RegulationFast Track (United States), Accelerated Approval (United States), Orphan Drug (United States), Orphan Drug (European Union), Orphan Drug (Japan), Conditional marketing approval (China), Priority Review (China)

Structure/Sequence

Molecular FormulaC34H45BrN4O4

InChIKeyUQRICAQPWZSJNF-UHFFFAOYSA-N

CAS Registry1467052-75-0

Clinical Trials associated with Tazemetostat Hydrobromide

NCT07209163

/ Not yet recruitingPhase 1/2IIT

An Open-label, Single-arm Study Evaluating the Safety and Efficacy of Tazemetostat in Combination With Linperlisib/Golidocitinib in Patients With Relapsed/Refractory Peripheral T-cell Lymphoma

In decades, the outcome of patients with peripherial T-cell lymphomas is dismal, especially in relapsed or refractory population. After failure to the frontline treatment, patients have limited treatment options and elderly population usually have no chance to undergo transplantation due to age or comorbidity, etc. EZH2 inhibitor like Tazemetostat or SHR 2554 has been demonstrated its anti-tumor activity in PTCL either alone or in combination with other targeted agents.
This study aims to explore the efficacy and safety of Tazemetostat in combination with Linperlisib/Golidocitinib in Patients With Relapsed/Refractory Peripheral T-cell Lymphoma in the patients with peripheral T-cell lymphoma according to next-generation sequesing results.

Start Date01 Oct 2025

Sponsor / Collaborator

Ruijin Hospital

NCT06824701

/ RecruitingPhase 1IIT

A Phase 1b Study of Tazemetostat in Combination With Zanubrutinib and Anti-CD20 Monoclonal Antibody in Relapsed or Refractory Indolent B-cell Non-Hodgkin Lymphomas (TARZAN Trial)

The purpose of this clinical trial is to learn if the study drug Tazemetostat combined with Zanubrutinib and anti-CD20 monoclonal antibody is safe and effective in treating patients with relapsed or refractory indolent B-cell non-Hodgkin lymphoma.

Start Date12 Sep 2025

Sponsor / Collaborator

University of Utah

[+1]

ChiCTR2500107892

/ RecruitingEarly Phase 1IIT

Evaluation of the Clinical Efficacy of Epigenetic Agents Combined with Immune Checkpoint Inhibitors in the Treatment of Pediatric-type Diffuse High-grade Gliomas

Start Date10 Sep 2025

Sponsor / Collaborator-

100 Clinical Results associated with Tazemetostat Hydrobromide

100 Translational Medicine associated with Tazemetostat Hydrobromide

100 Patents (Medical) associated with Tazemetostat Hydrobromide

418

Literatures (Medical) associated with Tazemetostat Hydrobromide

01 Dec 2025·FUNCTIONAL & INTEGRATIVE GENOMICS

Polycomb repressive complex 2 (PRC2) pathway’s role in cancer cell plasticity and drug resistance

Review

Author: Tabari, Mohammad Amin Khazeei ; Khan, Haroon ; Javan, Alireza ; Larsen, Danaé S ; Rezaee, Aryan ; Heidari, Mohammad Mahdi ; Sanaye, Pantea Majma ; Hadipour, Mahboube ; Daglia, Maria ; Goleij, Pouya

Polycomb Repressive Complex 2 (PRC2) is a central regulator of gene expression via the trimethylation of histone H3 on lysine 27. This epigenetic modification plays a crucial role in maintaining cell identity and controlling differentiation, while its dysregulation is closely linked to cancer progression. PRC2 silences tumor suppressor genes, promoting cell proliferation, metastasis, epithelial-mesenchymal transition, and cancer stem cell plasticity. Enhancement of zeste homolog 2 (EZH2) overexpression or gain-of-function mutations have been observed in several cancers, including lymphoma, breast, and prostate cancers, driving aggressive tumor behavior and drug resistance. In addition to EZH2, other PRC2 components, such as embryonic ectoderm development (EED) and suppressor of zeste 12, are essential for complex stability and function. EED, in particular, enhances EZH2 activity and has emerged as a therapeutic target. Inhibitors like MAK683 and EED226 disrupt EED's ability to maintain PRC2 activity, thereby reducing H3K27me3 levels and reactivating tumor suppressor genes. Valemetostat, a dual inhibitor of both EZH2 and EED, has shown promising results in aggressive cancers like diffuse large B-cell lymphoma and small-cell lung cancer, underlining the therapeutic potential of targeting multiple PRC2 components. PRC2's role extends beyond gene repression, as it contributes to metabolic reprogramming in tumors, regulating glycolysis and lipid synthesis to fuel cancer growth. Furthermore, PRC2 is implicated in chemoresistance, particularly by modulating DNA damage response and immune evasion. Tazemetostat, a selective EZH2 inhibitor, has demonstrated significant clinical efficacy in EZH2-mutant cancers, such as non-Hodgkin lymphomas and epithelioid sarcoma. However, the compensatory function of enhancer of zeste homolog 1 (EZH1) in some cancers requires dual inhibition strategies, as seen with agents like UNC1999 and Tulmimetostat, which target both EZH1 and EZH2. Given PRC2's multifaceted role in cancer biology, its inhibition represents a promising avenue for therapeutic intervention. The continued development of PRC2 inhibitors and exploration of their use in combination with standard chemotherapy or immunotherapy has great potential for improving patient outcomes in cancers driven by PRC2 dysregulation.

01 Nov 2025·Journal of Orthopaedic Translation

Epigenetic reprogramming via EZH2 inhibition rescues fibroadipose pathogenesis in secondary lymphedema through activating PPARγ signaling

Article

Author: Chen, Ziyu ; Yao, Zhi ; Liu, Pei ; Liao, Zhuangyao ; Zhang, Jianlin ; Zhou, Zhegang ; Yu, Longbiao ; Wei, Jiewen ; Li, Ye ; Wen, Jingjing ; Agarwal, Shailesh ; Wu, Mengfan ; Ma, Zetao ; Qian, Junyu ; Wang, Deli ; Yao, Yuefeng ; Xue, Lixiang ; Wei, Yihao ; Song, Lili ; Wu, Yuluan

Background:

Secondary lymphedema, a progressive disorder characterized by pathological fibroadipose tissue accumulation, is a common problem after cancer treatment and orthopedic surgery. It remains a therapeutic enigma due to its self-perpetuating fibrotic cascade and lack of disease-modifying therapies. While current therapeutic approaches focus on symptom management and volume reduction, they don't address the epigenetic reprogramming driving fibrotic commitment-a process recently linked to enhancer of zeste homolog 2 (EZH2). Although EZH2 inhibitor EPZ6438 has been approved for clinical application, its therapeutic potential in fibroadipose pathogenesis remains unexplored, leaving a critical gap in understanding epigenetic factors in lymphedema progression.

Methods:

Human skin tissue was collected from lymphedema patients and normal controls. Histological/immunofluorescence staining and RNA sequencing were performed. In vivo, a mouse hind limb secondary lymphedema model was established by lymphadenectomy. EZH2 inhibitors (EPZ6438, GSK126) were intraperitoneally injected. Skin samples were collected for histological assessment and immuno-staining. In vitro, adipose-derived mesenchymal stem cells (AdMSCs) were treated with transforming growth factor beta 1 (TGFβ1) and EZH2 inhibitors. Western blot, RT-qPCR and ChIP-qPCR were carried out.

Results:

Fibrous tissue was observed in lymphedema samples, with concomitant elevation of EZH2 and H3K27me3 levels in the nucleus. RNA sequencing and gene set enrichment analysis (GSEA) revealed significant downregulation of the peroxisome proliferator-activated receptor (PPAR) signaling in lymphedema tissue. Pharmacological inhibition of EZH2 significantly attenuated cutaneous thickening, fibroadipose layer expansion, and collagen deposition in the mouse lymphedema model. PPARγ was induced while phospho-SMAD2/3 activation was suppressed. In TGFβ1 stimulated AdMSCs, EZH2 inhibition upregulated PPARγ expression and inhibited fibrogenic differentiation of the cells.

Conclusion:

EZH2 inhibitors exerted potent anti-fibrotic effects in secondary lymphedema though activating PPARγ signaling, offering novel insights and strategies for fibrotic disorders.

The translational potential of this article:

This study demonstrated that targeted inhibition of the EZH2-PPARγ axis effectively inhibited fibrogenic differentiation of AdMSCs and reduced fibroadipose tissue in secondary lymphedema, indicating it is a promising strategy for secondary lymphedema treatment, offering novel insights and strategy for musculoskeletal fibrotic disorders.

01 Nov 2025·BIOMEDICINE & PHARMACOTHERAPY

Transcriptomic profiling of organoids derived from malignant effusions uncovers lncRNA MEG3 and target genes potentially involved in platinum resistance in serous ovarian carcinoma

Article

Author: Jensen, Lars Henrik ; Fokdal, Lars Ulrik ; Calanca, Naiade ; Steffensen, Karina Dahl ; Rogatto, Silvia Regina ; Villacis, Rolando André Rios ; Kuasne, Hellen ; Bizinelli, Daniela ; Aagaard, Mads Malik ; Côrtes, Luiza ; Rainho, Claudia Aparecida ; Maeda, Debora Kazumi

Serous ovarian carcinoma (SOC) is an aggressive disease, characterized by advanced-stage tumors that are often associated with relapse and poor outcomes. Although platinum-based chemotherapy is a cornerstone of the treatment, most of the relapsed tumors become resistant to these agents. We explored organoids derived from SOC malignant effusions to identify targets actionable by epigenetic drugs (epi-drugs) to enhance platinum response. Tumor-derived organoids (TDOs) were established using malignant effusions of SOC patients. Histological and transcriptomic (RNA-Seq) characterization (18 TDOs versus 7 normal ovarian samples) was performed, followed by cross-validation with external RNA-Seq datasets (337 SOC samples, 4 TDOs, and 180 normal tissues). Predicted interactions between long noncoding RNAs (lncRNAs) and epigenetic effectors were investigated. We selected the epi-drugs decitabine and tazemetostat, whose targets were overexpressed in SOC, to treat carboplatin-resistant SOC cell lines and TDOs. Subsequently, these models were challenged with carboplatin. Twelve lncRNAs and 168 protein-coding genes differentially expressed were involved in epigenetic regulation. Abnormal expression levels of lncRNA MEG3 and epigenetic effectors DNMT3B and EZH2 were confirmed in external datasets. Increased carboplatin sensitivity and MEG3 upregulation were observed after treating the cell lines and TDOs with epi-drugs. Altogether, our findings provide novel insights into using organoids derived from malignant effusions as preclinical models and hint at potential targets for overcoming platinum resistance in SOC.

News (Medical) associated with Tazemetostat Hydrobromide

08 Dec 2025

·www.globenewswire.com

HUTCHMED Announces Expanded Coverage on National Reimbursement Drug List and Inclusion in the First Commercial Insurance Drug List in China

HONG KONG and SHANGHAI and FLORHAM PARK, N.J., Dec. 08, 2025 (GLOBE NEWSWIRE) -- HUTCHMED (China) Limited (“HUTCHMED”) (Nasdaq/AIM:HCM; HKEX:13) today announces that following the contract renewal with the China National Healthcare Security Administration (“NHSA”), the updated National Reimbursement Drug List (“NRDL”) effective on January 1, 2026 will continue to include ELUNATE®, ORPATHYS® and SULANDA®. In addition, TAZVERIK® will be included in the first edition of the National Commercial Health Insurance Innovative Drug List (“Commercial Insurance Drug List”). ELUNATE® (fruquintinib) is included for the treatment of patients with advanced endometrial cancer with Mismatch Repair proficient (pMMR) tumors that have failed prior systemic therapy and are not candidates for curative surgery or radiation, in combination with TYVYT® (sintilimab injection). It is also renewed for the treatment of patients with metastatic colorectal cancer who have previously received fluoropyrimidine, oxaliplatin and irinotecan-based chemotherapy, and those who have previously received or are not suitable for receiving anti-VEGF therapy or anti-epidermal growth factor receptor (EGFR) therapy (RAS wild-type). ORPATHYS® (savolitinib) is included for treatment of adult patients with locally advanced or metastatic non-small cell lung cancer with MET exon 14 skipping alteration. SULANDA® (surufatinib) is renewed for the treatment of patients with unresectable; locally advanced or metastatic; progressive non-functional, well-differentiated (G1 or G2) pancreatic and non-pancreatic neuroendocrine tumors. TAZVERIK® (tazemetostat) is included in the Commercial Insurance Drug List for the treatment of adult patients with relapsed or refractory follicular lymphoma with EZH2 mutation who have received at least two prior systemic therapies. In July 2025, the NHSA issued the 2025 Adjustment Work Plan for the NRDL and the Commercial Health Insurance Innovative Drug List, announcing the establishment of the new Commercial Insurance Drug List. This list, together with the NRDL, forms a key component of China’s multi-level medical insurance system. This new list focuses on medicines with high innovation and significant clinical value that fall beyond the scope of basic medical insurance, including certain high-cost oncology drugs, gene therapies, and rare disease therapies, enabling reimbursement through commercial health insurance products such as high-limit medical insurance, inclusive health plans (“Huiminbao”) and group health insurance. This multi-layered reimbursement framework enhances patient access to breakthrough treatments while supporting the sustainable development of China’s innovative pharmaceutical sector. About NRDL The government in China has placed great importance on improving the affordability of drug treatments for the public. As of end of 2024, 1.33 billion people in China had basic medical insurance coverage, representing around 95% of the entire population. The NRDL is updated every year, and inclusion on the list is subject to renewal every two years. The NHSA annually convenes a broad network of experts in medicine, pharmacology, pharmacoeconomics and actuarial valuation to identify innovative medicines to consider for NRDL inclusion. Reimbursement of Category B medicines, including novel oncology medicines, requires varying degrees of copayment from patients, depending on their provinces or types of NHSA insurance scheme enrollment. About Fruquintinib Fruquintinib is a selective oral inhibitor of all three vascular endothelial growth factor receptors (“VEGFR”) -1, -2 and -3. Fruquintinib is co-developed and co-commercialized in China by HUTCHMED and Eli Lilly and Company under the brand name ELUNATE®. Takeda holds the exclusive worldwide license to further develop, commercialize, and manufacture fruquintinib outside mainland China, Hong Kong and Macau, marketing it under the brand name FRUZAQLA®. About Savolitinib Savolitinib is an oral, potent and highly selective MET tyrosine kinase inhibitor that has demonstrated clinical activity in advanced solid tumors. It blocks atypical activation of the MET receptor tyrosine kinase pathway that occurs because of mutations (such as exon 14 skipping alterations or other point mutations), gene amplification or protein overexpression. Savolitinib is being jointly developed by AstraZeneca and HUTCHMED, and commercialized by AstraZeneca under the brand name ORPATHYS®. About Surufatinib Surufatinib is a novel, oral angio-immuno kinase inhibitor that selectively inhibits the tyrosine kinase activity associated with VEGFRs and fibroblast growth factor receptor (FGFR), which both inhibit angiogenesis, and colony stimulating factor-1 receptor (CSF-1R), which regulates tumor-associated macrophages, promoting the body’s immune response against tumor cells. Surufatinib is marketed in China by HUTCHMED under the brand name SULANDA®. HUTCHMED currently retains all rights to surufatinib worldwide. About Tazemetostat Tazemetostat is a first-in-class methyltransferase inhibitor of EZH2 developed by Epizyme, an Ipsen company. HUTCHMED entered into a strategic collaboration with Epizyme to research, develop, manufacture and commercialize tazemetostat in Chinese Mainland, Hong Kong, Macau and Taiwan. About HUTCHMED HUTCHMED (Nasdaq/AIM:HCM; HKEX:13) is an innovative, commercial-stage, biopharmaceutical company. It is committed to the discovery and global development and commercialization of targeted therapies and immunotherapies for the treatment of cancer and immunological diseases. Since inception it has focused on bringing drug candidates from in-house discovery to patients around the world, with its first three medicines marketed in China, the first of which is also approved around the world including in the US, Europe and Japan. For more information, please visit: www.hutch-med.com or follow us on LinkedIn. Forward-Looking Statements This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the U.S. Private Securities Litigation Reform Act of 1995. These forward-looking statements reflect HUTCHMED’s current expectations regarding future events, including its expectations for the commercialization of fruquintinib, savolitinib, surufatinib and tazemetostat in China, the potential benefits and further clinical development of fruquintinib, savolitinib, surufatinib and tazemetostat, its expectations as to whether further studies would meet their primary or secondary endpoints, and its expectations as to the timing of the completion and the release of results from such studies. Forward-looking statements involve risks and uncertainties. Such risks and uncertainties include, among other things, assumptions regarding the commercial acceptance of fruquintinib, savolitinib, surufatinib and tazemetostat, the impact of the inclusion of fruquintinib, savolitinib and surufatinib on the NRDL and tazemetostat on the Commercial Health Insurance Innovative Drug List on sales of the drug and its pricing, clinical trial enrollment rates, timing and availability of subjects meeting a study’s inclusion and exclusion criteria, changes to clinical protocols or regulatory requirements, unexpected adverse events or safety issues, the ability of fruquintinib, savolitinib, surufatinib and tazemetostat to obtain regulatory approval for a targeted indication in different jurisdictions and the sufficiency of funding. In addition, as certain studies rely on the use of other drug products such as sintilimab as combination therapeutics, such risks and uncertainties include assumptions regarding their safety, efficacy, supply and continued regulatory approval. Existing and prospective investors are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. For further discussion of these and other risks, see HUTCHMED’s filings with the US Securities and Exchange Commission, The Stock Exchange of Hong Kong Limited and on AIM. HUTCHMED undertakes no obligation to update or revise the information contained in this press release, whether as a result of new information, future events or circumstances or otherwise. Medical Information This press release contains information about products that may not be available in all countries, or may be available under different trademarks, for different indications, in different dosages, or in different strengths. Nothing contained herein should be considered a solicitation, promotion or advertisement for any prescription drugs including the ones under development. CONTACTS Investor Enquiries+852 2121 8200 / ir@hutch-med.com Media Enquiries FTI Consulting –+44 20 3727 1030 / HUTCHMED@fticonsulting.comBen Atwell / Tim Stamper+44 7771 913 902 (Mobile) / +44 7421 898 348 (Mobile)Brunswick – Zhou Yi+852 9783 6894 (Mobile) / HUTCHMED@brunswickgroup.com Panmure LiberumNominated Advisor and Joint BrokerAtholl Tweedie / Emma Earl / Rupert Dearden+44 20 7886 2500 CavendishJoint BrokerGeoff Nash / Nigel Birks+44 20 7220 0500 Deutsche NumisJoint BrokerFreddie Barnfield / Jeffrey Wong / Duncan Monteith+44 20 7260 1000

License out/inImmunotherapyDrug Approval

25 Nov 2025

·www.businesswire.com

BostonGene to Showcase Transformative Impact of AI-Driven Profiling with Six Abstracts at the 67th American Society of Hematology Annual Meeting & Exposition

WALTHAM, Mass.--(BUSINESS WIRE)--BostonGene, a leading provider of AI-driven molecular and immune profiling solutions, today announced the selection of two abstracts for oral presentation, three abstracts for poster presentation and one abstract for online publication at the 67th American Society of Hematology (ASH) Annual Meeting and Exposition, which will be held December 6-9, 2025, in Orlando, Florida. BostonGene will exhibit in booth #1581. Our AI-powered tools, such as the Lymphly classifier and our B-cell-based marker provide the molecular precision required to de-risk clinical programs and ensure the right drug reaches the right patient subpopulation. “The research we are presenting highlights the critical need for advanced patient stratification in hematology. Our AI-powered tools, such as the Lymphly classifier and our B-cell-based marker provide the molecular precision required to de-risk clinical programs and ensure the right drug reaches the right patient subpopulation. This is about moving beyond conventional diagnostics to build a foundational, integrated approach for effective companion diagnostics and unified monitoring in drug studies,” said Nathan Fowler, MD, Chief Medical Officer at BostonGene. Details of the presentations are below: Oral presentations: Abstract number: 14219 Title: Acalabrutinib plus rituximab followed by brexucabtagene autoleucel for frontline treatment of high-risk mantle cell lymphoma: The WINDOW-3 clinical trial Date & time: December 7 — 5:45 PM – 6:00 PM Location: Tangerine Ballroom F2 Speaker: Preetesh Jain, MD, DM, PhD, The University of Texas MD Anderson Cancer Center The WINDOW-3 clinical trial evaluating acalabrutinib plus rituximab followed by brexucabtagene autoleucel CART in patients with high-risk mantle cell lymphoma (MCL) demonstrated strong efficacy and encouraging survival outcomes. BostonGene’s AI-based immunoprofiling revealed CART therapy in high-risk MCL led to drastic immune remodeling, with specific CART-cell types and memory subsets correlating with toxicity, indicating a key role in immune system monitoring for treatment-related toxicities. Research conducted in collaboration with MD Anderson Cancer Center Abstract number: 7242 Title: A phase 1b trial of the EZH2 inhibitor tazemetostat combined with CAR T cell therapy in B cell lymphomas Date & time: December 8 — 5:00 PM – 5:15 PM Location: OCCC - Tangerine Ballroom F3-4 Speaker: Samuel Yamshon, MD, Weill Cornell Medical College Based on the premise that inhibition of EZH2 prevents T cell exhaustion and modulates T cell activity, the phase I study administered tazemetostat with CAR-T in patients with B-cell lymphoma. The combination resulted in an impressive 100% response rate with no signal of additional toxicity. BostonGene’s novel immunophenotyping is being performed to demonstrate the immune modulatory effects of combination therapy, providing mechanistic rationale for further combination approaches. Research conducted in collaboration with Weill Cornell Medical Center Poster presentations: Abstract number: 1837 Title: Refining diffuse large B-cell lymphoma subtyping using Lymphly, an evidence-based classifier Date & time: December 6 — 5:30 PM - 7:30 PM Speaker: Nikita Kotlov, MS, BostonGene BostonGene developed Lymphly, an AI hierarchical classifier for diffuse large B-cell lymphoma (DLBCL), to resolve genetically heterogeneous and atypical tumors often missed by existing classifications. By integrating pathway-relevant genomic alterations into a transparent framework, Lymphly distinguishes both established and emerging subtypes, including high-risk TP53+ and MYC+ groups, offering refined molecular stratification for clinical trial design, treatment selection and targeted therapy development. Abstract number: 2692 Title: A genetic comparison of Epstein-Barr virus-associated polymorphic lymphoproliferative disorder and diffuse large B cell lymphoma Date & time: December 6 — 5:30 PM - 7:30 PM Speaker: Jennifer Chapman, MD, University of Miami and Sylvester Comprehensive Cancer Center BostonGene’s multimodal platform with integrated genomic, transcriptomic and immune data was used to analyze and compare Epstein-Barr virus (EBV)-positive lymphoproliferative disorder and diffuse large B-cell lymphoma. This study underscored the complexity of EBV-driven diseases and highlighted the need for improved classification strategies, demonstrating the potential of BostonGene’s AI-powered platform to advance precision diagnostics and improve patient outcomes. Research done in collaboration with the University of Miami Sylvester Cancer Institute Abstract number: 12996 Title: An immunometabolic companion biomarker to enhance FDG-PET interpretation and guide frontline therapy in follicular lymphoma Date & time: December 8 — 6:00 PM - 8:00 PM Speaker: Joshua W.D. Tobin, MD, MSc, Princess Alexandra Hospital, Mater Research Institute In collaboration with MD Anderson and several hospitals and academic institutions in Australia, BostonGene leveraged its multimodal pipeline to design a B cell-based candidate biomarker in patients with follicular lymphoma treated with bendamustine-based immunochemotherapy (ICT). Represented by centroblast (CB) scores, this biomarker identifies patients with high-grade disease who may respond to bendamustine-based ICT. Independent of and additive to pre-treatment PET, the CB score was highly prognostic suggesting a potential role for patient stratification. Research done in collaboration with the University of Queensland Online only Title: Replacing FISH with a comprehensive integrated approach for tumor genotyping and immune monitoring in multiple myeloma BostonGene’s integrated platform, combining whole exome and RNA sequencing of tumor (CD138⁺ plasma cells) and peripheral blood samples, reproduced FISH-detectable abnormalities (e.g., del17p/TP53 deletion or t(11;14) translocations) and revealed additional mutations, structural variants and immune signatures in multiple myeloma patients, including low-tumor-content samples. By overcoming limitations of conventional FISH, BostonGene’s approach may provide a scalable solution and broader diagnostic capabilities for unified genomic and immune monitoring in clinical trials and patient care. Research done in collaboration with the University of Miami Sylvester Cancer Institute In addition to the poster presentations, the abstracts are published online in the November supplemental issue of Blood. About BostonGene Corporation BostonGene is redefining cancer patient care and drug development through the integration of omnimodal data and artificial intelligence. Built and validated through an extensive real-world clinical testing network, BostonGene’s Foundation Model of cancer and the immune system integrates genomic, transcriptomic, and immune data with clinical outcomes to generate biologically grounded, actionable insights. These insights enable biopharma partners to design and de-risk trials, identify novel targets, and optimize therapeutic response prediction across all stages of development while simultaneously improving patient care through clinically integrated innovation. For more information, visit www.BostonGene.com.

ImmunotherapyClinical ResultPhase 1Cell TherapyASH

28 Apr 2025

·www.globenewswire.com

Arvinas Shares New Preclinical Combination Data for the PROTAC BCL6 Degrader, ARV-393, at the 2025 American Association for Cancer Research Annual Meeting

– ARV-393 demonstrated strong synergistic antitumor activity, including complete regressions, in combination with standard-of-care chemotherapy, biologics, and select investigational oral small molecule inhibitors – – Findings support continued evaluation of ARV-393 combinations in non-Hodgkin lymphoma – NEW HAVEN, Conn., April 28, 2025 (GLOBE NEWSWIRE) -- Arvinas, Inc. (Nasdaq: ARVN), a clinical-stage biotechnology company working to develop a new class of drugs based on targeted protein degradation, today presented data from preclinical combination studies of ARV-393, the company’s investigational PROteolysis TArgeting Chimera (PROTAC) B-cell lymphoma 6 protein (BCL6) degrader. BCL6 is a transcriptional repressor protein and a known driver of B-cell lymphomas. Data demonstrated synergistic antitumor activity, including complete regressions, in combination with standard of care (SOC) chemotherapy, SOC biologics, and investigational oral small molecule inhibitors (SMIs) in high grade B-cell lymphoma (HGBCL) and aggressive diffuse large B-cell lymphoma (DLBCL) models. The results from these preclinical studies were shared in a poster presentation at the 2025 American Association for Cancer Research (AACR) annual meeting in Chicago, Illinois. Key findings from the studies included: ARV-393 in combination with SOC chemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone [R-CHOP]), induced significantly greater tumor growth inhibition compared with rituximab, CHOP, R-CHOP, or ARV-393 alone, with complete tumor regressions in all mice treated with the ARV-393 and R-CHOP combination.ARV-393 in combination with SOC biologics targeting CD20 (rituximab), CD19 (tafasitamab), or CD79b (polatuzumab vedotin) resulted in tumor regressions and demonstrated significantly stronger tumor growth inhibition compared with each agent alone.In preclinical models, ARV-393 increased CD20 expression, providing additional support for the exploration of combinations with CD20-targeted agents and in the context of low or loss of CD20 expression.ARV-393 in combination with investigational small molecule inhibitors targeting clinically validated oncogenic drivers of lymphoma, such as BTK (acalabrutinib), BCL2 (venetoclax), or EZH2 (tazemetostat), resulted in superior tumor growth inhibition compared with each agent alone, with tumor regressions in all mice treated with the combinations. “Given that combination regimens are the foundation of lymphoma treatment, we are encouraged by the strength of these preclinical combination data, which demonstrate complete tumor regressions in aggressive lymphoma models,” said Noah Berkowitz, M.D., Ph.D., Chief Medical Officer at Arvinas. “We believe these preclinical data demonstrate potential for broad combinability of ARV-393 and provide a compelling rationale for considering combination strategies as we work to bring forward new therapeutic options for lymphoma patients.” A Phase 1 study of ARV-393 is enrolling patients with relapsed/refractory non-Hodgkin lymphoma, including DLBCL (NCT06393738). Additional detail on the ARV-393 data presentation at AACR 2025: Poster Title: ARV-393, a PROteolysis TArgeting Chimera (PROTAC) BCL6 Degrader, Combined With Biologics or Small-Molecule Inhibitors Induces Tumor Regressions in Diffuse Large B-Cell Lymphoma ModelsAbstract: 1655Session Title: Degraders and Glues 2 Session Type: Experimental and Molecular TherapeuticLocation: Poster Section 18Poster Board Number: 15Date: Monday, April 28, 2025Lecture Time: 9:00 a.m. – 12:00 p.m. CT About ARV-393ARV-393 is an investigational, orally bioavailable PROteolysis TArgeting Chimera (PROTAC) designed to degrade B-cell lymphoma 6 protein (BCL6), a transcriptional repressor and major driver of B-cell lymphomas. During B-cell development, tightly controlled BCL6 protein expression regulates >600 genes to facilitate rapid B-cell proliferation and tolerance of somatic hypermutation and gene recombination for antibody generation. Deregulated BCL6 expression is common in B-cell lymphoma and promotes cancer cell survival, proliferation, and genomic instability. PROTAC-mediated degradation has the potential to address the historically undruggable nature of BCL6. ARV-393 is currently in a Phase 1 clinical trial in patients with relapsed/refractory non-Hodgkin lymphoma. About ArvinasArvinas (Nasdaq: ARVN) is a clinical-stage biotechnology company dedicated to improving the lives of patients suffering from debilitating and life-threatening diseases. Through its PROteolysis TArgeting Chimera (PROTAC) protein degrader platform, the Company is pioneering the development of protein degradation therapies designed to harness the body’s natural protein disposal system to selectively and efficiently degrade and remove disease-causing proteins. Arvinas is currently progressing multiple investigational drugs through clinical development programs, including vepdegestrant, targeting the estrogen receptor for patients with locally advanced or metastatic ER+/HER2- breast cancer; ARV-393, targeting BCL6 for relapsed/refractory non-Hodgkin Lymphoma; and ARV-102, targeting LRRK2 for neurodegenerative disorders. Arvinas is headquartered in New Haven, Connecticut. For more information about Arvinas, visit www.arvinas.com and connect on LinkedIn and X. Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995 that involve substantial risks and uncertainties, including statements regarding the potential for Arvinas’ investigational oral PROteolysis TArgeting Chimera (PROTAC) degrader ARV-393 to treat relapsed/refractory non-Hodgkin lymphoma; the preclinical data for ARV-393 demonstrating the potential for broad combinability and supporting continued evaluation of ARV-393 combinations in non-Hodgkin lymphoma associated with B-cell lymphoma 6 protein (“BCL6”) dysfunction; and PROTAC-mediated degradation having the potential to address the historically undruggable nature of BCL6.. All statements, other than statements of historical facts, contained in this press release, including statements regarding Arvinas’ strategy, future operations, future financial position, future revenues, projected costs, prospects, plans and objectives of management, are forward-looking statements. The words “anticipate,” “believe,” “estimate,” “expect,” “intend,” “may,” “might,” “plan,” “predict,” “project,” “target,” “potential,” “will,” “would,” “could,” “should,” “continue,” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Arvinas may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on such forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements Arvinas makes as a result of various risks and uncertainties, including but not limited to: whether Arvinas will be able to successfully conduct and complete development for its product candidates, including ARV-393, including whether Arvinas initiates and completes clinical trials for its product candidates and receives results from its clinical trials on its expected timelines or at all; Arvinas’ ability to protect its intellectual property portfolio; whether Arvinas’ cash and cash equivalent resources will be sufficient to fund its foreseeable and unforeseeable operating expenses and capital expenditure requirements; and other important factors discussed in the “Risk Factors” section of Arvinas’ Annual Report on Form 10-K for the year ended December 31, 2024 and subsequent other reports on file with the U.S. Securities and Exchange Commission. The forward-looking statements contained in this press release reflect Arvinas’ current views with respect to future events, and Arvinas assumes no obligation to update any forward-looking statements, except as required by applicable law. These forward-looking statements should not be relied upon as representing Arvinas’ views as of any date subsequent to the date of this release. Contacts:Investors:Jeff Boyle+1 (347) 247-5089Jeff.Boyle@arvinas.com Media:Kirsten Owens+1 (203) 584-0307Kirsten.Owens@arvinas.com

Phase 1AACRPROTACs

100 Deals associated with Tazemetostat Hydrobromide

External Link

KEGG	Wiki	ATC	Drug Bank
D11485	Tazemetostat Hydrobromide	L01	DB12887

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Follicular Lymphoma	United States	Epizyme, Inc.	18 Jun 2020
Sarcoma	United States	Epizyme, Inc.	23 Jan 2020

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Refractory Follicular Lymphoma	Phase 3	United States	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	China	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Australia	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Belgium	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Brazil	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Canada	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	France	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Germany	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Hungary	Epizyme, Inc.	11 Jun 2020
Refractory Follicular Lymphoma	Phase 3	Italy	Epizyme, Inc.	11 Jun 2020

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ASH2025	Phase 1	B-Cell Lymphoma	13	Tazemetostat + CAR T cell therapy (DLBCL)	fxsvlebgsg(lkfgmwxxnk) = hzxuahygfp hsqfrmmocm (grvyrqbljr )	Positive	06 Dec 2025
				Tazemetostat + CAR T cell therapy (FL)	fxsvlebgsg(lkfgmwxxnk) = kbnnhmwtss hsqfrmmocm (grvyrqbljr )
NCT05467943 \| NCT04224493 (Pubmed \| EClinicalMedicine)	Phase 2	Follicular Lymphoma EZH2-mutant \| EZH2 wild-type	42	Tazemetostat 800 mg (EZH2 mutant)	gluzdzsxno(fyinhhbrcs) = nlwxosnqer srolqjrzdq (mpbjjutumw, 40.7 - 82.8) View more	Positive	01 Sep 2025
				Tazemetostat 800 mg (EZH2 wild-type)	gluzdzsxno(fyinhhbrcs) = flrxqbqepg srolqjrzdq (mpbjjutumw, 15.4 - 59.2) View more
NCT05467943 (EClinicalMedicine) Manual	Phase 2	Follicular Lymphoma EZH2 Mutation \| EZH2 Gene Mutation Negative	42	Tazemetostat 800 mg (EZH2 mutation)	wmjkzquaob(aqqzygcrxl) = rhyuxpiztf jtxyvicnxc (femagpwmhc, 40.7 - 82.8) View more	Positive	18 Aug 2025
				Tazemetostat 800 mg (EZH2 wild-type)	wmjkzquaob(aqqzygcrxl) = vngclcehjr jtxyvicnxc (femagpwmhc, 15.4 - 59.2) View more
ASCO2025	Not Applicable	Follicular Lymphoma \| Diffuse Large B-Cell Lymphoma	306	Tazemetostat as monotherapy	wvzbxabvcq(tsoozrvfgi) = pooled value of 84.5% at 12 months zfmeuutijp (ictugijjqi )	Positive	30 May 2025
				Tazemetostat in combination therapy
ASCO2025	Phase 1/2	B-Cell Lymphoma mutant EZH2	241	Tazemetostat 800 mg twice daily	uuyfuwsnak(fgdhipfibm) = ebyxslufbq rrnsudhnzg (sedztzjkol, 29.4 - 69.9) View more	Positive	30 May 2025
NCT05467943 (PF910, EHA2025)	Phase 2	Refractory Follicular Lymphoma EZH2MUT	22	TAZEMETOSTAT 800 mg	xfxpapelit(peekkuctnq) = ziwsytdgof dmkljhgsyo (iyboacgfhx, 40.7% - 82.8) View more	Positive	14 May 2025
NCT02601950 (CTgov)	Phase 2	Typical Teratoid Rhabdoid Tumor \| Chordoma \| Renal Medullary Carcinoma ... View more	267	tazemetostat (Rhabdoid Tumors: Cohort 1)	ehtxfvocvx = iuonazodyr dhekbbyvuq (lbzzvewyhq, ttopobdkqx - pkxmaicfuw) View more	-	11 Mar 2025
				tazemetostat (Other INI1-negative: Cohort 3)	ehtxfvocvx = igegjpoqke dhekbbyvuq (lbzzvewyhq, dvouojmfwo - ltcbctsdor) View more
NCT03348631 (CTgov)	Phase 2	Recurrent Ovarian Clear Cell Adenocarcinoma \| Endometrial Endometrioid Adenocarcinoma \| Recurrent ovarian cancer ... View more	62	Tazemetostat (Arm I: Treatment (Tazemetostat) in Endometrial Cancer Patients)	pzvehznouz = xeaxevenpm kuujhwthkl (qehzyvaeiy, trzizjedxk - sffqaxlpxb) View more	-	06 Mar 2025
				Tazemetostat (Arm II: Treatment (Tazemetostat) Ovarian in Cancer Patients)	pzvehznouz = fsutaqwfyg kuujhwthkl (qehzyvaeiy, raopaxjqzk - tncysuqeyx) View more
ASH2024	Not Applicable	Follicular Lymphoma	-	Tazemetostat 800mg BID	zwhqekmmfn(kwmomtrtfc) = leukopenia (n=2), neutropenia (n=1), anemia (n=1), atrial fibrillation (n=1), bone pain (n=1), infection (n=2), and infusion related reaction (n=1) vuxjmezvmq (yswfvyucid ) View more	-	09 Dec 2024
NCT04179864 (EZH-1101, ESMO2024) Manual	Phase 1/2	Metastatic castration-resistant prostate cancer	81	TAZ 1200 mg BID plus ENZ 160 mg QD	mpnclvfnmb(qttnpkdzsc) = uxcqnzkkxy pqonbazczl (buoxcixmqt, 8.5 - NE) View more	Negative	15 Sep 2024
				ENZ 160 mg QD	mpnclvfnmb(qttnpkdzsc) = edrvbipuvl pqonbazczl (buoxcixmqt, 6.6 - NE) View more

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