PIM1 inhibitors(Proto-oncogene serine/threonine-protein kinase Pim-1 inhibitors), PIM2 inhibitors(Serine/threonine-protein kinase pim-2 inhibitors), PIM3 inhibitors(Serine/threonine-protein kinase pim-3 inhibitors)

Therapeutic Areas

Hemic and Lymphatic DiseasesOther DiseasesNeoplasms+ [1]

Active Indication

Post-essential thrombocythemia myelofibrosisPost-polycythemia vera myelofibrosisTriple Negative Breast Cancer

Inactive Indication

Advanced Malignant Solid NeoplasmPrimary Myelofibrosis

Originator Organization

Tolero Pharmaceuticals, Inc.

Active Organization

Sumitomo Pharma America, Inc.

University of Virginia

Inactive Organization-

License Organization-

Drug Highest PhasePhase 1/2

First Approval Date-

RegulationFast Track (United States), Orphan Drug (United States), Orphan Drug (European Union), Orphan Drug (Japan)

Structure/Sequence

Molecular FormulaC22H25F3N4O

InChIKeyXRNVABDYQLHODA-JCNLHEQBSA-N

CAS Registry1361951-15-6

Sequence Code 15022948

Clinical Trials associated with Nuvisertib

NCT07492355

/ CompletedPhase 1

A Phase 1 Randomized Study in Healthy Adult Participants to Assess the Relative Bioavailability of and Effect of Food on TP-3654 Capsule Formulations

This clinical trial will determine the bioavailability and effect of food on TP-3654 in healthy adult participants.

Start Date04 Mar 2024

Sponsor / Collaborator

Sumitomo Pharma America, Inc.

NCT06389955

/ CompletedPhase 1

A Phase 1, Randomized, Study in Healthy Volunteers to Assess Relative Bioavailability and Effect of Food on Capsule and Tablet Formulations of TP-3654

This study comprised of 2 parts, Part A and Part B. Part B will only be conducted if the relative bioavailability of the tablet formulation was at least 70% of the capsule formulation.

Start Date22 May 2023

Sponsor / Collaborator

Sumitomo Pharma America, Inc.

NCT04176198

/ RecruitingPhase 1/2

A Phase 1/2, Open-Label, Dose-Escalation, Safety, Pharmacokinetic, and Pharmacodynamic Study of Oral Nuvisertib (TP-3654) in Patients With Intermediate or High-Risk Primary or Secondary Myelofibrosis

This study is a Phase 1/2, multicenter, dose-escalation, open-label trial to assess safety, tolerability, pharmacokinetics and pharmacodynamics of nuvisertib (TP-3654) in patients with intermediate or high-risk primary or secondary MF.

Start Date16 Dec 2019

Sponsor / Collaborator

Sumitomo Pharma America, Inc.

100 Clinical Results associated with Nuvisertib

100 Translational Medicine associated with Nuvisertib

100 Patents (Medical) associated with Nuvisertib

Literatures (Medical) associated with Nuvisertib

01 Aug 2025·JOURNAL OF BIOLOGICAL CHEMISTRY

Silencing PIM1 inhibits ENO1-induced AKT activation and attenuates fibrillogenesis during spinal cord injury-induced skeletal muscle atrophy

Article

Author: Jiaju Fu ; Chaoqin Wu ; Xiao Yu ; Shaohua Zhang ; Binyu Wang ; Jiang Cao ; Jie Chang ; Zi Wang ; Jingcheng Liu ; Xiaojian Cao ; Tao Sui

Spinal cord injury induces rapid and extensive skeletal muscle atrophy. During skeletal muscle atrophy, numerous extracellular matrix and fibroblasts accumulate, impairing muscle function. The proviral integration site for moloney murine leukemia virus kinases-1(PIM1) is considered a positive regulator of inflammation. In our study, we found that PIM1 was overexpressed in the fibrotic regions of the skeletal muscle following the spinal cord injury. We then explored the effects of the selective PIM1 inhibitor TP-3654 on fibrosis. TP-3654 decreased fibrosis by promoting fibroblast apoptosis, reducing proliferation and migration, and inhibiting tumor growth factor (TGF)-β classical and nonclassical signaling pathways. In vivo PIM1 pharmacological inhibition with TP-3654 alleviates skeletal muscle fibrosis, mitigating skeletal muscle atrophy by decreasing extracellular matrix formation, enhancing the cross-sectional area of muscle fibers, and increasing muscle weight. Furthermore, we found a potential interaction between PIM1 and the enolase 1 (ENO1)/protein kinase B (AKT) pathway. Downregulation of PIM1 expression in fibroblasts using drugs or siRNA leads to decreased ENO1 expression, concurrent with AKT phosphorylation reduction and suppressor of mothers against decapentaplegic (Smad) two-thirds dephosphorylation within the TGF-β classical pathway. In summary, PIM1 might be an important target gene for future skeletal muscle atrophy treatments.

01 Mar 2025·CANCER LETTERS

REDD1 is a determinant of the sensitivity of renal cell carcinoma cells to autophagy inhibition that can be therapeutically exploited by targeting PIM activity

Article

Author: Gamble, Madison E ; Espitia, Claudia M ; Wang, Wei ; Lee, Benjamin R ; Sureshkumar, Sruthi ; Carew, Jennifer S ; Carrera Espinoza, Maria Janina ; Nawrocki, Steffan T

Repurposing FDA approved drugs with off-target autophagy inhibition such as chloroquine/hydroxychloroquine (CQ, HCQ) has produced modest anticancer activity in clinical trials, due in part, to a failure to define predictive biomarkers that enable the selection of patients that best respond to this treatment strategy. We identified a new role for REDD1 as a determinant of sensitivity to autophagy inhibition in renal cell carcinoma (RCC). RNA sequencing, qRT-PCR, immunoblotting, gene silencing, knockout and overexpression studies revealed that REDD1 expression is a key regulator of cell death stimulated by autophagy inhibitors. Comprehensive in vitro and in vivo studies were conducted to evaluate the selectivity, tolerability, and efficacy of the PIM kinase inhibitor TP-3654 and CQ in preclinical models of RCC. Markers of autophagy inhibition and cell death were evaluated in tumor specimens. Transcriptomic analyses identified REDD1 (DDIT4) as a highly induced gene in RCC cells treated with the PIM kinase inhibitor TP-3654. Focused studies confirmed that PIM1 inhibition was sufficient to induce REDD1 and stimulate autophagy through the AMPK cascade. DDIT4 knockout and overexpression studies established its mechanistic role as a regulator of sensitivity to autophagy inhibition. Inhibition of autophagy with CQ synergistically enhanced the in vitro and in vivo anticancer activity of TP-3654. Our findings identify REDD1 as a novel determinant of the sensitivity of RCC cells to autophagy inhibition and support further investigation of PIM kinase inhibition as a precision strategy to drive sensitivity to autophagy-targeted therapies through REDD1 upregulation.

16 Feb 2024·Cancer research communications

Pim Kinase Inhibitors Increase Gilteritinib Cytotoxicity in FLT3-ITD Acute Myeloid Leukemia Through GSK-3β Activation and c-Myc and Mcl-1 Proteasomal Degradation

Article

Author: Lee, Jonelle K. ; Mustafa Ali, Moaath K. ; Scarpa, Mario ; Silvestri, Giovannino ; Baer, Maria R. ; Bailey, Christopher M. ; Wang, Yin ; Singh, Prerna ; Niyongere, Sandrine ; Chatterjee, Aditi ; Kapoor, Shivani

Abstract:

Acute myeloid leukemia (AML) with fms-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD) has poor outcomes. FLT3-ITD drives constitutive and aberrant FLT3 signaling, activating STAT5 and upregulating the downstream oncogenic serine/threonine kinase Pim-1. FLT3 inhibitors are in clinical use, but with limited and transient efficacy. We previously showed that concurrent treatment with Pim and FLT3 inhibitors increases apoptosis induction in FLT3-ITD–expressing cells through posttranslational downregulation of Mcl-1. Here we further elucidate the mechanism of action of this dual targeting strategy. Cytotoxicity, apoptosis and protein expression and turnover were measured in FLT3-ITD–expressing cell lines and AML patient blasts treated with the FLT3 inhibitor gilteritinib and/or the Pim inhibitors AZD1208 or TP-3654. Pim inhibitor and gilteritinib cotreatment increased apoptosis induction, produced synergistic cytotoxicity, downregulated c-Myc protein expression, earlier than Mcl-1, increased turnover of both proteins, which was rescued by proteasome inhibition, and increased efficacy and prolonged survival in an in vivo model. Gilteritinib and Pim inhibitor cotreatment of Ba/F3-ITD cells infected with T58A c-Myc or S159A Mcl-1 plasmids, preventing phosphorylation at these sites, did not downregulate these proteins, increase their turnover or increase apoptosis induction. Moreover, concurrent treatment with gilteritinib and Pim inhibitors dephosphorylated (activated) the serine/threonine kinase glycogen synthase kinase-3β (GSK-3β), and GSK-3β inhibition prevented c-Myc and Mcl-1 downregulation and decreased apoptosis induction. The data are consistent with c-Myc T58 and Mcl-1 S159 phosphorylation by activated GSK-3β as the mechanism of action of gilteritinib and Pim inhibitor combination treatment, further supporting GSK-3β activation as a therapeutic strategy in FLT3-ITD AML.

Significance::

FLT3-ITD is present in 25% of in AML, with continued poor outcomes. Combining Pim kinase inhibitors with the FDA-approved FLT3 inhibitor gilteritinib increases cytotoxicity in vitro and in vivo through activation of GSK-3β, which phosphorylates and posttranslationally downregulates c-Myc and Mcl-1. The data support efficacy of GSK-3β activation in FLT3-ITD AML, and also support development of a clinical trial combining the Pim inhibitor TP-3654 with gilteritinib.

News (Medical) associated with Nuvisertib

15 Jun 2026

·www.biospace.com

Sumitomo Pharma America Announces Encouraging Clinical and Translational Data at EHA 2026, Highlighting Investigational Combination Therapy in Relapsed/Refractory Myelofibrosis and New Research Findings in Menin Inhibition in Leukemia

– Preliminary clinical data on nuvisertib and momelotinib combination highlight encouraging clinical responses with 60% of evaluable patients achieving responses in spleen size, symptoms, and anemia at 24 weeks – – In addition to its primary activity as a PIM1 inhibitor, in vitro and biochemical data demonstrated that nuvisertib also binds to and inhibits ACVR1 – – New translational research in leukemia and menin inhibition has identified distinct MEN1 mutational signatures associated with acquired resistance to the menin inhibitor (MI) enzomenib – MARLBOROUGH, Mass.--(BUSINESS WIRE)-- Sumitomo Pharma America, Inc. (SMPA) today announced the presentation of new clinical and translational research at the European Hematology Association (EHA) 2026 Congress, held from June 11-14, 2026, in Stockholm, Sweden. Among the data is the first-ever disclosure of preliminary clinical data for the investigational PIM1 inhibitor nuvisertib in combination with momelotinib (MMB) for patients with myelofibrosis (MF), and new translational research into the mechanistic basis for hemoglobin improvement observed in patients with MF in an ongoing Phase 1/2 study with nuvisertib. Alongside these findings, SMPA is also sharing new data gathered around acquired resistance patterns observed with enzomenib in acute leukemia. “We are excited to present the preliminary data for our investigational combination of nuvisertib and momelotinib at EHA 2026, while also sharing learnings from our ongoing translational research of nuvisertib and enzomenib,” said Tsutomu Nakagawa, Ph.D., President and Chief Executive Officer of SMPA. “We appreciate this opportunity to share the latest data for these two programs with the oncology community, and these results reinforce our commitment to developing multi-faceted therapeutic approaches that address the most persistent challenges in treating hematologic malignancies.” Promising clinical response with nuvisertib and momelotinib in myelofibrosis James McCloskey, M.D., Interim Chief of the Division of Leukemia, John Theurer Cancer Center, Hackensack, USA, presented preliminary clinical data from the ongoing global Phase 1/2 study ( NCT04176198 ). As of December 6, 2025, a total of 26 patients with relapsed/refractory (R/R) MF and anemia were enrolled across four dose levels of nuvisertib (240, 360, 480, and 720 mg twice daily under fed condition) in combination with the approved dose of momelotinib in MF (200 mg once daily). This study population was particularly challenging to treat as every patient had previously received at least one approved Janus Kinase (JAK) inhibitor and 41% of patients carried high molecular risk (HMR) mutations. Despite these complexities, the combination appeared well tolerated with no dose-limiting toxicities (DLTs) observed. The most common treatment-related adverse events occurring in ≥20% patients were diarrhea, nausea, and thrombocytopenia. The most frequent treatment-related Grade 3 adverse event was thrombocytopenia without bleeding, which occurred in three patients. Of note, mean hemoglobin and platelet count levels remained stable throughout the 24-week treatment period. Among the efficacy evaluable patients who completed at least 12 weeks of treatment (n=15), the combination of nuvisertib and momelotinib demonstrated evidence of clinical activity. Spleen volume reduction of at least 25% (SVR25) was achieved by 73% of patients at Week 12 and reached 100% at Week 24 (n=5). Similarly, 53% of patients achieved a total symptom score reduction of at least 50% percent (TSS50) at Week 12 that further improved to 60% of patients at Week 24 (n=5). Anemia response by IWG ELN2024 criteria was observed in 50% of patients at any time. Most significantly, 60% of patients achieved a triple response at the Week 24 mark, meeting concurrent criteria for symptom reduction, spleen volume reduction, and anemia improvement. The development of nuvisertib and momelotinib combination therapy was driven by the need to address the pathways that drive MF progression more comprehensively. While standard treatments focus on inhibiting the JAK signaling pathway, research has shown that PIM1 expression is often upregulated in MF and can be driven by JAK-independent compensatory pathways, such as Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) and Ets Related Gene (ERG). These secondary pathways can allow the disease to survive and progress even during JAK inhibitor therapy. By combining nuvisertib with the JAK/Activin A Receptor Type 1 (ACVR1) inhibitor momelotinib, researchers aim to shut down these escape routes, potentially leading to deeper and more durable clinical responses for patients. New Nuvisertib translational research presented in MF Joseph M Scandura, M.D., Ph.D., Division of Hematology and Medical Oncology, Weill/Cornell Leukemia Program, New York, USA, presented translational research further elucidating the proposed mechanism of action of nuvisertib. In addition to its primary activity as a PIM1 inhibitor, in vitro and biochemical data demonstrated that nuvisertib also binds to and inhibits ACVR1, resulting in reduced hepcidin mRNA expression, a central regulator of iron homeostasis. Consistent with these findings, preliminary clinical data from a Phase 1/2 study of nuvisertib monotherapy showed reduced hepcidin levels in patients with R/R MF, providing a potential mechanistic explanation for the hemoglobin stability and improvement observed in patients with MF treated with nuvisertib. “Preliminary clinical data suggests that the combination of nuvisertib and momelotinib may provide a more comprehensive suppression of the disease pathways driving myelofibrosis,” said Raajit Rampal, M.D. Ph.D., Director of the Myeloproliferative Neoplasms Program at the Memorial Sloan Kettering Cancer Centre, New York, USA. “The promising symptom, spleen and anemia responses, coupled with the new nonclinical data on potential dual PIM1 and ACVR1 inhibitory activity by nuvisertib, suggest that this combination therapy may potentially offer meaningful clinical benefits for patients with myelofibrosis.” Translational research in leukemia and menin inhibition identifies E368K mutation as key resistance signature at relapse Also, during the conference, translational research in leukemia and menin inhibition was shared by Jevon Cutler, PhD, Assistant Professor of Cell, Developmental and Cancer Biology at the Oregon Health Sciences University School of Medicine, that identified distinct MEN1 mutational signatures associated with acquired resistance to the menin inhibitor (MI) enzomenib in patients with acute leukemia. Serial molecular profiling revealed that the E368K mutation was the predominant resistance signature identified at relapse, appearing in 53% of patients who relapsed after an initial response. Preclinical work predicted the E368K mutation to be the primary resistance mutation and that this mutation may not affect the other menin inhibitors; these findings support the further exploration of rational, sequential MI therapy to improve clinical outcomes for patients with acute leukemia. Presentation Details Abstract title Lead Author Investigational PIM1 Inhibitor Nuvisertib in Combination with Momelotinib Showed Promising Clinical Activity in Patients with Myelofibrosis and Anemia: Data from an Ongoing Global Phase 1/2 Study James McCloskey, MD Preclinical Evidence of Targeting ACVR1/Hepcidin by Nuvisertib, an Oral Investigational PIM1 Kinase Inhibitor, Suggests Potential Mechanistic Basis for Hemoglobin Benefit in Myelofibrosis Joseph M Scandura, MD, PhD Distinct MEN1 Mutational Signatures Are Associated with Acquired Resistance During MENIN-KMT2A Inhibition in a Phase 1 Enzomenib Trial Jevon Cutler, PhD About Sumitomo Pharma Sumitomo Pharma Co., Ltd. is a global pharmaceutical company based in Japan with key operations in the U.S. (Sumitomo Pharma America, Inc.) focused on addressing patient needs in oncology, urology, women's health, rare diseases, cell & gene therapies, and CNS. With products in the U.S., Canada, and Europe, and a diverse pipeline of early- to late-stage assets, we aim to accelerate discovery, research, and development to bring novel therapies to patients sooner. For more information on SMPA, visit our website or follow us on LinkedIn . The Sumitomo corporate symbol mark is a registered trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO PHARMA is a trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO is a registered trademark of Sumitomo Chemical Co., Ltd., used under license. Sumitomo Pharma America, Inc. is a U.S. subsidiary of Sumitomo Pharma Co., Ltd. ©2026 Sumitomo Pharma America, Inc. All rights reserved. Contacts For further information: SMPA CONTACT: Dave Murdoch, Sumitomo Pharma America, Inc., david.murdoch@us.sumitomo-pharma.com , +1 (774) 405-5570

Clinical ResultPhase 1

08 Dec 2025

·www.prnewswire.com

Sumitomo Pharma America Presents New Investigational Data on Enzomenib and Nuvisertib at the 2025 American Society of Hematology Annual Meeting and Exposition

New investigational data from Phase 1/2 study of enzomenib (DSP-5336) in patients with relapsed/refractory acute myeloid leukemia (AML) show clinical activity in various leukemia subtypes driven by genomic alterations Promising preliminary data, particularly in patients without prior venetoclax or menin inhibitor exposure, seen in Phase 1 study of enzomenib in combination with venetoclax and azacitidine in patients with relapsed/refractory AML Preliminary data from Phase 1/2 study of nuvisertib (TP-3654) in combination with momelotinib in patients with relapsed/refractory myelofibrosis (MF) with anemia show treatment combination appears to be well tolerated with early clinical activity and improvements in spleen and symptom responses MARLBOROUGH, Mass., Dec. 8, 2025 /PRNewswire/ -- Sumitomo Pharma America, Inc. (SMPA) today presented new clinical data supporting further development of enzomenib, an investigational, oral selective menin inhibitor being researched for the treatment of relapsed or refractory acute leukemia, and nuvisertib, an oral investigational highly selective small molecule PIM1 kinase inhibitor, being researched for the treatment of relapsed or refractory myelofibrosis (MF), at the 67th American Society of Hematology (ASH) Annual Meeting and Exposition. Updated Data Shared with the Use of Enzomenib in Acute Myeloid Leukemia Updated preliminary data were presented from the ongoing Phase 1/2 study of enzomenib monotherapy, which as of October 4, 2025, included 116 total patients with acute leukemia, most of whom (93.1%, 108/116) had acute myeloid leukemia (AML) with a median of two prior regimens. Genomic abnormalities of leukemia subtypes including KMT2A rearrangement (KMT2Ar) were documented in 61 patients (52.6%), NPM1 mutation (NPM1m) in 34 patients (29.3%), and other HOXA9/MEIS1-driven abnormalities in 21 patients (17.7%). Enzomenib was escalated from 40 mg twice a day (BID) to 400 mg BID with no dose-limiting toxicities (DLTs). Treatment-related adverse events (TRAEs) observed in at least 10% of patients were nausea (16.4%), and vomiting (11.2%). Differentiation syndrome (DS) was reported in 12.9% of patients and did not result in patient deaths, study discontinuations, or dose reductions of enzomenib. No treatment-related deaths were observed in the study. Dose-dependent increases in exposure were observed, particularly at doses greater than 140 mg BID. Little to no drug accumulation was observed, and CYP3A4 inhibitor azoles did not have a significant impact on exposure. In patients with KMT2Ar, dose optimization of 200, 300, and 400 mg BID is complete, and the RP2D has been determined as 300 mg BID. At RP2D, in patients with KMT2Ar who had not received prior treatment with a menin inhibitor (n = 15), the objective response rate (ORR) was 73.3% and CR+CRh was 40%. Across the optimization dose levels, the duration of CR+CRh (n = 11) was 12.5 months and in all optimization patients (n = 39) median overall survival (mOS) was 11.8 months. For patients with NPM1m AML, dose optimization is ongoing at 200, 300, and 400 mg BID with a focus on 200 and 300 mg BID in patients who have not received a prior menin inhibitor. In the NPM1m dose optimization population (n=25, pts who received ≥ 200 mg BID), ORR is 52% and CR+CR is 44% with a duration of CR+CRh of 5.7 months. The mOS was 8.5 months. "Despite improved understanding of the genetic factors of certain high-risk subtypes in acute leukemias, poor prognosis for patients remains a significant unmet need," said Naval G. Daver, M.D., professor and director of the Leukemia Research Alliance Program in the Department of Leukemia at MD Anderson Cancer Center in Houston. "The data from this ongoing Phase 1/2 study continue to show that enzomenib exhibits promising clinical activity, with encouraging overall and complete response rates, duration of response, and no significant drug interactions with azoles in patients with relapsed or refractory KMT2Ar or NPM1m AML. As an intentionally designed oral therapy to inhibit menin and KMT2A protein interaction, these encouraging clinical results combined with a promising safety profile support the potential of enzomenib as a therapeutic option for relapsed or refractory acute leukemia patients with KMT2A-rearranged or NPM1-mutated subtypes of the disease." Also presented were preliminary results of a Phase 1 study of enzomenib at dose levels of 140 mg, 200 mg, and 300 mg BID in combination with azacitidine and venetoclax (VEN/AZA) in patients with relapsed or refractory AML with KMT2Ar or NPM1m. VEN was administered on days 1-14 of a 28-day study cycle, AZA on days 1-7, and enzomenib was administered on days 1-28 with and without azole antifungal agents. A total of 40 patients were enrolled, of which 18 had KMT2Ar (45%) and 22 (55%) had NPM1m. The median number of prior regimens was 2, with 15 patients having received prior venetoclax (37.5%) and 11 patients (27.5%) a prior menin inhibitor. There were no DLTs observed in the 40 patients enrolled. Hematologic TRAEs related to any regimen component observed in at least 15% of patients included thrombocytopenia (45%), leukopenia (35%), neutropenia (30%), anemia (22.2%), and lymphopenia (15%). Non-hematologic TRAEs were nausea (25%), diarrhea (20%), and AST increased and constipation (15% each). Any-cause QT interval prolongation was reported in 4 patients (10%) with no grade 3 or higher events; no cases were considered related to enzomenib. There were also 4 events of non-serious DS with 0 events grade 3 or higher. Pharmacokinetic data indicated that there were no significant drug-drug interactions between enzomenib and VEN. As of the clinical data cutoff on October 4, 2025, clinical activity data is available for 26 of the 40 total patients as 11 patients were still in Cycle 1 (n = 9) or Cycle 2 (n = 2), and 3 patients had cutaneous leukemia without measurable disease in the bone marrow (bone marrow blasts <5%). Promising preliminary clinical activity has been observed, particularly in patients without prior VEN or menin inhibitor exposure (N=13). The ORR is 85% (11/13) and the composite complete remission (CRc) rate is 62% (8/13). Local MRD assessments were available in 9 patients and 7/9 (78%) achieved MRD negativity as of the cut-off. These data support evaluating enzomenib with VEN/AZA in patients with newly diagnosed AML. Study arms are being added to investigate the combination regimen for patients with newly diagnosed disease. Enzomenib will be administered at 200 mg or 300 mg BID using VEN/AZA administered according to the FDA label. Enrollment of newly diagnosed patients with KMT2Ar or NPM1m AML will begin in early 2026. Nuvisertib in Patients with Relapsed or Refractory (R/R) MF For the first time, clinical data were presented from the ongoing global Phase 1/2 study evaluating the safety and efficacy of nuvisertib in combination with momelotinib (MMB) in 18 patients with R/R MF with anemia. All enrolled patients in the study had previously been treated with a JAK inhibitor, the current standard of care for patients with MF, and 61% of patients had high molecular risk mutation. Preliminary data showed that the treatment with nuvisertib and MMB combination appeared well tolerated, with early clinical activity observed, including ³50% total symptom score reduction (TSS50 response) in 58% of patients with an absolute reduction in all individual symptoms, a spleen volume reduction ³ 25% (SVR25 response) in 50% of patients, anemia improvement, and cytokine modulation in patients with relapsed or refractory MF with anemia. These preliminary data, collected as of October 15, 2025, support further development of nuvisertib in combination with MMB as a potential treatment option for patients with MF. Additionally, data presented from the ongoing global Phase 1/2 study of nuvisertib in patients with relapsed or refractory MF (N=77) showed that nuvisertib monotherapy continued to be well tolerated with no DLTs and limited myelosuppression. The results showed that treatment with nuvisertib monotherapy led to SVR25 response in 20% of patients, TSS50 response in 45% of patients with absolute reduction in all individual symptoms. Data also showed that treatment with nuvisertib resulted in significant cytokine modulation over time, correlating with spleen and symptom responses and one-year overall survival rate of 81%. "Patients living with myelofibrosis with anemia usually have a dismal prognosis, still continue to face limited treatment options," said John Mascarenhas, M.D., Director of the Center of Excellence for Blood Cancers and Myeloid Disorders, Icahn School of Medicine at Mount Sinai, New York. "The promising preliminary results from the combination of nuvisertib and momelotinib underscore the urgent need for new therapeutic approaches that may offer meaningful clinical benefits to a difficult to treat disease." "We are excited to present the first-ever myelofibrosis data with a momelotinib-based combination, specifically nuvisertib in combination with momelotinib. The development of innovative therapies—both alone and in combination with other treatments—are critical for physicians and patients with blood cancers such as AML or MF who are in urgent need of new effective therapies," said Jatin Shah, M.D., Chief Medical Officer, Oncology, SMPA. "Based on these updated preliminary data presented at ASH, which continue to show promising clinical activity and safety profiles for both enzomenib and nuvisertib, we remain committed to accelerate the clinical development in these programs with the ultimate goal of improving patient outcomes." About Leukemia Leukemia is a type of cancer that forms in blood-forming tissue, characterized by the uncontrolled growth of blood cells, usually white blood cells, in the bone marrow. Acute leukemia, a form of leukemia, requires immediate treatment as blood cells multiply rapidly leading to a sudden onset of symptoms.1 Approximately 30% of patients with AML have NPM1 mutations,2 and 5%-10% of patients with AML have KMT2A rearrangements.3 About Myelofibrosis (MF) MF is a rare type of blood cancer that is characterized by the buildup of fibrous tissue in the bone marrow, which can affect the production of blood cells. This buildup is caused by dysregulation in the JAK signaling pathway. MF is a serious and rare disease with 0.7 new cases per 100,000 people worldwide each year.4 About Enzomenib (DSP-5336) Enzomenib is an investigational, oral, small molecule inhibitor of the menin and Lysine (K)-specific methyltransferase 2A (KMT2A) protein interaction, a key interaction in acute leukemia and other tumor cell proliferation and growth. Menin is a scaffold nuclear protein, which plays key roles in gene expression and protein interactions involved in many biological pathways, including cell growth, cell cycle, genomic stability, and hematopoiesis.5,6 In preclinical studies, enzomenib has shown selective growth inhibition in human acute leukemia cell lines with KMT2A rearrangements or NPM1 mutations.5,7 Enzomenib reduced the expression of the leukemia-associated genes HOXA9 and MEIS1 and increased the expression of the differentiation gene CD11b in human acute leukemia cell lines with KMT2A rearrangements and NPM1 mutation.8,9 The safety and efficacy of enzomenib is currently being clinically evaluated in a Phase 1/2 dose-escalation/dose-expansion study in patients with relapsed or refractory acute leukemia (NCT04988555). Additionally, the registrational Phase 2 Horizen-1 R/R mono AML/ALL (KMT2Ar + NPM1m) study is now open for enrollment. The FDA granted Orphan Drug Designation for enzomenib for the indication of acute myeloid leukemia in June 2022. The FDA granted Fast Track Designation for enzomenib for the indication of relapsed or refractory acute myeloid leukemia with KMT2Ar or NPM1m in June 2024. Japan's Pharmaceuticals and Medical Devices Agency (PMDA) granted Orphan Drug Designation for enzomenib for the indication of relapsed or refractory acute myeloid leukemia with KMT2Ar or NPM1m in September 2024. About Nuvisertib (TP-3654) Nuvisertib is an oral investigational selective inhibitor of PIM1 kinase, which has shown potential antitumor and antifibrotic activity through multiple pathways, including induction of apoptosis in preclinical models.10,11 Nuvisertib was observed to inhibit proliferation and increase apoptosis in murine and human hematopoietic cells expressing the clinically relevant JAK2 V617F mutation.10 Nuvisertib alone and in combination with ruxolitinib showed white blood cell and neutrophil count normalization and reduced spleen size and bone marrow fibrosis in JAK2 V617F and MPLW515L murine models of myelofibrosis.11 The safety and efficacy of nuvisertib is currently being clinically evaluated in a Phase 1/2 study in patients with intermediate- and high-risk myelofibrosis (NCT04176198). The FDA granted Orphan Drug Designation to nuvisertib for the indication of myelofibrosis in May 2022. The Japan Ministry of Health, Labour and Welfare (MHLW) granted Orphan Drug Designation to nuvisertib for the treatment of myelofibrosis in November 2024. The FDA granted Fast Track Designation to nuvisertib for the indication of myelofibrosis in July 2025. About Sumitomo Pharma Sumitomo Pharma Co., Ltd. is a global pharmaceutical company based in Japan with key operations in the U.S. (Sumitomo Pharma America, Inc.) and Canada (Sumitomo Pharma Canada, Inc.) focused on addressing patient needs in oncology, urology, women's health, rare diseases, cell & gene therapies and CNS. With several marketed products in the U.S., Canada, and Europe, and a diverse pipeline of early- to late-stage investigational assets, we aim to accelerate discovery, research, and development to bring novel therapies to patients sooner. For more information on SMPA, visit our website or follow us on LinkedIn. The Sumitomo corporate symbol mark is a trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO PHARMA is a trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO is a registered trademark of Sumitomo Chemical Co., Ltd., used under license. Sumitomo Pharma America, Inc., is a U.S. subsidiary of Sumitomo Pharma Co., Ltd. ©2025 Sumitomo Pharma America, Inc. All rights reserved. References Chennamadhavuni A, Lyengar V, Mukkamalla SKR, et al. Leukemia. [Updated 2023 Jan 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: Brandi ML, Agarwal SK, Perrier ND, Lines KE, Valk GD, Thakker RV. Multiple Endocrine Neoplasia Type 1: Latest Insights. Endocr Rev. 2021;42(2):133-170. doi:10.1210/endrev/bnaa031 Borkin D, Klossowski S, Pollock J, et al. Complexity of Blocking Bivalent Protein-Protein Interactions: Development of a Highly Potent Inhibitor of the Menin-Mixed-Lineage Leukemia Interaction. J Med Chem. 2018;61(11):4832-4850. doi:10.1021/acs.jmedchem.8b00071 Hernández-Boluda JC, Czerw T. Transplantation algorithm for myelofibrosis in 2022 and beyond. Best Pract Res Clin Haematol. 2022;35(2):101369. doi:10.1016/j.beha.2022.101369 Cierpicki T, Grembecka J. Challenges and opportunities in targeting the menin-MLL interaction. Future Med Chem. 2014;6(4):447-462. doi:10.4155/fmc.13.214 Matkar S, Thiel A, Hua X. Menin: a scaffold protein that controls gene expression and cell signaling. Trends Biochem Sci. 2013;38(8):394-402. doi:10.1016/j.tibs.2013.05.005 Kühn MW, Song E, Feng Z, et al. Targeting Chromatin Regulators Inhibits Leukemogenic Gene Expression in NPM1 Mutant Leukemia. Cancer Discov. 2016;6(10):1166-1181. doi:10.1158/2159-8290.CD-16-0237 Eguchi K, Shimizu T, Kato D, et al. Preclinical Evaluation of a Novel Orally Bioavailable Menin-MLL Interaction Inhibitor, DSP-5336, for the Treatment of Acute Leukemia Patients with MLL-Rearrangement or NPM1 Mutation. Blood 2021; 138 (Supplement 1): 3339. Available at: Daver N, Zeidner JF, Yuda J, et al. Phase 1/2 First-in-Human Study of the Menin-MLL Inhibitor DSP-5336 in Patients with Relapsed or Refractory Acute Leukemia. Blood 2023; 142 (Supplement 1): 2911. Available at: Dutta A, Nath D, Yang Y, et al. Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models. Leukemia. 2022;36(3):746-759. doi:10.1038/s41375-021-01464-2 Foulks JM, Carpenter KJ, Luo B, et al. A small-molecule inhibitor of PIM kinases as a potential treatment for urothelial carcinomas. Neoplasia. 2014;16(5):403-412. doi:10.1016/j.neo.2014.05.004 SOURCE Sumitomo Pharma America 21% more press release views with Request a Demo

Clinical ResultFast TrackOrphan DrugASHPhase 1

21 Nov 2025

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Hackensack Meridian John Theurer Cancer Center Unveils Research at the 67th American Society of Hematology Annual Meeting

Advances span leukemia, lymphoma, myeloma, myeloproliferative neoplasms, sickle cell disease, and AI-enabled diagnostics HACKENSACK, N.J., Nov. 21, 2025 /PRNewswire/ -- Investigators from Hackensack Meridian John Theurer Cancer Center (JTCC)—a leading research partner of the NCI-designated Lombardi Comprehensive Cancer Center at Georgetown University, and number one Cancer Center in New Jersey—will present 65 studies at the 67th American Society of Hematology (ASH) Annual Meeting, taking place December 6–9, 2025, in Orlando. This represents one of JTCC's largest and most diverse scientific contributions to ASH to date, highlighting innovations in cell therapy, targeted agents, AI-driven diagnostics, stem cell transplantation, and real-world evidence across virtually every hematologic disease area. "John Theurer Cancer Center continues to help shape the future of blood cancer care," said André Goy, MD, chair, physician-in-chief and vice president of oncology at Hackensack Meridian Health. "Our teams are redefining transplantation, advancing CAR-T science, and co-leading trials testing next-generation targeted therapies and immunotherapies. The depth and breadth of our ASH presentations underscore our mission: to bring transformational science rapidly to the clinic for patients with blood cancers and other serious blood disorders." Highlights of JTCC Research to be presented at ASH 2025 can be found here. Leukemia High event-free (EFS) and overall survival (OS) after non-total body irradiation (TBI) conditioning and allogeneic hematopoietic cell transplantation (HCT) in next-generation-sequencing minimal residual disease (NGS-MRD) negative B-acute lymphoblastic leukemia (B-ALL): Results from the EndRAD trial (PTCTC ONC1701) (ABSTRACT 25-12959) A phase 2 dose confirmation trial of oral ASTX030, a combination of oral azacitidine with cedazuridine among patients with myelodysplastic syndromes, chronic myelomonocytic leukemia, and acute myeloid leukemia (ABSTRACT 25-7509) Ziftomenib in combination with venetoclax and azacitidine in relapsed/refractory NPM1-m or KMT2A-r acute myeloid leukemia: Updated phase 1a/b safety and clinical activity results from KOMET-007 (ABSTRACT 25-3910) MRD-guided therapy of sonrotoclax (BGB-11417) + obinutuzumab (O) in patients with treatment-naive CLL: Initial results from an ongoing phase 1/1b study, BGB-11417-101 (ABSTRACT 25-7489) Real world outcomes of bispecific T-cell engagers in plasma cell leukemia (ABSTRACT 25-4651) Etoposide can be safely removed from induction chemotherapy without impacting survival for pediatric acute myeloid leukemia – a report from the Children's oncology group study AAML1831 (ABSTRACT 25-12270) Updated response and safety analyses from a Phase 1 study of ivosidenib combined with intensive chemotherapy in patients with newly diagnosed (ND) Acute Myeloid Leukemia with isocitrate dehydrogenase (IDH)1 mutation (ABSTRACT 25-421) AI-derived prediction of response and relapse to venetoclax plus hypomethylating agent based therapy in Acute Myeloid Leukemia (ABSTRACT 25-14588) TSC-101 eliminates recipient hematopoietic cells and demonstrates potential for improved relapse-free survival in patients with AML, ALL, or MDS undergoing allogeneic HCT: Updated results from the Phase 1 (ALLOHA) trial (ABSTRACT 25-12098) Trials in progress: Design of a registrational Phase 2 trial (ALLOHA) using an external control arm for TSC-101 for prevention of relapse post allogeneic HCT in patients with ALL, AML, or MDS (ABSTRACT 25-13827) Developing artificial intelligence-based transcriptomic signature for selecting patients with HOXA-MEIS1 pathway abnormalities for the treatment with menin inhibitors (ABSTRACT 25-4126) Evaluation of ventoclax initiation prophylaxis and monitoring outcomes at each dose level and time point in patients with chronic lymphocytic leukemia: A real-world experience (ABSTRACT 25-2129) Developing transcriptomic signature for IDH1 and IDH2 acute leukemia and the demonstration of high prevalence of these signatures in mutation-negative leukemia (ABSTRACT 25-4127) Impact of DUSP22 and TP63 rearrangements in patients with ALK-negative ALCL treated with frontline BV-CH(E)P (ABSTRACT 25-1798) Harnessing repressive LEF1/ β-catenin complexes to overcome drug resistance in chronic lymphocytic leukemia (ABSTRACT 25-14485) Reducing Acute Myeloid Leukemia resistance to CAR T cell therapy by epigenetic activation of the tumor inflammasome-pyroptosis signaling (ABSTRACT 25-13458) Lymphoma Epcoritamab + R-mini-CHOP results in 2-year remissions and high MRD negativity rates in elderly patients with newly diagnosed DLBCL: Results from the EPCORE NHL-2 trial (ABSTRACT 25-3828) Epcoritamab with rituximab + lenalidomide (R2) and epcoritamab maintenance deliver deep and durable remissions in previously untreated (1L) follicular lymphoma (FL): 3-year outcomes from epcore NHL-2 arms 6 and 7 (ABSTRACT 25-2787) Liquid-biopsy mutation landscape and its concordance with skin biopsies in cutaneous T-cell lymphoma (ABSTRACT 25-2858) ZUMA-25 preliminary analysis: A Phase 2 study of brexucabtagene autoleucel (brexu-cel) in patients (Pts) with relapsed/refractory (R/R) Burkitt lymphoma (BL), substudy C (ABSTRACT 25-2841) Final results of a phase 1 trial with soquelitinib (SQL), a selective interleukin-2-inducible T cell kinase (ITK) inhibitor for treatment of relapsed/refractory (R/R) T cell lymphomas (TCL) (ABSTRACT 25-2574) Acalabrutinib plus venetoclax and rituximab in patients with treatment-naive (TN) mantle cell lymphoma (MCL): Results from the Phase 2 TrAVeRse study (ABSTRACT 25-7289) Two-year update of ZUMA-2 Cohort 3: Brexucabtagene autoleucel (Brexu-cel) in patients (pts) with relapsed/refractory mantle cell lymphoma (R/R MCL) who had not received prior Bruton tyrosine kinase inhibitor (BTKi) therapy (ABSTRACT 25-2240) Phase 2 bellwave-003 cohort f: Updated clinical outcomes of nemtabrutinib in participants with relapsed or refractory marginal zone lymphoma (ABSTRACT 25-2322) A real-world analysis of safety and outcomes with first line nivolumab in combination with doxorubicin, vinblastine, and dacarbazine (NAVD) in patients with classic Hodgkin lymphoma (cHL) – a multicenter cohort study (ABSTRACT 25-2368) Safety and efficacy of brexucabtagene autoleucel in elderly patients with relapsed or refractory Mantle Cell Lymphoma: A retrospective, multicenter, international study (ABSTRACT 25-2034) Developing artificial intelligence-based transcriptomic signature for the diagnosis of dark zone lymphoma in patients without MYC gene rearrangement (ABSTRACT 25-7855) A multicenter real-world analysis of combined chemotherapy followed by consolidative radiation versus chemotherapy alone in the management of early-stage Hodgkin lymphoma – the HODGKIN25 study (ABSTRACT 25-1471) Nivolumab with doxorubicin, vinblastine, and dacarbazine (NAVD) in older adults with classic Hodgkin lymphoma: Do S1826 results hold up in the real world? (ABSTRACT 25-7840) First-line salvage therapies in relapsed/refractory large B-cell lymphoma after second- or third-line CD19-directed CAR T-cell therapy (ABSTRACT 25-3402) Multicenter, randomized Phase II study of epcoritamab for patients with large B-cell lymphomas achieving a partial response after CD19-directed CAR T-cell therapy: Trial in progress (ABSTRACT 25-15528) Zanubrutinib + obinutuzumab + sonrotoclax in patients with treatment-naive chronic lymphocytic leukemia/small lymphocytic lymphoma (TN CLL/SLL): Initial results from an ongoing phase 1/1b study, BGB-11417-101 (ABSTRACT 25-4113) Sustained remissions beyond 4 years with epcoritamab monotherapy: Long term follow-up results from the pivotal EPCORE NHL-1 trial in patients with relapsed or refractory large B-cell lymphoma (ABSTRACT 25-7543) Multiple Myeloma Real-world outcomes with elranatamab in multiple myeloma: A multi-center analysis from the United States multiple myeloma immunotherapy consortium (ABSTRACT 25-2557) Phase 1 study of ktx-1001, a first-in-class oral MMSET/NSD2 inhibitor, demonstrates clinical activity in relapsed/refractory multiple myeloma (ABSTRACT 25-2077) Phase 2 registrational study of anitocabtagene autoleucel for the treatment of patients with relapsed and/or refractory multiple myeloma: Updated results from iMMagine--1 (ABSTRACT 25-4541) Alterations in the gut microbiome and the association of butyrate producers with progression-free survival in multiple myeloma patients undergoing autologous stem cell transplantation (ABSTRACT 25-14794) Talquetamab outcomes in relapsed/refractory myeloma with extramedullary and paraskeletal soft tissue plasmacytomas (ABSTRACT 25-7804) Safety and efficacy of talquetamab in patients with relapsed and refractory multiple myeloma (RRMM) with and without renal impairment (ABSTRACT 25-7724) Enhancing the safety of ciltacabtagene autoleucel in relapsed multiple myeloma (MM): Identification of potentially modifiable risk-factors associated with delayed neurotoxicity and non-relapse mortality (ABSTRACT 25-2357) An open-label, multi-center Phase 2 study to assess the safety and efficacy of burixafor (GPC-100) and propranolol with G-CSF for the mobilization of hematopoietic progenitor cells in patients with multiple myeloma (ABSTRACT 25-14982) Prospective real-world evaluation of SKY92 for risk stratification in multiple myeloma: Comparison with updated ims/IMWG criteria in the prommis study (ABSTRACT 25-8818) Pomalidomide salvage in T-cell engager monotherapy failures: Real-world experience with talquetamab or elranatamab with pomalidomide combinations in heavily pretreated multiple myeloma (ABSTRACT 25-10539) Prolonged elranatamab treatment interruption in patients with relapsed or refractory multiple myeloma (RRMM) is feasible: A retrospective analysis from MagnetisMM-3 (ABSTRACT 25-8338) Talquetamab, a GPRC5D×CD3 bispecific antibody, in combination with pomalidomide in patients with Relapsed/Refractory multiple myeloma: Updated safety and efficacy results from the Phase 1b monumental-2 study (ABSTRACT 25-11949) Prospective study of fluoroquinolone resistance colonization in patients undergoing autologous hematopoietic stem cell transplantation in the treatment of multiple myeloma (ABSTRACT 25-13625) Identifying high-risk profiles and adverse prognoses in relapsed/refractory multiple myeloma treated with bispecific antibodies: A real-world analysis of 943 treatment initiations (ABSTRACT 25-8860) Intratumoral cellular immunotherapy with autologous hyperactivated M1 SIRP α -low macrophages in non-Hodgkin lymphoma: Clinical results from a first-in-human Phase 1 study (ABSTRACT 25-8309) Real-world disease burden and treatment patterns among triple-class–exposed patients with relapsed/refractory multiple myeloma and extramedullary disease in the US: A retrospective analysis using Flatiron Health electronic medical records (ABSTRACT 25-9053) Shared immune features correspond to high-risk multiple myeloma across multiple human subtypes and murine models (ABSTRACT 25-13910) Real-world efficacy and safety of teclistamab in relapsed or refractory multiple myeloma: Results from 87 patients treated by the polish myeloma group (ABSTRACT 25-11305) Myeloproliferative Neoplasms Preliminary data from the Phase I/II study of nuvisertib, an oral investigational selective PIM1 inhibitor, in combination with momelotinib showed clinical responses in patients with relapsed/refractory myelofibrosis (ABSTRACT 25-3882) Safety and efficacy results from A phase 1b study of R289, a dual irak 1/4 inhibitor, in patients with Relapsed/Refractory (R/R) lower risk myelodysplastic syndrome (LR-MDS) (ABSTRACT 25-13480) Nuvisertib, an oral investigational selective PIM1 kinase inhibitor, showed clinical responses strongly correlating with cytokine modulation in patients with relapsed/refractory myelofibrosis in the ongoing global phase I/II study (ABSTRACT 25-2614) Bone marrow microenvironment overlap between vexas and myelodysplastic syndrome demonstrated by targeted transcriptomic and artificial intelligence (ABSTRACT 25-7376) Noncancerous Blood Disorders Reduced intensity haploidentical bone marrow transplantation in children with severe sickle cell disease (SCD): BMT CTN 1507 (ABSTRACT 25-11982) End-of-study results from the ICON3 pines trial, a phase 3, randomized trial of eltrombopag vs. standard first-line treatment for newly diagnosed immune thrombocytopenia in children (ABSTRACT 25-4324) The real-world safety and efficacy of BCMA-directed chimeric antigen receptor T-cell therapy in systemic AL amyloidosis (ABSTRACT 25-2732) Robust HbF induction and improvement of anemia and hemolysis with base editing in sickle cell disease: Safety and efficacy findings from the ongoing BEACON study (ABSTRACT 25-2531) Children and adolescents with sickle cell disease demonstrate improved health-related quality of life and low decisional regret after hematopoietic cell transplantation: A sickle cell transplant advocacy and research alliance (STAR) study (ABSTRACT 25-12128) Increased age-adjusted mortality rates from hemophagocytic lymphohistiocytosis (HLH), 2010-2023 (ABSTRACT 25-7365) Rapid decrease in age-adjusted mortality rates associated with ITP following eltrombopag and romiplostim approvals, but not in TMA following eculizumab approval, 1999-2023 (ABSTRACT 25-9103) Technology B- and T-cell clonality using peripheral blood cell-free RNA (cfRNA) in liquid biopsy (ABSTRACT 25-7865) Not so exclusive: Co-mutations in JAK2, MPL and CALR define distinct hematologic and clonal signatures (ABSTRACT 25-10661) Temporal control of CAR expression enables thymic generation of autoreactive T cells targeting tumor-associated antigens (ABSTRACT 25-8390) About Hackensack Meridian John Theurer Cancer Center Hackensack Meridian John Theurer Cancer Center at Hackensack University Medical Center is recognized as New Jersey's #1 cancer center in New Jersey by U.S. News & World Report. They are also the largest and most comprehensive center dedicated to diagnosis, treatment, management, research, screening, and preventive care as well as survivorship of patients with all types of cancers. The 16 specialized divisions covering the complete spectrum of cancer care have developed a close-knit team of medical, research, nursing, and support staff with specialized expertise that translates into more advanced, focused care for all patients. Each year, more people in the New Jersey/New York metropolitan area turn to John Theurer Cancer Center for cancer care than to any other facility in New Jersey. John Theurer Cancer Center is part of the NCI-designated Lombardi Comprehensive Cancer Center at Georgetown University. Housed within a 781-bed not-for-profit teaching, tertiary care, and research hospital, John Theurer Cancer Center provides state-of-the-art technological advances, compassionate care, research innovations, medical expertise, and a full range of aftercare services that distinguish John Theurer Cancer Center from other facilities. The center expanded to Jersey Shore University Medical Center, serving patients in southern New Jersey and parts of Pennsylvania. Toms River Regional Cancer Center and Saint Joseph's Health are affiliated with the cancer center. For additional information, please visit . SOURCE Hackensack Meridian John Theurer Cancer Center 21% more press release views with Request a Demo

Clinical ResultPhase 2Phase 1ImmunotherapyASH

100 Deals associated with Nuvisertib

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Indication	Highest Phase	Country/Location	Organization	Date
Post-essential thrombocythemia myelofibrosis	Phase 2	United States	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Japan	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Australia	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Belgium	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Canada	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	France	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Germany	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Italy	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	Spain	Sumitomo Pharma America, Inc.	16 Dec 2019
Post-essential thrombocythemia myelofibrosis	Phase 2	United Kingdom	Sumitomo Pharma America, Inc.	16 Dec 2019

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04176198 (EHA2026)	Phase 1/2	Myelofibrosis	26	Nuvisertib + Momelotinib (fed) (Myelofibrosis + Anemia + Relapsed/Refractory)	jdlmypapck(ixmdcahsyc) = wlljivzpmr mriqjhaqds (fhbbfvtump ) View more	Positive	12 May 2026
NCT04176198 (ASH2025)	Phase 1/2	Recurrent Myelofibrosis	77	Nuvisertib	ufvxmbshnu(lmkuxaewzd) = okjkjhpeud eoynctbrsj (vbctuquivf ) View more	Positive	06 Dec 2025
NCT04176198 (Phase I/II study of Nuvisertib, EHA2025)	Phase 1/2	Myelofibrosis	77	Nuvisertib 480 mg QD	uctxbuewor(gwpgxxegpk) = ybhllpcely pvoawooaqp (qwwyfsjkqo ) View more	-	14 May 2025
NCT04176198 (Phase I/II study of Nuvisertib, EHA2025)	Phase 1/2	Myelofibrosis	77	Nuvisertib 720 mg BID	lgckycukjc(brwtngudfx) = xbiulldaxn rpsgjsohvm (bijwtipvkx ) View more	-	14 May 2025
NCT04176198 (ASH2024) Manual	Phase 1/2	Myelofibrosis	65	Nuvisertib (TP-3654) monotherapy	brwnrkgurr(gebepgjqfp) = Gr 1/2 nausea, vomiting, and diarrhea. Gr ≥3 TRAE occurring in ≥3 pts included PLT count decreased (n=4; 3 pts had BL Gr 2 and 1 pt Gr 1 PLT count decreased). mehrsuoyqu (fmocndkfsc ) View more	Positive	08 Dec 2024
ASH2024	Not Applicable	Myelofibrosis	-	Nuvisertib (TP-3654)	bvtgmbtumz(rkiupmyyxe) = 6 of 18 (33%) evaluable pts showed ≥1 grade reduction in BM fibrosis correlating with 3 of 6 (50%) showing anemia and platelet response, and 5 of 6 (83%) were on active treatment for ≥1 year manlhxhhkx (tudknzwpdu ) View more	-	08 Dec 2024
NCT04176198 (ASH2023)	Phase 1/2	Refractory Myelofibrosis	23	TP-3654	gkqkjpuvxq(mpvudfimvo) = bncnpmvsbw ifhmmcjikj (jetggkbarf ) View more	-	10 Dec 2023
SOHO2023	Not Applicable	Recurrent Myelofibrosis	-	TP-3654	wnuhkdcrpw(djcqejyvsq) = diarrhea reported as a common treatment-related adverse event (TRAE) hbsdhfglyp (wopklwmncz ) View more	-	01 Sep 2023
NCT04176198 (EHA2023)	Phase 1/2	Refractory Myelofibrosis	15	TP-3654	ckrtbhillf(osqefjhsca) = qhntqfhxoo uhjazfdume (mxolhxqtpm ) View more	-	08 Jun 2023
NCT04176198 (ASH 12022 \| ASH 22022) Manual	Phase 1/2	Primary Myelofibrosis	8	TP-3654	bcynuzinoe(idfpwywofd) = trpvtdcnbj cowijcvpuk (xgojibbean ) View more	Positive	15 Nov 2022
ASCO2020	Phase 1	Advanced Malignant Solid Neoplasm	10	TP-3654 480 mg	rcshykmhvv(owtascmree) = Grade 3 AEs were scrotum wound infection, altered mental status, anemia, fall, and lower extremity edema, none were related to study drug and all were manageable with supportive care. xafevcmqve (kxykcwqvad )	Positive	25 May 2020
ASCO2020	Phase 1	Advanced Malignant Solid Neoplasm	10	TP-3654 720 mg		Positive	25 May 2020

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