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])

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

On October 22, 2025 Aurigene Oncology Limited, a clinical-stage biopharmaceutical company developing novel therapies in oncology, reported that it will present new data from its proprietary Targeted Protein Degradation (TPD) and Proximity Inducer Platform (A-PROX) 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) being held at the Hynes Convention Centerin Boston, MA, from October 22–26, 2025.

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Aurigene’s A-PROX platform integrates library screening, direct-to-biology chemistries, proprietary ternary complex assays, modelling algorithms, and structure-based design to accelerate the discovery and optimization of both protein degraders, molecular glues and proximity inducers.

Through this integrated approach, Aurigene has advanced a strong pre-clinical portfolio of next-generation degraders, including a SMARCA2-selective degrader, which recently received Investigational New Drug (IND) approval from the United States Food and Drug Administration (FDA); a pan-KRAS degrader; a SMARCA4-selective degrader; and a p300 degrader.

"Our A-PROX platform represents a significant step forward in the rational discovery of targeted protein degraders and molecular glues," said Dr. Murali Ramachandra, CEO of Aurigene Oncology Ltd. "We are excited to share our progress at the AACR (Free AACR Whitepaper)-NCI-EORTC conference and continue advancing differentiated therapies that have the potential to transform cancer treatment."

These programmes underscore Aurigene’s capability to deliver potent, paralogue-selective, and mutant-agnostic degraders, enabling the targeting of previously undruggable oncology pathways. Aurigene’s proprietary long-acting injectable (LAI) formulation has enabled infrequent intravenous dosing, just once every three weeks for most molecules, while maintaining excellent efficacy.

Poster Presentations

Title: Identification of an orally bio-available SMARCA2 selective degrader for treatment of SMARCA4 mutant cancers
Presenting Author: Susanta Samajdar
Presentation Date/Time: Oct 25 12:30-4PM ET
Abstract Number: C025

This presentation describes the identification and characterization of an orally bioavailable SMARCA2 degrader with good potency and selectivity over SMARCA4. SMARCA2 and SMARCA4 regulate chromatin architecture by mobilizing and repositioning nucleosomes on DNA, which is critical for various genomic functions, including transcriptional regulation, DNA recombination and repair, and mitotic chromosome segregation. Loss-of-function mutations or silencing of SMARCA4 are frequently observed in multiple cancer types, where tumorigenesis becomes dependent on the residual SMARCA2 degrader with good potency and selectivity over SMARCA4. In this study, the lead SMARCA2 degrader demonstrated potent antitumor activity, driven by efficient SMARCA2 degradation, in multiple SMARCA4-deficient cell line-derived xenograft (CDX) models at well-tolerated dose levels. Additionally, with the use of Aurigene’s proprietary long-acting injectable (LAI) formulation, AUR110, a candidate with US-FDA clearance for first-in-human studies, has shown potent and comparable anti-tumor activity following once every three week intravenous dosing.

Aurigene will also be showcasing other pipeline programmes in poster presentations at the conference, including:

Title: Discovery and development of a highly differentiated, efficacious, first-in-class anti-SIRPα/β dual antibody with single agent phagocytosis activity
Presenting Author: Subhra Chakrabarty
Presentation Date/Time: Oct 24 12:30-4PM ET
Abstract Number: B077

Title: Discovery and preclinical characterization of novel macrocyclic KIF18A inhibitors for treatment of chromosomally instable tumors
Presenting Author: Susanta Samajdar
Presentation Date/Time: Oct 23 12:30-4PM ET
Abstract Number: A030

Title: Development of a Differentiated, Best-in-Class oral Cbl-b inhibitor with Robust Immune Activation and Favourable Safety for Cancer Immunotherapy
Presenting Author: Susanta Samajdar
Presentation Date/Time: Oct 25 12:30-4PM ET
Abstract Number: C059

(Press release, Aurigene Discovery Technologies, OCT 22, 2025, View Source [SID1234656893])

On October 22, 2025 IASO Biotherapeutics ("IASO Bio"), a biopharmaceutical company focused on the discovery, development, production, and commercialization of novel cell therapies, reported that the Blood published the latest results of its independently developed fully human anti-GPRC5D CAR-T cell therapy, RD118, for the treatment of relapsed/refractory multiple myeloma (R/R MM). The study demonstrates that RD118 exhibited significant efficacy and a manageable safety profile in heavily pretreated R/R MM patients, offering new therapeutic hope for the patients with a poor prognosis.

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The study entitled ‘Fully Human anti-GPRC5D CAR T-Cell Therapy RD118 Induces Durable Remissions in Relapsed/Refractory Multiple Myeloma’ has been published in Blood. Full text available at: View Source This is an open-label, phase 1 dose-escalation and expansion study to evaluate the efficacy and safety of RD118 in the treatment of R/R MM, which was conducted at Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, and Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (registered as NCT05759793 and NCT05219721).

A total of eighteen patients received RD118 infusion in this study, including 17 with R/R MM and 1 with a history of primary plasma cell leukemia (pPCL) who had relapsed after achieving complete remission. Among the 18 patients, the median age was 59.5 years, and the median line of prior therapies was 5. High-risk features included double-hit cytogenetics (50%), triple-class refractoriness (50%), penta-class refractoriness (22.2%), and prior anti-BCMA CAR-T therapy (38.9%). Following lymphodepletion with fludarabine and cyclophosphamide, patients received a single infusion of RD118 at one of three dose levels (1.0, 2.0, or 3.0×106 cells/kg) during the dose-escalation phase or 2.0×106 cells/kg in the expansion cohort. At a median follow-up of 17.0 months, results show that:

Efficacy: The overall response rate (ORR) was 94.4%, with 72.2% of patients achieving complete response or stringent complete responses (CR/sCR). Among the seven patients who had received prior BCMA-directed CAR T-cell therapy, the ORR was 85.7%, with 5 patients (71.4%) achieving CR/sCR. All three patients with extramedullary disease and the patient with pPCL achieved sCR and remained in remission at last follow-up. The median progression-free survival (PFS) was 18.2 months, with 12-month PFS and overall survival (OS) rates of 82.1% and 93.3%, respectively.

Safety: Cytokine release syndrome (CRS) occurred in 88.9% of patients, primarily grade 1-2. Only one patient developed grade 3 or higher CRS, which rapidly recovered with intensive management. One patient developed grade 3 immune effector cell–associated neurotoxicity (ICANS) which resolved within 72 hours. No cerebellar toxicities or treatment-related deaths were reported

Conclusion ：Fully human anti-GPRC5D CAR-T therapy RD118 demonstrated a 94.4% ORR and a median PFS of 18.2 months with a manageable safety profile in heavily over pretreated R/R MM, including patients who relapsed after prior anti-BCMA CAR-T therapy.

Professor Mi Jianqing from Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, commented: "Multiple myeloma remains an incurable malignant plasma cell disorder. While anti-BCMA CAR-T therapy has greatly transformed the treatment for relapsed/refractory patients, challenges such as antigen escape often leads to relapse, highlighting the need for novel targets to overcome these limitations. GPRC5D has attracted significant attention due to its high expression, specificity, and independence from BCMA. The current study results have validated its potential: among patients previously treated with anti-BCMA CAR-T therapy, RD118 achieved an 85.7% overall response rate, with 71.4% of patients reaching complete response, demonstrating that GPRC5D is a highly promising novel therapeutic target."

Professor Chunrui Li from Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, commented: "The innovative design of RD118 is the foundation of its outstanding clinical performance. RD118 is a novel GPRC5D-directed CAR-T that incorporates a fully human nanobody (VHH) as its antigen-binding domain. This design provides distinct advantages over conventional scFv, it is expected to lower immunogenicity, and potentially enhanced persistence, offering a new approach to overcome the safety limitations of existing comparable therapies. Meanwhile, the construct also includes a 4-1BB and a CD3ζsignal domains, which support expansion and sustained anti-tumor activity. Together, these features position RD118 as a highly competitive next-generation CAR-T product."

Ms. Jinhua Zhang, Founder, Chairwoman and CEO of IASO Bio, remarked: "We are delighted that the remarkable research results of IASO Bio’s independently developed anti-GPRC5D CAR-T product, RD118, for the treatment of R/R MM have been published in the prestigious international journal Blood. This achievement marks another significant milestone for the product following the IND approval from China’s NMPA in June 2024. The treatment landscape for multiple myeloma requires continuous innovation, and GPRC5D, alongside BCMA, are represents a crucial therapeutic target in this field. Developed based on our fully human antibody platform, RD118 is designed to provide a new treatment option for patients. It offers renewed hope particularly for those who have relapsed after prior anti-BCMA CAR-T therapy. This publication will further motivate us to advance the clinical development of RD118, with the goal of delivering this innovative therapy to more patients worldwide."

About RD118

RD118 is an autologous T-cell immunotherapy product targeting G protein-coupled receptor class C group 5 member D (GPRC5D). It can identify and eliminate malignant tumor cells expressing GPRC5D. GPRC5D is highly expressed on multiple myeloma cells. However, in normal tissues, its expression is limited to plasma cells and hair follicle cells. Such a feature has made GPRC5D a promising safe and effective target for the treatment of multiple myeloma.

The antigen recognition domain of RD118 is developed from IASO Bio’s proprietary fully human single-domain antibody library. It has advantages of high affinity, high specificity, and low immunogenicity. The intracellular domain is a fusion of 4-1BB (CD137) and CD3ζ signaling domains. RD118 has been subjected to extensive development and optimization in terms of antibody screening and structure design. The candidate molecule has demonstrated excellent in vitro cytotoxic activity and in vivo tumor suppression ability. Additionally, it has good expansion capability and persistence in vivo, indicating high development potential.

(Press release, IASO Biotherapeutics, OCT 22, 2025, View Source [SID1234656909])

On October 22, 2025 BioNTech SE (Nasdaq: BNTX, "BioNTech") reported it had commenced its public exchange offer (the "Offer") for all outstanding shares of CureVac N.V. (Nasdaq: CVAC, "CureVac"). The Offer is being made pursuant to the previously announced purchase agreement between BioNTech and CureVac, dated as of June 12, 2025 (the "Purchase Agreement"). Upon closing, the transaction will bring together two pioneers in mRNA science with complementary capabilities and technologies to advance the development of innovative and transformative investigational mRNA-based cancer immunotherapies for patients in need.

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With the acquisition, BioNTech aims to strengthen its research, development, manufacturing, and commercialization capabilities, complementing its expertise in mRNA design, delivery formulations, and mRNA manufacturing. The transaction marks a milestone in the execution of BioNTech’s oncology strategy, which focuses on two pan-tumor programs: mRNA-based cancer immunotherapy candidates, and pumitamig (BNT327), a PD-L1xVEGF-A bispecific antibody candidate. BioNTech’s all-stock acquisition of CureVac is expected to create long-term value for shareholders of both companies, building on BioNTech’s proven track record in mRNA research, development, manufacturing, and commercialization.

Under the terms of the Purchase Agreement, each CureVac share will be exchanged for approximately $5.46 in BioNTech American Depositary Shares ("ADSs"), resulting in an implied aggregate equity value for CureVac of approximately $1.25 billion (subject to the adjustments described below). The consideration is subject to a collar mechanism, such that if the 10-day volume weighted average price of a BioNTech ADS ending on, and including, the fifth business day prior to the closing of the Offer ("VWAP") is greater than or equal to $126.55, each CureVac share will be exchanged (the "Exchange Ratio") for 0.04318 of a BioNTech ADS, and if the VWAP is less than or equal to $84.37, the Exchange Ratio will be 0.06476 of a BioNTech ADS. For the duration of the Offer, an indicative Exchange Ratio will be available at www.envisionreports.com/CureVacOffer.

CureVac shareholders who want to participate in the Offer should contact their broker, dealer, or other nominee through which they hold their CureVac shares for further information. Any CureVac shareholder who has any questions, including regarding how to participate, may reach out to the information agent for the Offer, Georgeson LLC, at +1 888 686 7195 (toll free in the US), +1 732 353 1948 (collect) or [email protected].

The Offer will expire at 9:00 a.m. (New York City time) on December 3, 2025, unless extended or terminated earlier, in each case in accordance with the terms of the Purchase Agreement. The Offer is subject to various conditions, including at least 80% of CureVac’s shares (threshold may be reduced to 75% unilaterally by BioNTech under certain circumstances) being tendered into the Offer and accepted for payment and the receipt of required regulatory approvals.

As promptly as practicable following the expiration of the Offer, including the contemplated subsequent offering period, BioNTech and CureVac will effectuate a corporate reorganization of CureVac and its subsidiaries, resulting in BioNTech owning 100% of CureVac’s business. As part of this corporate reorganization, any holders of CureVac shares who do not participate in the Offer will receive the same consideration as they would have received had they participated in the Offer; however, BioNTech ADSs (and cash in lieu of fractional BioNTech ADSs) received pursuant to such reorganization may be subject to Dutch dividend withholding tax at a rate of 15%. The exchange agent may withhold and sell BioNTech ADSs to satisfy any such withholding tax.

In connection with the commencement of the Offer, CureVac will convene an extraordinary general meeting of shareholders (the "EGM") to be held on November 25, 2025. The EGM will be called to vote on certain resolutions by the CureVac shareholders relating to the proposed transaction with BioNTech, including the post-offer corporate reorganization of CureVac and its subsidiaries, and the appointment of new members to the management and supervisory boards, each as further to be set out in the agenda and explanatory notes that will be made available to CureVac’s shareholders. The convening notice, agenda, explanatory notes, and other relevant materials for the EGM will be made available free of charge at CureVac’s registered office and on its website (View Source). The registration date for CureVac shareholders is October 28, 2025. CureVac shareholders will be able to attend and vote at the EGM, either in person or by proxy, subject to the procedures set forth in the convening notice, in particular complying with the notification cut-off date on November 20, 2025. The adoption of the proposed resolutions relating to the post-offer reorganization and the post-closing composition of the management and supervisory boards at the EGM is a condition to the expiration of the Offer.

Should you need help or have questions relating to the EGM and to vote your shares, please contact CureVac’s information agent, Sodali, at [email protected] or +49 69 95179985.

BioNTech has filed a registration statement on Form F-4 and amendments thereto (the "Registration Statement") with the U.S. Securities and Exchange Commission (the "SEC"), which has not yet become effective. BioNTech has filed with the SEC a Tender Offer Statement on Schedule TO, including as exhibits an offer to exchange/prospectus and letter of transmittal, which include the terms of the Offer. Additionally, CureVac has filed a Solicitation/Recommendation Statement on Schedule 14D-9 with the SEC containing the recommendation of its management board and supervisory board that CureVac shareholders tender their shares into the Offer. The Schedule TO, Registration Statement, Schedule 14D-9, their exhibits and other Offer materials can be obtained free of charge at the website maintained by the SEC at www.sec.gov or by contacting Georgeson LLC, the information agent for the Offer, as set out above.

(Press release, BioNTech, OCT 22, 2025, View Source [SID1234656894])