On November 4, 2026 Genprex, Inc. ("Genprex" or the "Company") (NASDAQ: GNPX), a clinical-stage biotechnology company developing gene therapies designed to restore tumor-suppressor function in cancer and insulin-producing function in diabetes, reported new research identifying TROP2 expression as a potential predictive biomarker of response to its lead drug candidate, Reqorsa (quaratusugene ozeplasmid), a gene therapy product, will be presented at the 2026 EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics, taking place November 18-20, 2026 in Barcelona, Spain.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

The research collaborators found that low TROP2 expression was consistently associated with resistance to REQORSA across multiple preclinical models of non-small cell lung cancer (NSCLC). This finding was also supported by analysis of pretreatment tumor biopsies from patients enrolled in a clinical trial evaluating REQORSA.

"Discovering an applicable biomarker of response is a meaningful step toward a more precise approach to treating lung cancer with REQORSA," said Ryan Confer, President and Chief Executive Officer of Genprex. "These data show that low TROP2 expression was associated with primary resistance across multiple preclinical models, and this was supported by analysis of patient biopsies from a clinical trial. If confirmed in further studies, TROP2 could not only help us enhance our clinical trials by recruiting and selecting more applicable patients, but, more importantly, benefit future patients by ultimately delivering potentially more effective, personalized treatment options. This work reflects our commitment to a precision-medicine approach to treating lung cancer."

The TUSC2 tumor suppressor protein expression is downregulated or absent in more than 80% of NSCLC cases and nearly all small cell lung cancers. Previous studies have shown that REQORSA has antitumor activity, including in models resistant to targeted therapies and in immunotherapy-resistant KRAS/LKB1-mutant NSCLC. REQORSA’s effects are mediated by inhibiting MAPK and mTOR signaling, inducing cell-cycle arrest and apoptosis, and activating antitumor immune responses.

Key findings from the research include:

TROP2 expression associated with resistance: Approximately 50% of 10 NSCLC cell lines and 50% of 12 patient derived organoid models evaluated showed primary resistance to TUSC2 gene delivery. Protein-expression analyses consistently identified low TROP2 expression as a marker associated with resistance across multiple preclinical models.
Supporting clinical evidence: Analysis of pretreatment tumor biopsies from patients enrolled in a TUSC2 gene therapy clinical trial supported the association between TROP2 expression and treatment response.
TROP2 modulation influenced treatment sensitivity: Experimental manipulation of TROP2 expression altered TUSC2-induced cancer cell death, suggesting that TROP2-dependent signaling may play a role in therapeutic response. Further research is underway to understand these context-dependent effects.
Collectively, the findings identify TROP2 as a potential predictive biomarker for response to REQORSA and suggest that modulating TROP2 signaling may be a novel strategy to enhance the therapeutic efficacy of REQORSA in NSCLC. While these findings provide preclinical and supportive clinical evidence, additional research and prospective clinical evaluation will be required to establish TROP2’s predictive utility in patients receiving REQORSA.

The featured Genprex-supported poster is to be presented at the 2026 EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics:

Title: TROP2 Predicts Response to TUSC2 Gene Therapy (Quaratusugene Ozeplasmid) and Its Modulation Sensitizes Non-Small Cell Lung Cancer to Treatment

Conference: 2026 EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics

Topic: Drug Resistance and Modifiers

Session Date and Time: Wednesday, Nov. 18, 2026

Time: 12:00–6:00 p.m. CET

Abstract Number: 108

Poster Board Number: PB-108

Location: CCIB, Barcelona, Spain

The EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) 2026 poster is expected to be available on Genprex’s website following the presentation, subject to applicable conference disclosure requirements.

About Reqorsa Gene Therapy

Reqorsa (quaratusugene ozeplasmid), a gene therapy product, consists of a plasmid containing the TUSC2 gene encapsulated in non-viral lipid-based nanoparticles in a lipoplex form (the Company’s Oncoprex Delivery System), which has a positive charge. REQORSA is injected intravenously and specifically targets cancer cells. REQORSA is designed to deliver the functioning TUSC2 gene to negatively charged cancer cells while minimizing uptake by normal tissue. Laboratory studies conducted at MD Anderson show that the uptake of TUSC2 in tumor cells in vitro after REQORSA treatment was 10 to 33 times the uptake in normal cells.

(Press release, Genprex, NOV 4, 2026, View Source [SID1234674166])

On November 4, 2026 FORE Biotherapeutics, a registration stage company dedicated to developing targeted therapies to treat patients with cancer, reported two abstracts that have been selected for presentation at two prestigious oncology medical meetings. The first is an oral presentation highlighting long-term efficacy and safety data from a Phase 1/2a study evaluating plixorafenib in patients with BRAF V600 primary CNS tumors and will be presented at the upcoming Society for Neuro-Oncology (SNO) 2026 Annual Meeting taking place in Philadelphia November 12-15, 2026. The second is a poster presentation featuring new preclinical data supporting plixorafenib’s unique mechanism of action and its potential as a future treatment for BRAF-altered colorectal cancer (CRC) and will be presented at the 38th EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium (ENA 2026) taking place in Barcelona November 18-20, 2026.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Stacie Peacock Shepherd, M.D., Ph.D., Chief Medical Officer of Fore, commented: "The data being presented at SNO this year are exciting because they show that plixorafenib has sustained response and activity in patients with BRAF-altered CNS tumors, including treatment durations exceeding 4 years, with a manageable safety profile with no cumulative or late-onset toxicities, and without the class-associated adverse events commonly observed with first generation RAF inhibitors."

"BRAF V600 mutation occurs in approximately 8% of colorectal cancer and is a highly aggressive tumor with poor prognosis due to limited responses and intrinsic and acquired resistance. As a novel paradox and dimer breaker BRAF inhibitor, we believe plixorafenib’s unique mechanism of action has the potential to be the ideal combination partner to mitigate resistance in colorectal cancer. At ENA this year, we will be presenting new preclinical data that demonstrates single-agent plixorafenib activity following standard therapies, along with compelling synergistic efficacy in vitro when combined with pan-RAS inhibition or widely used standard-of-care agents, including in resistant cell lines. We look forward to sharing all of these data with the scientific and medical communities later this month," concluded Dr. Peacock.

Oral Presentation Details at SNO 2026:

Title: Long-term safety and efficacy of plixorafenib in patients with BRAF-altered CNS neoplasms from the phase 1/2a PLX120-03 study
Presenter: Macarena De La Fuente, M.D., Sylvester Comprehensive Cancer Center, University of Miami
Abstract Number: CTNI-09
Session: Clinical Trials Oral Abstracts Session I
Date and Time: Friday, November 13, 2026, 10:54 – 10:59 a.m. ET

Poster Presentation Details at ENA 2026:

Title: Determinants of response and rational combination strategies for plixorafenib (PLX8394/FORE8394) in models of BRAF-altered colorectal cancer
Lead Author: Jessica Jang, Ph.D., Director, Translational Science, Fore Biotherapeutics
Poster Number: PB-117
Poster Session: Molecular Targeted Agents
Date and Time: Thursday, November 19, 2026, 1:00 – 3:00 p.m. CET

About Plixorafenib

Plixorafenib is a novel BRAF inhibitor, with a unique mechanism of action that functions both as a dimer and paradox breaker, and that has demonstrated a differentiated and compelling monotherapy profile in clinical studies. Plixorafenib received Breakthrough Therapy Designation by the U.S. Food and Drug Administration in April 2026. In a previously conducted Phase 1/2 study in patients with MAPK inhibitor naïve BRAF V600 primary recurrent CNS tumors (n=9), plixorafenib monotherapy demonstrated an ORR of 67% and a clinical benefit rate of greater than 75%. In patients with V600 alterations who were MAPK inhibitor naïve, plixorafenib achieved a 42% response rate with prolonged duration of response (mDOR 17.8 months), with a clinical benefit rate of >70%. Plixorafenib also demonstrated a favorable safety and tolerability profile across tumor types, including relative to existing standard of care treatments for various BRAF altered tumors, with a discontinuation rate due to drug-related adverse events of less than 2%. Fore believes plixorafenib has the potential to overcome the limitations and tolerability challenges of currently available BRAF inhibitors, including high rates of rash, hemorrhage and growth effects in younger patients, through its unique mechanism of action targeting both BRAF Class I and Class II alterations, while avoiding the limitations of the earlier generation BRAF inhibitors that led to rapid recurrence of disease and the need for combination with a MEK inhibitor.

(Press release, Fore Biotherapeutics, NOV 4, 2026, View Source [SID1234674165])

On November 4, 2026 Tangram Therapeutics ("Tangram"), a company committed to unlocking transformative RNAi medicines for meaningful patient impact, reported that preclinical data from TGM-148, a novel GalOmic medicine for bleeding disorders, will be presented in an oral session at the 68th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting, taking place 12–15 December 2026 in New Orleans, Louisiana.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

TGM-148 silences Protein Z-dependent Protease Inhibitor (ZPI), a natural regulator of coagulation. It is designed to combine robust hemostatic efficacy with low thrombotic risk and infrequent administration (four or fewer subcutaneous doses a year) to substantially reduce the burden of prophylaxis. In preclinical proof-of-concept studies, TGM-148 demonstrated efficacy in four distinct genetic disease models, including a model of von Willebrand disease (VWD), the planned entry indication.

Tangram’s oral presentation at ASH (Free ASH Whitepaper) will highlight TGM-148’s unique, context-dependent mechanism of action. In non-human primate plasma depleted of factor VIII, modeling a deficiency that causes hemophilia A and is common in VWD, TGM-148 dose-dependently enhanced thrombin generation. In non-depleted plasma, TGM-148 had no effect on thrombin generation, consistent with ZPI’s adaptive role in regulating coagulation. In addition, TGM-148 was well tolerated up to the highest dose tested in a repeat-dose toxicology study in healthy non-human primates, supporting a wide therapeutic window. Together, these findings demonstrate TGM-148’s potential to restore hemostatic balance in people with bleeding disorders without increasing thrombotic risk.

"We are pleased to present data at ASH (Free ASH Whitepaper) showcasing TGM-148’s context-dependent mechanism of action, which was a key reason we chose to pursue this novel target. With this differentiated mechanism, and the prospect of quarterly or less frequent dosing, TGM-148 has the potential to offer effective, patient-friendly prophylaxis with a wide therapeutic window", said Alan Whitmore, BM BCh, FFPM, PhD, Chief Scientific Officer of Tangram.

"People living with bleeding disorders need more prophylactic options, and the data Tangram will be presenting highlight the potential of TGM-148 as a novel approach. I am excited to see it progress through clinical development to evaluate ZPI silencing as a viable mechanism for rebalancing hemostasis." added Robert F. Sidonio, Jr MD, MSc, Pediatric Hematologist at Hemophilia of Georgia Pediatric Center for Bleeding and Clotting Disorders, Emory University School of Medicine.

Presentation Details

Title: TGM-148, a Novel GalNAc-siRNA Targeting ZPI, Demonstrates Context-dependent Hemostatic Rebalancing in Cynomolgus Monkeys
Publication Number: 953
Session Name: 801. Gene Therapies: Beyond Transplant: The Expanding Role of Gene Therapy in Hematology
Session Date & Time: 14 December, 14:45-16:15
Location: MCCNO – 388-390

About TGM-148
TGM-148 is a first-on-target GalOmic GalNAc-conjugated small interfering RNA (GalNAc-siRNA) designed to selectively silence Protein Z-dependent Protease Inhibitor (ZPI) in the liver, where it is produced before circulating in the blood. Its context-dependent mechanism of action aims to enhance clotting in response to bleeding in those with bleeding disorders, while maintaining a favorable safety profile.

In preclinical studies, TGM-148 demonstrated efficacy in four genetic bleeding disorder models and was well tolerated at supratherapeutic doses in wildtype animals. Together, these findings support TGM-148’s wide therapeutic window and provide a strong rationale for its development across a broad range of bleeding disorders, with VWD selected as the first indication. By offering the potential for quarterly or less frequent subcutaneous administration, TGM-148 is also designed to lower the barriers to prophylaxis, supporting broader uptake, better outcomes, and improved quality of life for patients.

(Press release, e-Therapeutics, NOV 4, 2026, View Source [SID1234674164])

On November 4, 2026 Cullinan Therapeutics, Inc. (Nasdaq: CGEM), a clinical-stage biopharmaceutical company accelerating potential first- or best-in-class, disease-modifying T cell engagers in autoimmune diseases and cancer, reported that two of its T cell engager programs, CLN-049, a FLT3xCD3 T cell engager, and velinotamig (CLN-803), a BCMAxCD3 T cell engager, will be featured across four poster presentations at the 68th American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting and Exposition, being held December 12-15 in New Orleans, Louisiana.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

Cullinan will present updated data from the CLN-049 Phase 1 dose escalation study in patients with relapsed or refractory acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS). The abstract reports the anti-leukemic activity of the selected Phase 2 target doses of 6 µg/kg and 12 µg/kg, and a favorable safety profile for the double step-up dosing regimen. Updated dose escalation results for the selected Phase 2 regimens will be further detailed in the poster presentation.

Additional posters include a Trial in Progress for CLN-049 in combination with azacitidine and venetoclax in newly diagnosed AML and a Trial in Progress for velinotamig in immune thrombocytopenia and warm autoimmune hemolytic anemia, which is also supported by a poster with new preclinical data demonstrating that velinotamig selectively targets BCMA-expressing B-lineage cells that drive autoimmune cytopenias.

Presentation Details

CLN-049 Poster Presentations

Title: Updated anti-leukemia activity from a Phase 1 study of CLN-049, a novel anti-FLT3 x anti-CD3 bispecific T cell engager, in relapsed/refractory (R/R) acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS)
Session Name: 616. Acute Myeloid Leukemias: Investigational Drug and Cellular Therapies: Poster II
Session Date: December 13, 2026
Session Time: 6:00 p.m. – 8:00 p.m.

Session Location: MCCNO – Hall F
Poster Number: 3385

Title: Trials in Progress: A multicenter Phase 1b study of the bispecific T-cell engager CLN-049 in combination with venetoclax and azacitidine in patients with newly diagnosed acute myeloid leukemia (AML)

Session Name: 616. Acute Myeloid Leukemias: Investigational Drug and Cellular Therapies: Poster I
Session Date: December 12, 2026
Session Time: 5:30 p.m. – 7:30 p.m.

Session Location: MCCNO – Hall F

Poster Number: 1640

Velinotamig (CLN-803) Poster Presentations 

Title: Velinotamig (CLN-803), a BCMA×CD3 Bispecific T-cell Engager, Targets B Cells and Plasma Cells That Drive Autoimmune Cytopenias

Session Name: 703. Cellular Immunotherapies Other Than CAR-T Cells: Basic and Translational: Poster I
Session Date: December 12, 2026
Session Time: 5:30 p.m. – 7:30 p.m.
Session Location: MCCNO – Hall F

Poster Number: 2384

Title: Trials in Progress: A Phase 1b/2a, Open-label Study of a Novel Subcutaneously Administered BCMAxCD3 T-Cell Engager Velinotamig in Relapsed/Refractory Immune Thrombocytopenia and Warm Autoimmune Hemolytic Anemia

Session Name: 311. Disorders of Platelet Number or Function: Clinical and Epidemiological: Poster II
Session Date: December 13, 2026
Session Time: 6:00 p.m. – 8:00 p.m.
Session Location: MCCNO – Hall F

Poster Number: 3001

About CLN-049

CLN-049 is a novel, investigational FLT3xCD3 T cell engager. CLN-049 is designed to target FLT3-expressing leukemia cells, offering a new immunotherapeutic approach for treating acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). CLN-049 binds to both mutated and non-mutated FLT3, allowing targeted action regardless of FLT3 mutational status, making the investigational treatment widely applicable to a broad population.

CLN-049 is being studied in a Phase 1/2, open-label, multicenter, multiple ascending dose study evaluating safety, tolerability, pharmacokinetics (PK), pharmacodynamics (PD), and preliminary efficacy of intravenously (IV) administered CLN-049 in patients with relapsed/refractory AML or MDS (NCT05143996).

CLN-049 is also being studied in a Phase 1/2, open-label, multicenter, dose escalation and dose expansion study to evaluate the safety, tolerability, PK, and PD of IV-administered CLN-049 in combination with azacitidine and venetoclax in patients with newly diagnosed AML (NCT07722767).

CLN-049 has received Orphan Drug designation and Fast Track designation from the U.S. FDA for the treatment of relapsed/refractory AML.

About Acute Myeloid Leukemia (AML)

Acute myeloid leukemia (AML) is a cancer of the blood and bone marrow, and the most common form of acute leukemia in adults.1 It is characterized by the rapid growth of abnormal white blood cells that crowd out healthy cells, leading to infections, fatigue, and bleeding.2 Each year in the U.S., approximately 23,000 people are diagnosed with AML, and about half as many lives are lost to the disease.3 Globally, AML affects an estimated 145,000 people annually, with approximately 130,000 deaths.4

Despite recent advances, outcomes for patients with AML remain poor, particularly for those with relapsed or refractory disease, where five-year survival is 10% or less.5 Patients with high-risk genetic features, such as complex karyotype or TP53 mutations, face especially limited options.6,7 Intensive treatments like chemotherapy and stem cell transplantation may be inaccessible for many older patients due to severe side effects.7 Currently, there are no approved immunotherapies for AML, underscoring the urgent need for novel therapeutic approaches that can improve outcomes for patients and their families facing this life-threatening disease.8

About Velinotamig (CLN-803, GR1803) 

Velinotamig is a BCMAxCD3 T cell engager designed to redirect cytotoxic T cells to target BCMA-expressing cells including pathogenic, autoantibody-producing plasma cells. Velinotamig is engineered with high-affinity binding to BCMA and lower-affinity binding to CD3, with the goal of enhancing target cell depletion while minimizing non-specific T cell activation and associated cytokine-related toxicity. By targeting BCMA-expressing cells, velinotamig has the potential to address autoimmune diseases driven by pathogenic autoantibodies. 

Cullinan holds a global (ex-Greater China), all indication, exclusive license to velinotamig from Genrix Bio. Genrix Bio is evaluating velinotamig in a Phase 1b/2a clinical trial in patients with refractory systemic lupus erythematosus (SLE) in China. Cullinan Therapeutics is evaluating subcutaneously administered velinotamig in a global Phase 1b/2a study in patients with relapsing and refractory immune thrombocytopenia and warm autoimmune hemolytic anemia (NCT07738822).

About Immune Thrombocytopenia (ITP)

Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disease characterized by increased platelet destruction and impaired platelet production.9 Platelets play a critical role in blood clotting, and reduced platelet levels can lead to bruising, bleeding, debilitating fatigue, and impaired health-related quality of life.9,10 In severe cases, bleeding may be life-threatening.9 ITP may present as an acute, self-limited condition or follow a chronic and relapsing course, particularly in adults.9 In the U.S., the prevalence of chronic primary ITP among adults has been estimated at 23.6 per 100,000 people, or approximately 62,000 adults.11 Although currently available therapies can help manage platelet counts and reduce bleeding risk, many patients continue to experience relapses and the burden of ongoing disease management.9,10

About Warm Autoimmune Hemolytic Anemia (wAIHA)

Warm autoimmune hemolytic anemia (wAIHA) is a rare autoimmune disease in which warm-reactive autoantibodies cause the premature destruction of red blood cells, resulting in anemia.12 People living with wAIHA may experience debilitating fatigue, shortness of breath, jaundice, and other complications of anemia. The disease can be serious and potentially life-threatening.12 The prevalence of wAIHA among adults in the U.S. is estimated at approximately 33,300 adults.13,14 Achieving sustained disease control can remain challenging, particularly for patients with relapsing or refractory wAIHA, underscoring the need for additional treatment options.

(Press release, Cullinan Oncology, NOV 4, 2026, View Source [SID1234674163])

On November 4, 2026 Citius Oncology, Inc. ("Citius Oncology" or the "Company") (Nasdaq: CTOR) reported health-related quality of life (HRQoL) results from pivotal Study 302 (NCT01871727) of LYMPHIR (denileukin diftitox-cxdl) in adults with relapsed or refractory (r/r) cutaneous T-cell lymphoma (CTCL). Christiane Querfeld, MD, PhD, of City of Hope, delivered an oral presentation at the European Organisation for Research and Treatment of Cancer Cutaneous Lymphoma Tumour Group (EORTC-CLTG) 2026 Annual Meeting, held October 8–10, 2026, in Berlin, Germany.

Schedule your 30 min Free 1stOncology Demo!
Discover why more than 1,500 members use 1stOncology™ to excel in:

Early/Late Stage Pipeline Development - Target Scouting - Clinical Biomarkers - Indication Selection & Expansion - BD&L Contacts - Conference Reports - Combinatorial Drug Settings - Companion Diagnostics - Drug Repositioning - First-in-class Analysis - Competitive Analysis - Deals & Licensing

                  Schedule Your 30 min Free Demo!

"Patients and physicians have told us that both clinical response and quality of life matter in CTCL treatment," said Leonard Mazur, Chairman and Chief Executive Officer of Citius Oncology. "These data add the patient’s voice to the efficacy and durability shown in our pivotal trial. We were pleased to share the data at the EORTC-CLTG conference in Berlin and are proud to partner with the Cutaneous Lymphoma Foundation on its November 2026 workshop to put quality of life at the center of CTCL care."

"CTCL is a disease of the skin which symptomatic patients must deal with 24/7. Painful, itchy lesions take a real toll on their well-being," said Dr. Myron Czuczman, Chief Medical Officer of Citius Oncology. "In Study 302, patients who responded to denileukin diftitox-cxdl reported sustained quality of life improvements, and nearly a third of heavily pretreated patients with significant itch noted its decrease. We believe these findings underscore how important quality of life considerations are as practitioners choose between various treatment options for their patients with relapsed or refractory CTCL."

Study 302 is the open-label, single-arm, multicenter registrational trial that supported the U.S. Food and Drug Administration (FDA) approval of LYMPHIR. Adult patients with Stage I-III CTCL who had received at least one prior systemic treatment received LYMPHIR 9 mcg/kg as a one-hour intravenous infusion on Days 1–5 of each 21-day cycle, for up to eight cycles.

Quality of life was an exploratory objective, assessed with two validated patient-reported outcome (PRO) instruments: the disease-specific Skindex-29 and the general Functional Assessment of Cancer Therapy – General (FACT-G). Pruritus was measured on a 100-mm visual analog scale (VAS). All analyses were descriptive. The study was not designed or powered to evaluate quality of life outcomes, no formal statistical comparisons were performed, and these results are not included in the LYMPHIR Prescribing Information.

Key findings included:

● Skin-related quality of life: Among responders (n=25) in the primary analysis set (Stage I-III, n=69), mean change from baseline in Skindex-29 Total Score ranged from −5.38 to −13.69 points across assessments, compared with slightly positive to near-zero changes among non-responders (lower scores indicate better quality of life). In the full analysis set (Stage I–IV, n=81), sustained quality of life improvements among responders over non-responders were consistent across all three Skindex-29 domains: symptoms, emotions, and functioning.

● Overall quality of life: Among responders in the primary analysis set, FACT-G Total Score showed a sustained benefit at the end of treatment, with a mean change from baseline of +3.21 at the end of treatment, compared with −2.28 for non-responders.

● Pruritus: Among 41 heavily pretreated patients with a baseline itch score of 20 mm or greater, 13 (32%; 95% CI, 18.1–48.1) achieved a clinically meaningful improvement, defined as a decrease of at least 20 mm sustained for four weeks or longer.

Citius Oncology is also partnering with the Cutaneous Lymphoma Foundation on the Foundation’s first-ever Quality of Life Workshop, to be held in November 2026. The working meeting will bring together patients and care partners, clinicians, researchers, advocacy organizations, and industry representatives to set priorities, standardize how quality of life is measured in cutaneous lymphoma, and build a shared roadmap for patient care and well-being. More information about the workshop is available at www.clfoundation.org/quality-life-workshop.

About LYMPHIR (denileukin diftitox-cxdl)

LYMPHIR is a targeted immunotherapy for relapsed or refractory cutaneous T-cell lymphoma (CTCL) indicated for use in Stage I–III disease after at least one prior systemic therapy. It is a recombinant fusion protein that combines the IL-2 receptor binding domain with diphtheria toxin (DT) fragments. The agent specifically binds to IL-2 receptors on the cell surface, causing DT fragments that have entered cells to inhibit protein synthesis, resulting in cell death. Denileukin diftitox-cxdl has demonstrated the ability to deplete immunosuppressive regulatory T lymphocytes (Tregs) and antitumor activity through a direct cytocidal action on IL-2R-expressing tumors. LYMPHIR was approved by the FDA and subsequently launched in the U.S. in December 2025. For more information, please visit www.lymphirhcp.com.

(Press release, Citius Pharmaceuticals, NOV 4, 2026, View Source [SID1234674162])