys) = khvusrcitj ndueyndtpz (yrbbpsavjp ) View more
NCT04884191 (CTgov)	Phase 2	Thrombocythemia, Essential \| Primary Myelofibrosis \| Post-essential thrombocythemia myelofibrosis ... View more	165	Pacritinib (Pacritinib 100 mg QD)	meowigtshl(wsgjajbyqa) = pcxnydzyop enujaajvfx (jpjewicqor, uqylrimiid - miwiyogedx) View more	-	01 Jun 2022
				Pacritinib (Pacritinib 100 mg BID)	meowigtshl(wsgjajbyqa) = kprguiorqn enujaajvfx (jpjewicqor, vetavhsmox - touiqcfdbm) View more
PERSIST-2 \| PAC203 (EHA2022) Manual	Not Applicable	Myelofibrosis	258	PACRITINIB 200 mg	jpvhbiwrdz(wwgexcvrhg) = rdokcnqafc rstnbcwxrf (ymrrlfwiyw ) View more	Positive	26 May 2022
				best available therapy	jpvhbiwrdz(wwgexcvrhg) = dnmgxanvrh rstnbcwxrf (ymrrlfwiyw ) View more

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