On March 18, 2026 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 at the upcoming 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting being held April 17-22, 2026 in San Diego, California. The collaborators will present positive preclinical data from studies of its lead drug candidate, Reqorsa Gene Therapy (quaratusugene ozeplasmid, also referred to as Quar Oze), for the treatment of lung cancer.

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"The selection of three distinct abstracts for presentation at the 2026 American Association for Cancer Research (AACR) (Free AACR Whitepaper) underscores the robust preclinical evidence supporting REQORSA’s multi-faceted potential in the treatment of cancer," said Ryan Confer, President and Chief Executive Officer at Genprex. "These findings advance our understanding of TUSC2’s therapeutic mechanisms and its impact on lung cancer. Additionally, the identification of TROP2 and PTEN as potential biomarkers of response to TUSC2 gene therapy in non-small cell lung cancer is a pivotal development, providing insights that could refine patient selection strategies and optimize the therapeutic efficacy of REQORSA in a clinical setting."

The featured Genprex-supported posters to be presented at AACR (Free AACR Whitepaper) 2026:

Title: "TROP2 and PTEN are biomarkers of primary resistance to TUSC2 gene therapy in non-small cell lung cancer (NSCLC)"

Session Category: Experimental and Molecular Therapeutics

Session Title: Mechanisms of Drug Resistance 1

Session Date and Time: April 19, 2026 from 2-5 p.m. PT

Location: Poster Section 16

Poster Board Number: 24

Abstract Presentation Number: 391

In this study, researchers established models primarily resistant to TUSC2 gene therapy (REQORSA or Quar Oze) to find biomarkers indicative of TUSC2 gene therapy resistance in NSCLC cell lines, PDX-derived organoids (PDXOs), and patient-derived xenografts (PDXs). A panel of 10 NSCLC cell lines screened for TUSC2 sensitivity showed resistance in 50% of the cell lines, as assessed by annexin V staining and colony formation assays. Researchers evaluated TUSC2 sensitivity in 12 NSCLC PDXOs using ATP-based viability assays in 3D culture following TUSC2 or empty vector transfection. While some PDXOs were highly responsive to TUSC2 within 72 hours post-transfection, 50% of PDXOs exhibited primary resistance. TC314AR (Acquired Resistance) PDX tumors and xenograft models (A549AR, H1299AR, H23AR) were developed, grown in NSG mice, and then treated with TUSC2 gene therapy. 20-30% of tumors in every model showed resistance, with no significant reduction in size compared to the control tumors after treatment. Protein expression profiling using reverse-phase protein array (RPPA) analysis of 500 proteins showed distinct expression signatures, with several candidate biomarkers significantly altered in resistant cell lines and PDXOs. RPPA analysis of residual tumors from both the xenograft and PDX models revealed significant but model-specific alterations in protein expression between responders and non-responders. Comparative analyses across the three models showed low expression of TROP2 and high expression of PTEN as potential biomarkers of primary resistance. Overexpression of TROP2 in H1299 and H460 cells increased TUSC2-induced apoptosis. These findings suggest that TROP2 and PTEN may serve as biomarkers to predict TUSC2 response and guide therapeutic strategies in NSCLC.

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

Session Category: Experimental and Molecular Therapeutics

Session Title: RNA, Gene and Cell Therapies, and Enabling Assay Technologies

Session Date and Time: April 19, 2026 from 2-5 p.m. PT

Location: Poster Section 19

Poster Board Number: 12

Abstract Presentation Number: 469

In this study, researchers evaluated TUSC2 expression in a range of ALK+ cell lines and patient-derived organoids (PDOs), both prior to and following exposure to quaratusugene ozeplasmid (Quar Oze). The findings show that Quar Oze-driven TUSC2 overexpression initiates a robust pro-apoptotic response in ALK-positive (ALK+) models, not only in cells that are sensitive but also with acquired resistance (generated in the lab) to the ALK inhibitor, alectinib. This is evidenced by increased pro-apoptotic markers and lower cell viability when Quar Oze is used in combination with alectinib. To further assess the Quar Oze and alectinib combination, researchers tested it in two in vivo models: (1) an alectinib-sensitive model using subcutaneous injection of NCI-H2228 ALK+ cells into nude mice, and (2) an alectinib-resistant model using ALK167 PDX implants in NSG mice. Once tumors reached ~ 100 mm³, mice were randomized into four groups: vehicle control; Quar Oze alone (25 μg/mouse, IV, every three days); alectinib alone (0.5 mg/kg for sensitive or 15 mg/kg for resistant, oral, daily); and Quar Oze plus alectinib at the same doses. In the sensitive model, tumors in the alectinib-treated group shrank by 60%. Notably, treatment with Quar Oze alone, and particularly Quar Oze combined with alectinib, resulted in 79% tumor shrinkage (p value 0.0135 versus control), demonstrating a 23% improved outcome compared to alectinib alone. This suggests that Quar Oze might serve as a valuable adjunct therapy, especially for patients who have advanced disease and/or experience resistance to TKIs.

In the resistant model, the Quar Oze and alectinib combination produced a synergistic effect, achieving the greatest tumor reduction and improved overall survival (p value 0.0001 versus control), further supporting the clinical potential of this therapeutic strategy in ALK+ NSCLC. Altogether, the in vitro and in vivo studies indicate that Quar Oze-mediated TUSC2 overexpression in ALK+ NSCLC effectively curtails tumor growth and proliferation via activation of apoptotic pathways, providing a compelling rationale for progressing toward a clinical trial.

Title: "Restoring TUSC2 function boosts NK cell cytotoxicity and antitumor immunity in vivo and in vitro"

Session Category: Immunology

Session Title: Immune Cell Biology and Tumor-Immune Crosstalk

Session Date and Time: April 19, 2026 from 2-5 p.m. PT

Location: Poster Section 8

Poster Board Number: 7

Abstract Presentation Number: 164

Tusc2 knockout (Tusc2 KO) and wild-type (Tusc2 WT) mice were challenged with syngeneic tumor cells (344SQ) and treated with TUSC2-expressing lipoparticles (quaratusugene ozeplasmid, Quar Oze). The therapeutic group received Quar Oze after tumor establishment starting at day 8 from cell line injection, while the prophylaxis group received Quar Oze before tumor establishment, starting 2 days before injection of cell lines. Control groups received empty lipoparticles. After three weeks from cell line injection, tumor volumes were assessed, and mice were euthanized for collection of tumors, spleens, and tumor-draining lymph nodes (TDLN). Immune cell phenotypes and cytotoxic markers were analyzed using flow cytometry. In vitro studies evaluated NK cell cytotoxic function following Quar Oze treatment by measuring CD107a degranulation and CellTrace Violet–based proliferation. In the therapeutic treatment group, 67% of Tusc2 KO mice and 33% of Tusc2 WT mice achieved complete tumor regression, with all remaining mice showing significant tumor reduction compared with controls. Prophylactic administration did not induce complete tumor clearance but consistently reduced tumor growth across all mice. Immune profiling of the tumor microenvironment revealed that Quar Oze robustly enhanced NK cell cytotoxicity, particularly increasing granzyme B and perforin expression. In vitro assays confirmed that TUSC2 restoration significantly increased NK cell degranulation and proliferation, supporting the in vivo findings.

In conclusion, TUSC2 acts as a critical enhancer of innate antitumor immunity by boosting NK cell cytotoxic function. Therapeutic delivery of TUSC2 via Quar Oze suppresses tumor progression and, in many cases, drives complete tumor elimination. These results highlight TUSC2 as a potent immunomodulatory tumor suppressor and support its development as a dual-function therapeutic that directly targets tumor cells while also activating NK cell–mediated immunity.

About TUSC2

TUSC2 is the tumor suppressor gene used in REQORSA (quaratusugene ozeplasmid or Quar Oze). REQORSA consists of a TUSC2 gene expressing plasmid 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 show that the uptake of TUSC2 in tumor cells in vitro after REQORSA treatment was 10 to 33 times the uptake in normal cells.

The aforementioned 2026 AACR (Free AACR Whitepaper) posters will be available on Genprex’s website following the completion of their live presentations.

(Press release, Genprex, MAR 18, 2026, View Source [SID1234663700])

On March 18, 2026 Sichuan Kelun-Biotech Biopharmaceutical Co., Ltd. ("Kelun-Biotech" or the "Company", 6990.HK), reported that the final OS analysis from the pivotal study (OptiTROP-Lung03) of sacituzumab tirumotecan (sac-TMT, also known as SKB264/MK-2870) (佳泰莱), a TROP2 ADC has been selected as a Late-Breaking Abstract (LBA) (Presentation Number: LBA4) at the 2026 European Lung Cancer Congress (ELCC) to be held in Copenhagen, Denmark, from March 25 to 28, 2026 (local time). Professor Yunpeng Yang from the Sun Yat-sen University Cancer Center will present the findings to the global research community during a Mini Oral Session. The abstract was published on the ESMO (Free ESMO Whitepaper) Open.

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The OptiTROP-Lung03 study was designed to evaluate the efficacy and safety profile of sac-TMT monotherapy (5 mg/kg every other week) versus docetaxel for the treatment of patients with locally advanced or metastatic EGFR-mutant NSCLC who have previously treated with an EGFR-TKI and platinum-based chemotherapy. Previously reported results presented at the ASCO (Free ASCO Whitepaper) 2025 meeting in 137 randomized participants demonstrated that sac-TMT achieved statistically significant and clinically meaningful improvements in progression-free survival (PFS) and overall survival (OS) compared to docetaxel——the hazard ratio (HR) for BICR-assessed PFS was 0.30 (95% CI: 0.20–0.46, one-sided p<0.001) and HR for OS was 0.49 (95% CI: 0.27–0.88, one-sided p=0.007)[1]. Based on these positive results, sac-TMT received approval from the National Medical Products Administration (NMPA) for this indication, which has also been included in China’s National Reimbursement Drug List (NRDL).

At the 2026 ELCC, the final OS analysis, along with updated PFS and additional data from the OptiTROP-Lung03 study will be presented. As of December 11, 2025, the median follow-up was 23.8 months. Key highlights are as follows:

In the docetaxel control group, 41.3% of patients crossed over to receive sac-TMT after disease progression.
Considering the impact of OS from crossover treatment in the control group, adjusted and analysed by the pre-specified rank-preserving structural failure time (RPSFT) model, the median OS was 20.0 months in the sac-TMT group vs 11.2 months in the docetaxel group (HR 0.45, 95% CI: 0.28–0.73), with 18-month OS rate of 54.7% vs 9.1%. Without adjustment for subsequent sac-TMT treatment in the control group, median OS was 20.0 months vs 13.5 months (HR 0.63, 95% CI: 0.40–0.98).
Median PFS assessed by investigators (INV) was 7.9 months vs 2.8 months (HR 0.23, 95% CI: 0.15-0.35).
Notably, based on another study, the OptiTROP-Lung04 study, sac-TMT has been approved by the NMPA for the treatment of advanced or metastatic EGFR-mutant NSCLC after progression on EGFR-TKI therapy, with the findings concurrently published in The New England Journal of Medicine[2]. In this study among the EGFR-mutant NSCLC population who have progressed after prior EGFR-TKI and platinum-based chemotherapy, sac-TMT demonstrated a statistically significant and clinically meaningful increase in overall survival，with a median OS of 20 months. The consistent positive findings from two pivotal registrational studies further reinforce sac-TMT’s leading position in the treatment landscape for pre-treated EGFR-mutant NSCLC, offering a more definitive and long-term survival benefit option for patients with advanced lung cancer.

About Sac-TMT

Sac-TMT, a core product of the Company, is a novel human TROP2 ADC in which the Company has proprietary intellectual property rights, targeting advanced solid tumors such as NSCLC, breast cancer (BC), gastric cancer (GC), gynecological tumors, among others. Sac-TMT is developed with a novel linker to conjugate the payload, a belotecan-derivative topoisomerase I inhibitor with a drug-to-antibody-ratio (DAR) of 7.4. Sac-TMT specifically recognizes TROP2 on the surface of tumor cells by recombinant anti-TROP2 humanized monoclonal antibodies, which is then endocytosed by tumor cells and releases the payload KL610023 intracellularly. KL610023, as a topoisomerase I inhibitor, induces DNA damage to tumor cells, which in turn leads to cell-cycle arrest and apoptosis. In addition, it also releases KL610023 in the tumor microenvironment. Given that KL610023 is membrane permeable, it can enable a bystander effect, or in other words kill adjacent tumor cells.

In May 2022, the Company licensed the exclusive rights to MSD (the tradename of Merck & Co., Inc, Rahway, NJ, USA) to develop, use, manufacture and commercialize sac-TMT in all territories outside of Greater China (which includes Mainland China, Hong Kong, Macao and Taiwan).

To date, four indications for sac-TMT have been approved and marketed in China for: EGFR mutant-positive locally advanced or metastatic non-squamous NSCLC following progression on EGFR-TKI therapy and platinum-based chemotherapy; unresectable locally advanced or metastatic TNBC who have received at least two prior systemic therapies (at least one of them for advanced or metastatic setting); EGFR mutant-positive locally advanced or metastatic non-squamous NSCLC who progressed after treatment with EGFR-TKI therapy; unresectable or metastatic HR+/HER2- (IHC 0, IHC 1+ or IHC 2+/ISH-) BC who have received prior ET and at least one line of chemotherapy in advanced setting. The first two indications listed above have been included in China’s National Reimbursement Drug List (NRDL). This inclusion is expected to bring clinical benefits to a greater number of patients with BC and NSCLC. Additionally, sac-TMT has been granted six Breakthrough Therapy Designations (BTDs) by the NMPA.

Sac-TMT is the world’s first TROP2 ADC drug approved for marketing in lung cancer. As of today, Kelun-Biotech has initiated 9 registrational clinical studies in China. MSD is evaluating 17 ongoing Phase III global clinical studies of sac-TMT as a monotherapy or with pembrolizumab or other anti-cancer agents for several types of cancer. These studies are sponsored and led by MSD.

(Press release, Kelun, MAR 18, 2026, View Source [SID1234663716])

On March 18, 2026 Greenwich LifeSciences, Inc. (Nasdaq: GLSI) (the "Company"), a clinical-stage biopharmaceutical company focused on its Phase III clinical trial, FLAMINGO-01, which is evaluating Fast Track designated GLSI-100, an immunotherapy to prevent breast cancer recurrences, reported an update on the upcoming AACR (Free AACR Whitepaper) Meeting 2026.

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Two abstracts and two posters were accepted for presentation. The titles and authors of the abstracts are as follows:

Abstract Number: CT138 – Poster Section 52 on April 20, 2026, 2-5pm

Abstract Title: Preliminary delayed-type-hypersensitivity immune response results from open-label arm of on-going Phase III study to evaluate the efficacy and safety of GLSI-100 (GP2 + GM-CSF) in breast cancer patients with residual disease or high-risk PCR after both neo-adjuvant and postoperative adjuvant anti-HER2 therapy, Flamingo-01

Snehal S. Patel1, Jaye Thompson1, F. Joseph Daugherty1, Francois-Clement Bidard2, William J. Gradishar3, Marcus Schmidt4, Miguel Martin5, Joyce A. O’Shaughnessy6, Hope S. Rugo7, Cesar A. Santa-Maria8, Laura M. Spring9, Mothaffar F. Rimawi10

1Greenwich LifeSciences, Stafford, TX,2Institut Curie, Paris, France,3Northwestern University, Chicago, IL,4University Medical Center Mainz, Mainz, Germany,5GEICAM, Madrid, Spain,6Sarah Cannon Research Institute, Dallas, TX,7City of Hope Comprehensive Cancer Center, Duarte, CA,8Johns Hopkins University, Baltimore, MD,9Massachusetts General Hospital, Boston, MA,10Lester and Sue Smith Breast Center, Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX

This will be the first abstract and poster from FLAMINGO-01 with statistically significant immune response data, potentially with subgroup analysis by the most prevalent HLA types. A positive immune response is an indicator that the immune system has been activated against recurring cancer cells, potentially leading to the prevention of metastatic breast cancer and improved long term survival.
Immune responses to GP2 were measured at baseline and over time using delayed-type-hypersensitivity (DTH) skin tests and other methods. The DTH skin test measures the diameter of the skin immune response to GP2 in millimeters, 48-72 hours after intradermal injection of a low concentration of GP2 without GM-CSF.

Abstract Number: CT227 – Poster Section 51 on April 21, 2026, 9am-12pm

Abstract Title: Phase III study to evaluate the efficacy and safety of GLSI-100 (GP2 + GM-CSF) in breast cancer patients with residual disease or high-risk PCR after both neo-adjuvant and postoperative adjuvant anti-HER2 therapy, Flamingo-01

Jaye Thompson1, Snehal Patel1, Mira Patel1, Anu Tammareddi1, F. Joseph Daugherty1, Mothaffar F. Rimawi2

1Greenwich LifeSciences, Stafford, TX,2Lester and Sue Smith Breast Center, Dan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX

This abstract and poster will continue to update principal investigators at the conference about the study design of FLAMINGO-01.

The Steering Committee authoring abstract CT138 is comprised of the following experts in the field of breast cancer oncology representing prominent teaching hospitals in the US and 4 of the largest breast oncology networks in the US, Germany, France, and Spain:

Dr. Mothaffar F. Rimawi – Professor of Medicine at the Baylor College of Medicine and Executive Medical Director and Co-Leader, Breast Cancer Program of the Dan L Duncan Comprehensive Cancer Center
Dr. Francois-Clement Bidard – Professor of Medical Oncology, UVSQ/Paris Saclay University, Head of Breast Cancer Group, Institut Curie, Vice-Chair of the French Breast Cancer research group UCBG (Unicancer)
Dr. William J. Gradishar – Professor of Medicine at the Feinberg School of Medicine at Northwestern University, Chief of Hematology and Oncology in the Department of Medicine, and Betsy Bramsen Professor of Breast Oncology
Dr. Sibylle Loibl – Professor (apl) Goethe University Frankfurt/M, Clinical Consultant Centre for Haematology and Oncology/Bethanien Frankfurt/M, CEO of GBG Forschungs GmbH & Chair of the German Breast Group (GBG)
Dr. Miguel Martin – Professor of Medicine, Head, Medical Oncology Service, Gregorio Marañón General University Hospital, Complutense University, Madrid, CEO of GEICAM
Dr. Joyce A. O’Shaughnessy – Celebrating Women Chair in Breast Cancer, Baylor University Medical Center and Chair, Breast Cancer Program, Texas Oncology, US Oncology, Dallas, Texas
Dr. Hope S. Rugo – Director, Women’s Cancers Program, Division Chief, Breast Medical Oncology, Professor, Department of Medical Oncology & Therapeutics Research, City of Hope Comprehensive Cancer Center, Professor Emeritus, University of California, San Francisco
Dr. Cesar A. Santa-Maria – Associate Professor of Oncology, Breast and Gynecological Malignancies Group, Director of Breast Cancer Trials, Johns Hopkins Sidney Kimmel Comprehensive Cancer Center
Dr. Laura M. Spring – Assistant Professor, Medicine, Harvard Medical School, Attending Physician, Medical Oncology, Massachusetts General Hospital

About the AACR (Free AACR Whitepaper) Annual Meeting 2026

The AACR (Free AACR Whitepaper) is the first and largest cancer research organization dedicated to accelerating the conquest of cancer and has more than 61,000 members residing in 143 countries and territories. The AACR (Free AACR Whitepaper) Annual Meeting is the focal point of the cancer research community, where scientists, clinicians, other health care professionals, survivors, patients, and advocates gather to share the latest advances in cancer science and medicine. From population science and prevention; to cancer biology, translational, and clinical studies; to survivorship and advocacy; the AACR (Free AACR Whitepaper) Annual Meeting highlights the work of the best minds in cancer research from institutions all over the world.

About FLAMINGO-01 Open Label Phase III Data

More than 1,000 patients have been screened with a current screen rate of approximately 800 patients per year. The 250 patient non-HLA-A*02 arm is now fully enrolled, where all patients received GLSI-100, which is 5 times more treated patients and recurrence rate data than the approximately 50 patients treated in the Phase IIb trial. The Primary Immunization Series (PIS), which includes the first 6 GLSI-100 injections over the first 6 months and is required to reach peak protection, is followed by 5 booster injections given every 6 months to prolong the immune response, thereby providing longer-term protection.

In the non-HLA-A*02 arm, a preliminary analysis of recurrence rates after the PIS is completed shows an approximately 70-80% reduction in recurrence rate.
This observation is trending similarly to the Phase IIb trial results and hazard ratio where HLA-A*02 patients were treated and where breast cancer recurrences were reduced up to 80% compared to a 20-50% reduction in recurrence rate by other approved products.
The immune response at baseline prior to any GLSI-100 treatment, the increasing immune response during the PIS, and the safety profile of non-HLA-A*02 patients is trending similarly to the HLA-A*02 arms of FLAMINGO-01 and to the Phase IIb study.

Analysis of the open label data from FLAMINGO-01 has been conducted in a manner that maintains the study blind. The open label recurrence rate, immune response, and safety data is based on the patients enrolled to date in FLAMINGO-01 and the data provided by the clinical sites so far, which is not completed or fully reviewed, and is thus preliminary. While comparing any preliminary FLAMINGO-01 data to the Phase IIb clinical trial data may be possible, these preliminary results are not a prediction of future results, and the results at the end of the study may differ.

About GLSI-100 Phase IIb Study

In the prospective, randomized, single-blinded, placebo-controlled, multi-center (16 sites led by MD Anderson Cancer Center) Phase IIb clinical trial of HLA-A*02 breast cancer patients, 46 HER2/neu 3+ over-expressor patients were treated with GLSI-100, and 50 placebo patients were treated with GM-CSF alone. After 5 years of follow-up, there was an 80% or greater reduction in cancer recurrences in the HER2/neu 3+ patients who were treated with GLSI-100, followed, and remained disease free over the first 6 months, which we believe is the time required to reach peak immunity and thus maximum efficacy and protection. The Phase IIb results can be summarized as follows:

80% or greater reduction in metastatic breast cancer recurrence rate over 5 years of follow-up with a peak immune response at 6 months and well-tolerated safety profile.
The PIS elicited a potent immune response as measured by local skin tests and immunological assays.

About FLAMINGO-01 and GLSI-100

FLAMINGO-01 (NCT05232916) is a Phase III clinical trial designed to evaluate the safety and efficacy of Fast Track designated GLSI-100 (GP2 + GM-CSF) in HER2 positive breast cancer patients who had residual disease or high-risk pathologic complete response at surgery and who have completed both neoadjuvant and postoperative adjuvant trastuzumab based treatment. The trial is led by Baylor College of Medicine and currently includes US and European clinical sites from university-based hospitals and academic and cooperative networks with plans to open up to 150 sites globally. In the double-blinded arms of the Phase III trial, approximately 500 HLA-A*02 patients are planned to be randomized to GLSI-100 or placebo, and up to 250 patients of other HLA types are planned to be treated with GLSI-100 in a third arm. The trial has been designed to detect a hazard ratio of 0.3 in invasive breast cancer-free survival, where 28 events will be required. An interim analysis for superiority and futility will be conducted when at least half of those events, 14, have occurred. This sample size provides 80% power if the annual rate of events in placebo-treated subjects is 2.4% or greater.

For more information on FLAMINGO-01, please visit the Company’s website here and clinicaltrials.gov here. Contact information and an interactive map of the majority of participating clinical sites can be viewed under the "Contacts and Locations" section. Please note that the interactive map is not viewable on mobile screens. Related questions and participation interest can be emailed to: [email protected]

About Breast Cancer and HER2/neu Positivity

One in eight U.S. women will develop invasive breast cancer over her lifetime, with approximately 300,000 new breast cancer patients and 4 million breast cancer survivors. HER2 (human epidermal growth factor receptor 2) protein is a cell surface receptor protein that is expressed in a variety of common cancers, including in 75% of breast cancers at low (1+), intermediate (2+), and high (3+ or over-expressor) levels.

(Press release, Greenwich LifeSciences, MAR 18, 2026, View Source [SID1234663701])

On March 18, 2026 Sapience Therapeutics, Inc., a clinical-stage biotechnology company focused on the discovery and development of peptide therapeutics to address oncogenic and immune dysregulation that drive cancer, reported three poster presentations at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22, 2026, in San Diego, California. Sapience will present clinical and non-clinical results from ST316, a first-in-class antagonist of β-catenin, as well as results from its preclinical Fra1 antagonist peptide (FraAP) program, a first-in-class antagonist of the activator protein 1 (AP-1) complex.

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Poster Presentation Details:

Title: "ST316, a first in class β-catenin antagonist, demonstrates safety and efficacy in metastatic colorectal cancer (mCRC)"
Session Title: Phase II and Phase III Clinical Trials
Location: Poster Section 52, Poster Board Number 20
Abstract Number: CT156
Date and Time: Monday, April 20, 2026, 2:00PM – 5:00PM PST

Title: "Antagonism of β-catenin/BCL9 interaction suppresses polymorphonuclear myeloid-derived suppressor cell generation and maintenance"
Session Title: Oncogenic Pathways and Cancer Immunity
Location: Poster Section 7, Poster Board Number 5
Abstract Number: 5562
Date and Time: Tuesday, April 21, 2026, 2:00PM – 5:00PM PST

Title: "Targeted antagonism of the activator protein 1 transcription factor complex results in potent anti-tumor activity in HNSCC models"
Session Title: Oncogenic Transcription Factors and Cancer Programs
Location: Poster Section 24, Poster Board Number 17
Abstract Number: 4767
Date and Time: Tuesday, April 21, 2026, 9:00AM – 12:00PM PST

More information can be found on the AACR (Free AACR Whitepaper) Annual Meeting 2026 website.

About ST316

ST316 is a first-in-class antagonist of the interaction between β-catenin and its co-activator, BCL9, a complex responsible for driving oncogene expression and immune exclusion in multiple cancers where aberrant Wnt/β-catenin pathway signaling is observed. Aberrant activation of the Wnt/β-catenin pathway is a critical driver of tumor progression and immune evasion in tumors including colorectal cancer (CRC). Targeting this pathway is challenging for multiple reasons including its role in normal tissue physiology. BCL9 is a co-activator essential for oncogenic β-catenin activity, but not its physiologic functions, highlighting the β-catenin/BCL9 interaction as a therapeutic target. ST316 was designed to selectively disrupt the β-catenin and BCL9/9L interaction, resulting in disruption of oncogenic Wnt/β-catenin transcriptional activity and potent antitumor activity, with no negative impact on intestinal or bone physiology.

ST316-101 (NCT05848739) is a first-in-human, open-label, Phase 1/2 dose escalation and expansion study designed to determine the safety, tolerability, PK, PD and early efficacy of ST316. The Phase 1 dose escalation portion of the study tested various dose levels of ST316 in patients with selected advanced solid tumors that are known to harbor abnormalities of the Wnt/β-catenin signaling pathway, including colorectal cancer (CRC). ST316 is currently being evaluated in the Phase 2 portion of the study in CRC patients in combination with relevant standards of care and in multiple lines of treatment. The U.S. Food and Drug Administration (FDA) has granted Orphan Drug Designation to ST316 for the treatment of familial adenomatous polyposis (FAP).

(Press release, Sapience Therapeutics, MAR 18, 2026, View Source [SID1234663717])

On March 18, 2026 Sandoz (SIX:SDZ/OTCQX:SDZNY), the global leader in affordable medicines, reported a major license, development and commercialization partnership agreement with Samsung Bioepis Co., Ltd., marking a significant step to broaden patient access to high-quality biosimilar medicines worldwide.

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The agreement paves the way for the two companies to partner on up to five biosimilar assets. The first asset will be a vedolizumab biosimilar, which is in early-stage development. The reference medicine, Entyvio* (vedolizumab), is used to treat adult patients with Crohn’s disease, ulcerative colitis or pouchitis2,3.

Under the terms of the agreement, Sandoz will have exclusive rights to commercialize globally, except in China, Hong Kong, Taiwan, Macau and Republic of Korea. Samsung Bioepis will be responsible for development, regulatory submissions in key markets and manufacturing. Both companies have agreed to keep the financial details of the agreement confidential.

The partnership could expand the leading Sandoz pipeline to up to 32 assets and reinforces its commitment to capturing a significant share of the projected global biosimilar loss-of-exclusivity market opportunity, estimated at around USD 320 billion over the next decade1.

Richard Saynor, Chief Executive Officer, Sandoz, said: "This partnership underscores our unwavering commitment to expanding access to affordable, high-quality medicines for patients worldwide. It is another important step toward capitalizing on the unprecedented biosimilar market opportunity over the next decade while also strengthening our partnership with Samsung Bioepis."

Today’s news builds on the successful global partnership between the two companies first established in September 2023 for Pyzchiva (ustekinumab), which Sandoz launched in Europe in July 2024 and in the US in February 2025. The Pyzchiva collaboration is unaffected by the partnership announced today. In December 2025, the companies also signed an agreement for the commercialization of Epysqli, a biosimilar to eculizumab (Soliris**), for the Middle East and Africa region.

Sandoz continues to develop its leading pipeline of biosimilar medicines, building on its experience as the pioneer and global leader with a portfolio of 13 molecules available in nearly 100 countries.

(Press release, Sandoz, MAR 18, 2026, View Source [SID1234663630])