Delving into the Latest Updates on Ruxolitinib Phosphate with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

Jakabi, RUX, Ruxolitinab

+ [13]

Target

JAK1 x JAK2

Mechanism

JAK1 inhibitors(Tyrosine-protein kinase JAK1 inhibitors), JAK2 inhibitors(Tyrosine-protein kinase JAK2 inhibitors)

Therapeutic Areas

NeoplasmsImmune System DiseasesCongenital Disorders+ [8]

Active Indication

Nonsegmental vitiligoDermatitis, AtopicThrombocythemia, Essential+ [54]

Inactive Indication

acute leukemiaAdenocarcinoma of LungAdvanced Malignant Solid Neoplasm+ [30]

Originator Organization

Eli Lilly & Co.

Active Organization

Incyte Corp.

AbbVie, Inc.Novartis Europharm Ltd.

+ [13]

Inactive Organization

Novartis AG

Maruho Co., Ltd.

Drug Highest PhaseApproved

First Approval Date

US (16 Nov 2011),

Myelofibrosis

RegulationOrphan Drug (US), Orphan Drug (AU), Priority Review (AU), Accelerated assessment (EU), Orphan Drug (JP)

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Structure

Molecular FormulaC17H21N6O4P

InChIKeyJFMWPOCYMYGEDM-XFULWGLBSA-N

CAS Registry1092939-17-7

JOURNAL/nrgr/04.03/01300535-202509000-00023/figure1/v/2024-11-05T132919Z/r/image-tiff Although microglial polarization and neuroinflammation are crucial cellular responses after traumatic brain injury, the fundamental regulatory and functional mechanisms remain insufficiently understood. As potent anti-inflammatory agents, the use of glucocorticoids in traumatic brain injury is still controversial, and their regulatory effects on microglial polarization are not yet known. In the present study, we sought to determine whether exacerbation of traumatic brain injury caused by high-dose dexamethasone is related to its regulatory effects on microglial polarization and its mechanisms of action. In vitro cultured BV2 cells and primary microglia and a controlled cortical impact mouse model were used to investigate the effects of dexamethasone on microglial polarization. Lipopolysaccharide, dexamethasone, RU486 (a glucocorticoid receptor antagonist), and ruxolitinib (a Janus kinase 1 antagonist) were administered. RNA-sequencing data obtained from a C57BL/6 mouse model of traumatic brain injury were used to identify potential targets of dexamethasone. The Morris water maze, quantitative reverse transcription-polymerase chain reaction, western blotting, immunofluorescence and confocal microscopy analysis, and TUNEL, Nissl, and Golgi staining were performed to investigate our hypothesis. High-throughput sequencing results showed that arginase 1, a marker of M2 microglia, was significantly downregulated in the dexamethasone group compared with the traumatic brain injury group at 3 days post–traumatic brain injury. Thus dexamethasone inhibited M1 and M2 microglia, with a more pronounced inhibitory effect on M2 microglia in vitro and in vivo. Glucocorticoid receptor plays an indispensable role in microglial polarization after dexamethasone treatment following traumatic brain injury. Additionally, glucocorticoid receptor activation increased the number of apoptotic cells and neuronal death, and also decreased the density of dendritic spines. A possible downstream receptor signaling mechanism is the GR/JAK1/STAT3 pathway. Overactivation of glucocorticoid receptor by high-dose dexamethasone reduced the expression of M2 microglia, which plays an anti-inflammatory role. In contrast, inhibiting the activation of glucocorticoid receptor reduced the number of apoptotic glia and neurons and decreased the loss of dendritic spines after traumatic brain injury. Dexamethasone may exert its neurotoxic effects by inhibiting M2 microglia through the GR/JAK1/STAT3 signaling pathway.

31 Dec 2024·Hematology

Presence of triple positive driver mutations in JAK2, CALR and MPL in primary myelofibrosis: a case report and literature review

Review

Author: Chen, Juan ; Zhang, Hao ; Liu, Bei ; Zhao, Long ; Ma, Haizhen

BACKGROUND:

Primary myelofibrosis (PMF) is the most advanced subtype among the classic Philadelphia chromosomenegative myeloproliferative neoplasms (MPNs). A majority of patients carry one of three mutually-exclusive somatic driver mutations: JAK2 (60-65%), CALR (20-25%), or MPL (5%). Co-occurrence of these mutations is rarely reported. Here we report a case with a triple positive combination of JAK2, CALR and MPL driver mutations.

CASE PRESENTATION:

A 69-year-old male was admitted to hospital for acute exacerbation of chronic obstructive pulmonary disease (COPD) and was found to have splenomegaly and leukocytosis. Nextgeneration revealed JAK2, CALR, MPL mutations, and additional variants in SF3B1, SRSF2, and STAG2. The patient was diagnosed with PMF and treated with ruxolitinib and COPD therapy. Due to nausea, the ruxolitinib dose was reduced. After therapy, spleen volume decreased and hematologic responses were poor. Another genetic mutation of ASXL1 was later found. After adjusting the medication and adding antiemetics, the patient's condition improved.

CONCLUSIONS:

The rare coexistence of JAK2, CALR, and MPL mutations challenges the assumption of their mutual exclusivity. Further study of these mutations is essential for developing better treatment strategies.

31 Dec 2024·OncoImmunology

Interplay between oncolytic measles virus, macrophages and cancer cells induces a proinflammatory tumor microenvironment

Article

Author: Boisgerault, Nicolas ; Fresquet, Judith ; Berland, Laurine ; Treps, Lucas ; Blanquart, Christophe ; Tangy, Frédéric ; Jouand, Nicolas ; Fonteneau, Jean-François ; Nader, Joëlle ; Hirigoyen, Ugo ; Chatelain, Camille ; Pons-Tostivint, Elvire ; Fradin, Delphine ; Combredet, Chantal ; Grard, Marion ; Petithomme, Tacien

Attenuated measles virus (MV) exerts its oncolytic activity in malignant pleural mesothelioma (MPM) cells that lack type-I interferon (IFN-I) production or responsiveness. However, other cells in the tumor microenvironment (TME), such as myeloid cells, possess functional antiviral pathways. In this study, we aimed to characterize the interplay between MV and the myeloid cells in human MPM. We cocultured MPM cell lines with monocytes or macrophages and infected them with MV. We analyzed the transcriptome of each cell type and studied their secretion and phenotypes by high-dimensional flow cytometry. We also measured transgene expression using an MV encoding GFP (MV-GFP). We show that MPM cells drive the differentiation of monocytes into M2-like macrophages. These macrophages inhibit GFP expression in tumor cells harboring a defect in IFN-I production and a functional signaling downstream of the IFN-I receptor, while having minimal effects on GFP expression in tumor cells with defect of responsiveness to IFN-I. Interestingly, inhibition of the IFN-I signaling by ruxolitinib restores GFP expression in tumor cells. Upon MV infection, cocultured macrophages express antiviral pro-inflammatory genes and induce the expression of IFN-stimulated genes in tumor cells. MV also increases the expression of HLA and costimulatory molecules on macrophages and their phagocytic activity. Finally, MV induces the secretion of inflammatory cytokines, especially IFN-I, and PD-L1 expression in tumor cells and macrophages. These results show that macrophages reduce viral proteins expression in some MPM cell lines through their IFN-I production and generate a pro-inflammatory interplay that may stimulate the patient's anti-tumor immune response.

376

News (Medical) associated with Ruxolitinib Phosphate

07 Nov 2024

·www.globenewswire.com

Secura Bio Announces Poster Presentation Highlighting New COPIKTRA® (duvelisib) Data for the Treatment of Patients With Peripheral T-Cell Lymphoma and Other Advanced Hematologic Malignancies at the 2024 American Society of Hematology Meeting

Nov. 06, 2024 -- Secura Bio, Inc. (www.securabio.com), an integrated pharmaceutical company dedicated to the worldwide development and commercialization of impactful oncology therapies, today announced a poster presentation highlighting new data on the investigational use of COPIKTRA® (duvelisib) both as a single agent and in combination therapy for the treatment of Peripheral T-cell Lymphoma (PTCL) and advanced hematologic malignancies at the upcoming 2024 American Society of Hematology (ASH) Annual Meeting taking place on December 7-10, 2024 in San Diego, CA. The poster, entitled: Duvelisib in Patients with Relapsed/Refractory Peripheral T-cell Lymphoma: Final Results from the Phase 2 PRIMO Trial highlights the outcomes of 123 patients in the PRIMO dose expansion phase of the PRIMO clinical trial and will be presented by Dr. Neha Mehta-Shah, Washington University School of Medicine, on Sunday, December 8, 2024, from 6:00 PM to 8:00 PM (PST) in the San Diego Convention Center, Halls G-H. The abstract is now available here. The PRIMO clinical trial was a global, multicenter, open-label, parallel cohort, Phase 2 study sponsored by Secura Bio, Inc., that evaluated COPIKTRA for the treatment of adult patients with relapsed or refractory (R/R) Peripheral T-cell Lymphoma (PTCL). Based on the dose optimization phase results, an expansion group of 123 patients was added in which COPIKTRA was dosed at 75 mg twice daily for two cycles, followed by 25 mg twice daily. COPIKTRA will also be highlighted in a number of other poster presentations evaluating combination therapy, including: Dr Alison Moskowitz, Memorial Sloan Kettering Cancer Center, will be presenting an oral presentation entitled Dual-targeted therapy with ruxolitinib plus duvelisib for T-cell lymphoma. Dr Moskowitz will be presenting on Sunday, December 8, 2024, from 9:30 AM - 11:00 AM (PST) in the San Diego Convention Center, Ballroom 20CD Dr Jennifer Crombie, Dana-Farber Cancer Institute, will be presenting a poster entitled A Phase 2 Study of Duvelisib and Venetoclax in Patients with Relapsed or Refractory (R/R) Chronic Lymphocytic Leukemia (CLL) or Richter’s Syndrome (RS) on Monday, December 9, 2024, from 6:00 PM - 8:00 PM (PST) in the San Diego Convention Center, Halls G-H Dr Hayder Saeed, Moffitt Cancer Center, will be presenting a poster entitled A Phase I Study Of Duvelisib In Combination With Oral Azacitidine (BMS-986345) In Lymphoid Malignancy on Sunday, December 8, 2024, from 6:00 PM - 8:00 PM (PST) in the San Diego Convention Center, Halls G-H Dr Josie Ford, Massachusetts General Hospital, will be presenting a poster entitled Real-World Evidence for Duvelisib and Romidepsin Combination in Patients with Relapsed/Refractory Peripheral T-Cell Lymphomas on Monday, December 9, 2024, from 6:00 PM - 8:00 PM (PST) in the San Diego Convention Center, Halls G-H Peripheral T-cell lymphoma (PTCL) is a rare, aggressive type of non-Hodgkin lymphoma that develops in mature white blood cells that circulate through the bloodstream and lymphatic system. PTCL accounts for between 10-15% of all non-Hodgkin lymphomas and generally affects people aged 60 years and older. Although there are many different subtypes of peripheral T-cell lymphoma, they often present in a similar way, with widespread, enlarged, typically painless lymph nodes in the neck, armpit, and/or groin. There are currently no well-established standards of care for patients with relapsed or refractory disease. COPIKTRA is an oral inhibitor of phosphoinositide 3-kinase (PI3K), and the first United States FDA approved dual inhibitor of PI3K-delta and PI3K-gamma, two enzymes known to help support the growth and survival of malignant cells. PI3K signaling may lead to the proliferation of malignant cells and is thought to play a role in the formation and maintenance of a supportive tumor microenvironment. COPIKTRA is a kinase inhibitor indicated for the treatment of adult patients with relapsed or refractory chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) after at least two prior lines of systemic therapy. Limitations of Use: COPIKTRA is not indicated or recommended for the treatment of any patients with CLL or SLL as initial or second line treatment due to an increased risk of treatment-related mortality. COPIKTRA is also being investigated for the treatment of lymphomas, including peripheral T-cell lymphomas (PTCL). COPIKTRA has been given Fast Track status in the United States for the treatment of adult patients with PTCL who have received at least one prior therapy. Additionally, COPIKTRA has received an Orphan Drug Designation for use in the treatment of T-cell lymphomas. Treatment of T-cell lymphomas is a disease category for which COPIKTRA is not currently indicated. COPIKTRA is being investigated in combination with other agents across several types of solid and hematologic malignancies, through investigator-sponsored studies. For more information on COPIKTRA, please visit https://copiktra.com/. Information about duvelisib clinical trials can be found on https://www.clinicaltrials.gov/. Secura Bio is an integrated, commercial-stage pharmaceutical company dedicated to the worldwide development and commercialization of significant oncology therapies for physicians and their patients. Its product, COPIKTRA, is currently approved for the treatment of multiple B-cell malignancies and is also being investigated for the treatment of PTCL, for which it has received Fast Track status in the United States and is being investigated in combination with other agents through investigator-sponsored studies. For more information on Secura Bio, please visit https://www.securabio.com/. The content above comes from the network. if any infringement, please contact us to modify.

Fast TrackOrphan DrugDrug ApprovalClinical Result

07 Nov 2024

·www.prnewswire.com

Cellenkos Announces Oral Presentation at ASH Annual Meeting 2024 Highlighting Phase 1b Clinical Data of CK0804 in Myelofibrosis

- CK0804 is an off-the-shelf, allogeneic, non-HLA matched, CXCR4 enriched, T regulatory cell therapy product. - Multiple doses of CK0804 can be safely infused in myelofibrosis patients - CK0804 reduces symptom burden and induces spleen volume reduction in patients with myelofibrosis who have suboptimal response to prior lines of therapy HOUSTON, Nov. 7, 2024 /PRNewswire/ -- Cellenkos® Inc., a clinical-stage biotechnology company focused on developing allogeneic, off-the-shelf, T regulatory (Treg) cell therapies for inflammatory disease areas of high unmet needs and autoimmune disorders, today announced that its CK0804 Phase 1b study data in myelofibrosis has been selected for oral presentation at the 66th Annual Meeting & Exposition of the American Society of Hematology (ASH), December 7-10, 2024, in San Diego, California. The oral presentation will feature the safety and efficacy data from Cellenkos' Phase 1b trial evaluating CK0804 in patients with myelofibrosis who have suboptimal responses to prior therapies, including ruxolitinib. CK0804 is an off-the-shelf, allogeneic, non-HLA matched, CXCR4-enriched Treg cell therapy and is administered in fixed dose of 100 million cells infused every 28 days for 6 doses. CK0804 has shown early promise in addressing this high unmet medical need. Oral Presentation Details () Session Name: 634. Myeloproliferative Syndromes: Clinical and Epidemiological: Advancing MPN Care: Innovative Therapies and Clinical Breakthroughs in Myelofibrosis Date: Monday, December 9, 2024 Time: 5:00 PM (Presentation) Location: Manchester Grand Hyatt San Diego, Harbor Ballroom DEFG Publication Number: 999 Title: A Phase Ib, Open-Label Study of Add-on Therapy with CK0804 in Participants with Myelofibrosis and Suboptimal Response to Ruxolitinib Submission ID: 211587 The study data to be presented demonstrates the safety and efficacy of CK0804 in patients with myelofibrosis who had previously failed standard treatments. Key findings from the trial include significant improvements in symptom burden, spleen volume reduction, blood transfusion dependence, and systemic inflammatory cytokine levels. Importantly, CK0804 was well-tolerated, with no significant drug-related adverse events observed, aside from one patient with a sulfa drug allergy who had an infusion reaction. Study Highlights Nine patients, with a median of two (range, 1-6) prior lines of treatment, were treated with CK0804. Improvements in fatigue and overall symptom burden were reported by all patients, with four out of six evaluable patients showing spleen volume reduction (SVR). Two patients who were transfusion-dependent showed a reduction in their monthly need for transfusions by the end of the treatment period. Longitudinal data indicates sustained benefits, including improvements in hemoglobin levels and inflammatory markers. Following the initial success of the Phase 1b trial, the Data Safety Monitoring Board has approved an expansion cohort to further explore the safety and efficacy of CK0804. This expansion includes an induction phase of four weekly doses, followed by five monthly doses, and active participant enrollment is ongoing (NCT05423691). About Myelofibrosis Myelofibrosis is a rare, chronic, and progressive blood cancer that causes scar tissue to form in the bone marrow, disrupting the production of normal blood cells. Patients with myelofibrosis often experience debilitating symptoms such as fatigue, spleen enlargement, and night sweats. Approximately 16,000 to 18,500 people in the U.S. are living with myelofibrosis, and those who fail to respond adequately to current treatments including ruxolitinib, face limited options and a poor prognosis. Inflammation is a key driver for disease pathogenesis and progression in myelofibrosis. About CK0804 CK0804 is an investigational, allogeneic, off-the-shelf Treg cell therapy that leverages the CXCR4/CXCL12 axis to suppress inflammatory cytokines implicated in myelofibrosis pathogenesis. CXCR4 enriched Tregs home faster to bone marrow compared to unmanipulated Tregs. Derived from clinical-grade umbilical cord blood and manufactured using Cellenkos' proprietary CRANE® process, CK0804 does not require HLA matching, making it an ideal therapeutic option for patients in need of prompt intervention. The therapy is administered intravenously and can be infused in an outpatient setting. About Cellenkos, Inc. Cellenkos is a clinical-stage biotechnology company based in Houston, Texas, focused on developing off-the-shelf Treg cell therapies for rare inflammatory diseases and autoimmune disorders. The company's portfolio includes four clinical-stage candidates: CK0801 for aplastic anemia: durable transfusion independence. CK0802 for COVID-19 ARDS: survival benefit CK0803 for amyotrophic lateral sclerosis (ALS): slowing of ALSFRSR score decline and decrease in neurofilament CK0804 for myelofibrosis: decrease in symptom burden and spleen volume reduction Cellenkos' Treg therapies, derived from umbilical cord blood, are designed to provide powerful anti-inflammatory effects and long-lasting immune modulation without the need for donor matching. The company is committed to advancing the development of these promising therapies to improve the lives of patients with rare and underserved conditions. For more information, please visit . Contact: Ting Huang [email protected] SOURCE Cellenkos, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Cell TherapyPhase 1ASHClinical Result

06 Nov 2024

·www.pharmamanufacturing.com

Court blocks Sun Pharma's JAK inhibitor U.S. launch

Sun Pharmaceutical Industries announced that a U.S. District Court has granted a preliminary injunction preventing the company from launching its product, Leqselvi, in the U.S. The injunction, issued by the District Court of New Jersey on November 1, 2024, halts the launch of Leqselvi until further court action or the expiration of the relevant patent. Incyte initiated the legal action that led to the injunction against Sun Pharma’s Leqselvi, claiming that the drug infringes on its patent related to deuterated forms of ruxolitinib, a Janus kinase (JAK) inhibitor. Incyte’s argument centers on Leqselvi's formulation, which they allege overlaps with the intellectual property protections they hold. The court decision stems from a motion filed earlier this year by Sun, which sought to address ongoing litigation regarding Leqselvi launch. The injunction restricts Sun from proceeding with its product release, impacting the company's timeline for introducing the drug to the U.S. market. Sun Pharmaceuticals has expressed disagreement with the ruling and plans to file an immediate appeal. The company maintains that it aims to resolve the matter promptly to bring Leqselvito patients, pending a favorable court outcome.

Patent Infringement

100 Deals associated with Ruxolitinib Phosphate

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External Link

KEGG	Wiki	ATC	Drug Bank
D09960	Ruxolitinib Phosphate	L01XE18	DB08877

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Nonsegmental vitiligo	US	Incyte Corp.	18 Jul 2022
Dermatitis, Atopic	US	Incyte Corp.	21 Sep 2021
Thrombocythemia, Essential	CN	Novartis Europharm Ltd.	10 Mar 2017
Acute Graft Versus Host Disease	EU	Novartis Europharm Ltd.	23 Aug 2012
Acute Graft Versus Host Disease	IS	Novartis Europharm Ltd.	23 Aug 2012
Acute Graft Versus Host Disease	LI	Novartis Europharm Ltd.	23 Aug 2012
Acute Graft Versus Host Disease	NO	Novartis Europharm Ltd.	23 Aug 2012
Chronic graft-versus-host disease	EU	Novartis Europharm Ltd.	23 Aug 2012
Chronic graft-versus-host disease	IS	Novartis Europharm Ltd.	23 Aug 2012
Chronic graft-versus-host disease	LI	Novartis Europharm Ltd.	23 Aug 2012
Chronic graft-versus-host disease	NO	Novartis Europharm Ltd.	23 Aug 2012
Graft vs Host Disease	EU	Novartis Europharm Ltd.	23 Aug 2012
Graft vs Host Disease	IS	Novartis Europharm Ltd.	23 Aug 2012
Graft vs Host Disease	LI	Novartis Europharm Ltd.	23 Aug 2012
Graft vs Host Disease	NO	Novartis Europharm Ltd.	23 Aug 2012
Polycythemia Vera	EU	Novartis Europharm Ltd.	23 Aug 2012
Polycythemia Vera	IS	Novartis Europharm Ltd.	23 Aug 2012
Polycythemia Vera	LI	Novartis Europharm Ltd.	23 Aug 2012
Polycythemia Vera	NO	Novartis Europharm Ltd.	23 Aug 2012
Post-essential thrombocythemia myelofibrosis	EU	Novartis Europharm Ltd.	23 Aug 2012

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
prurigo nodularis	Phase 3	US	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	AR	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	BE	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	CA	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	CL	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	FR	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	DE	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	IT	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	NL	Incyte Corp.	10 Mar 2023
prurigo nodularis	Phase 3	PL	Incyte Corp.	10 Mar 2023

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT05371964 (IMproveMF, ASH2024) Manual	Phase 1	Myelofibrosis	13	Imetelstat+ruxolitinib	cfoywygygz(cgwrsxlqyk) = None dtugspqfoi (cdkpmymcuk ) View more	Positive	09 Dec 2024
NCT03153982 (CTgov)	Phase 2	Squamous Cell Carcinoma of Head and Neck	16	Ruxolitinib	usrzvwlvxb(ynodznyadv) = khygkwoilc fywqfooxrd (acvhjcvrzj, nykltuigaq - lqpdatbnki) View more	-	30 Oct 2024
NCT02713386 (NRG-GY007 \| NRG Oncology Group Study, CTgov)	Phase 1/2	Primary peritoneal carcinoma \| Primary Peritoneal High-Grade Serous Adenocarcinoma \| Fallopian Tube Clear Cell Adenocarcinoma ... View more	147	Therapeutic Conventional Surgery+Carboplatin+Paclitaxel (Arm I (Paclitaxel and Carboplatin))	jqbvywtfxb(lpplusveqc) = ilqwcpjbid uuzcwjxygi (tfbpnjunfd, ldmaxwgeit - owrrpmjmth) View more	-	24 Oct 2024
				Therapeutic Conventional Surgery+Carboplatin+Paclitaxel+Ruxolitinib Phosphate (Arm II (Ruxolitinib, Paclitaxel, and Carboplatin))	jqbvywtfxb(lpplusveqc) = iqvbzvxelc uuzcwjxygi (tfbpnjunfd, suyszjxndw - mqkgyyxkib) View more
NCT04061876 (Pubmed) Manual	Phase 3	Acute Graft Versus Host Disease First line	198	Ruxolitinib + Methylprednisolone	oqnkbbgfgi(orqreqhqpr) = gcajhxqfaw hjelnhmelx (tucnqnwfkb ) View more	Positive	23 Oct 2024
				Methylprednisolone	oqnkbbgfgi(orqreqhqpr) = gdzvipflfk hjelnhmelx (tucnqnwfkb ) View more
NCT05293717 (CTgov)	Phase 1/2	Chronic dermatitis \| Inflammation	16	Ruxolitinib	oxkdnkemut(wremllgpfr) = ryypehklyr wpwnknbcza (ltehohelia, mmrhmgtrjo - vmneilxhho) View more	-	15 Oct 2024
NCT04582604 (Pubmed \| Ann Hematol)	Phase 2	Acute Myeloid Leukemia measurable residual disease (MRD)	37	Ruxolitinib	gjypwsegjx(uhatziqoxr) = pqaveewkbc wedcgtipqu (kggzmxjbqg ) View more	Positive	07 Sep 2024
				Decitabine	gjypwsegjx(uhatziqoxr) = fukzrfyncb wedcgtipqu (kggzmxjbqg ) View more
NCT03745638 \| NCT03745651 (Pubmed) Manual	Phase 3	Dermatitis, Atopic	32	Ruxolitinib cream (during the long-term safety)	umnarmsfol(ypxtcewtwc) = trgwaqclxi bjysbjldtn (gdxgcdiqvg ) View more	Positive	12 Jul 2024
				vehicle (during the long-term safety)	umnarmsfol(ypxtcewtwc) = afxsfslfqy bjysbjldtn (gdxgcdiqvg )
NCT03745638 \| NCT03745651 (Pubmed) Manual	Phase 3	Dermatitis, Atopic	245	Ruxolitinib Cream 1.5%	omnxoffzcr(vnbhemvmjf) = cbrfhxuprw eqqxfzmdna (dbrsljgkzq ) View more	Positive	01 Jul 2024
				Vehicle	omnxoffzcr(vnbhemvmjf) = aqoszfrcny eqqxfzmdna (dbrsljgkzq ) View more
NCT01594216 (CTgov)	Phase 2	Estrogen receptor positive breast cancer	25	Ruxolitinib+Exemestane (First Stage)	qawitiizqk(dvbnsqorqk) = sbdkgsxfdi uoqaglacgx (ggzdvrglcc, snykyhqihe - eugivcysmb) View more	-	12 Jun 2024
				Ruxolitinib+Exemestane (Second Stage)	qawitiizqk(dvbnsqorqk) = dddswynxjb uoqaglacgx (ggzdvrglcc, xesmnjvokv - esajpfyoop) View more
NCT04921969 (TruE-AD3, CTgov)	Phase 3	Alzheimer Disease, Familial, Type 3 \| Dermatitis, Atopic	330	VC (VC Period: Vehicle Cream BID)	dwxvdpsqni(rlycwwzrog) = rxieolzfmd fahldkgrnu (mmunfrgcqi, qvmkskswrx - ekrgdaftre) View more	-	10 Jun 2024
				Ruxolitinib (VC Period: Ruxolitinib 0.75% Cream BID)	dwxvdpsqni(rlycwwzrog) = eadxdqcgra fahldkgrnu (mmunfrgcqi, ypbqeojuso - xtshourvti) View more