A Phase 2/3 Randomized Trial Investigating Daratumumab on a Modified Augmented BFM (aBFM) Backbone in Newly Diagnosed T-Lymphoblastic Leukemia (T-ALL) and T-Lymphoblastic Lymphoma (T-LL)

This phase II/III trial tests the addition of daratumumab to chemotherapy for treating patients with newly-diagnosed T-ALL and T-LL. Daratumumab is in a class of medications called monoclonal antibodies. It binds to a protein called CD38, which is found on some types of immune cells and cancer cells. Daratumumab may block CD38 and help the immune system kill cancer cells. Chemotherapy drugs work in different ways to stop the growth of cancer cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Giving chemotherapy with daratumumab may kill more cancer cells.

Start Date28 Jun 2026

Sponsor / Collaborator

The Children's Oncology Group Foundation, Inc.

NCT07220187

/ Not yet recruitingPhase 3IIT

A Randomized Phase III Study of Pirtobrutinib Plus R-CHOP vs. R-CHOP for Participants With Previously Untreated Richter Transformation (PIRAMID)

This phase III trial compares the effect of adding pirtobrutinib to the usual treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) to R-CHOP alone for the treatment of Richter transformation, which is when chronic lymphocytic leukemia or small lymphocytic lymphoma turns into large B-cell lymphoma, a more aggressive (faster-growing) form of lymphoma. Pirtobrutinib may stop the growth of cancer cells by blocking some of the enzymes needed for cell growth. Rituximab is a monoclonal antibody. It binds to a protein called CD20, which is found on B cells (a type of white blood cell) and some types of cancer cells. This may help the immune system kill cancer cells. Cyclophosphamide is in a class of medications called alkylating agents. It works by damaging the cell's DNA and may kill cancer cells. It may also lower the body's immune response. Doxorubicin is in a class of medications called anthracyclines. Doxorubicin damages the cell's DNA and may kill cancer cells. It also blocks a certain enzyme needed for cell division and DNA repair. Vincristine is in a class of medications called vinca alkaloids. It works by stopping cancer cells from growing and dividing and may kill them. Prednisone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Adding pirtobrutinib to R-CHOP may kill more cancer cells than R-CHOP alone in patients with Richter transformation.

Start Date02 May 2026

Sponsor / Collaborator

SWOG

[+1]

NCT07278856

/ Not yet recruitingPhase 1IIT

Ruxolitinib in Combination With Chemotherapy for Untreated Nodal T-Follicular Helper (TFH) Cell Lymphomas

This phase I trial tests the safety, side effects and best dose of ruxolitinib in combination with cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) chemotherapy and how well the combination works in treating patients with untreated nodal T-follicular helper (TFH) cell lymphoma. Ruxolitinib phosphate blocks a protein called janus kinase, which may help keep abnormal blood cells or cancer cells from growing. It may also lower the body's immune response. Ruxolitinib phosphate is a type of tyrosine kinase inhibitor. Cyclophosphamide is in a class of medications called alkylating agents. It works by damaging the cell's deoxyribonucleic acid (DNA) and may kill cancer cells. It may also lower the body's immune response. Doxorubicin damages the cell's DNA and may kill cancer cells. It also blocks a certain enzyme needed for cell division and DNA repair. Doxorubicin is a type of anthracycline antitumor antibiotic. Vincristine is in a class of medications called vinca alkaloids. It works by stopping cancer cells from growing and dividing and may kill them. Prednisone is in a class of medications called corticosteroids. It is used to reduce inflammation and lower the body's immune response to help lessen the side effects of chemotherapy drugs. Giving ruxolitinib in combination with CHOP chemotherapy may be safe, tolerable, and/or effective in treating patients with untreated nodal TFH cell lymphoma.

Start Date27 Apr 2026

Sponsor / Collaborator

City of Hope National Medical Center

[+1]

100 Clinical Results associated with Vincristine Sulfate

100 Translational Medicine associated with Vincristine Sulfate

100 Patents (Medical) associated with Vincristine Sulfate

12,869

Literatures (Medical) associated with Vincristine Sulfate

01 Feb 2026·Current Neuropharmacology

Celastrol Ameliorates Vincristine-induced Neuropathic Pain by Inhibiting Spinal Astrocyte Hyperactivation-mediated Inflammation, Oxidative Stress, and Apoptosis

Article

Author: Hu, Ya-Hui ; Xu, Jing ; Li, Yun-Man ; Li, Gui-Zhou

Background::

Neurotoxicity is the severe adverse reaction induced by chemotherapy drugs, characterized by neuropathic pain. However, there is a notable lack of therapeutic drugs for chemotherapy-induced neuropathic pain (CINP). Celastrol, a naturally occurring terpenoid active compound extracted from the roots of Tripterygium wilfordii Hook f., exhibits a neuroprotective effect, yet its therapeutic potential in CINP has not been reported.

Objective::

In this study, with vincristine-induced neuropathic pain (VINP) as a model, we aimed to investigate the therapeutic effect of celastrol on VINP and its specific mechanisms.

Methods::

Vincristine (VCR, 0.1 mg/kg, intraperitoneal injection) was used to induce a neuropathic pain model. Celastrol (0.5, 1.0, and 2.0 mg/kg, intraperitoneal injection) was administered to assess its therapeutic effects on vincristine-induced neuropathic pain (VINP). Transmission electron microscopy (TEM) was employed to examine damage to the sciatic nerve fibers and mitochondria. Flow cytometry was used to detect mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and cell apoptosis. Primary astrocyte cultures were utilized further to validate the therapeutic mechanisms of celastrol in VINP.

Results::

Here, we demonstrate that celastrol inhibits vincristine (VCR)-induced activation of spinal astrocytes by suppressing CaMKII phosphorylation. Additionally, celastrol alleviates the Cx43- dependent inflammation caused by VCR through the inhibition of the CaMKII/NF-κB signaling pathway. Concurrently, celastrol modulates the production of reactive oxygen species (ROS) and the expression of apoptosis-related proteins (Cleaved Caspase-3, Bax, and Bcl-2) by suppressing the phosphorylation of CaMKII in astrocytes, thereby ameliorating the mitochondrial damage and cell apoptosis caused by VCR.

Conclusion::

Our findings reveal that celastrol exerts therapeutic effects on VINP through its antiinflammatory, antioxidant, and anti-apoptotic properties. Furthermore, we preliminarily explore the molecular mechanisms underlying these effects, thereby providing a scientific basis for celastrol as a potential therapeutic agent for CINP.

01 Feb 2026·BIOCHEMICAL GENETICS

Computational Elucidation of Hub Genes and Pathways Correlated with the Development of 5-Fluorouracil Resistance in HCT 116 Colorectal Carcinoma Cell Line

Article

Author: Lim, Siew Huah ; Tan, Chun Hoe ; Sim, Kae Shin

Colorectal cancer (CRC) is the third most deadly cancer diagnosed in both men and women. 5-Fluorouracil (5-FU) treatment frequently causes the CRC cells to become chemoresistance, which has a negative impact on prognosis. Using bioinformatic techniques, this work describes important genes and biological pathways linked to 5-FU resistance in CRC cells. In our studies, a 5-FU-resistant HCT 116 cell line exhibiting elevated TYMS was created and validated using various tests. Bioinformatic studies were conducted to determine which differentially expressed genes (DEGs) were responsible for the establishment of 5-FU resistance in the same cell line. After screening 3949 DEGs from the two public datasets (GSE196900 and GSE153412), 471 overlapping DEGs in 5-FU-resistant HCT 116 cells were chosen. These overlapping DEGs were used to build the PPI network, and a major cluster module containing 21 genes was found. Subsequently, using three topological analysis algorithms, 10 hub genes were identified, which included HLA-DRA, HLA-DRB1, CXCR4, MMP9, CDH1, SMAD3, VIM, SYK, ZEB1, and SELL. Their roles were ascertained by utilizing Gene Ontology keywords and pathway enrichment studies. Our results also demonstrated that the miRNA and transcription factors (TFs) that had the strongest connection with the hub genes were hsa-mir-26a-5p, hsa-mir-30a-5p, RELA, and NFKB1. Ultimately, 84 FDA-approved drugs that target those hub genes were found to potentially treat 5-FU resistance CRC. Our research's findings increase our understanding of the fundamental factors that contribute to the prevalence of 5-FU resistance CRC, which could ultimately assist in the identification of valuable malignancy biomarkers and targeted treatment approaches based on key regulatory pathways.

27 Jan 2026·Blood Advances

Population-wide introduction of dose-adjusted EPOCH-R in high-grade B-cell lymphoma with MYC / BCL2 rearrangements, DLBCL morphology

Article

Author: Slack, Graham W. ; Jiang, Aixiang ; Collinge, Brett ; Ben-Neriah, Susana ; Alduaij, Waleed ; Farinha, Pedro ; Mungall, Andrew J. ; Scott, David W. ; Champagne, Jean-Nicolas ; Meissner, Barbara ; Hilton, Laura K. ; Freeman, Ciara L. ; Craig, Jeffrey W. ; Boyle, Merrill ; Villa, Diego ; Gerrie, Alina S. ; Steidl, Christian ; Savage, Kerry J. ; Sehn, Laurie H.

Abstract:

High-grade B-cell lymphoma with "double-hit" MYC and BCL2 rearrangements (HGBCL-DH-BCL2) is associated with poor outcomes following standard chemoimmunotherapy, prompting dose-intensive regimen use. However, the benefit of intensification is unclear due to rarity precluding randomized trials, and selection bias in retrospective comparisons. In 2015, BC Cancer introduced a provincial guideline recommending dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (DA-EPOCH-R) for fit patients aged ≤75 years with HGBCL-DH-BCL2 identified by routine cytogenetic testing. To assess this guideline’s impact, we compared the outcomes of patients with de novo HGBCL-DH-BCL2 tumors of diffuse large B-cell lymphoma (DLBCL) morphology across 2 eras. The DA-EPOCH-R era (2015-2020) included patients diagnosed after guideline implementation. The historic era (2005-2010) included patients identified from a historic province-wide cohort of patients with DLBCL morphology tumors that underwent universal cytogenetic testing in a research setting, predominantly treated with standard chemoimmunotherapy. Two-year overall survival (OS) was significantly improved in the DA-EPOCH-R vs historic era (75% vs 47%, P = .008) in HGBCL-DH-BCL2, whereas OS remained unchanged in DLBCL, not otherwise specified (78% vs 76%, P = .17). Within HGBCL-DH-BCL2, tumors harboring immunoglobulin MYC partner loci (43%) and those expressing the dark-zone signature (77%) were associated with the most substantial survival improvements. In a contemporary cohort of HGBCL-DH-BCL2 histologically transformed from follicular lymphoma (FL) in the DA-EPOCH-R era, outcomes of patients who were chemoimmunotherapy-naïve were comparable to those with de novo disease, whereas patients treated with chemoimmunotherapy for FL prior to transformation had poor outcomes. These data support using DA-EPOCH-R in select patients with HGBCL-DH-BCL2 of DLBCL morphology.

124

News (Medical) associated with Vincristine Sulfate

11 Feb 2026

·captortherapeutics.com

Captor reports: Targeted degradation of GSPT1 in preclinical models of high-risk neuroblastoma

Neuroblastoma remains one of the most devastating childhood cancers, accounting for nearly 15% of oncological deaths in this age group. As a tumor originating from the stem cells of the sympathetic nervous system, its progression can vary wildly - from mild forms that may regress spontaneously to aggressive types requiring complex treatment. Latest data obtained by Captor in collaboration with Lund University indicates the potential application of Targeted Protein Degradation (TPD) technology in treating neuroblastoma with MYCN gene amplification. Future research into GSPT1 protein degraders may contribute to improving the chances of effective treatment. Neuroblastoma and the fate of the MYCN gene Neuroblastoma is a solid tumor most located in the adrenal glands or sympathetic ganglia. A particularly critical clinical challenge is the subgroup of patients with MYCN gene amplification (MYCN-amplified neuroblastoma). This gene, present in excessive copies in approximately 20-30% of patients, acts as a master regulator of tumor growth, making cancer exceptionally aggressive and resistant to standard chemotherapy. Symptoms can be non-specific, ranging from swallowing difficulties and vomiting to general malaise. Consequently, it is often mistaken for less serious conditions. Rapid detection and the implementation of effective treatment are crucial for the prognosis. In Poland, about 70 new cases are diagnosed annually, while global incidence reaches over 5,000 children per year. Up to a quarter of diagnosed cases involve MYCN amplification; in this population, the prognosis is uncertain, and 5-year survival often does not exceed 50%. The amplification of the MYCN oncogene is a hallmark of neuroblastoma aggressiveness. The rapid multiplication of gene copies leads to the overproduction of the MYCN protein, a transcription factor. The presence of elevated levels of this protein results in the constitutive activation of genes driving the cell cycle. Additionally, MYCN induces intensive glycolysis and ribosome synthesis, leading to uncontrolled cancer cell proliferation. A key element of this aggressive phenotype is the suppression of apoptosis (programmed cell death) mechanisms, rendering the cancer cells resistant to the cytotoxic effects of standard chemotherapy. Intensive therapy according to the COJEC protocol Due to its structure, the MYCN protein is considered pharmacologically "undruggable," so neuroblastoma treatment strategies focus on achieving maximum cytoreduction in the shortest possible time. The current standard of care for children with high-risk neuroblastoma in Europe is the Rapid COJEC, developed by SIOP Europe. This is an intensive, multi-drug chemotherapy protocol consisting of eight courses administered at short, 10-day intervals. It includes cytostatic drugs such as cisplatin, vincristine, carboplatin, etoposide, and cyclophosphamide, which cause DNA damage, prevent repair, and halt mitotic cell division. The high dose intensity of the COJEC is designed to break the cancer cells' resistance to death by accumulating genetic damage faster than the cell can repair it. While this protocol achieves an initial response in many patients, it carries significant limitations. The intensity of treatment leads to severe side effects, such as profound myelosuppression, nephrotoxicity and ototoxicity (hearing loss). A significant portion of patients do not achieve full remission, and the disease often returns in a chemoresistant form. Severe infectious complications frequently make it impossible to continue such an intensive regimen. For patients successfully treated via COJEC, the price of success is often very high. Most survivors face serious late-term effects, including growth problems, thyroid dysfunction, infertility (particularly after cyclophosphamide), and an increased risk of heart failure later in life. Regarding the therapy's efficacy, despite maximizing dose intensity in the COJEC protocol, survival rates in the highest-risk group have plateaued. Further dose increases are impossible due to the risk of patient death from treatment toxicity. Despite targeting the mechanisms behind tumorigenesis, the COJEC protocol lacks specificity toward healthy tissues. Conversely, the search for more precise therapeutic strategies is limited by the inability to target the MYCN oncogene directly. One possible direction is to modulate related cellular mechanisms characteristic of cancer cells using indirect and potentially milder therapeutic interventions. GSPT1 protein degradation and its consequences A recent article published in the Journal of Experimental & Clinical Cancer Research presents findings on the therapeutic potential of GSPT1 protein degraders in treating chemoresistant MYCN-amplified neuroblastoma. The GSPT1 protein is a factor responsible for the correct termination of protein synthesis and the regulation of the cell's transition through the division cycle. In oncological diseases, the role of this protein becomes critical, as its excess allows aggressive cancer cells to multiply uncontrollably and mass-produce the oncoproteins necessary for their survival. Initial analyses showed that high GSPT1 expression strictly correlates with the presence of MYCN amplification and a poorer prognosis in neuroblastoma. Therefore, directly targeting and degrading GSPT1 could be a key aspect in developing new therapies. Reducing GSPT1 levels induces proteotoxic stress and a protein synthesis block in cancer cells, effectively bypassing the pharmacological inaccessibility of the MYCN oncogene and inducing cell death. Preclinical results of the CTX-18 degrader and curative perspectives The study details the mechanism and consequences of GSPT1 protein degradation triggered by molecular glue degraders developed by Captor Therapeutics. These molecular glues induce the proximity of GSPT1 and cereblon protein (an E3 ligase). The formation of a complex between these proteins results in GSPT1 being redirected to the proteasome and removed by the cellular protein degradation system. In preclinical studies, the compound CTX-18 demonstrated efficacy that goes beyond the tumor growth inhibition seen in classic therapies. In xenograph models (mice transplanted with donor cancer cells) with induced chemoresistant neuroblastoma, CTX-18 achieved the desired pharmacological effects. Low oral doses of the degrader led to rapid disease remission and the complete disappearance of tumors. Unlike COJEC chemotherapy, which slows disease progression, the application of CTX-18 allowed the animals to survive without recurrence for over 150 days, resulting in a long-lasting effect. CTX-18 targets GSPT1, and a secondary effect of its degradation is a drastic reduction in the level of the MYCN protein itself. In the long term, these results may point toward the possibility of developing curative treatment with reduced toxicity; however, they currently remain at the preclinical research stage. Potential benefits of targeted GSPT1 degradation Introducing targeted protein degradation technology to neuroblastoma treatment opens entirely new perspectives for patients. Neuroblastoma, which most often affects children and infants, represents a massive diagnostic and therapeutic challenge. The results provide the foundation for a new therapeutic approach that could significantly improve patient quality of life by limiting the toxicity of standard protocols and minimizing the risk of complications. While the results of the studies conducted so far are very promising, further research is necessary to confirm the efficacy and safety of targeted protein degradation technology in treating neuroblastoma. The development of the CTX-18 degrader has the potential to fill a significant therapeutic gap in pediatric oncology as a potential first-in-class therapy. Positive preclinical results, supported by years of developed know-how, provide the basis for continuing research projects in the field of targeted protein degradation.

PROTACs

19 Jan 2026

·www.biospace.com

Genmab Announces Topline Results for Epcoritamab (DuoBody® CD3xCD20) from Phase 3 EPCORE® DLBCL-1 Trial in Patients with Relapsed/Refractory Diffuse Large B-cell Lymphoma (DLBCL)

Company Announcement Based on the topline results from the EPCORE ® DLBCL-1 trial, Genmab will engage global regulatory authorities to discuss next steps COPENHAGEN, Denmark; January 16, 2026 – Genmab A/S (Nasdaq: GMAB) today announced topline results from the Phase 3 EPCORE DLBCL-1 trial evaluating epcoritamab, a T-cell engaging bispecific antibody administered subcutaneously, which demonstrated an improvement in progression-free survival (PFS) (HR: 0.74 [95% CI 0.60 to 0.92]) * in patients treated with epcoritamab monotherapy. Additionally, improvements were observed in the complete response rate, duration of response, and time to next treatment among patients treated with epcoritamab monotherapy. EPCORE DLBCL-1 is the first Phase 3 study to demonstrate an improvement in PFS in patients with relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) who were treated with a CD3xCD20 T-cell engaging bispecific monotherapy. The study demonstrated an overall survival (OS) of HR: 0.96 [95% CI 0.77 to 1.20], which did not reach statistical significance. The global study enrolled 483 patients with R/R DLBCL with at least one prior line of therapy (73% had received two or more prior lines) who were ineligible for high-dose chemotherapy and autologous stem cell transplant (HDT-ASCT). The study evaluated the safety and efficacy of epcoritamab monotherapy compared to investigator’s choice of either rituximab plus gemcitabine and oxaliplatin (R-GemOx), or bendamustine plus rituximab (BR). The adverse events observed in this study appear consistent with the known safety pro epcoritamab. Further analysis of the results is ongoing, including the potential impact of various factors, such as the COVID-19 pandemic and increasing availability of novel anti-lymphoma therapies. The full trial results will be submitted for presentation at a future medical meeting. Genmab and AbbVie will engage with global regulatory authorities to discuss next steps. Data is anticipated in 2026 from two Phase 3 trials evaluating fixed duration epcoritamab in patients with DLBCL, including EPCORE DLBCL-2, a front-line study evaluating epcoritamab in combination with standard-of-care rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine, and prednisone (R-CHOP), and EPCORE DLBCL-4, evaluating epcoritamab in combination with lenalidomide versus chemo-immunotherapy in patients with relapsed or refractory DLBCL. “The EPCORE DLBCL-1 trial is the first Phase 3 study evaluating a bispecific antibody monotherapy to demonstrate improvements in progression-free survival in patients with relapsed or refractory DLBCL,” said Jan van de Winkel, Ph.D., Chief Executive Officer of Genmab. “The results from this global trial contribute to the growing body of evidence supporting epcoritamab and build upon the robust foundation established by epcoritamab, which has been used to treat thousands of patients in need of additional therapeutic options. Together with our partner, AbbVie, we remain deeply committed to advancing the development of epcoritamab as a potential core therapy across a broad range of B-cell malignancies.” Epcoritamab (approved under the brand name EPKINLY ® in countries including the U.S. and Japan, and as TEPKINLY ® in the European Union) has received regulatory approval in certain lymphoma indications in more than 65 countries. Genmab and AbbVie remain committed to advancing the potential of epcoritamab, with ongoing clinical programs evaluating the therapy as a monotherapy and in combination regimens across treatment lines and a broad range of hematologic malignancies. *Based on intent-to-treat principle. About Diffuse Large B-Cell Lymphoma Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma (NHL) worldwide, accounting for approximately 25-30 percent of all NHL cases. i , ii In the U.S., there are approximately 25,000 new cases of DLBCL diagnosed each year. iii DLBCL can arise in lymph nodes as well as in organs outside of the lymphatic system, occurs more commonly in the elderly and is slightly more prevalent in men. iv , v DLBCL is a fast-growing type of NHL, a cancer that develops in the lymphatic system and affects B-cell lymphocytes, a type of white blood cell. For many people living with DLBCL, their cancer either relapses, which means it may return after treatment, or becomes refractory, meaning it does not respond to treatment. Although new therapies have become available, treatment management can remain a challenge. iv , vi About the EPCORE DLBCL-1 Trial EPCORE DLBCL-1 ( NCT04628494 ) is a global Phase 3 open label, multi-center, randomized trial to evaluate the efficacy of epcoritamab (GEN3013, DuoBody ® -CD3xCD20) compared to investigator's choice of chemotherapy, either rituximab plus gemcitabine plus and oxaliplatin (R-GemOx), or bendamustine plus rituximab (BR), in patients with relapsed or refractory DLBCL who are ineligible for high-dose chemotherapy and autologous stem cell transplant (HDT-ASCT). The trial started on January 13, 2021, and is ongoing. More information on this trial can be found at . About Epcoritamab Epcoritamab is an IgG1-bispecific antibody created using Genmab's proprietary DuoBody technology and administered subcutaneously. Genmab's DuoBody-CD3 technology is designed to direct cytotoxic T cells selectively to elicit an immune response toward target cell types. Epcoritamab is designed to simultaneously bind to CD3 on T cells and CD20 on B cells and induces T-cell-mediated killing of CD20+ cells. vii Epcoritamab (approved under the brand name EPKINLY ® in the U.S. and Japan, and TEPKINLY ® in the EU) has received regulatory approval in certain lymphoma indications in several territories. Where approved, epcoritamab is a readily accessible therapy. Epcoritamab is being co-developed by Genmab and AbbVie as part of the companies' oncology collaboration. The companies will share commercial responsibilities in the U.S. and Japan, with AbbVie responsible for further global commercialization. Both companies will pursue additional international regulatory approvals for the investigational R/R FL indication and additional approvals for the R/R DLBCL indication. Genmab and AbbVie continue to evaluate the use of epcoritamab as a monotherapy, and in combination, across lines of therapy in a range of hematologic malignancies. This includes three ongoing Phase 3, open-label, randomized trials, among them a trial evaluating epcoritamab in combination with R-CHOP in adult patients with newly diagnosed DLBCL ( NCT05578976 ), a trial evaluating epcoritamab in combination with lenalidomide compared to chemotherapy infusion in patients with R/R DLBCL ( NCT06508658 ), and a trial evaluating epcoritamab in combination with lenalidomide and rituximab (R 2 ) compared to chemoimmunotherapy in patients with previously untreated FL ( NCT06191744 ). The safety and efficacy of epcoritamab has not been established for these investigational uses. Please visit for more information. About Genmab Genmab is an international biotechnology company dedicated to improving the lives of people with cancer and other serious diseases through innovative antibody medicines. For over 25 years, its passionate, innovative and collaborative team has advanced a broad range of antibody-based therapeutic formats, including bispecific antibodies, antibody–drug conjugates (ADCs), immune-modulating antibodies and other next-generation modalities. Genmab’s science powers eight approved antibody medicines, and the company is advancing a strong late-stage clinical pipeline, including wholly owned programs, with the goal of delivering transformative medicines to patients. Established in 1999, Genmab is headquartered in Copenhagen, Denmark, with international presence across North America, Europe and Asia Pacific. For more information, please visit Genmab.com and follow us on LinkedIn and X . Contact: Marisol Peron, Senior Vice President, Global Communications & Corporate Affairs T: +1 609 524 0065; E: mmp@genmab.com Andrew Carlsen, Vice President, Head of Investor Relations T: +45 3377 9558; E: acn@genmab.com This Company Announcement contains forward looking statements. The words “believe,” “expect,” “anticipate,” “intend” and “plan” and similar expressions identify forward looking statements. Actual results or performance may differ materially from any future results or performance expressed or implied by such statements. The important factors that could cause our actual results or performance to differ materially include, among others, risks associated with preclinical and clinical development of products, uncertainties related to the outcome and conduct of clinical trials including unforeseen safety issues, uncertainties related to product manufacturing, the lack of market acceptance of our products, our inability to manage growth, the competitive environment in relation to our business area and markets, our inability to attract and retain suitably qualified personnel, the unenforceability or lack of protection of our patents and proprietary rights, our relationships with affiliated entities, changes and developments in technology which may render our products or technologies obsolete, and other factors. For a further discussion of these risks, please refer to the risk management sections in Genmab’s most recent financial reports, which are available on and the risk factors included in Genmab’s most recent Annual Report on Form 20-F and other filings with the U.S. Securities and Exchange Commission (SEC), which are available at . Genmab does not undertake any obligation to update or revise forward looking statements in this Company Announcement nor to confirm such statements to reflect subsequent events or circumstances after the date made or in relation to actual results, unless required by law. Genmab A/S and/or its subsidiaries own the following trademarks: Genmab ® ; the Y-shaped Genmab logo ® ; Genmab in combination with the Y-shaped Genmab logo ® ; HuMax ® ; DuoBody ® ; HexaBody ® ; DuoHexaBody ® , HexElect ® and KYSO™. EPCORE ® , EPKINLY ® , TEPKINLY ® and their designs are trademarks of AbbVie Biotechnology Ltd. i Lymphoma Research Foundation. Diffuse Large B-Cell Lymphoma. Accessed December 2025. ii Padala, et al. Diffuse Large B-Cell Lymphoma. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan. 2023 Apr 24. iii Leukemia and Lymphoma Society. Diffuse Large B-Cell Lymphoma (DLBCL). Accessed November 2024. iv Sehn, et al. Diffuse Large B-Cell Lymphoma. N Engl J Med . 2021;384:842-858. doi: 10.1056/NEJMra2027612. v Kanas, et al. Epidemiology of Diffuse Large B-Cell Lymphoma (DLBCL) and Follicular Lymphoma (FL) in the United States and Western Europe: Population-Level Projections for 2020-2025. Leuk Lymphoma . 2022;63(1):54-63. doi: 10.1080/10428194.2021.1975188. vi Crump, et al. Outcomes in Refractory Diffuse Large B-Cell Lymphoma: Results From the International SCHOLAR-1 Study. Blood . 2017;130(16):1800-1808. doi: 10.1182/blood-2017-03-769620. vii Engelberts PJ, Hiemstra IH, de Jong B, et al. DuoBody-CD3xCD20 induces potent T-cell-mediated killing of malignant B cells in preclinical models and provides opportunities for subcutaneous dosing. EBioMedicine. 2020;52:102625. DOI: 10.1016/j.ebiom.2019.102625. Company Announcement no. 01 CVR no. 2102 3884 LEI Code 529900MTJPDPE4MHJ122 Genmab A/S Carl Jacobsens Vej 30 2500 Valby Denmark Attachment 011626_CA01_EPCORE DLBCL-1 TOPLINE

Phase 3ImmunotherapyClinical ResultDrug Approval

19 Jan 2026

·www.biospace.com

AbbVie, Genmab’s Bispecific Misses Key Overall Survival Endpoint in Phase III Lymphoma Study

iStock, Wel_nofri Despite the late-stage miss, analysts maintained confidence in the Epkinly program, with Truist Securities saying the result “doesn’t waver our optimism” regarding the bispecific antibody’s ongoing frontline trial. AbbVie and Genmab’s bispecific antibody Epkinly did not significantly improve overall survival in a late-stage study of patients with a specific type of relapsed or refractory diffuse large B cell lymphoma. Analysts appeared to find these results discouraging but maintained faith in the Epkinly franchise. In a note to investors on Friday, William Blair called the outcome “unfortunate” but added that it “doesn’t detract from key second/first-line DLBCL readouts in 2026.” Similarly, while Truist Securities found the overall survival (OS) miss “disappointing,” the analysts said in a Friday note that it “doesn’t waver our optimism on [Epkinly’s] frontline trial.” The Phase III EPCORE DLBCL-1 trial, which is still ongoing, has enrolled 483 patients with relapsed or refractory disease who can’t undergo high-dose chemotherapy or autologous stem cell transplantation. Results announced on Friday showed a 4% improvement in OS in patients treated with Epkinly versus those given an investigator’s choice of chemotherapy. This effect did not reach statistical significance. The FDA is considering OS as a primary endpoint for EPCORE DLBCL-1, William Bair explained on Friday. The analysts added that failing to elicit a significant benefit here has raised questions/concerns from investors as to whether the current relapsed or refractory diffuse large B-cell lymphoma (r/r DLBCL) indication, approved under the accelerated pathway in May 2023 , is at risk. As an accelerated nod, Epkinly’s continued approval in this indication depends on the verification of its clinical benefit in a Phase III confirmatory study. Despite the miss, “we believe it is unlikely Epkinly would lose accelerated approval in DLBCL,” the analysts added. Beyond OS, Epkinly did show a significant improvement in progression-free survival, cutting the risk of disease progression or death by 26% compared to chemotherapy. The bispecific also led to improvements in other endpoints, including complete response rate, duration of response and time to next treatment. With these findings, AbbVie and Genmab said they will approach global health authorities to determine the best path forward for Epkinly in this indication. The two companies originally partnered in June 2020 to collaborate on the development of Epkinly and today share commercialization responsibilities in the U.S. In DLBCL, the companies are also running the Phase III EPCORE-DLBCL-4 study, which is assessing Epkinly in combination with lenalidomide against chemo-immunotherapy, according to Friday’s release . There is also the late-stage EPCORE DLBCL-2, combining Epkinly with rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine and prednisone. Both studies are set to read out this year.

Phase 3ImmunotherapyAccelerated ApprovalPhase 2Clinical Result

100 Deals associated with Vincristine Sulfate

External Link

KEGG	Wiki	ATC	Drug Bank
D02197	Vincristine Sulfate	L01CA02	DB00541

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Pheochromocytoma	Japan	Nippon Kayaku Co., Ltd.	26 Mar 2013
Extensive stage Small Cell Lung Cancer	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Female Genital Neoplasms	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Mycosis Fungoides	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Osteosarcoma	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Rhabdomyosarcoma	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Uterine Cervical Cancer	Brazil	Libbs Farmacêutica Ltda.	20 Nov 2006
Astrocytoma	Japan	Nippon Kayaku Co., Ltd.	14 Feb 2005
Glioma	Japan	Nippon Kayaku Co., Ltd.	14 Feb 2005
Ewing Sarcoma	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
Leukemia	China	Yangzhou Pharmaceutical Co., Ltd.	01 Jan 1982
Leukemia	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
Melanoma	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
Neuroblastoma	China	Yangzhou Pharmaceutical Co., Ltd.	01 Jan 1982
Neuroblastoma	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
Small Cell Lung Cancer	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
Wilms Tumor	China	Jiangsu Qinfen Pharmaceutical Co., Ltd.	01 Jan 1982
acute leukemia	Japan	Eli Lilly Japan KK	18 Apr 1968
Chronic leukemia	Japan	Eli Lilly Japan KK	18 Apr 1968
Acute Lymphoblastic Leukemia	United States	Eli Lilly & Co.	10 Jul 1963

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Adult Lymphoblastic Lymphoma	Phase 2	United States	Amgen, Inc.	23 Jan 2025
Adult Lymphoblastic Lymphoma	Phase 2	United States	Pfizer Inc.	23 Jan 2025
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma	Phase 2	United States	Pfizer Inc.	23 Jan 2025
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma	Phase 2	United States	Amgen, Inc.	23 Jan 2025
Classical Hodgkin's Lymphoma	Phase 2	United States	Teva Pharmaceuticals USA, Inc.	12 Dec 2018
Classical Hodgkin's Lymphoma	Phase 2	United States	Seagen, Inc.	12 Dec 2018
Ph-Like Acute Lymphoblastic Leukemia	Phase 2	United States	Spectrum Pharmaceuticals, Inc.	05 Mar 2013
Bone Cancer	Phase 2	United States	Amgen, Inc.	01 May 2011
Philadelphia Chromosome Negative Acute Lymphoblastic Leukemia	Phase 2	Germany	Talon Therapeutics, Inc.	16 Nov 2007
Aggressive B-Cell Non-Hodgkin Lymphoma	Phase 2	France	Zeneus Pharma Ltd.	01 Oct 2002

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03504644 (EA9152, CTgov)	Phase 1/2	Recurrent B Acute Lymphoblastic Leukemia \| Precursor B-lymphoblastic lymphoma/leukemia refractory \| Recurrent T Lymphoblastic Lymphoma ... View more	40	Computed Tomography+Venetoclax+Vincristine Sulfate+Vincristine Liposomal	jfxtfqghoy(idqbilkkaf) = zajcwabirz iyshwdlvij (vdmlzajorb, nujxzkwhhj - psraxehkxk) View more	-	25 Feb 2026
NCT01777152 (ECHELON-2, Pubmed \| Blood Adv)	Phase 3	Peripheral T-Cell Lymphoma	452	BV-CHP	noxzdvmdoj(courxrhbzx): HR = 0.38 (95.0% CI, 0.16 - 0.94) View more	Positive	09 Dec 2025
				CHOP
ASH2025	Not Applicable	Diffuse Large B-Cell Lymphoma	428	Rituximab+Cyclophosphamide+Doxorubicin+Vincristine+Prednisone	uvbcrmlisi(qbhxcyjxxl) = ywgtwnjbdj fqmkvgwfuu (ldyczftewh ) View more	Positive	06 Dec 2025
NCT06207123 (ASH2025)	Phase 1/2	T-cell Acute Lymphoblastic Leukemia/Lymphoma	21	LP-118+Ponatinib+Vincristine+Dexamethasone	rweewvskjt(iujpkzteju) = pccrntidlt rbicixfuhi (tkjfoliglo )	Positive	06 Dec 2025
ASH2025	Not Applicable	Diffuse Large B-Cell Lymphoma	46	R-CHOP therapy (R-CHOP with XRT)	ghtavthdsd(wndwhcrgmj) = whhsdefyjo vbbvasqvhq (xxxsdbrekg ) View more	Positive	06 Dec 2025
				R-CHOP therapy (without XRT)	ghtavthdsd(wndwhcrgmj) = ahbovzbzme vbbvasqvhq (xxxsdbrekg ) View more
NCT03023046 (ASH2025)	Phase 2	Acute Lymphoblastic Leukemia First line	53	DA-EPOCH±R±TKI (Ph+)	jqngbjoifz(dkphejqotz) = kcvbppdqsa nvmyzcurmf (khxohqcykn, 22 - 59) View more	Positive	06 Dec 2025
				DA-EPOCH±R±TKI (Ph-)	jqngbjoifz(dkphejqotz) = aicipoudoy nvmyzcurmf (khxohqcykn, 12 - 48) View more
NCT00136435 (CTgov)	Phase 2	Acute Lymphoblastic Leukemia	100	L-asparaginase	amqpaimrcm = pobkrnlqzh vavhdetvks (iwseppmxwf, vcsisxggzn - juxknyujtr) View more	-	20 Oct 2025
ESMO2025	Not Applicable	Enteropathy-Associated T-Cell Lymphoma	56	mNewcastle regimen	hwlllqtprz(cxpbfjtnlb) = vyaharltty lfhykkpeiu (hwruycnrza ) View more	Positive	17 Oct 2025
				CHOP-like regimens	hwlllqtprz(cxpbfjtnlb) = pxfbypgdkf lfhykkpeiu (hwruycnrza ) View more
NCT00278408 (UNFOLDER, CTgov)	Phase 3	CD20 positive B-Cell Lymphoma	700	R-CHOP-21 (Interventional: 6 R-CHOP-21 for Patients With Radiotherapy Indication)	ekteabsurh = rdrulokggg nppqkkosku (bztjljcfjt, whoiammrev - twxnxnyxtv) View more	-	26 Aug 2025
				R-CHOP-14 (Interventional: 6 R-CHOP-14 for Patients With Radiotherapy Indication)	ekteabsurh = ljwyzkyyhk nppqkkosku (bztjljcfjt, niamvnccep - hoixtjvobm) View more
NCT00878254 (CTgov)	Phase 2	Mantle-Cell Lymphoma	25	Mesna+Etoposide+Cyclophosphamide+Leucovorin+G-CSF+Doxorubicin+ifosfamide+Methotrexate+Rituximab+Vincristine+Cytarabine	zkrwohuwqm(gevkizpzqf) = edsoexfasi hqifkmtvpn (vylowcufgq, kkdcxxgetf - wfhtusmakh) View more	-	23 Jul 2025

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