MANAGEMENT'S DISCUSSION AND ANALYSIS OF FINANCIAL CONDITION AND RESULTS OF OPERATION

CAUTIONARY STATEMENT REGARDING FORWARD-LOOKING STATEMENT NOTICE

This Quarterly Report on Form 10-Q and other reports filed by the Company from time to time with the Securities and Exchange Commission contains or may contain certain forward-looking statements and information that are based upon beliefs of, and information currently available to the Company's management as well as estimates and assumptions made by the Company's management. Readers are cautioned not to place undue reliance on these forward-looking statements, which are only predictions and speak only as of the date hereof. For this purpose, any statements contained in this Quarterly Report on Form 10-Q that are not statements of historical fact may be deemed to be forward-looking statements. Without limiting the foregoing, words such as "may," "will," "expect," "believe," "anticipate," "estimate" or "continue" or comparable terminology are intended to identify forward-looking statements. These statements by their nature involve substantial risks and uncertainties, and actual results may differ materially depending on a variety of factors, many of which are not within our control. These factors include but are not limited to economic conditions generally and in the industries in which we may participate; competition within our chosen industry, including competition from much larger competitors; technological advances and failure to successfully develop business relationships. Although we believe that the expectations reflected in the forward-looking statements are reasonable, we cannot guarantee future results, levels of activity, performance, or achievements. Except as required by applicable law, including the securities laws of the United States, we do not intend to update any of the forward-looking statements to conform these statements to actual results.

Description of Business

We are a clinical-stage biopharmaceutical company pioneering the development of targeted radiotherapies to address significant unmet medical needs in oncology. We are focused on employing a biology-driven approach to develop differentiated, first-in-class radiopharmaceutical therapeutics for patients with solid tumors and hematologic malignancies. Our mission is to transform cancer treatment by delivering innovative, high-value, radioconjugates that maximize therapeutic efficacy while minimizing toxicity to healthy tissue by combining our deep understanding of tumor biology and translational medicine with our expertise in radiochemistry.

Since our inception, we have focused on developing innovative and differentiated radiotherapies. Our pipeline of both early and later stage development programs is a testimony to our approach in three areas with: (1) two novel solid tumor product candidates, ATNM-400 and Actimab-A, with pan-tumor potential, (2) Actimab-A, which is also being developed as a therapeutic backbone for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) in partnership with the National Cancer Institute (NCI), and (3) two targeted conditioning agents, Iomab-B for bone marrow transplant and Iomab-ACT for cell & gene therapies. Our solid tumor asset, ATNM-400, targets a novel antigen distinct from PSMA, with demonstrated preclinical activity across metastatic castration-resistant prostate cancer (mCRPC), non-small cell lung cancer (NSCLC), and breast cancer. Actimab-A targets myeloid derived suppressor cells (MDSCs) and is being studied in multiple solid tumors in combination with immune checkpoint inhibitors where MDSCs are known to act as an efficacy deterrent for these agents. Our hematology franchise includes: Actimab-A, a CD33-targeted therapy; as well as, Iomab-B and Iomab-ACT which are CD45-targeting conditioning agents. Both Actimab-A and Iomab-B are Phase 2/3 ready assets and are supported by extensive validation in over 15 clinical trials in which more than 500 patients were treated. We have several ongoing clinical studies across our pipeline. We expect to report data from ongoing company- and investigator-sponsored clinical studies for ATNM-400, Actimab-A for MDSC's and Iomab-ACT in 4Q:2026 and over the course of 2027.

ATNM-400: First-in-Class Pan-Tumor Radiotherapy

ATNM-400 is our lead solid tumor program, representing a first-in-class Ac-225 antibody radioconjugate targeting a novel, undisclosed antigen with expression across multiple solid tumor types. The ATNM-400 target is implicated in disease biology during tumor progression and is also overexpressed when tumors become resistant to many approved therapies in multiple solid tumors. We are developing ATNM-400 as a potential pan-cancer, biology-driven therapy - alone or in combination with standard-of-care agents - for large, treatment resistant-solid tumor populations across prostate, NSCLC, breast cancer and potentially other sizable cancer indications.

Our translational data demonstrated that ATNM-400 is superior to the active ingredients in the many of the most commonly prescribed approved therapies in prostate cancer, NSCLC and breast cancer when tested in a wide variety of preclinical models:

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Prostate Cancer: PSMA-targeted agents (177Lu-PSMA-617 (the active ingredient in Pluvicto®) and 225Ac-PSMA-617) and ARPIs (enzalutamide, apalutamide, darolutamide) in the mCRPC setting of prostate cancer;

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NSCLC: EGFR inhibitors (osimertinib), osimertinib with chemotherapy, TROP-2 ADC (Dato-DXd), EGFR-cMET bispecific (amivantamab), HER3-EGFR bispecific antibody drug conjugate (ADC) (izalontamab brengitecan, in development) in EGFR-mutant NSCLC, and KRAS-G12C inhibitors (sotorasib and adagrasib) in KRAS-G12C mutant NSCLC; and

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Breast Cancer: HER2 therapies (trastuzumab and T-DXd) in HER2 resistant breast cancer and endocrine therapy (tamoxifen) in tamoxifen-resistant breast cancer.

These preclinical translational data show that ATNM-400 works well as monotherapy but is even better in combination in resistant settings where the target is overexpressed as part of the resistance mechanism of several of the approved standard-of-care drugs. Evidence of ATNM-400 target expression has been observed ranging from 60%-80% of mCRPC, >90% of NSCLC, and 50-70% of breast cancer patient tumors, representing a significant addressable population of well over a hundred thousand patients in the United States based on existing datasets. We believe this number may expand as we continue our work to demonstrate the potential of ATNM-400 in various additional disease and treatment settings.

In addition, we have developed a theranostic strategy utilizing Zr-89 as a companion imaging agent to enable patient selection and tumor visualization. We believe this approach allows for non-invasive assessment of target expression and drug biodistribution prior to therapeutic administration, potentially enhancing the therapeutic index by selecting patients most likely to respond.

Market Opportunity

ATNM-400 Is Designed to Address Large, Treatment Resistant Patient Populations Across Prostate, Lung and Breast Cancer - Indications in Which Approved Targeted Therapies Generated More Than $30 Billion in Worldwide Sales in 2025

We are developing ATNM-400 as a mutation- and pathway-agnostic radiotherapeutic - as a monotherapy or in combination with standard of care - for large, treatment resistant solid tumor populations, with initial focus on prostate cancer, non-small cell lung cancer (NSCLC) and breast cancer. These diseases have been selected for initial clinical development driven by a common scientific and commercial rationale. Each disease represents a large, well-established market due to targeted agents and yet a major underserved opportunity once their resistance to these therapies develops. The antigen targeted by ATNM-400 is expressed in all these disease areas and its expression further increases in many cases as the existing therapies fail. Several of these therapies have blockbuster sales generated by treating a large number of patients. ATNM-400 target expression is reported in a majority of prostate cancer, NSCLC and breast cancer tumors based on immunohistochemistry datasets, which we estimate corresponds to an addressable population of well over 350,000 patients per year in the United States across these three indications and considerably more worldwide. We believe this addressable population may expand as we evaluate ATNM-400 in additional indications and treatment settings.

Prostate Cancer

Prostate cancer is the most frequently diagnosed cancer in men in the United States. According to the American Cancer Society, approximately 333,830 men in the United States were estimated to be diagnosed with prostate cancer in 2026, representing approximately 30% of all cancer diagnoses in men. While localized prostate cancer is frequently curable, metastatic disease is not: approximately 5% to 7% of patients present with metastatic disease at initial diagnosis, and approximately 20% to 30% of patients initially diagnosed with localized disease subsequently progress to metastatic disease, for which available therapies slow, but do not cure, disease progression.

Because prostate cancer cells rely on androgens for growth, most patients receive androgen receptor pathway inhibitor (ARPI) therapy, including enzalutamide (Xtandi^®), apalutamide (Erleada^®) and darolutamide (Nubeqa^®), which generated more than $6.3 billion, $3.6 billion and $2.7 billion in worldwide sales, respectively, in 2025. We estimate that up to approximately 50,000 to 60,000 men in the United States progress following ARPI therapy each year. Collectively, ARPIs generated more than $12 billion in worldwide sales in 2025.

Since the March 2022 approval of the PSMA-directed radioligand therapy Pluvicto^® (with active ingredient Lu177-PSMA-617), targeted radiotherapy has become a prominent component of the metastatic castration-resistant prostate cancer (mCRPC) treatment paradigm. Pluvicto^®, marketed by Novartis, generated approximately $2.0 billion in worldwide sales in 2025, and its addressable population has expanded from approximately 44,000 patients toward approximately 86,500 patients with successive label expansions into earlier lines of therapy. More than 30 PSMA-targeted radiotherapies are currently in various stages of development. Notwithstanding this activity, we believe a significant unmet need remains: we estimate that approximately 30% of patients with mCRPC have low or no PSMA expression and are therefore poorly served by PSMA-directed radioligand therapies, and re-treatment with PSMA-directed agents may be limited by reduced PSMA surface expression and increased tumor heterogeneity following initial PSMA-targeted therapy. In addition, because PSMA is expressed in the salivary glands, PSMA-directed radiotherapies are associated with xerostomia, a quality-of-life limitation that is particularly relevant for Ac-225-based PSMA agents.

Because ATNM-400 is directed against a novel, non-PSMA antigen and acts independently of both androgen receptor (AR) signaling and PSMA expression, we believe it is positioned to address the full metastatic castration-resistant prostate cancer (mCRPC) treatment continuum. This includes patients whose disease has progressed on androgen receptor pathway inhibitors (ARPIs), as well as patients with PSMA-low or PSMA-negative tumors, for whom there are very limited commercially available targeted radiotherapy options. Together, these patient populations represent a combined opportunity that we estimate exceeds 100,000 patients annually in the United States and may be addressable with ATNM-400 as either a monotherapy or in combination with existing standards of care.

Non-Small Cell Lung Cancer

Lung cancer is the leading cause of cancer death worldwide. Approximately 229,410 new cases of lung cancer were estimated to be diagnosed in the United States in 2026, and NSCLC accounts for approximately 85% of the more than two million lung cancer cases diagnosed globally each year. Approximately 70% are either diagnosed with advanced/metastatic disease or progress to advanced metastatic disease. NSCLC is a large and heterogeneous market in which no single mutation dominates. EGFR and KRAS mutations together account for approximately 50% to 60% of NSCLC cases, and existing therapies are segmented by mutation subtype and ultimately limited by acquired resistance.

Beyond EGFR and KRAS Driver Mutations the NSCLC Market is Fragmented

Source: Adapted from Fregni M, et al. Int J Mol Sci. 2022;23:7213, based on Skoulidis F and Heymach JV. Nat Rev Cancer. 2019;19:495-509

Current targeted therapies illustrate both the scale of the market and the treatment resistant- unmet need. In EGFR-mutant NSCLC, nearly all patients receive osimertinib (Tagrisso^®) as first-line therapy; osimertinib generated approximately $7.3 billion in worldwide sales in 2025. Disease progression on osimertinib is common and the resistance mechanisms are highly heterogeneous; in the second-line setting, amivantamab (Rybrevant^®) plus chemotherapy became a National Comprehensive Cancer Network (NCCN)- preferred regimen following its September 2024 approval, and datopotamab deruxtecan (Datroway^®, a TROP-2 antibody-drug conjugate) received accelerated approval in patients with prior platinum chemotherapy in June 2025, yet a significant unmet need remains for durable options beyond chemotherapy. Separately, the KRAS-inhibitor class in NSCLC, led by sotorasib (Lumakras^®) and adagrasib (Krazati^®), is conservatively projected to exceed $3 billion in peak sales by 2032.

We believe ATNM-400 is well suited to this fragmented market. Based on prior immunohistochemistry studies, the antigen targeted by ATNM-400 is expressed in approximately 98% of NSCLC tumors, is highly expressed in approximately 70%, is conserved across EGFR-, KRAS- and other driver-defined subgroups, and is further increased in tumors that have become resistant to EGFR, KRAS and immune-checkpoint therapies. Because ATNM-400 addresses NSCLC as a broad, target-defined population rather than as another mutation-specific therapy for a single molecular subset, we believe its mutation-agnostic profile positions it to participate in these large, established markets as a backbone therapy - enhancing the standard of care in combination while also reaching the broader NSCLC population beyond any single mutation.

Breast Cancer

Breast cancer is the most frequently diagnosed cancer among women in the United States. The National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program estimates that approximately 321,910 women will be diagnosed with invasive breast cancer in 2026. Approximately 200,000 women were living with metastatic breast cancer in the United States in 2025, a figure expected to grow to approximately 250,000 by 2030.

Hormone receptor-positive, HER2 negative (HR+/HER2−) breast cancer is the largest molecular subtype, accounting for approximately 70% of newly diagnosed cases. Endocrine therapy is the backbone of treatment, with endocrine therapy plus a CDK4/6 inhibitor preferred for most patients in the first-line metastatic setting. Approximately half of patients experience disease progression or death within two years, and the substantial majority progress within five years. Following progression, treatment is guided by prior therapy and biomarkers such as ESR1, PIK3CA, AKT1, PTEN, and germline BRCA1/2 alterations. Patients with ESR1-mutated disease may receive elacestrant, imlunestrant, or vepdegestrant, which was approved in May 2026 as the first proteolysis-targeting chimera in oncology. Gedatolisib-based therapy provides another pathway-targeted option for patients with PIK3CA-wild-type disease, while trastuzumab deruxtecan is approved following endocrine therapy for HR+, HER2 low or HER2 ultralow disease. Although post-endocrine options have expanded, these approvals were based on progression-free survival benefits generally measured in months. Median PFS across approved second-line regimens ranges from approximately four to thirteen months, and substantially all patients ultimately progress. In later lines, datopotamab deruxtecan is approved following endocrine-based therapy and chemotherapy, while sacituzumab govitecan is approved following endocrine therapy and at least two additional metastatic systemic regimens. Despite these advances, substantial need remains for therapies that overcome resistance and provide more durable disease control across successive lines of treatment.

HER2 positive (HER2+) breast cancer accounts for approximately 15% of breast cancers. Although HER2 directed therapies have substantially improved outcomes, metastatic disease generally remains incurable, and resistance develops across successive regimens. Central nervous system progression is a major unmet need, with up to 50% of patients developing brain metastases during the course of disease. Trastuzumab deruxtecan plus pertuzumab was approved in December 2025 as a first-line treatment for unresectable or metastatic HER2+ breast cancer. Taxane chemotherapy with trastuzumab and pertuzumab remains an option for selected patients. Trastuzumab deruxtecan plus pertuzumab achieved a median PFS of 40.7 months, compared with 26.9 months for the taxane-based regimen. Nevertheless, approximately 30% of patients experienced progression or death within two years, and half were expected to do so within approximately three and a half years. For patients with HR+, HER2+ disease controlled after induction therapy, palbociclib with trastuzumab, endocrine therapy, and optional pertuzumab was approved in June 2026 as maintenance treatment. Following progression, treatment depends on prior HER2 directed therapy and the presence or risk of central nervous system disease. Trastuzumab deruxtecan remains an established second-line option after first-line taxane, trastuzumab, and pertuzumab. However, the optimal sequence after progression on a first-line trastuzumab deruxtecan-containing regimen has not been established. Later-line options include tucatinib with trastuzumab and capecitabine, particularly for patients with brain metastases, and other HER2 directed regimens. New agents are needed that remain active following resistance to HER2 directed antibody-drug conjugates and across successive lines of treatment.

Triple-negative breast cancer (TNBC), defined by the absence of estrogen receptor, progesterone receptor, and HER2 overexpression or amplification, accounts for approximately 10% to 15% of breast cancers. TNBC is more aggressive than HR+ breast cancer, carries a higher risk of early distal recurrence, and lacks endocrine and HER2 directed treatment options. First-line treatment is informed by PD-L1 expression and germline BRCA1/2 mutation status. For patients with PD-L1-positive disease, immune-checkpoint inhibition combined with systemic therapy is a common strategy. In June 2026, sacituzumab govitecan was approved with pembrolizumab for PD-L1-positive unresectable locally advanced or metastatic TNBC and as monotherapy for patients who are not candidates for PD-1- or PD-L1-directed therapy. Datopotamab deruxtecan was also approved in May 2026 for patients who are not candidates for checkpoint inhibition. Despite these advances, more than half of patients are expected to experience progression or death within one year of starting first-line treatment. With TROP-2-directed antibody-drug conjugates now used in the first-line setting, no prospectively validated preferred sequence has been established after progression. Subsequent treatment may include chemotherapy, PARP inhibition for eligible patients with germline BRCA1/2 mutations, or clinical trials. This sequencing gap and the biological heterogeneity of TNBC support the need for therapies with mechanisms distinct from TROP-2-directed cytotoxic delivery.

The antigen targeted by ATNM-400 is expressed across multiple breast cancer subtypes, including HR+/HER2−, HER2+ (including HR+ and HR-), and triple-negative disease. Based on our preclinical findings, target expression is also retained or increased in tumor models that have developed resistance to selected standard therapies. We believe ATNM-400's target-driven, subtype-agnostic profile could position it to address treatment-resistant breast cancer populations as either a monotherapy or in combination with established standards of care.

ATNM-400 Positioned to Address HR+/HER2-, HER2+ and TNBC Breast Cancer Subtypes After Resistance to Standard of Care

Source: American Cancer Society, Cancer Facts & Figures 2026 (Atlanta: American Cancer Society, 2026), estimated new cases of invasive breast cancer in U.S. women, 2026. Subtype distribution derived from age-adjusted incidence rates for 2019-2023, National Cancer Institute, SEER Cancer Stat Facts: Female Breast Cancer Subtypes.

ATNM-400 Preclinical Data in Large Solid Tumor Indications

Our preclinical development program has generated encouraging efficacy and mechanism-of-action data across multiple indication-specific animal models of solid tumors including prostate cancer, NSCLC and breast cancer:

ATNM-400 in Prostate Cancer

ATNM-400 is a first-in-class Ac-225 antibody radioconjugate directed against a novel, non-PSMA antigen implicated in aggressive prostate cancer biology and overexpressed as tumors progress and develop resistance to standard-of-care therapies. Because ATNM-400 acts independently of both androgen-receptor signaling and PSMA expression, we believe it has the potential to address patients across the metastatic castration-resistant prostate cancer, or mCRPC, treatment continuum.

Key Findings and Therapeutic Positioning in Metastatic Castration-Resistant Prostate Cancer

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Broad monotherapy activity across PSMA expression levels. ATNM-400 demonstrated anti-tumor activity in PSMA-high, PSMA-low and PSMA-negative mCRPC models. It showed greater efficacy than 177Lu-PSMA-617 across these models, including in PSMA-low and PSMA-negative disease where PSMA-directed therapies may have limited activity, and greater efficacy than 225Ac-PSMA-617 in the PSMA-low model.

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Strong activity in PSMA-high disease with no xerostomia limitation expected. In the PSMA-high model, ATNM-400 demonstrated activity comparable to 225Ac-PSMA-617 and achieved comparable tumor control to 177Lu-PSMA-617 at approximately one-thousandth of the administered radioactivity. However, since the ATNM-400 target is not expressed in the salivary glands, we do not expect ATNM-400 to cause the xerostomia associated with PSMA-directed therapies.

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Activity following PSMA-directed therapy. ATNM-400 retained anti-tumor activity after progression on 177Lu-PSMA-617 and produced more durable tumor control and prolonged survival relative to 177Lu-PSMA-617, supporting its potential use in patients who have exhausted PSMA-directed radioligand therapy.

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Activity in ARPI-resistant disease. ATNM-400 demonstrated greater tumor growth inhibition than the approved ARPIs enzalutamide, apalutamide and darolutamide in ARPI-resistant models and retained activity following progression on enzalutamide.

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Enhanced activity in combination with ARPIs. Combinations of ATNM-400 with enzalutamide, apalutamide or darolutamide produced enhanced tumor growth inhibition, tumor regression and durable complete responses. These findings are supported by evidence that ARPI resistance increases ATNM-400 target expression, providing a mechanistic rationale for the observed combination activity.

We believe these findings support the potential development of ATNM-400 as a monotherapy or in combination with ARPIs across a broad mCRPC population, including patients with ARPI-resistant, PSMA-low or PSMA-negative disease, as well as patients with PSMA-high disease who may benefit from a differentiated safety profile.

Supporting Data in Metastatic Resistant Prostate Cancer Models

ATNM-400 Is Directed Against a Non-PSMA Target With the Potential to Treat More Patients Across Lines of Prostate Cancer Therapy

ATNM-400 Demonstrated Robust Tumor Growth Inhibition and was Superior to PSMA-Targeted Agents Across PSMA-High (C4-2), PSMA-Low (22Rv1) and PSMA-Negative (DU145) Prostate Cancer Models

ATNM-400 had robust efficacy in prostate cancer xenograft mouse models with high, low and no PSMA and was superior to 177-Lu-PSMA-617 in all the models and to 225Ac-PSMA-617 in the Low-PSMA model. ATNM-400 had comparable efficacy to 225Ac-PSMA-617 in the High-PSMA model. Given that 30% mCRPC patients have low or no PSMA expression and up to 70% of patients do not respond to Pluvicto^® and nearly all patients progress on Pluvicto^® in <12 months, our data in 177-Lu-PSMA-617, the active ingredient in Pluvicto^®, suggests that ATNM-400 has the potential to treat a broader population of mCRPC patients.

ATNM-400 retained anti-tumor activity in prostate cancer models after tumors had progressed on 177Lu-PSMA-617. Following tumor progression on 177Lu-PSMA-617, ATNM-400 produced continued tumor growth inhibition, supporting its potential to treat patients who have exhausted PSMA-directed radioligand therapy.

ATNM-400 Demonstrated Robust Efficacy After 177Lu-PSMA-617 Failure in Prostate Cancer Model

Beyond tumor growth inhibition, ATNM-400 conferred a survival benefit relative to PSMA-directed radioligand therapy. In preclinical prostate cancer models, animals treated with ATNM-400 survived longer than those treated with 177Lu-PSMA-617, consistent with the greater and more durable tumor control described above and achieved it at approximately one-thousandth of the administered radioactivity.

ATNM-400 Improved Survival vs 177Lu-PSMA-617 in Prostate Cancer Model

ATNM-400 demonstrated activity in prostate cancer cells and tumors resistant to all three approved androgen-receptor pathway inhibitors (ARPIs) - enzalutamide, apalutamide, and darolutamide. Across these studies, ATNM-400 delivered tumor control as either a single-bolus or repeat-dose regimen with a consistent safety profile and minimal off-target toxicity, which we believe indicates dosing flexibility and a wide therapeutic window.

In an ARPI-resistant model, ATNM-400 as a monotherapy and in combination with enzalutamide produced greater tumor growth inhibition and prolonged survival than enzalutamide alone that correlated well with overall survival. In the combination arm, 40% of the mice had complete cures that were durable up to 100 days post- treatment. The latter can be explained by mechanistic synergy since it has been published that enzalutamide resistance increases ATNM-400 target expression in prostate cancer models and in tumor biopsies from mCRPC patients.

ATNM-400 Monotherapy Demonstrated Superiority to Enzalutamide in ARPI-resistant Prostate Cancer Model and Had Complete Cures with Combination Activity

ATNM-400 Showed Survival Benefit vs Enzalutamide
Monotherapy and Combination

Following disease progression on enzalutamide, ATNM-400 produced continued tumor growth inhibition, supporting its potential to treat patients who have exhausted ARPIs.

ATNM-400 Displayed Strong Efficacy After Enzalutamide Failure

In data presented at the Society of Nuclear Medicine and Molecular Imaging (SNMMI) 2026 Annual Meeting in June 2026, as a monotherapy in the ARPI-resistant 22Rv1 model, ATNM-400 achieved 94% tumor growth inhibition, compared with 32% for apalutamide and 5% for darolutamide, and in combination with either apalutamide or darolutamide achieved 107% tumor growth inhibition (representing tumor regression), with durable complete responses in a majority of treated animals.

ATNM-400 Monotherapy Had Strong Tumor Growth Inhibition in the ARPI-Resistant 22Rv1 Prostate Cancer Model Resistant to Darolutamide and Apalutamide

ATNM-400 Combination with Darolutamide or Apalutamide Demonstrated Strong Tumor Growth Inhibition and Achieved Complete Responses (CRs) in the ARPI-Resistant 22Rv1 Prostate Cancer Model

ATNM-400 in Non-Small Cell Lung Cancer (NSCLC)

ATNM-400 is being developed as a potential mutation-agnostic targeted radiotherapy for non-small cell lung cancer (NSCLC). Its target is broadly expressed across NSCLC, including EGFR- and KRAS-mutant disease, and is further increased following resistance to targeted therapies. Because ATNM-400 acts independently of a tumor's driver mutation or signaling pathway, we believe it has the potential to address a broad, target-defined NSCLC population.

Key Findings and Therapeutic Positioning in Non-Small Cell Lung Cancer

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Target-specific activity across major NSCLC driver mutations. ATNM-400 demonstrated target-specific binding, internalization and tumor uptake across EGFR-mutant and multiple KRAS-mutant models, supporting activity driven by target expression rather than by a particular driver mutation.

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Greater activity than therapies used across EGFR-mutant treatment settings. In an EGFR-mutant model, ATNM-400 demonstrated greater tumor growth inhibition than the active ingredient in the key approved therapies used across first-, second- and third-line settings, including osimertinib, amivantamab and datopotamab deruxtecan.

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Enhanced activity in combination with osimertinib. Combining ATNM-400 with osimertinib produced tumor regression and complete responses exceeding either agent alone. Osimertinib increased ATNM-400 target expression, providing a mechanistic rationale for the observed combination activity.

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Monotherapy and combination activity across KRAS-mutant disease. ATNM-400 demonstrated activity in both KRAS G12C- and KRAS G13D-mutant models, including greater activity than approved KRAS G12C inhibitors and tumor regression in combination with sotorasib and adagrasib. Sotorasib and adagrasib also increased ATNM-400 target expression, supporting the potential for combination use.

We believe these findings support the potential development of ATNM-400 as a monotherapy or combination backbone across EGFR- and KRAS-mutant NSCLC and potentially the broader target-positive NSCLC population.

ATNM-400 vs Standard of Care Therapies Across EGFR- and KRAS-Mutant NSCLC Models

Supporting Data in NSCLC

In an EGFR-mutant model (NCI-H1975, harboring L858R and T790M mutations), ATNM-400 monotherapy achieved 75% tumor growth inhibition, compared with 40% for osimertinib, and the combination of ATNM-400 plus osimertinib achieved 107% tumor growth inhibition (representing tumor regression) with complete cures in 100% of treated animals.

ATNM-400 Monotherapy Showed Strong Tumor Growth Inhibition and Combination with Osimertinib Achieved Complete Responses in the EGFR-Mutant NSCLC Model

Osimertinib treatment increased ATNM-400 target expression both in vitro and in vivo, which we believe provides a mechanistic rationale for why the combination of osimertinib with ATNM-400 works even better than ATNM-400 monotherapy alone. Furthermore, in vitro studies also demonstrated that Osimertinib upregulated the ATNM-400 target in NCI-H1975 cells, enhancing ATNM-400 cytotoxicity when dosed in combination.

Increased Target Expression Post-Osimertinib Treatment	ATNM-400 Post-Osimertinib

In the same EGFR-mutant model, ATNM-400 monotherapy also demonstrated greater anti-tumor activity than the approved agents datopotamab deruxtecan (a TROP-2 antibody drug conjugate), amivantamab (an EGFR-cMET bispecific antibody), and izalontamab brengitecan (a HER3-EGFR bispecific antibody-drug conjugate that is currently in development).

ATNM-400 Demonstrated 3-5x Greater Tumor Growth Inhibition vs Osimertinib or Dato-DXd or Amivantamab in EGFR-mutant NSCLC Model

ATNM-400 Demonstrated Superior Tumor Growth Inhibition Compared to Dato-DXd or Izalontamab Brengitecan in EGFR-mutant NSCLC Model

In data presented at the Society of Nuclear Medicine and Molecular Imaging (SNMMI) 2026 Annual Meeting in June 2026, ATNM-400 demonstrated activity across KRAS-mutant NSCLC models spanning distinct KRAS alleles. In a KRAS G12C model (NCI-H358), ATNM-400 monotherapy achieved 92% tumor growth inhibition, compared with 0% for the approved KRAS G12C inhibitor sotorasib, and the combination of ATNM-400 plus sotorasib achieved 90% tumor growth inhibition. In the same G12C model, the combination of ATNM-400 with adagrasib achieved 110% tumor growth inhibition (indicating regression) compared to 71% for adagrasib alone.

ATNM-400 Showed Superior Efficacy versus Approved KRAS G12C Inhibitors in KRAS G12C-Mutant NSCLC Model

Treatment with the approved KRAS G12C inhibitors sotorasib and adagrasib increased ATNM-400 target expression by up to approximately 3.5- and 3.8-fold, respectively (p<0.0001). The addition of ATNM-400 reduced cancer-cell viability beyond KRAS G12C inhibitors alone - demonstrating the same target-expression-increasing, synergy-enabling biology previously observed with the EGFR inhibitor osimertinib.

Sotorasib and Adagrasib Increase ATNM-400 Target Expression in a Dose-Dependent Manner in the KRAS G12C-Mutant NCI-H358 NSCLC Model

Positron-emission-tomography imaging of Zr-89-labeled ATNM-400 confirmed target-specific tumor uptake in a KRAS G12C model with low uptake in healthy normal tissues.

Zr-89-ATNM-400 PET Imaging Showed Tumor-specific Uptake that is Blocked by Unlabeled Cold Antibody Demonstrating Specificity in the KRAS G12C-Mutant NSCLC Model

In a target-positive KRAS G13D-mutant NSCLC model (Calu-3), single doses of 20 uCi/kg or 40 uCi/kg of ATNM-400 reduced tumor volume below baseline, corresponding to 124% and 135% tumor growth inhibition which translates to tumor regression. The unlabeled antibody produced minimal tumor growth inhibition relative to vehicle - indicating that anti-tumor activity is driven by the Ac-225 payload rather than by antibody-mediated target engagement alone.

ATNM-400 Had Dose-Dependent Tumor Growth Inhibition in the KRAS G13D-Mutant NSCLC Model

ATNM-400 in Breast Cancer

ATNM-400's target antigen is overexpressed across breast cancer subtypes, including HR+/HER2-, HER2+ (including HR+ and HR-), and triple-negative breast cancer, and is retained or increased following resistance to endocrine and HER2+-directed therapies. Because ATNM-400 acts through a pathway-independent mechanism, we believe it has the potential to address multiple treatment-resistant breast cancer populations as a monotherapy or in combination with existing standards of care. In addition, we do not believe ATNM-400 carries the risks of interstitial lung disease (ILD) associated with ADCs carrying the deruxtecan payload.

Key Findings and Therapeutic Positioning in Breast Cancer

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Activity in treatment-resistant HER2+ disease. In a trastuzumab-resistant HER2+ model, ATNM-400 demonstrated strong monotherapy activity and enhanced activity in combination with trastuzumab, with efficacy comparable to trastuzumab deruxtecan in the evaluated model. Increased ATNM-400 target expression in HER2 resistant disease provides a mechanistic rationale for this activity.

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Activity in triple-negative breast cancer. ATNM-400 monotherapy produced tumor regression in a TNBC model, supporting its potential in a disease subtype with limited targeted treatment options.

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Activity following HER2 directed therapy failure. ATNM-400 retained durable anti-tumor activity after trastuzumab progression and demonstrated greater activity than trastuzumab deruxtecan in the post-trastuzumab-failure setting without the risks of ILD associated with ADCs addressing the indication.

	●	Activity in endocrine-resistant HR+ disease. ATNM-400 demonstrated dose-dependent activity in an endocrine-resistant HR+ model, supporting activity independent of HER2 status and endocrine sensitivity.
	●	Combination activity in endocrine treatment-resistant disease. Following tamoxifen failure, sequential treatment with ATNM-400 drove a dose-dependent, near-complete loss of cancer-cell viability, supporting ATNM-400's potential to deepen response after endocrine therapy failure.

We believe these findings support the potential development of ATNM-400 across breast cancer subtypes, with particularly differentiated opportunities in TNBC and treatment-resistant HER2+ disease, as well as additional potential in endocrine-resistant HR+ disease.

Supporting Data in Breast Cancer Models

In a trastuzumab-resistant HER2+ model (BT474-Clone5), ATNM-400 monotherapy achieved 97% tumor growth inhibition and, in combination with trastuzumab, achieved 100% tumor growth inhibition (representing tumor regression) - comparable to the approved HER2 antibody-drug conjugate trastuzumab deruxtecan, without the higher risks of interstitial lung disease associated with ADC with the deruxtecan payload. ATNM-400 monotherapy drove tumor regression (103% tumor growth inhibition) in a triple-negative model (MDA-MB-468). Similar to referenced KRAS G13D studies in NSCLC, unlabeled antibody produced minimal tumor growth inhibition relative to vehicle - again indicating that anti-tumor activity is driven by ATNM-400's Ac-225 payload versus antibody-mediated target engagement.

ATNM-400 Monotherapy and Combinations Eradicate Trastuzumab-Resistant Tumors and Triple-Negative Breast Cancer (TNBC)

Trastuzumab-Resistant HER2+ Model BT474-Clone5	MDA-MB-468 (TNBC) Breast Cancer Model

In the post-trastuzumab-failure setting, ATNM-400 retained durable anti-tumor activity (93% tumor growth inhibition), exceeding trastuzumab deruxtecan (64%), further demonstrating utility after resistance to approved drugs.

ATNM-400 Demonstrated Efficacy After Trastuzumab and HER2-DXd Failures in Trastuzumab-resistant Breast Cancer Model

ATNM-400 demonstrated dose-dependent activity in an endocrine-resistant HR+ model (MCF7), consistent with activity that is independent of HER2 status and endocrine sensitivity.

ATNM-400 Showed Dose-Dependent Tumor Growth Inhibition in MCF7 (HR+) Breast Cancer

In an endocrine-resistant (HR+) setting modeling patients who have failed prior tamoxifen, ATNM-400, when given sequentially after tamoxifen exposure, drove a tamoxifen dose-dependent, near-complete loss of cancer-cell viability - reducing viability to as low as approximately 3%.

ATNM-400 Significantly Decreased Cancer Cell Viability Post-Tamoxifen Failures

Actimab-A for MDSCs: Novel Immunomodulatory Approach in Solid Tumors

Actimab-A (lintuzumab-Ac-225) is a CD33-targeted actinium-225 radioconjugate that we are developing to enhance checkpoint inhibitor efficacy by depleting immunosuppressive CD33+ myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. MDSCs are a heterogeneous population of immature myeloid cells that accumulate in solid tumors and suppress anti-tumor T-cell responses, representing a well-validated mechanism of resistance to PD-1/PD-L1 checkpoint inhibitors. By selectively eliminating these suppressive cells with targeted alpha-particle therapy, Actimab-A is designed to dismantle this barrier and restore an environment in which checkpoint blockade can drive meaningful Tcell-mediated tumor killing. This positions Actimab-A as a differentiated immunomodulatory approach intended to expand the population of patients who benefit from checkpoint inhibitors, including those with tumors historically considered immunologically "cold."

Actimab-A Depletion of MDSCs: Resensitizing PD-1 Inhibitors for T Cell Activation

Clinical studies have demonstrated that patients with high circulating MDSC levels have significantly reduced progression-free and overall survival on PD-1 therapy compared to patients with low MDSC levels.

Low MDSCs Associated With Statistically Significant Improvement in PFS and OS

(Bronte et al., Frontiers in Immunology 2022)

Our preclinical studies have suggested that Actimab-A: (1) selectively homes to tumor-resident CD33+ MDSCs in vivo; (2) are cytotoxic to patient-derived MDSCs ex vivo; and (3) rescue T-cell proliferation and anti-tumor immune responses ex vivo following MDSC depletion. We believe these data provide mechanistic support for combining Actimab-A with PD-1 inhibitors to overcome MDSC-mediated resistance.

Actimab-A (Lintuzumab-Ac225) was shown to deplete MDSCs in our studies. Actimab-A was also shown to restore T-cell proliferation in a dose dependent manner.

Actimab-A Depletes Human MDSCs In Vivo	Actimab-A Facilitates T cell Proliferation

We intend to conduct a Phase 1b basket trial evaluating Actimab-A in combination with pembrolizumab (Keytruda^®) or nivolumab (Opdivo^®) in patients with R/R locally advanced or metastatic head and neck squamous cell carcinoma (HNSCC), NSCLC, glioblastoma (GBM), and microsatellite instability (MSI)-high colorectal cancer. These tumor types were selected based on high MDSC infiltration and limited response rates to PD-1 monotherapy. The trial design incorporates comprehensive correlative biomarker assessments to evaluate MDSC depletion in both tumor microenvironment and peripheral blood, as well as T-cell activity restoration.

Patients eligible to be enrolled in the trial must have MDSC-rich tumor types, be checkpoint inhibitor-naïve, be at least 18 years of age, and demonstrate PD-1/PD-L1 expression. Primary endpoints include safety and tolerability of the combination, with secondary endpoints including ORR, PFS, and OS. Biomarker endpoints will evaluate the pattern of CD33+ MDSC depletion and T-cell activity in both tumor tissue and peripheral blood samples. Clinical outcomes will be compared against real-world data from similar patient populations treated with PD-1 monotherapy. We expect to report initial data from this trial in 2H:2026 or 1H:2027. In addition, we are also evaluating clinical opportunities with other immune checkpoint inhibitors in GBM and NSCLC.

Hematology Programs

Actimab-A: Backbone Therapy for AML and MDS

In hematologic malignancies, we are developing Actimab-A as a mutation-agnostic backbone therapy for AML and high-risk MDS. CD33 is expressed on leukemic blasts in the majority of AML patients and represents an established therapeutic target validated by the approval of gemtuzumab ozogamicin (Mylotarg^®). However, antibody-drug conjugates like Mylotarg^® can have limitations, including hepatotoxicity and limited efficacy in certain patient populations. Actimab-A, delivering the highly potent alpha-emitter Ac-225 to CD33+ cells, represents a differentiated approach designed to provide superior efficacy while maintaining a favorable safety profile. Supporting this backbone positioning, preclinical and translational studies have demonstrated that Actimab-A is cytotoxic in primary AML patient samples irrespective of FLT3, KMT2A, NPM1, IDH1, or TP53 mutation status. The combinations of Actimab-A with agents from each of the three major classes of AML standard-of-care therapies, including the menin inhibitor revumenib, the FLT3 inhibitor gilteritinib, and the hypomethylating agent azacitidine, potentiate AML cell death, supporting a backbone strategy. Actimab-A was shown to produce consistent transcriptional reprogramming, including activation of p53-associated stress response and apoptosis pathways and downregulation of proliferative programs such as MYC targets and G2/M checkpoint signatures.

We have completed a Phase 1b clinical trial evaluating Actimab-A in combination with CLAG-M chemotherapy in R/R AML patients, results of which were published in a peer-reviewed journal Leukemia in February 2025. The trial enrolled high-risk patients including those with TP53 mutations, prior venetoclax treatment failure, and patients who had prior allogeneic transplant. Results demonstrated high rates of measurable residual disease (MRD)-negative complete remissions and improved survival outcomes compared to historical controls.

Among patients treated with Actimab-A plus CLAG-M, 70% of those deemed eligible for transplant proceeded to bone marrow transplant, and this population achieved a 24-month median overall survival. These results compare favorably to published data showing less than 2-4 month median overall survival in TP53-mutated or prior venetoclax-treated R/R AML patient populations. The combination was well-tolerated with a safety profile consistent with CLAG-M chemotherapy alone and no dose-limiting toxicities observed.

We have discussed with the Food and Drug Administration (FDA) and believe we are aligned on a Phase 2/3 trial design to evaluate Actimab-A plus CLAG-M in R/R AML patients eligible for first or second salvage therapy. We are actively seeking a strategic partner to execute this trial. We believe the trial design allows for enrollment of a broad R/R AML population while enriching for patients most likely to benefit based on Phase 1b results.

Actimab-A + CLAG-M Phase 2/3 Trial Design

Actimab-A Development Programs: Beyond R/R AML, we are developing Actimab-A in conjunction with the National Cancer Institute, or NCI across multiple AML and MDS treatment settings and exploring its potential in additional areas:

●

Frontline AML Triplet Combination: Evaluating Actimab-A as a backbone therapy in combination with standard induction regimen of venetoclax and a hypomethylating agent in newly diagnosed AML patients. This mutation-agnostic approach could provide benefit across the broad frontline AML population.

●

Combination with Targeted Therapies: Developing Actimab-A combinations with FLT3 inhibitors, IDH1/2 inhibitors, and menin inhibitors in genomically-defined AML patient subsets. These combinations leverage Actimab-A's mutation-agnostic mechanism while potentially enhancing efficacy through complementary mechanisms of action.

●

High-Risk MDS Monotherapy: Evaluating Actimab-A as monotherapy in high-risk MDS patients who have failed hypomethylating agent therapy, representing a patient population with very limited treatment options and poor outcomes.

●

Maintenance Therapy: The potential exists for Actimab-A as maintenance therapy following achievement of remission to prevent relapse in AML and MDS patients.

The programs are supported by our Cooperative Research and Development Agreement (CRADA) with the NCI, which enables cost-effective clinical development while retaining commercial rights to Actimab-A.

On April 21, 2026, preclinical translational data with Actimab-A were presented at the AACR Annual Meeting in San Diego, California. The presentation highlighted the following:

Transcriptional Reprogramming as a Key Mechanism for Actimab-A Combination Activity

●

Combination treatment produced consistent pathway-level changes compared with monotherapy, with gene set enrichment analysis (GSEA) showing enhanced myeloid differentiation signatures when Actimab-A was added to revumenib, gilteritinib, and azacitidine, agents from each of the three major classes of AML standard-of-care therapies.

●

Across models, combinations were associated with downregulation of proliferative programs, including MYC target genes, E2F targets, and G2/M checkpoint signatures, together with enrichment of p53-associated stress response and apoptosis pathways.

●

We believe these findings indicate that Actimab-A combinations reprogram AML cells from proliferation toward differentiation and apoptosis, potentially providing a mechanistic basis for deeper and more durable MRD-negative responses and supporting Actimab-A's role as a universal combination backbone across AML treatment settings.

Gene Set Enrichment Analysis Demonstrated Broad Activity of Actimab-A Combinations Versus AML Standard of Care Therapies Alone

Combinations with Revumenib and Azacitidine Sensitize AML Cells to Actimab-A and Support Frontline Triplet Rationale

●

Actimab-A demonstrated robust cytotoxicity in primary AML patient samples independent of FLT3, KMT2A, NPM1, IDH1, IDH2, or TP53 mutation status, supporting its potential applicability across the full AML patient population, including TP53-mutant patients who lack effective targeted options.

●

Combining Actimab-A with standard-of-care therapies, including revumenib (menin inhibitor), gilteritinib (FLT3 inhibitor), and azacitidine (hypomethylating agent), enhanced anti-leukemic efficacy across models, demonstrating synergy with agents representing each of the three pillars of modern AML care and, we believe, further support Actimab-A's positioning as a combination partner across frontline, relapsed/refractory, and unfit AML populations.

Actimab-A Combination with SOC Enhance Cytotoxicity in Primary AML Patient Samples

Iomab-ACT: Universal Conditioning for Cell and Gene Therapies

Iomab-ACT is our CD45-targeted conditioning platform being developed as a universal conditioning agent to improve access and outcomes for cell and gene therapies, including CAR-T, allogeneic hematopoietic stem cell transplant, and gene therapy. The cell and gene therapy field has been limited by the need for lymphodepleting chemotherapy conditioning, which is associated with significant toxicities and can limit the patient populations eligible for these potentially curative treatments.

Iomab-ACT is designed to provide targeted lymphodepletion and myeloablation when necessary while avoiding the off-target toxicities associated with chemotherapy conditioning. By delivering targeted radiation specifically to CD45+ hematopoietic cells, Iomab-ACT aims to create an optimal environment for therapeutic cell engraftment while minimizing treatment-related morbidity and mortality.

We currently have three active clinical trials evaluating Iomab-ACT:

●

Phase 1/2 Trial in Commercial CAR-T: Evaluating Iomab-ACT as conditioning prior to commercial CAR-T therapy in patients with relapsed/refractory non-Hodgkin's lymphoma. The primary endpoint is engraftment and key secondary endpoints are incidence of Cytokine Release Syndrome (CRS) and Immune Effector Cell-Associated Neurotoxicity Syndrome (ICANS), which are two potentially fatal adverse events associated with CAR-T cell therapy.

●

Phase 1 Trial in experimental CAR-T: Evaluating Iomab-ACT as conditioning prior to CD19 CAR-T cell therapy in patients with relapsed /refractory B-cell malignancies.

●

Phase 1 Trial in Sickle Cell Disease BMT: Evaluating Iomab-ACT as conditioning for allogeneic bone marrow transplant in patients with sickle cell disease.

Iomab-B: Targeted Conditioning for Bone Marrow Transplant in R/R AML

Iomab-B (apamistamab-I-131) is a CD45-targeted radioimmunotherapy designed to enable bone marrow transplant in R/R AML patients who are ineligible for conventional myeloablative conditioning due to age, comorbidities, or prior treatment-related toxicities. CD45 is expressed on all hematopoietic cells, enabling Iomab-B to deliver targeted radiation to bone marrow while sparing non-hematopoietic organs from radiation exposure.

Conventional stem cell transplant conditioning regimens utilize high-dose chemotherapy, with or without total body irradiation, to ablate the patient's hematopoietic system and create space for donor cell engraftment. These regimens are associated with significant toxicities including mucositis, hepatotoxicity, pulmonary toxicity, and treatment-related mortality. Many elderly patients and those with comorbidities are deemed ineligible for these intensive conditioning regimens, limiting access to potentially curative transplant therapy.

Iomab-B has been evaluated in over 500 patients across multiple clinical trials, including the Phase 3 SIERRA trial in R/R AML patients. The SIERRA trial demonstrated that Iomab-B enabled successful donor cell engraftment in elderly R/R AML patients who would otherwise be ineligible for conventional conditioning. The study met the primary endpoint of durable complete remission (dCR). While the study did not meet the secondary endpoint of OS due to the cross-over of two-thirds of the patients from the control arm to the Iomab-B arm, it provided important insights into optimal patient selection and trial design for future development.

We have discussed our Phase 2/3 trial design with FDA and, based on the feedback, we believe we are aligned on a Phase 2/3 trial design in an expanded R/R AML patient population that includes all patients age 18 and older with R/R AML. This expanded population reflects learnings from SIERRA regarding optimal patient selection. We believe the trial design allows us to leverage both the Phase 2 results and the SIERRA database to support regulatory submissions.

Iomab-B benefits from composition of matter patents extending to 2038, a well-established network of 24 clinical sites from the SIERRA trial that maintains strong interest in the program, and potential for market expansion beyond R/R AML. Preclinical and clinical data support potential development in five additional disease indications including acute lymphoblastic leukemia, myelodysplastic syndromes, chronic myeloid leukemia, multiple myeloma, and lymphoma, representing a total addressable market of approximately 150,000 patients who could benefit from improved bone marrow transplant conditioning.

We are actively seeking a strategic partner to advance Iomab-B through pivotal development and commercialization.

Our Platform and Capabilities

Radiochemistry and Translational Science Capabilities

We have assembled a team with expertise in radiopharmaceutical discovery and development, spanning target selection, radioconjugate design, preclinical evaluation, and clinical development. Our capabilities include:

●

Target Selection and Validation: Comprehensive target assessment including expression profiling in tumor versus normal, binding and internalization kinetics, and competitive landscape analysis to identify optimal targets for radiopharmaceutical development.

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Radioconjugate Design and Optimization: Medicinal chemistry expertise in chelator selection, linker design, and conjugation chemistry to optimize tumor uptake, retention, and biodistribution while minimizing normal organ exposure.

●

Preclinical Pharmacology: In vitro and in vivo models to assess binding affinity, internalization, tumor penetration, radiation dosimetry, and anti-tumor efficacy across diverse tumor types.

●

Translational Biomarkers: Development of imaging companion diagnostics, circulating biomarkers, and tissue-based assessments to enable patient selection and monitor treatment response.

We believe these capabilities enable us to efficiently advance programs from target selection through clinical development while maintaining high quality standards and generating comprehensive translational data packages to guide clinical development and support regulatory submissions and partnership discussions.

Clinical Development Operations

We conduct company-sponsored clinical development activities through a combination of internal personnel and third-party service providers in the United States and selected international jurisdictions where we operate through subsidiaries and/or contract research organizations. Our clinical development capabilities include clinical trial planning and execution, regulatory affairs, clinical monitoring, pharmacovigilance, medical oversight, data management, biostatistics and investigational product logistics. We work with contract research organizations, clinical investigators, central laboratories and other specialized vendors to support patient enrollment, study execution and regulatory compliance across our development programs.

We believe this operating model provides flexibility to efficiently advance multiple clinical programs while maintaining quality oversight, operational scalability and regulatory compliance. We expect to report data from ongoing company- and investigator-sponsored clinical studies for ATNM-400, Actimab-A for MDSC's and Iomab-ACT in 4Q:2026 and over the course of 2027.

Ac-225 Production and Radiopharmaceutical Manufacturing

We have developed proprietary cyclotron-based technology for commercial-scale production of Ac-225, one of the most critical bottlenecks in radiopharmaceutical development. Our production method generates high-purity Ac-225 with radiochemical purity equivalent to the gold-standard thorium-229 decay method, while avoiding the generation of long-lived radioactive contaminants such as Ac-227. This production technology is protected by patents and if operationalized may represent a significant competitive and cost advantage.

We are currently completing construction of a radiopharmaceutical manufacturing facility designed to manufacture Ac-225-based final drug products for clinical supply. The facility, expected to be operational in 2H:2026, incorporates purpose-built infrastructure for alpha-emitter handling and a flexible manufacturing suite capable of supporting multiple trials.

We have also established an end-to-end supply chain spanning isotope production through patient administration. Our clinical development infrastructure supports company-sponsored clinical development activities conducted in the United States and selected international jurisdictions through relationships with isotope suppliers, contract development and manufacturing organizations and specialized radiopharmaceutical logistics providers. We maintain supply agreements with multiple redundant isotope suppliers, relationships with multiple contract manufacturing organizations, and a distribution network to approximately 50 leading cancer centers amassed via the execution of several Phase 1 - 3 clinical trials. This supply chain infrastructure provides geographic coverage across major metropolitan areas, minimizes risk of supply disruption, and positions us to reliably serve patient demand at clinical scale.

Intellectual Property

We strive to protect and enhance the proprietary technologies that we believe are important to our business, including seeking, maintaining and defending patent rights, whether developed internally or licensed from third parties. Our policy is to seek to protect our proprietary position by, among other methods, filing U.S. and foreign patent applications related to our proprietary technology, inventions and improvements that are important for the development and implementation of our business. We also rely on trade secrets, know-how, continuing technological innovation and in-licensing opportunities to develop, strengthen and maintain our proprietary position. Our intellectual property portfolio comprises approximately 250 patents and patent applications across multiple jurisdictions. Our patent estate includes:

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Composition of Matter Patents: Covering our key product candidates including Iomab-B, Iomab-ACT, and ATNM-400.

●

Method of Use Patents: Covering specific therapeutic applications, combination therapies, and treatment protocols for our product candidates Actimab-A, Iomab-B, Iomab-ACT, and ATNM-400, as well as preclinical pipeline candidates.

●

Manufacturing and Process Patents: Protecting our cyclotron-based Ac-225 production technology, radiopharmaceutical manufacturing processes, and formulation technologies.

●

Platform Technology Patents: Protecting core technologies applicable across multiple programs including chelator chemistry, targeting approaches, and bioconjugation methods.

Our patents provide market exclusivity in major territories including the United States, Europe, Canada, Japan, and key emerging markets. We actively monitor and enforce our intellectual property rights and investigate potential infringement of our proprietary technologies. In addition to patents, we maintain proprietary know-how and trade secrets relating to our radiopharmaceutical development platform, manufacturing processes, and clinical development strategies. We seek to protect this information through confidentiality agreements with employees, consultants, advisors, and collaborative partners. We also rely on regulatory exclusivity to protect our products from competition. In the United States, biologics such as our antibody radioconjugates may be eligible for 12 years of market exclusivity under the Biologics Price Competition and Innovation Act. If any of our product candidates are approved for orphan indications, we may be eligible for seven years of market exclusivity in the United States, and similar exclusivity periods in other territories.

Manufacturing and Supply Chain

Our manufacturing strategy combines internal capabilities with external partnerships to create a flexible, redundant, and cost-effective supply chain capable of supporting both clinical development and commercial supply. This hybrid approach provides us with strategic flexibility, supply reliability, and the ability to scale production to meet patient demand.

Internal Manufacturing Capabilities

We are completing construction of a state-of-the-art cGMP radiopharmaceutical manufacturing facility located in New York, expected to be operational in 2H:2026. This facility has been purpose-built for alpha-emitter handling and radiopharmaceutical production with the following capabilities:

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Therapeutic Drug Product Manufacturing: production suites for radioconjugate synthesis, formulation, fill-finish, and quality control testing, designed to support multiple simultaneous programs.

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Quality Control and Analytics: Comprehensive analytical capabilities including radiochemical purity testing, stability assessment, sterility testing, and release testing in accordance with regulatory requirements.

●

Radiation Safety Infrastructure: Shielded manufacturing suites and a comprehensive radiation safety program to protect personnel and environment.

External Manufacturing Partnerships

We have established partnerships with multiple contract manufacturing organizations providing geographic redundancy and production flexibility to support company-sponsored clinical development activities in the United States and selected international jurisdictions. These partnerships, together with relationships with specialized isotope suppliers and radiopharmaceutical logistics providers, support investigational product manufacturing, distribution and clinical supply while providing operational redundancy and continuity of supply as the Company expands its internal manufacturing capabilities:

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Isotope Supply: We maintain supply agreements with multiple domestic and international suppliers of Ac-225 and other radioisotopes, providing priority access and redundancy to ensure reliable supply.

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Contract Manufacturing: We have qualified multiple contract manufacturers capable of producing our drug products under cGMP conditions. These partnerships provide backup capacity, geographic diversity, and specialized capabilities complementing our internal manufacturing.

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Distribution Partners: We have established relationships with specialized radiopharmaceutical logistics providers capable of cold-chain distribution, real-time tracking, and just-in-time delivery to clinical sites and commercial administration centers.

Supply Chain Management

Our supply chain team has established systems and processes to coordinate the complex logistics of radiopharmaceutical production and distribution:

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Demand Forecasting: Predictive models incorporating clinical trial enrollment, commercial demand projections, and inventory optimization to ensure adequate supply while minimizing waste.

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Production Scheduling: Coordinated scheduling across isotope production, drug product manufacturing, quality testing, and distribution to optimize efficiency and minimize decay losses.

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Real-Time Tracking: Systems to monitor location, temperature, and radiation levels throughout the supply chain from production through patient administration.

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Regulatory Compliance: Procedures ensuring compliance with FDA, NRC, Department of Transportation, and international regulations governing radioactive material handling, transportation, and administration.

Our manufacturing and supply chain capabilities position us to support ongoing clinical development activities conducted in multiple jurisdictions and future commercial operations while maintaining flexibility to respond to changing demand.

Human Capital

As of August 6, 2026, we had 27 full-time employees, 13 of whom have Ph.D. or M.D. degrees and 23 of whom are engaged in research and development and clinical development activities. We believe that we have been successful to date in attracting skilled and experienced personnel despite the competitive hiring environment in the industry. Our employees are not covered by a collective bargaining agreement, and we believe that our relationship with our employees is excellent. We continue to engage external consultants on an as-needed basis to supplement existing staff.

Results of Operations - Three Months Ended June 30, 2026 Compared to Three Months Ended June 30, 2025

The following table sets forth, for the periods indicated, data derived from our statements of operations:

		For the Three Months Ended June 30
(in thousands)		2026				2025
Revenue:
Revenue		$	-			$	-
Other revenue			35,000				-
Total revenue			35,000				-
Operating expenses:
Research and development, net of reimbursements			5,377				4,879
General and administrative			2,058				2,624
Total operating expenses			7,435				7,503
Other income:
Interest income - net			336				625
Total other income			336				625
Income/(loss) before income taxes			27,901				(6,878	)
Income tax expense			-				-
Net income/(loss)		$	27,901			$	(6,878	)

Revenue

We recorded no commercial revenue for the three months ended June 30, 2026 and June 30, 2025, respectively.

Other revenue

On April 7, 2022, we entered into a License Agreement with Immedica, pursuant to which Immedica licensed the exclusive product rights for commercialization of Iomab-B in certain countries in the EUMENA region. Upon signing, we were entitled to an upfront, non-refundable payment of $35 million from Immedica, which was received in May 2022. Under the terms of the License Agreement, we are eligible to receive certain regulatory and commercial milestone payments and royalties on net sales of the product in certain countries that may result from the License Agreement. We continue to retain commercialization rights in the U.S. and the rest of the world. The $35 million upfront payment was initially recorded as Long-term license revenue - deferred due to uncertainty regarding Immedica's ability to obtain regulatory approval of the product by the European Medicines Agency. Subsequently, Immedica notified us that it would not pursue regulatory approval of Iomab-B in the licensed territories. In the current period, based on the facts and circumstances, we concluded that Immedica's right to asserting a claim related to the $35 million had expired. Accordingly, the condition previously constraining recognition of the $35 million upfront payment no longer existed and that the non-refundable payment was no longer subject to a significant reversal. Therefore, we recognized the previously deferred $35 million upfront payment as revenue in June 2026.

Research and development expense, net of reimbursements

Research and development expenses include costs associated with preclinical and clinical development activities conducted in the United States and selected international jurisdictions, including clinical site costs, contract research organizations, manufacturing, isotope supply, investigational product logistics, regulatory support and pharmacovigilance. Certain international clinical development activities are conducted through the Company's wholly owned Australian subsidiary, Actinium Pharmaceuticals Australia Pty Ltd. The Company has applied for available Australian research and development tax incentives associated with qualifying research activities.

Research and development expenses, net of reimbursements, of $5.4 million for the three months ended June 30, 2026 increased by $0.5 million from $4.9 million for the three months ended June 30, 2025, primarily due to increased preclinical expenses of $0.3 million, increased Chemistry, manufacturing and controls, or CMC, expenses and clinical expenses of $0.6 million, partially offset by lower compensation expense of $0.4 million due to lower headcount. In the second quarter of 2025, we conducted a workforce optimization that reduced our headcount by approximately fourteen percent and announced a strategic pipeline prioritization which resulted in additional departures in 2025.

General and administrative expense

General and administrative expense of $2.1 million for the three months ended June 30, 2026 decreased by $0.5 million from $2.6 million for the three months ended June 30, 2025 primarily due to a decrease in compensation expense of $0.4 million due to lower headcount and a decrease in non-cash stock-based compensation expense of $0.1 million.

Other income

Other income is comprised of net interest income in both reporting periods. The amount for the three months ended June 30, 2026 of $0.3 million decreased from $0.6 million for the three months ended June 30, 2025 primarily due to a lower average cash balance during the three months ended June 30, 2026 compared to the prior-year period.

Income tax expense

Income tax expense was $0 for the three months ended June 30, 2026 and 2025. Despite reporting profit before income taxes of $27.9 million for the three months ended June 30, 2026, no income tax expense was recorded as we have sufficient net operating losses that are available to offset net taxable income. The Company's estimated annual effective income tax rate is 0%, compared to the U.S. federal statutory rate of 21%. The difference is attributable to the full valuation allowance maintained against the Company's net deferred tax assets. Based on the Company's history of cumulative losses and the uncertainty of generating sufficient future taxable income to utilize its deferred tax assets, management has determined that it is more likely than not that the net deferred tax assets will not be realized.

Net income / (loss)

Net income of $27.9 million for the three months ended June 30, 2026 increased by $34.8 million from a net loss of $6.9 million for the three months ended June 30, 2025 driven by the recognition of $35.0 million of revenue previously deferred in connection with the commercialization agreement with Immedica.

Results of Operations - Six Months Ended June 30, 2026 Compared to Six Months Ended June 30, 2025

The following table sets forth, for the periods indicated, data derived from our statements of operations:

		For the Six Months Ended June 30,
(in thousands)		2026				2025
Revenue:
Revenue		$	-			$	-
Other revenue			35,000				-
Total revenue			35,000				-
Operating expenses:
Research and development, net of reimbursements			9,578				12,579
General and administrative			3,760				11,562
Total operating expenses			13,338				24,141
Other income:
Interest income - net			717				1,325
Total other income			717				1,325
Income/(loss) before income taxes			22,379				(22,816	)
Income tax expense			-				-
Net income/(loss)		$	22,379			$	(22,816	)

Revenue

We recorded no commercial revenue for the six months ended June 30, 2026 and June 30, 2025, respectively.

Other revenue

As noted above, we recognized $35 million as revenue in the six months ended June 30, 2026 related to the Immedica collaboration.

Stock-based compensation expense

On March 31, 2025, our Board of Directors approved the cancellation of certain stock options to purchase an aggregate of 4.9 million shares of common stock held by certain current employees and directors that were initially granted under our Amended and Restated 2013 Stock Plan and our 2019 Stock Plan. The cancellation of these stock options resulted in the recording of $8.7 million in non-cash stock compensation expense for the six months ended June 30, 2025, $2.1 million in Research and development expense and $6.6 million in General and administrative expense.

Research and development expense, net of reimbursements

Research and development expenses, net of reimbursements, of $9.6 million for the six months ended June 30, 2026 decreased by $3.0 million from $12.6 million for the six months ended June 30, 2025. The cancellation of stock options in March 2025 described above resulted in lower non-cash stock-based compensation expense of $2.1 million for the six months ended June 30, 2026 compared with the six months ended June 30, 2025. In addition, there was lower compensation cost of $0.9 million due to lower headcount.

General and administrative expense

General and administrative expense of $3.8 million for the six months ended June 30, 2026 decreased by $7.8 million from $11.6 million for the six months ended June 30, 2025. Lower non-cash stock-based compensation expense of $6.9 million for the six months ended June 30, 2026 compared with the same period in 2025 was primarily driven by the cancellation of stock options in March 2025, discussed above. In addition, in comparison to the prior-year period, compensation expense decreased $0.9 million due to lower headcount.

Other income

Other income is comprised of net interest income in both reporting periods. The amount for the six months ended June 30, 2026 of $0.7 million decreased from $1.3 million for the six months ended June 30, 2025 primarily due to a lower average cash balance during the six months ended June 30, 2026 compared to the prior-year period.

Income tax expense

Income tax expense was $0 for the six months ended June 30, 2026 and 2025. Despite reporting income before income taxes of $22.4 million for the six months ended June 30, 2026, no income tax expense was recorded. The Company's estimated annual effective income tax rate is 0%, compared to the U.S. federal statutory rate of 21%.

Net income/(loss)

Net income of $22.4 million for the six months ended June 30, 2026 increased by $45.2 million from a net loss of $22.8 million for the six months ended June 30, 2025, driven by the recognition of $35.0 million of revenue previously deferred in connection with the commercialization agreement with Immedica, lower stock-based compensation of $9.0 million discussed above and lower compensation expense of $1.8 million due to lower headcount, slightly offset by lower other income of $0.6 million.

Liquidity and Capital Resources

The following table sets forth selected cash flow information for the periods indicated:

		For the Six Months Ended June 30,
(in thousands)		2026				2025
Cash used in operating activities		$	(11,049	)		$	(12,966	)
Cash used in investing activities			(480	)			-
Cash used in financing activities			(5	)			(5	)
Effect of foreign currency rates on cash			13				-
Net change in cash, cash equivalents and restricted cash		$	(11,521	)		$	(12,971	)

Net cash used in operating activities for the six months ended June 30, 2026 was $11.0 million, a decrease of $2.0 million from $13.0 million in the prior-year period, primarily resulting from lower compensation expense as a result of lower headcount for the six months ended June 30, 2026 compared to the prior-year period.

Cash used in investing activities for the six months ended June 30, 2026 was $0.5 million related to the construction of modular removable manufacturing improvements within our leased manufacturing facility. There was no cash used in investing activities for the six months ended June 30, 2025.

Cash used in financing activities for the six months ended June 30, 2026 and June 30, 2025 was $5 thousand and $5 thousand, respectively.

In August 2020, we entered into the Capital on Demand™ Sales Agreement with JonesTrading Institutional Services LLC, or JonesTrading, pursuant to which we are able to sell, from time to time, through or to JonesTrading, up to an aggregate of $200 million of our common stock. On June 28, 2022, we entered into an Amended and Restated Capital on Demand™ Sales Agreement, or the A&R Sales Agreement, with JonesTrading and B. Riley Securities, Inc. ("B. Riley"). The A&R Sales Agreement modifies the original Capital on Demand™ Sales Agreement to include B. Riley as an additional sales agent thereunder. Shares of common stock were offered pursuant to a shelf registration statement on Form S-3 (File No. 333-242322) filed with the SEC on August 7, 2020 (the "Prior Shelf Registration Statement"). On August 11, 2023, we filed a registration statement on Form S-3 (File No. 333-273911), which was amended on February 2, 2024, and declared effective on February 5, 2024, to replace the Prior Shelf Registration Statement, including a base prospectus which covers the offering, issuance and sale of up to $500 million of common stock, preferred stock, warrants, units and/or subscription rights; and a sales agreement prospectus covering the offering, issuance and sale of up to a maximum aggregate offering price of $200 million of common stock that may be issued and sold under the A&R Sales Agreement. There was no sale of shares of common stock during the six months ended June 30, 2026 and 2025, respectively.

As of the date of filing this report, we expect that our existing resources will be sufficient to fund our planned operations for more than 12 months following the date of this report.

Notice of Delisting or Failure to Satisfy a Continued Listing Rule or Standard

On May 27, 2026, the Company received a notice from NYSE American LLC indicating that we are not in compliance with the continued listing standards set forth in Section 1003(a)(ii) of the NYSE American Company Guide, which requires a listed company to maintain stockholders' equity of $4.0 million or more if it has reported losses from continuing operations and/or net losses in three of its four most recent fiscal years. As of March 31, 2026, the Company reported stockholders' equity of $2.3 million and had net losses in its last five fiscal years ended December 31, 2025. As of June 30, 2026, the Company reported stockholders' equity of $30.3 million.

In connection with its non-compliance with Sections 1003(a)(ii) and (iii) of the Company Guide, the Company was required to submit a plan by June 26, 2026, advising of actions it has taken or will take to regain compliance with the continued listing standards by November 27, 2027, or the Plan Period Deadline. If NYSE Regulation determines to accept the plan, we will be notified in writing and will be subject to periodic reviews including quarterly monitoring for compliance with the plan. Note that typically, NYSE considers a company compliant if it meets the listing requirements for two consecutive quarters. Subsequent to filing of this current Form 10-Q, we expect to be in technical compliance based on our stockholder equity and expect to remain so thereafter.

On June 18, 2026, we submitted our compliance plan to NYSE American, outlining certain actions management intends to take in effort to restore compliance with applicable listing standards. If the plan is not accepted, delisting proceedings will commence. Furthermore, if the plan is accepted but the Company is not in compliance with the continued listing standards by the Plan Period Deadline, or if the Company does not make progress consistent with the plan during the plan period, NYSE American staff will initiate delisting proceedings as appropriate. The Company may appeal a staff delisting determination in accordance with Section 1010 and Part 12 of the Company Guide.

The Notice has no immediate effect on the listing or trading of the Company's common stock, which will continue to trade on NYSE American under the symbol "ATNM," subject to the Company's compliance with the other continued listing requirements of NYSE American, and will continue to trade with a ".BC" indicator to denote that the Company is below compliance.

There can be no assurance that the Company will be able to regain or maintain compliance with the applicable continued listing standards, that NYSE American will accept the Company's Plan, that the Company will be able to comply with the terms of any accepted Plan, or that the Company will be able to maintain the listing of its common stock on NYSE American.

Critical Accounting Estimates

Our management's discussion and analysis of financial condition and results of operations is based on our consolidated financial statements, which have been prepared in accordance with accounting principles generally accepted in the United States ("GAAP"). The preparation of these financial statements requires us to make estimates and judgments that affect the reported amounts of assets, liabilities and expenses and the disclosure of contingent assets and liabilities in our consolidated financial statements during the reporting periods. These items are monitored and analyzed by us for changes in facts and circumstances, and material changes in these estimates could occur in the future. We base our estimates on historical experience, known trends and events, and on various other factors that we believe are reasonable under the circumstances, the results of which form the basis for making judgments about the carrying value of assets and liabilities that are not readily apparent from other sources. Changes in estimates are reflected in reported results for the period in which they become known. Actual results may differ materially from these estimates under different assumptions or conditions. The Company does not have any critical accounting estimates.

Recently Issued Accounting Pronouncements

In September 2025, the FASB issued ASU 2025-07, Derivatives and Hedging (Topic 815) and Revenue from Contracts with Customers (Topic 606): Derivatives Scope Refinements and Scope Clarification for Share-Based Noncash Consideration from a Customer in a Revenue Contract, which excludes from derivative accounting non-exchange-traded contracts with underlying terms that are based on operations or activities specific to one of the parties to the contract. However, this scope exception does not apply to (1) variables based on a market rate, market price, or market index, (2) variables based on the price or performance of a financial asset or financial liability of one of the parties to the contract, (3) contracts (or features) involving the issuer's own equity that are evaluated under the guidance in Subtopic 815-40, Derivatives and Hedging-Contracts in Entity's Own Equity, and (4) call options and put options on debt instruments. We can apply the amendments in AUS 2025-07 either (1) prospectively to new contracts entered into on or after the date of adoption or (2) on a modified retrospective basis through a cumulative-effect adjustment to the opening balance of retained earnings as of the beginning of the annual reporting period of adoption for contracts existing as of the beginning of the annual reporting period of adoption. The amendments in ASU 2025-07 are effective January 1, 2027, for annual reporting periods, including interim periods within annual reporting periods. Early adoption is permitted. We are evaluating the impact of ASU 2025-07 on our financial statements.

In May 2025, FASB issued ASU 2025-04, Compensation-Stock Compensation (Topic 718) and Revenue from Contracts with Customers (Topic 606): Clarifications to Share-Based Consideration Payable to a Customer, which revises the Master Glossary definition of the term "performance condition" for share-based consideration payable to a customer to include conditions, such as vesting conditions, that are based on the volume or monetary amount of a customer's purchases or potential purchases of goods or services from the grantor, including over a specified period of time. The revised definition also incorporates performance targets based on purchases made by other parties that purchase the grantor's goods or services from the grantor's customers. The revised definition of the term performance condition cannot be applied by analogy to awards granted to employees and non-employees in exchange for goods or services to be used or consumed in the grantor's own operations. ASU 2025-04 eliminates the policy election permitting a grantor to account for forfeitures as they occur for share-based awards granted to a customer. Separate policy elections for forfeitures remain available for share-based payment awards with service conditions granted to employees and non-employees in exchange for goods or services to be used or consumed in the grantor's own operations. ASU 2025-04 further clarifies that a grantor should not apply the guidance in Topic 606 on constraining estimates of variable consideration to share-based consideration payable to a customer. ASU 2025-04 permits a grantor to apply the new guidance on either a modified retrospective or a retrospective basis. The amendments in ASU 2025-04 are effective January 1, 2027, for annual reporting periods, including interim periods within annual reporting periods. We are evaluating the impact of ASU 2025-04 on our financial statements.

In November 2024, FASB issued ASU 2024-03, Income Statement-Reporting Comprehensive Income-Expense Disaggregation Disclosures (Subtopic 220-40), to improve the disaggregation of expenses within the consolidated statement of operations. The amendments in ASU 2024-03 require disclosures in the notes to the consolidated financial statements and specified information about certain costs and expenses. The amendments require that at each interim and annual reporting period an entity disclose (a) employee compensation, (b) depreciation, and (c) intangible asset amortization included in each relevant expense caption; include certain amounts that are already required to be disclosed under current GAAP in the same disclosure as the other disaggregation requirements; and disclose a qualitative description of the amounts remaining in relevant expense captions that are not separately disaggregated quantitatively. The amendments in ASU 2024-03 are effective January 1, 2027 and effective for interim periods beginning January 1, 2028, either on a prospective or retrospective basis. We are evaluating the impact of ASU 2024-03 on our financial statements.

In December 2025, the FASB issued ASU 2025-11, Interim Reporting (Topic 270): Narrow-Scope Improvements. This update clarifies interim disclosure requirements and centralizes such requirements within Topic 270. Among other changes, ASU 2025-11 introduces a disclosure principle requiring entities to provide information about significant events or changes since the end of the last annual reporting period that have a material impact, clarifies when duplicative annual disclosures may be omitted from interim reports, and aligns interim reporting requirements with applicable SEC guidance for registrants. This guidance is effective for interim reporting periods within annual reporting periods beginning after December 15, 2027. Early adoption is permitted. The amendments in ASU 2025-11 should be applied prospectively. We are currently assessing the impact on its condensed consolidated financial statements and disclosures.

Known Trends, Events and Uncertainties

The Company is subject to risks and uncertainties common to companies in the biopharmaceutical industry, including but not limited to, risks associated with completing preclinical studies and clinical trials, receiving regulatory approvals for product candidates, development by competitors of new biopharmaceutical products, dependence on key personnel, protection of proprietary technology, compliance with government regulations and the ability to secure additional capital to fund operations. In addition, the consequences of the ongoing geopolitical conflicts, such as the ongoing conflict between Russia and Ukraine and the ongoing conflicts in the Middle East, including related sanctions and countermeasures, and the effects of rising global inflation, are difficult to predict, and could adversely impact geopolitical and macroeconomic conditions, the global economy, and contribute to increased market volatility, which may in turn adversely affect our business and operations. In the past, U.S. federal government shutdowns, such as the shutdown that began on October 1, 2025 and ended on November 12, 2025, have curtailed operations of key agencies such as the FDA and the NIH, which includes the NCI. Future shutdowns may result in delays or disrupt our ability to advance clinical development of the current and planned clinical trials under our CRADA, obtain regulatory interactions/approvals, or secure government-funded grants. Additionally, changes to U.S. policy implemented by the U.S. Congress, the Trump administration or any new administration have impacted and may in the future impact, among other things, the U.S. and global economy, tariffs, international trade relations, unemployment, immigration, healthcare, taxation, the U.S. regulatory environment, inflation and other areas. Although we cannot predict the impact, if any, of these changes to our business, they could adversely affect our business. For a further discussion of factors that may affect future operating results see the sections entitled "Risk Factors" and "Cautionary Statement Regarding Forward-Looking Statement Notice."

Other than as discussed above and elsewhere in this report, we are not aware of any trends, events or uncertainties that are likely to have a material effect on our financial condition.