NASDAQ: TCRT

Small Molecule Oral Obesity and Metabolic Disorders Program

We are advancing our internally developed, preclinical small molecule program for the treatment of obesity and related metabolic disorders through a non-hormonal mechanism. This program focuses on discovering and developing novel, orally administered therapeutics with the potential for a differentiated and complementary profile compared to currently available therapies. While other pipeline therapies for obesity explore alternative hormonal pathways such as amylin or dual GIP/GLP-1 receptor agonism, our approach is focused on a non-hormonal mechanism of action.

Key findings from two separate DIO studies (non-GLP) are summarized below (nominal reported p-values are unadjusted for multiple comparisons):

DIO Study 1

The purpose of the first study was to evaluate the pharmacokinetics (PK) and tolerability of ALN1003 and to assess early proof-of-concept anti-obesity efficacy including changes in weight, metabolic biomarkers, and adipose remodeling. Mice received low, controlled oral doses of ALN1003, split into two doses each day. Measurements included daily body weight, food and water consumption at the cage level, and metabolic markers (blood collection after a 4-6 hour fast at end of study). All animals were observed prior to and after each dose administration. There were 12 mice in each group, with mice housed 3 per cage.

Relative to DIO controls, mean percent change in body weight for ALN1003-treated mice peaked at -12.9% (p<0.0001) on Day 34 and was

-10.3% (p<0.0001) after 48 days of treatment. Peak reductions in absolute weight loss were observed by Day 13 and remained lower than DIO controls through Day 48 (p<0.0001 at selected timepoints).

Food and water consumption: ALN1003 reduced cumulative food consumption versus DIO control (347.5 g/cage vs 425.0 g/cage; nominal p<0.05). ALN1003 reduced water consumption (445.8 mL/cage vs 494.5 mL/cage; not statistically significant).

Liver and Fat Tissue: In this study, ALN1003 reduced liver weight compared to untreated mice by 43% (p<0.0001) and by 39% when expressed as a percentage of body weight (p<0.0001). Long-term administration of ALN1003 was associated with lower ALT (alanine aminotransferase; p<0.0001), AST (aspartate aminotransferase; nominal p<0.0001) and ALP (alkaline phosphatase; p<0.0001), with a trend toward lower total bilirubin (nominal p=0.058) compared to untreated mice.

An unblinded macroscopic visual review of organ morphology was conducted comparing the liver and adipose tissues of the DIO control to the ALN1003 treatment group. Relative to DIO controls, ALN1003-treated animals exhibited smaller, deep reddish-brown livers; reduced epididymal white adipose tissue (eWAT) and inguinal white adipose tissue (iWAT) depots consistent with decreased adiposity; and darker interscapular BAT with appearance consistent with reduced “whitening” of BAT.

Tolerability: ALN1003 was generally well tolerated throughout the study. Mild, short-term, reversible hypolocomotion was observed after dosing in approximately one-half of dose administrations. There were no similar observations in DIO control animals.

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DIO Study 2

The second study conducted was a pilot study to evaluate palatability, tolerability, anti-obesity effects, body composition and PK of ALN1003 administered orally in drinking water at three dose levels in DIO mice. The study comprised a treatment period of 14 days and a PK period of 4 days. ALN1003 was administered at three dose levels: low, medium and high. The middle and highest planned doses were 3 and 9 times higher than the low dose, respectively. Measurements included daily body weight, food and water consumption at the cage level, and metabolic parameters (blood collection after a 4-6 hour fast at end of study). All animals were observed each day. There were 6 mice in each group (2 mice per cage).

Food and water consumption: ALN1003 reduced cumulative food intake in a dose-dependent manner over the 14-day treatment period. Cumulative food consumption in grams per cage was 84.5g, 80.8g, 76.7g and 56.7g (nominal p<0.05) for the DIO control, low, medium and high doses, respectively. Cumulative food consumption when normalized to body weight per cage was 87.9g, 85.6g, 86.7g and 73.6g for the DIO control, low, medium and high doses, respectively. ALN1003 reduced water intake significantly over the 14-day treatment period. Cumulative water consumption in milliliters per cage was 112.8 mL, 80.1 mL (nominal p<0.05), 71.1 mL (p<0.0001) and 63.5 mL (p<0.0001) for the DIO control, low, medium and high doses, respectively. Cumulative water consumption when normalized to body weight per cage was 116.9 mL, 84.9 mL, 80.5 mL and 80.3 mL for the DIO control, low, medium and high doses, respectively. Actual dose consumed is dependent on how much water mice drink. Actual doses consumed during the 14-day treatment period were consistent with planned doses, with variances to planned doses of +7.3%, -0.3% and -6.9% in the low, medium and high dose groups, respectively.

Body composition was assessed using a Bruker MinispecTMLF90II Body Composition Analyzer (Bruker BioSpin, Billerica, MA, USA) and demonstrated dose-related changes that were driven primarily by fat loss but also included the loss of lean and fluid mass. The table below summarizes the mean percentage change from baseline through Day 17 in fat, lean and fluid as a % of body weight (BW) and mass in grams:

Mean % Change:

Control

Low

Medium

High

D17 Fat% of BW

+2.4%

-1.5%

-5.4%

-21.9%c

D17 Lean% of BW

-1.3%

+2.4%

+4.6%

+17.2%c

D17 Fluid% of BW

+0.4%

-9.3%

-12.0%

-25.7%b

D17 Fat in grams

+4.7% (+0.9g)

-1.8% (-0.4g)

-12.3% (-2.5g)b

-44.6% (-8.9g)c

D17 Lean grams

+1.9% (+0.5g)

+2.2% (+0.6g)

-4.1% (-1.1g)a

-18.8% (-5.0g)c

D17 Fluid grams

+2.7% (+0.1g)

-9.6% (-0.4g)

-18.8% (-0.7g)a

-47.3% (-1.8g)c

Significance of comparison to Control group: a: nominal p<0.05; b: nominal p<0.001; c: p<0.0001

Liver and Fat Tissue: At end of study Day 18, including the 14-day treatment period plus the PK period, dose-related reductions in liver weights compared to DIO control were -6.8%, -20.5% and -55.0% (nominal p<0.01) in the low, medium and high dose groups, respectively. Reductions in liver weights expressed as a percentage of body weight relative to DIO control were -2.6%, -12.0% and -32.6% (nominal p<0.05). Liver enzymes showed no statistically significant change after 18 days; gross liver appearance suggested reduced fat accumulation. Histological analyses of liver and adipose tissues are planned.

An unblinded macroscopic visual review of organ morphology was conducted comparing the liver and adipose tissues of the DIO control to the high dose group. This analysis showed reductions in white fat depots (such as epididymal white adipose tissue, or eWAT, and inguinal white adipose tissue, or iWAT) and an interscapular BAT appearance consistent with reduced “whitening” in the ALN1003 tissues vs DIO control. Review of liver images suggested less visible fat accumulation and smaller, deep red-brown livers compared to DIO control.

Metabolic parameters: In this study, the highest-dose group showed lower blood sugar (glucose; 197 mg/dL in high dose vs 320 mg/dL in DIO control; p<0.0001) and lower total cholesterol (162 mg/dL in high dose vs 209 mg/dL in DIO control; nominal p<0.05). HDL-C (high-density lipoprotein cholesterol), the dominant lipoprotein in DIO mice, also decreased to 130 mg/dL in high dose vs 165 mg/dL in DIO control; nominal p<0.05.

Tolerability: ALN1003 was generally well tolerated throughout the study; however, on Day 16 (during the PK portion of the study), two mice in the high-dose group were noted to be slightly dehydrated for the remainder of the study, although they otherwise appeared normal.

Important Context and Model Limitations

Behavior-coupled dosing in unrestricted (ad libitum) drinking-water studies: In this paradigm, ALN1003 caused dose-related loss of appetite and thirst (anorexia/hypodipsia), leading to avoidance of medicated water. Despite actual doses consumed approximating planned doses in this study, reductions in drinking may confound attribution of weight loss solely to drug exposure in this model.

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Development Roadmap

The findings from these two studies support the Company’s strategy to focus on additional preclinical studies and CMC activities to optimize formulations while maintaining effective overall drug levels. We are also planning to conduct studies to better understand mechanisms of ALN1003, including measuring liver fat levels and scoring MASLD severity of the liver in a blinded manner. We are planning to further refine manufacturing processes and to run a small-scale production run based on these improvements. Thereafter, a larger scale production run is planned. In parallel, the Company has initiated a computational chemistry program to design, make, and test ALN1003 variations to strengthen the Company’s intellectual property and assess next-generation compounds. These initiatives, including large animal pharmacokinetic studies, will inform plans to conduct IND enabling studies.

The advancement of this program is subject to numerous risks and uncertainties inherent in early-stage drug development. Subject to favorable data from these preclinical studies and our ability to secure additional capital, we plan to advance a selected development candidate into formal investigational new drug (IND)-enabling studies. We intend to actively explore strategic financing and collaboration opportunities to fund the continued development of this program.

Obesity Market

Obesity remains one of the most critical and rapidly escalating global health challenges. Prevalence continues to rise across nearly all regions, with particularly high and still increasing rates in the United States, Europe, the Middle East, and parts of Asia. Importantly, obesity is no longer viewed solely as a lifestyle issue but as a chronic, relapsing, multisystem disease that drives long‑term morbidity, mortality, and healthcare costs.

The burden of obesity is amplified by its strong causal links to a wide spectrum of comorbidities, including type 2 diabetes, cardiovascular disease, chronic kidney disease, and liver disorders—most notably Metabolic Dysfunction–Associated Steatotic Liver Disease (MASLD)—as well as several cancers. Increasing evidence also links obesity to neurological and neurodegenerative conditions, including vascular dementia and Alzheimer’s disease, further expanding its societal and economic impact. As a result, obesity sits at the center of converging metabolic, inflammatory, cardiovascular, and oncologic disease pathways, making it a major focus for health systems and biopharma innovation.

The global obesity therapeutics market is undergoing unprecedented expansion. In 2026, analyst revisions now project the market reaching $150 billion by 2030, reflecting one of the fastest growth trajectories in pharmaceutical history. This acceleration is driven by rising prevalence across all age groups, earlier diagnosis, increased recognition of obesity as a treatable disease, and a historic shift in reimbursement policies, including expanded coverage under Medicare for patients with established cardiovascular risk.

Key additional growth drivers include the expansion of obesity treatment beyond simple weight loss into the prevention of downstream cardiometabolic and liver disease. There is also a notable shift toward long‑term, chronic management paradigms and the emergence of "oral revolutions," where highly effective pill-based formulations are broadening adoption among younger and needle-hesitant populations.

The market has been fundamentally reshaped by the rapid adoption of incretin‑based therapies, particularly GLP‑1 receptor agonists and multi-receptor agonists (e.g., Ozempic™, Wegovy™, Zepbound™). These agents have demonstrated unprecedented weight‑loss efficacy and emerging benefits across cardiovascular and renal outcomes.

Despite transforming obesity care, hormone‑based therapies have important limitations, including high cost, gastrointestinal tolerability issues, and uncertainty around lifelong use. Critically, data reveals a clinically meaningful rate of non‑response, affecting approximately 10–30% of patients who fail to achieve ≥5% weight loss despite adequate dosing. This highlights the biological heterogeneity of obesity and underscores the urgent need for complementary or non‑hormonal approaches, particularly for patients who hit metabolic plateaus or cannot tolerate hormonal side effects.

As obesity increasingly affects younger populations and becomes a true lifelong condition, there is growing recognition that additional therapeutic modalities will be required to complement or substitute hormone‑based approaches. Within this evolving landscape, there is strong interest in non‑hormonal alternatives that offer differentiated safety profiles and easier chronic use. Programs positioned in this space are essential for expanding the treatable population and supporting the next phase of sustainable, long-term disease management.

Legacy Cell Therapy Programs

We were historically involved in developing adoptive T-cell receptor (TCR) engineered T-cell therapies (TCR-T) targeting solid tumors using our proprietary non-viral Sleeping Beauty gene transfer platform and hunTR TCR discovery engine. These programs were being developed in collaboration with The University of Texas MD Anderson Cancer Center in a Phase 1/2 TCR-T Library Trial. In August 2023, due to substantial development costs and the challenging financing environment, we announced a strategic reprioritization and discontinued further clinical development of our TCR-T programs. Efforts to consummate a sale or out-license transaction of this intellectual property portfolio have been unsuccessful to date.

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Preclinical and Clinical Development

Manufacturing

We have no internal manufacturing capability and outsource the production of active pharmaceutical ingredient (API) and drug product for our preclinical small-molecule obesity program to third-party contract development and manufacturing organizations (CDMOs) with experience in small-molecule synthesis and production. We currently rely on a limited number of CDMOs for API supply, and we may depend on single or limited sources for certain raw materials or specialized services. We are engaged in chemistry, manufacturing, and controls (CMC) activities to support formulation optimization, small-scale production, and future IND-enabling studies. Reliance on third-party manufacturers involves risks, including potential delays in supply, quality or purity issues, regulatory compliance challenges, and increased costs.

Intellectual Property

Our goal is to obtain, maintain and enforce patent and trade secret protection for our product candidates, formulations, processes, methods and other proprietary technologies. We strive to preserve our trade secrets and other confidential information and to operate without infringing the proprietary rights of other parties. Our policy is to actively seek the strongest possible intellectual property protection for our technology and product candidates through a combination of license agreements and owned patents, both in the United States and abroad.

Obesity and Metabolic Disorders Program

For our small-molecule obesity program (including lead candidate ALN1003), we are pursuing intellectual property protection through pending and planned patent applications directed to compositions of matter, methods of use, formulations, and related technologies. We have initiated a computational chemistry effort to conceive, manufacture and evaluate analogs of our product candidates to expand and strengthen our patent portfolio. As with our legacy assets, we currently have no issued patents protecting the obesity and metabolic disorders program, and protection is limited to pending applications and trade secret safeguards.

Legacy TCR-T Programs

As of December 31, 2025, we have six families of pending patent applications covering aspects of our historical TCR-T library, products, and processes (including Sleeping Beauty gene transfer and hunTR TCR discovery technologies). We currently hold no issued patents in this area.

General IP Strategy & Risks

Patent terms vary by jurisdiction and depend on filing or grant dates, claim scope, and legal remedies available. Under the Hatch-Waxman Act, certain patents may qualify for up to five years of term extension (not exceeding 14 years from approval) to offset development and regulatory delays, subject to USPTO/FDA review. We intend to pursue such extensions where applicable, but there is no assurance of success.

We also rely on trade secrets and confidentiality agreements to protect unpatentable know-how, proprietary methods, and other confidential information. Employees, consultants, and contractors are generally required to assign inventions to us and enter into confidentiality obligations.

Our IP position is subject to significant risks, including challenges to patentability, enforceability, or validity; third-party infringement claims; and dependence on licensed rights (see License Agreements below). Please refer to Item 1A, “Risk Factors — Risks Related to Our Intellectual Property” for a detailed discussion of these and other risks that could materially impair our ability to protect or commercialize our technologies and candidates.

License Agreements

We have historically relied on license and research agreements to access key technologies for our former TCR-T cell therapy programs. The most material of these agreements are summarized below. We no longer have active clinical development under these arrangements following our August 2023 strategic reprioritization and wind-down of the TCR-T Library Phase 1/2 Trial.

MD Anderson License and Research Agreements

In January 2015, we entered into an exclusive worldwide license agreement (the “MD Anderson License”) with The University of Texas MD Anderson Cancer Center (“MD Anderson”) for certain technologies related to non-viral gene transfer, genetic modification of immune cells, TCRs, and other cellular therapy approaches. In August 2015, we, together with Precigen (formerly Intrexon), entered into a research and development agreement (the “2015 R&D Agreement”) to facilitate the transfer and development of these technologies. Precigen’s rights were later assigned to us.

The MD Anderson License and related agreements were amended several times to extend terms and adjust funding obligations. In October 2019, we entered into a separate 2019 R&D Agreement focused on TCR library expansion and clinical development. Under these arrangements, we funded specified research and development activities and agreed to pay royalties on net sales of resulting TCR products (if any), as well as

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potential milestone payments tied to clinical and regulatory progress (aggregate potential milestones up to $36.5 million, with only $3.0 million due prior to first marketing approval).

The MD Anderson License term continues until the later of the expiration of all licensed patents or 20 years from the agreement date, after which we retain a perpetual, royalty-free license. MD Anderson retains certain rights to terminate or convert licenses to non-exclusive under specified conditions (e.g., failure to meet diligence requirements or commercial efforts). Either party may terminate for uncured material breach or certain insolvency events.

Current Status

Following our August 2023 strategic reprioritization and wind-down of the TCR-T Library Phase 1/2 Trial, we are no longer conducting clinical development under these agreements. Efforts to consummate a sale or out-license transaction of this intellectual property portfolio have been unsuccessful to date.

In December 2025, we entered into a Settlement and Release Agreement with MD Anderson to fully resolve outstanding invoices and payment disputes arising from historical activities under the 2015 and 2019 R&D Agreements. Under the terms of the settlement, we agreed to make payments totaling $285,000 in six installments through May 30, 2026, in full satisfaction of all amounts due. The agreement includes mutual general releases (subject to customary exceptions) and does not affect our retained intellectual property rights under the MD Anderson License.

Risks

Our ability to realize value from these legacy agreements and related IP is subject to significant risks, including termination rights, diligence requirements, and third-party claims. For a full discussion, see Item 1A, “Risk Factors — Risks Related to Our Intellectual Property” and “Risks Related to Our Strategic Reprioritization.”

Governmental Regulation and Product Approval

Government authorities in the United States (at the federal, state and local level) and in other countries and jurisdictions extensively regulate, among other things, the research, development, preclinical and clinical testing, manufacturing, quality control, labeling, packaging, storage, record-keeping, promotion, advertising, sale, distribution, post-approval monitoring and reporting, marketing and export and import of pharmaceutical products such as those we are developing. Our product candidates must be approved by the FDA before they may be legally marketed in the United States and by the appropriate foreign regulatory agency before they may be legally marketed in foreign countries. Generally, our activities in other countries will be subject to regulation that is similar in nature and scope as that imposed in the United States, although there can be important differences. The process for obtaining regulatory marketing approvals and the subsequent compliance with applicable federal, state, local and foreign statutes and regulations require the expenditure of substantial time and financial resources.

U.S. Regulatory Process

In the United States, the FDA regulates small-molecule drugs under the Federal Food, Drug, and Cosmetic Act and implementing regulations. Before human testing can begin, we must submit an Investigational New Drug application (IND) to the FDA containing preclinical data, manufacturing information, and a proposed clinical protocol. The IND becomes effective 30 days after submission unless the FDA places a clinical hold. We have not yet filed an IND for any product candidate and are currently in the preclinical stage.

Clinical development typically occurs in three phases: Phase 1 (safety in healthy volunteers or patients), Phase 2 (preliminary efficacy and dosing), and Phase 3 (confirmatory efficacy and safety in larger populations). Clinical trials must comply with Good Clinical Practices (GCP) and be overseen by institutional review boards (IRBs). Before marketing approval, we would submit a New Drug Application (NDA) demonstrating safety and efficacy, followed by FDA review, potential advisory committee input, and facility inspections for compliance with current Good Manufacturing Practices (cGMP). Approval may be subject to restrictions, post-marketing studies (Phase 4), or Risk Evaluation and Mitigation Strategies (REMS).

Even if approved, marketed products remain subject to ongoing FDA regulation, including adverse event reporting, labeling changes, and manufacturing inspections. Failure to comply with regulatory requirements can result in warning letters, product recalls, clinical holds, approval withdrawal, or civil/criminal penalties.

Coverage, Pricing, and Reimbursement

Significant uncertainty exists regarding third-party payor coverage and reimbursement for any product candidates that may receive marketing approval. In the United States, third-party payors (government programs, private insurers) increasingly challenge pricing, medical necessity, and cost-effectiveness. Inadequate reimbursement could limit market acceptance and our ability to generate revenue.

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Other Laws

We are subject to federal and state healthcare fraud and abuse laws (e.g., Anti-Kickback Statute, False Claims Act), as well as foreign equivalents, which restrict certain business practices and relationships with healthcare providers and payors. Compliance with these laws involves significant costs and risks.

The regulatory process is subject to change, including through new legislation or FDA policies, which could delay or prevent approval of our product candidates. For a more detailed discussion of these and other regulatory risks, see Item 1A, “Risk Factors — Risks Related to Our Ability to Commercialize Our Product Candidates.”

Competition

The obesity treatment market is highly competitive and rapidly evolving. We are developing an oral, small-molecule candidate (ALN1003) with a differentiated, non-hormonal, non-incretin approach. However, numerous pharmaceutical and biotechnology companies are actively developing or marketing competing obesity treatments, including GLP-1 receptor agonists, dual/triple agonists, and other mechanisms. Many of these competitors have significantly greater financial resources, clinical development experience, manufacturing capabilities, regulatory expertise, and commercial infrastructure than we do. Key competitors in the obesity space include (but are not limited to) companies such as Novo Nordisk, Eli Lilly, Amgen, Pfizer, Viking Therapeutics, Structure Therapeutics, and others.

If competitors develop and commercialize products that are more effective, safer, better tolerated, easier to administer, or less expensive than our candidates, or if they obtain regulatory approval more quickly, our potential market opportunity could be significantly reduced. Competitive factors that may affect any future product include efficacy, safety, tolerability, ease of administration, price, reimbursement, and market access.

Employees and Human Capital Resources

As of March 31, 2026, we had one full-time employee and no part-time employees. Our employee is not subject to a collective bargaining agreement.

Given our current size and strategic focus, we rely heavily on consultants and external advisors to perform key functions, including finance, legal, regulatory, and preclinical development activities. Several material consulting agreements remain in place to support business continuity and execution of our obesity program and strategic alternatives review.

Our human capital strategy emphasizes retaining and incentivizing our limited internal team while effectively managing consultant relationships to advance our objectives with constrained resources. We maintain equity incentive plans (including the 2020 Equity Incentive Plan) to attract, retain, and motivate employees, consultants, and directors through stock-based compensation awards and, where applicable, cash-based performance bonuses.

The small size of our workforce and dependence on consultants increase execution risk for our remaining programs and strategic initiatives.

Departure of Dale Curtis Hogue, Jr. as Chief Executive Officer and Director

On July 1, 2025, Dale Curtis Hogue, Jr. notified the Company of his resignation from the board of directors (the “Board”) of Alaunos Company and his position as Chief Executive Officer, effective immediately. His departure was not due to any disagreement with the Company.

On the same day, Mr. Hogue entered into a Consulting Agreement with the Company, effective July 1, 2025 (the “Consulting Agreement”), pursuant to which Mr. Hogue will continue providing strategic and advisory services to the Company. The Consulting Agreement will continue until terminated by either party. The Consulting Agreement provides for compensation at a fixed rate of $250 per hour and reimbursement by the Company for any usual and customary expenses incurred by Mr. Hogue in connection with performing services pursuant to the Consulting Agreement.

Mr. Weis Engagement

Effective July 2, 2025, the Company entered into an employment agreement with Mr. Weis in connection with his appointment as Chief Executive Officer.

Pursuant to the employment agreement, Mr. Weis is entitled to an annual base salary of $275,000. In addition, Mr. Weis was granted an option to purchase 130,000 shares of the Company’s common stock at an exercise price of $5.06 per share. One-fourth of the option vested and became exercisable on the grant date, and the remaining three-fourths vest in equal installments over three years on each quarterly anniversary of the grant date, beginning October 2, 2025, subject to Mr. Weis’s continued employment with the Company through each applicable vesting date. Any unvested portion of the option will be forfeited upon the termination of Mr. Weis’s employment with the Company. The option grant is

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governed by the Company’s 2020 Equity Incentive Plan and the applicable stock option agreement thereunder.

Appointment of Michael A. Jerman

On July 15, 2025, the board of directors of the Company appointed Mr. Michael A. Jerman, as a director of the Company. Mr. Jerman filled the vacancy created by Mr. Dale Curtis Hogue’s resignation. Mr. Jerman was also appointed to the Audit Committee and the Compensation Committee of the Board, replacing Mr. Holger Weis, who was appointed Chief Executive Officer of the Company. Mr. Jerman serves as the chair of the Audit Committee. The Board has determined that Mr. Jerman meets the requirements for independence under the applicable listing standards of the Nasdaq Stock Market LLC and the Securities and Exchange Act of 1934, as amended.

Departure of Melinda Lackey as Legal & Administration, Corporate Secretary

On July 16, 2025, Melinda Lackey notified the Company that, pursuant to Section 1 of the November 11, 2023 Consulting Agreement (the “Agreement”) between the parties, she was terminating the agreement, effective 30 days from the date of the notice, or August 15, 2025 (the “Effective Date”). Concurrent with this notice, Ms. Lackey resigned as Legal and Administrative Officer and as the Company’s corporate secretary as of the Effective Date. Ms. Lackey's departure is not the result of any disagreement with the Company on any matter related to the Company's operations, policies or procedures.

Appointment of Ferdinand Groenewald as Corporate Secretary

On August 14, 2025, the Board of Directors of the Company appointed Mr. Ferdinand Groenewald as Corporate Secretary effective upon the resignation of Ms. Lackey.

Corporate Information

We originally incorporated in Colorado in September 1998 (under the name Net Escapes, Inc.) and later changed our name to “EasyWeb, Inc.” in February 1999. We re-incorporated in Delaware on May 16, 2005 under the same name. On September 13, 2005, we completed a “reverse” acquisition of privately held Ziopharm, Inc., a Delaware corporation. To effect this transaction, we caused ZIO Acquisition Corp., our wholly-owned subsidiary, to merge with and into Ziopharm, Inc., with Ziopharm, Inc. surviving as our wholly owned subsidiary. Following the merger, we caused Ziopharm, Inc. to merge with and into us and we changed our name to “Ziopharm Oncology, Inc.” As a result, Ziopharm, Inc. became the registrant with the Securities and Exchange Commission, or the SEC, and the historical financial statements of Ziopharm, Inc. became our historical financial statements. On January 25, 2022, we filed a Certificate of Amendment to our Amended and Restated Certificate of Incorporation with the Delaware Secretary of State to change our name to Alaunos Therapeutics, Inc.

Our principal executive offices are located at 501 E. Las Olas Blvd., Suite 300, Fort Lauderdale, Florida 33301, and our telephone number is (346) 355-4099.

Available Information

Our website address is www.alaunos.com. Our website and information included in or linked to our website are not part of this Annual Report on Form 10-K. We file reports with the SEC, which we make available on our website free of charge. These reports include annual reports on Form 10-K, quarterly reports on Form 10-Q, current reports on Form 8-K and amendments to such reports, each of which is provided on our website as soon as reasonably practicable after we electronically file such materials with or furnish them to the SEC. In addition, the SEC maintains a website (www.sec.gov) that contains reports, proxy and information statements and other information regarding issuers, like us, that file electronically with the SEC.

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