Genprex Collaborators to Present Positive Preclinical Data on the Use of Reqorsa® Gene Therapy for the Treatment of Lung Cancer at the 2025 AACR-NCI-EROTC International Conference on Molecular Targets and Cancer Therapeutics

On October 23, 2025 Genprex, Inc. ("Genprex" or the "Company") (NASDAQ: GNPX), a clinical-stage gene therapy company focused on developing life-changing therapies for patients with cancer and diabetes, reported that its research collaborators will present positive preclinical data at the upcoming 2025 AACR (Free AACR Whitepaper)-NCI-EROTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper) taking place October 22-26, 2025 at the Hynes Convention Center in Boston. The collaborators will present positive preclinical data from a study of Genprex’s lead drug candidate, Reqorsa Gene Therapy (quaratusugene ozeplasmid), for the treatment of ALK-EML4 positive non-small cell lung cancer (NSCLC).

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"We are delighted to have our academic partners present this compelling preclinical evidence that supports the therapeutic use of REQORSA in ALK Positive NSCLC," said Ryan Confer, President and Chief Executive Officer at Genprex. "Our researchers found that REQORSA alone or in combination with alectinib was able to shrink tumors by 79 percent, suggesting that REQORSA may be active as a single agent and may also be an ideal companion drug for patients with advanced disease. These data support a pathway for a potential future clinical trial for REQORSA."

The featured Genprex-supported poster to be presented at the 2025 EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics:

Title: "Quaratusugene ozeplasmid mediated TUSC2 upregulation in EML4-ALK bearing non-small cell lung carcinoma induces apoptosis and is highly effective in preclinical studies"

Collaborator: The University of Michigan Rogel Cancer Center

Session: Poster Session C

Session Date and Time: Saturday, October 25, 2025 from 12:30 – 4:00 p.m. ET

The featured Genprex-supported abstract to be presented at the 2025 EORTC-NCI-AACR (Free EORTC-NCI-AACR Whitepaper) Symposium on Molecular Targets and Cancer Therapeutics:

NSCLC bearing the EML4-ALK fusion (Echinoderm microtubule-associated protein-like 4- Anaplastic Lymphoma Kinase) occurs in approximately 5% of NSCLC. Tumors bearing the fusion are sensitive to ALK Tyrosine Kinase Inhibitors (TKIs), that form the first and second line of treatment for these patients. However, ALK+ lung cancers invariably develop resistance to ALK inhibitors, creating the need for newer treatment strategies.

Tumor Suppressor Candidate 2 (TUSC2) is a tumor suppressor gene that is known to have low endogenous expression in NSCLC. REQORSA Gene Therapy, referred to as quaratusugene ozeplasmid (QO) in the abstract and developed by Genprex, is a gene therapy (TUSC2 plasmid encapsulated in non-viral lipid nanoparticles) that upregulates TUSC2 expression in cancer cells by delivering the functional TUSC2 gene.

Researchers evaluated TUSC2 expression in several ALK+ cell lines and patient derived organoids (PDOs), both before and after exposure to QO. The studies indicate that QO mediated overexpression of TUSC2 significantly induced apoptosis in ALK+ cell lines and PDOs, as demonstrated by increase in caspase 3/7 activity of the cells, increased protein expression of pro-apoptotic markers, reduced colony formation ability of the cells, and increased DNA fragmentation. Furthermore, researchers have observed a robust pro-apoptotic response in ALK+ NSCLC cell lines with acquired resistance to the ALK inhibitor, alectinib, resulting in reduced cell viability when treated with QO and alectinib in combination. To better understand how QO and alectinib work in combination, researcher subcutaneously injected NCI-H2228 ALK+ cells into nude mice and when the tumors developed to approximately 100mm3, mice were randomized into 4 groups. Mice from group 1 were treated with vehicle control, group 2 were treated with QO (25ug/mouse, i.v., every three days), group 3 were treated with alectinib (0.5mg/kg/mouse, oral gavage, every day) and group 4 were treated with QO and alectinib in combination at the same concentration and frequency of dosing for up to a month.

The results showed that alectinib shrunk tumors by 60% (group 3). However, QO alone (group 2) and in combination with alectinib (group 4) were able to shrink the tumors by 79%. This finding showed that QO has a 23% improved outcome than alectinib, leading to the hypothesis that QO may be an ideal companion drug for patients with advanced disease or a treatment for patients who cannot tolerate alectinib. Researchers are also currently monitoring the mice for survival, and tumor measurements recorded at 2 weeks after the end of treatment indicate that tumors in mice that received single drug treatment are regrowing faster than tumors in mice that received combined treatment of QO and alectinib, further emphasizing the clinical relevance of this novel combination in ALK+ NSCLC.

Taken together, the in vitro and in vivo data suggest that QO mediated overexpression of TUSC2 in ALK+ NSCLC is effective in decreasing growth and proliferation through the activation of apoptotic pathways, thereby paving the way for a potential clinical trial.

About Reqorsa Gene Therapy

REQORSA (quaratusugene ozeplasmid) 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, OCT 23, 2025, View Source [SID1234656943])

BridGene Biosciences to Present Three Posters at the 2025 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics

On October 23, 2025 BridGene Biosciences, Inc., a leader in the discovery of small molecule drugs for traditionally "hard-to-drug" targets, announced today that three abstracts have been accepted for presentation at the AACR (Free AACR Whitepaper)-NCI-EORTC AACR-NCI-EORTC (Free AACR-NCI-EORTC Whitepaper) International Conference on Molecular Targets and Cancer Therapeutics (EORTC-NCI-AACR) (Free ASGCT Whitepaper) (Free EORTC-NCI-AACR Whitepaper), taking place October 22-26, 2025, in Boston, Massachusetts. The presentations showcase new discoveries from BridGene’s proprietary IMTAC (Isobaric Mass Tagged Affinity Characterization) chemoproteomics platform, including the identification of a novel covalent FGFR3 inhibitor, a first-in-class PAX8 inhibitor, and data illustrating the breadth and precision of IMTAC in mapping covalent ligandable sites across the proteome.

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BridGene will present findings from its study titled "Discovery of a Highly Potent and Selective Covalent FGFR3 Inhibitor," which details the identification and preclinical evaluation of a selective FGFR3 inhibitor discovered using the company’s IMTAC chemoproteomics platform. The compound demonstrated irreversible binding to a previously uncharacterized cysteine residue in FGFR3, resulting in sustained inhibition of FGFR3 phosphorylation and downstream ERK signaling. In cellular models harboring FGFR3 alterations, the inhibitor exhibited nanomolar potency and strong antiproliferative effects, while maintaining high selectivity over other FGFR family members. These data support the potential of covalent FGFR3 inhibition as a novel therapeutic strategy for FGFR3-driven cancers and further validate BridGene’s chemoproteomic approach for uncovering druggable sites in challenging targets.

BridGene will present findings from its study titled "IMTAC: A Proteome-Wide Live-Cell Screening Platform for Discovering Covalent Binders to Diverse Targets Including GPCRs, Phosphatases, and More." The research showcases how BridGene’s proprietary IMTAC platform integrates a highly diverse covalent small molecule library with advanced live-cell chemical proteomics and quantitative mass spectrometry to identify direct, on-target binding events under native cellular conditions. The platform enables proteome-wide selectivity profiling, minimizes false positives, and reveals transient, novel binding pockets that are undetectable in traditional assays.

Using IMTAC, BridGene identified covalent binders across multiple challenging target classes, including GPCRs, phosphatases, and kinases. In GPCR studies, BGP-1951 inhibited serotonin-induced calcium influx through 5-HT₂A while avoiding common CNS toxicity profiles, and BGP-2992 acted as a positive allosteric modulator of CXCR4 signaling with therapeutic potential in neuroinflammation. Among phosphatases, BGP-15341 inhibited ENPP1 enzymatic activity at nanomolar potency, and BGP-1900 selectively bound PTPN2, offering a path toward targeted degradation strategies. In kinase assays, BGP-21172 showed strong selectivity for CDK7, and two ADK binders—BGP-1892 and BGP-13486—demonstrated nanomolar activity in target engagement assays.

BridGene will present findings from "Discovery of a Covalent Inhibitor Targeting PAX8-Driven Ovarian Cancer" highlighting the identification of BGP-31609, a covalent small molecule inhibitor discovered through the IMTAC platform. BGP-31609 binds irreversibly to a single cysteine residue within the DNA-binding domain of PAX8, disrupting transcriptional activity and reducing the expression of downstream oncogenic targets including FGF18 and CCNA2. In biochemical and cellular assays, the compound showed dose-dependent inhibition of DNA binding in EMSA and selective suppression of PAX8-driven luciferase activity with minimal off-target effects. Importantly, BGP-31609 inhibited proliferation of PAX8-high OVCAR3 ovarian cancer cells while sparing PAX8-negative A549 cells, demonstrating target selectivity. These results establish BGP-31609 as a validated covalent binder to an historically undruggable transcription factor and a promising lead for treating PAX8-dependent malignancies.

"We’re excited to share these new discoveries that further validate the strength and versatility of our IMTAC chemoproteomics platform," stated Ping Cao, Ph.D., CEO and co-founder of BridGene Biosciences. "The data we’re presenting at AACR (Free AACR Whitepaper)-NCI-EORTC illustrate how IMTAC can uncover previously hidden binding sites and enable the development of covalent inhibitors against some of the most challenging oncology targets. These findings reflect our commitment to expanding what’s possible in small molecule drug discovery and to translating this science into meaningful therapies for patients."

The three poster presentations will be available on the AACR (Free AACR Whitepaper)-NCI-EORTC conference website following the sessions. BridGene’s scientific team will be available to discuss the data and the continued advancement of the company’s IMTAC platform in driving discovery of covalent small molecule drugs for previously undruggable targets.

Abstract Title:

Discovery of a Highly Potent and Selective Covalent FGFR3 Inhibitor

Session:

Poster Session B

Date and Time:

Friday, October 24, 12:30-4pm

Location:

Hynes Convention Center, Boston – Level 2, Exhibit Hall D

Abstract Title:

IMTAC: A Proteome-Wide Live-Cell Screening Platform for Discovering Covalent Binders to Diverse Targets Including GPCRs, Phosphatases, and More

Session:

Poster Session C

Date and Time:

Saturday, October 25, 12:30-4pm

Location:

Hynes Convention Center, Boston – Level 2, Exhibit Hall D

Abstract Title:

Discovery of a Covalent Inhibitor Targeting PAX8-Driven Ovarian Cancer

Session:

Poster Session B

Date and Time:

Friday, October 24, 12:30-4pm

Location:

Hynes Convention Center, Boston – Level 2, Exhibit Hall D

Genprex Announces Registered Direct Offering of up to $8.2 Million Priced At-The-Market Under Nasdaq Rules

On October 23, 2025 Genprex, Inc. ("Genprex" or the "Company") (NASDAQ: GNPX), a clinical-stage gene therapy company focused on developing life-changing therapies for patients with cancer and diabetes, reported that it has entered into definitive agreements for the issuance and sale of 243,622 shares of common stock at a purchase price of $11.21 per share in a registered direct offering priced at-the-market under Nasdaq rules. In a concurrent private placement, the Company will issue unregistered short-term warrants to purchase an aggregate of up to 487,244 shares of common stock at an exercise price of $11.00 per share that will be immediately exercisable upon issuance and will expire twenty-four months from the effective date of a registration statement registering for resale the shares of common stock underlying the warrants. The closing of the offering is expected to occur on or about October 24, 2025, subject to the satisfaction of customary closing conditions.

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H.C. Wainwright & Co. is acting as the exclusive placement agent for the offering.

The gross proceeds to the Company from the offering are expected to be approximately $2.7 million before deducting placement agent fees and other offering expenses payable by the Company. The potential additional gross proceeds to the Company from the short-term warrants, if fully-exercised on a cash basis, will be approximately $5.5 million. No assurance can be given that any of such short-term warrants will be exercised for cash or at all. The Company intends to use the net proceeds from the offering for working capital and general corporate purposes.

The shares of common stock offered in the registered direct offering (but not the unregistered short-term warrants issued in the concurrent private placement nor the shares of common stock underlying the unregistered short-term warrants) described above are being offered by the Company pursuant to a "shelf" registration statement on Form S-3 (File No. 333-271386) that was declared effective by the Securities and Exchange Commission (the "SEC") on June 9, 2023. The offering of the shares of common stock in the registered direct offering is being made only by means of a prospectus, including a prospectus supplement, forming a part of the effective registration statement. A final prospectus supplement and accompanying prospectus relating to the registered direct offering will be filed with the SEC. Electronic copies of the final prospectus supplement and accompanying prospectus may be obtained, when available, on the SEC’s website at View Source or by contacting H.C. Wainwright & Co., LLC at 430 Park Avenue, 3rd Floor, New York, New York 10022, by phone at (212) 856-5711 or e-mail at [email protected].

The unregistered warrants described above and the shares of common stock issuable upon exercise of such warrants are being offered in a private placement under Section 4(a)(2) of the Securities Act of 1933, as amended (the "Securities Act"), and/or Regulation D promulgated thereunder and have not been registered under the Securities Act, or applicable state securities laws. Accordingly, the unregistered warrants and underlying shares of common stock may not be offered or sold in the United States except pursuant to an effective registration statement or an applicable exemption from the registration requirements of the Securities Act and such applicable state securities laws.

This press release does not constitute an offer to sell or the solicitation of an offer to buy these securities, nor shall there be any sale of these securities in any state or jurisdiction in which such offer, solicitation or sale would be unlawful prior to the registration or qualification under the securities laws of any such state or jurisdiction.

(Press release, Genprex, OCT 23, 2025, View Source [SID1234656944])

HanchorBio’s Novel CD47-SIRPα Therapeutic HCB101 Accepted for Publication in Prestigious Journal of Hematology & Oncology

On October 23, 2025 HanchorBio Inc. (TPEx: 7827), a global clinical-stage biotechnology company developing next-generation immunotherapies, reported that its manuscript describing the discovery and preclinical development of HCB101, an engineered SIRPα-Fc fusion protein, has been published in the Journal of Hematology & Oncology (SCI Impact Factor 40.4; for reference, leading journals in the field of immuno-oncology include Journal of Clinical Oncology (impact factor 41.9), The Lancet Oncology (35.9), and Nature Cancer (28.5)).

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The publication, titled "HCB101: A Novel Potent Ligand-Trap Fc-fusion Protein Targeting the CD47-SIRPα Pathway with High Safety and Preclinical Efficacy for Hematological and Solid Tumors," describes the rational protein engineering that enabled HCB101 to restore macrophage-mediated phagocytosis and bridge innate and adaptive immune responses while reducing red blood cell binding. In preclinical studies, HCB101 showed broad activity across more than 80 xenograft and PDX tumor animal models with a safety profile that differs from first- and second-generation CD47-targeting agents.

Notably, a US competitor focusing on CD47/SIRPα published findings in JHO in November 2020, reporting on a third-generation anti-CD47–SIRPα therapy. This underscores the journal’s strong recognition within the field. The continued publication of anti-CD47 biologics in JHO highlights both the scientific importance of ongoing advancements and the journal’s role as a leading international platform for preclinical and translational research on anti-CD47 therapies.

"Publication in the Journal of Hematology & Oncology affirms the scientific rigor and innovation behind HCB101 and emphasizes its differentiated preclinical foundation," said Scott Liu, PhD, Chairman, CEO, and Founder of HanchorBio. "Importantly, these insights are being directly translated into clinical studies: combined with standard-of-care, HCB101 has demonstrated a clear dose-dependent efficacy profile in 2L gastric cancer, culminating in a nearly 90% partial response rate at 5.12 and 8.0 mg/kg. In parallel, we have now escalated monotherapy dosing to 30 mg/kg without safety concerns. These milestones highlight HCB101’s potential to serve as a backbone immunotherapy across solid tumors and hematologic malignancies and lay the groundwork for expanding into autoimmune indications where CD47-SIRPα biology is also potentially useful in creating a new B-cell depletion therapy."

Clinical Progress Strengthens Differentiated Best-in-Class Profile
HCB101 is currently being evaluated in multinational Phase 1 and Phase 1b/2a trials:

Monotherapy (HCB101-101, NCT05892718):
The Safety Review Committee (SRC) has reviewed the safety data up to 30 mg/kg weekly and found no dose-limiting toxicities, confirming a wide therapeutic window. Early signs of efficacy included two confirmed partial responses (PRs) in head and neck squamous cell carcinoma and marginal zone lymphoma, along with stable disease (SD) in nine patients, including over 40 weeks of disease control in platinum-resistant ovarian cancer.
Combination (HCB101-201, NCT06771622):
In the triplet regimen for 2L-gastric cancer (HCB101 + ramucirumab + paclitaxel), emerging activity was first observed at 2.56 mg/kg, where evaluable patients achieved SD with modest tumor shrinkage, averaging a 6% reduction in tumor size in the dose cohort. At 5.12 mg/kg, all three evaluable patients achieved confirmed PRs (33%–46% tumor reductions). At 8.0 mg/kg, all three evaluable patients have now achieved confirmed PRs (tumor shrinkage up to -78%) after extended follow-up. Together, these results represent a nearly 90% confirmed response rate (6 of 7 patients) at ≥ 5.12 mg/kg dose level — a striking outcome in a setting where the typical overall response rate (ORR) for the SOC is only 26.5%.
"The data now published in JHO validate the design strategy that made HCB101 possible – balancing high efficacy with a clean safety margin where earlier CD47-targeting agents failed," added Wenwu Zhai, PhD, Chief Scientific Officer of HanchorBio. "Seeing those preclinical insights translate into durable monotherapy activity and remarkable combination dose-dependent responses in gastric cancer provides confidence not only for oncology but also for new areas such as autoimmunity. HCB101’s differentiated mechanism and safety profile open the door to rational combinations and next-generation applications well beyond cancer."

About HCB101: A Differentiated CD47-SIPRα Blockade
HCB101 is a 3.5th-generation, affinity-optimized SIRPα-Fc fusion protein with intact IgG4 effector function, developed using HanchorBio’s proprietary FBDB platform. Engineered for selective CD47 blinding on tumors with low affinity for red blood cells, HCB101 avoids the hematologic toxicities commonly associated with anti-CD47 monoclonal antibodies, while preserving strong antibody-dependent cellular phagocytosis (ADCP) and innate-to-adaptive immune bridging.

Key Differentiators of HCB101:

Enhanced safety: Low RBC binding minimizes anemia and thrombocytopenia risk.
Robust immune activation: Engineered to enhance ADCP and innate-to-adaptive bridging.
Broad tumor applicability: Demonstrated activity in >80 PDX/CDX preclinical models.
Clinical translation: Early efficacy as monotherapy with durable disease control, and 100% ORR and disease control rate (DCR) at the middle dose cohort in combination with standard-of-care for 2L-gastric cancer.

(Press release, Hanchor Bio, OCT 23, 2025, View Source;oncology-302592241.html [SID1234656961])

Blenrep approved by US FDA for use in treatment of relapsed/refractory multiple myeloma

On October 23, 2025 GSK plc (LSE/NYSE: GSK) reported the US Food and Drug Administration (FDA) has approved Blenrep (belantamab mafodotin-blmf) in combination with bortezomib and dexamethasone (BVd) for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least two prior lines of therapy, including a proteasome inhibitor (PI) and an immunomodulatory (IMID) agent.

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The Blenrep approval is supported by data from the pivotal DREAMM-7 phase III trial. In patients who had two or more prior lines of therapy (3L+), including a PI and an IMID, Blenrep in combination demonstrated a clinically meaningful 51% reduction in the risk of death [HR 0.49, 95% confidence interval (CI): 0.32-0.76] and a tripled median progression-free survival (PFS) of 31.3 months [95% CI: 23.5-NR)] versus 10.4 months [95% CI: 7.0-13.4] for a daratumumab-based triplet (DVd) [HR 0.31, 95% CI: 0.21-0.47]. The safety and tolerability profiles of the Blenrep combination were broadly consistent with the known profiles of the individual agents.2

Tony Wood, Chief Scientific Officer, GSK, said: "Today’s FDA approval of Blenrep is another significant milestone, providing potential for superior efficacy, including overall survival, to US patients. There is an urgent need for new and novel therapies, as nearly all patients with multiple myeloma experience relapse and re-treating with the same mechanism of action often leads to suboptimal outcomes. As the only anti-BCMA agent that can be administered across healthcare settings, including in community centres where 70% of patients receive care, Blenrep fulfils a major patient need. We believe Blenrep can redefine treatment for patients with multiple myeloma in all parts of the world, and we are accelerating its development in earlier lines of therapy to support its use across all stages of this difficult-to-treat cancer."

Working closely with the FDA, Blenrep is available through a new, streamlined Risk Evaluation and Mitigation Strategy (REMS). The new REMS supports appropriate use and patient safety while reducing administrative burden through simplified patient forms, removal of duplicative checklists and efficient communication between HCPs and either optometrists or ophthalmologists monitoring eye care. GSK will also offer Together with GSK, an optional patient support programme available to all US patients prescribed Blenrep.

Data from the DREAMM (DRiving Excellence in Approaches to Multiple Myeloma) clinical trial programme will be submitted to the National Comprehensive Cancer Network (NCCN) guidelines this year. Recent results from the DREAMM studies, alongside emerging real-world evidence, provide a growing body of data for Blenrep.5,6

Sagar Lonial, MD, Chief Medical Officer, Winship Cancer Institute of Emory University in Atlanta, Georgia, Chair of Emory Department of Hematology and Medical Oncology, said: "With the approval of Blenrep, we now have a community-accessible BCMA-targeting agent with the potential to improve outcomes for patients following two or more prior lines of treatment, where options are limited. This approval marks an important advance in the US relapsed/refractory treatment landscape."

Michael Andreini, President and Chief Executive Officer of the Multiple Myeloma Research Foundation and the Multiple Myeloma Research Consortium, said: "The reality for most patients with multiple myeloma is a relentless cycle of remission and relapse, as their disease becomes refractory to treatments. Patients urgently need more effective treatment options that can offer more quality time with their loved ones. We see the potential for Blenrep in combination to help patients achieve this."

GSK is advancing the DREAMM clinical programme to demonstrate Blenrep’s potential benefit in earlier lines of treatment. Follow-up continues for overall survival (OS) in both DREAMM-7 and DREAMM-8 with data expected in early 2028, including in patients who have received only one prior line of therapy. DREAMM-10, a phase III trial in newly diagnosed transplant-ineligible patients, which represent over 70% of patients starting therapy, was initiated in Q4-2024.4 Interim efficacy and safety data for Blenrep as a first line treatment are expected in early 2028 with enrolment expanded to US sites to increase US patient representation in the study population. GSK continues to work with the FDA for US patients.

Approvals outside of the US
Blenrep combinations are approved in 2L+ relapsed or refractory multiple myeloma in the European Union7, UK8, Japan9, Canada, Switzerland and Brazil. Applications are currently under review in other markets globally, including China10 where the application is based on the results of DREAMM-7 and has been granted Breakthrough Therapy Designation and Priority Review.

About multiple myeloma
Multiple myeloma is the third most common blood cancer globally and is generally considered treatable but not curable.11,12 There are approximately 180,000 new cases of multiple myeloma diagnosed globally each year. Research into new therapies is needed as multiple myeloma commonly becomes refractory to available treatments.13 Many patients with multiple myeloma, including approximately 70% in the US, are treated in a community cancer setting, leaving an urgent need for new, effective therapies with manageable side effects that can be administered outside of an academic centre.3,15,16

About Blenrep
Blenrep is a monoclonal ADC (antibody-drug conjugate) comprising a humanised BCMA (B-cell maturation antigen) conjugated to the cytotoxic agent auristatin F via a non-cleavable linker. The drug linker technology is licensed from Seagen Inc.; the monoclonal antibody is produced using POTELLIGENT Technology licensed from BioWa Inc., a member of the Kyowa Kirin Group.

Indication
In the US, Blenrep is indicated in combination with bortezomib and dexamethasone (BVd) for the treatment of adult patients with relapsed or refractory multiple myeloma who have received at least two prior lines of therapy, including a proteasome inhibitor and an immunomodulatory agent.

Please see accompanying US Prescribing Information which will soon be available here17.

About DREAMM-7
DREAMM-7 is a multicentre, open-label, randomised phase III clinical trial evaluating the efficacy and safety of belantamab mafodotin combined with bortezomib plus dexamethasone (BVd) compared to daratumumab combined with bortezomib plus dexamethasone (DVd) in patients with relapsed or refractory multiple myeloma who previously were treated with at least one prior line of multiple myeloma therapy, with documented disease progression during or after their most recent therapy. The trial enrolled 494 participants who were randomised 1:1 to receive either BVd or DVd. Belantamab mafodotin was administered at a dose of 2.5mg/kg intravenously every three weeks in combination for the first eight cycles and then continued as a single agent. The primary endpoint was PFS as per an independent review committee, with secondary endpoints including OS, duration of response (DOR), and minimal residual disease (MRD) negativity rate as assessed by next-generation sequencing. Other secondary endpoints include overall response rate (ORR), safety, and patient reported and quality of life outcomes.

PFS results17 were presented at the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Plenary Series in February 2024 and published in the New England Journal of Medicine. OS results18 were presented at the American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting in December 2024.

About DREAMM-10
DREAMM-10 is a multicentre, open-label, randomised phase III clinical trial in newly diagnosed transplant ineligible patients with multiple myeloma, evaluating belantamab mafodotin plus lenalidomide and dexamethasone (BRd) versus daratumumab plus lenalidomide and dexamethasone (DRd).

(Press release, GlaxoSmithKline, OCT 23, 2025, View Source [SID1234656945])