Quarterly Report for Quarter Ending March 31, 2026 (Form 10-Q)

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.

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, non-PSMA targeting 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.

Our preclinical translational data demonstrated that ATNM-400 is superior to:

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PSMA-targeted agents (177Lu-PSMA-617 (the active ingredient in Pluvicto®)) or ARPIs (enzalutamide) in the mCRPC setting of prostate cancer;

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EGFR inhibitors (osimertinib), osimertinib with chemotherapy, TROP-2 ADC (Dato-DXd), EGFR-cMET bispecific (amivantamab), and HER3-EGFR bispecific ADC (izalontamab brengitecan, in development) in EGFR-mutant NSCLC; and to

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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. Evidence of target expression has been observed ranging from 60%-80%+ in mCRPC, NSCLC, and breast cancer patient tumors, representing a significant addressable population of well over a hundred thousand patients in the United States based on our 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.

Our preclinical development program has generated encouraging efficacy and mechanism-of-action data across multiple indication-specific animal models:

Prostate Cancer

ATNM-400 demonstrated specific tumor uptake and decreased tumor cell proliferation across preclinical models representative of clinically relevant mCRPC settings spanning ARPI-resistant disease as well as PSMA-high (C4-2), PSMA-low (22Rv1) and PSMA-negative (DU145) states. The results demonstrate ATNM-400's PSMA-independent mechanism of action which provides an alternative which can address key limitations of current PSMA-targeted radioligand therapies. In these models, ATNM-400 showed significantly greater efficacy than both 177Lu-PSMA-617 (the active ingredient in Pluvicto®) and next-generation 225Ac-PSMA-617 in PSMA-low 22Rv1 prostate cancer xenograft models that are resistant to ARPI therapy. We believe greater efficacy against 225Ac-PSMA-617 suggests the importance of the ATNM-400 target as the energy delivered by the Ac-225 payload is the same. Efficacy was also observed in PSMA-negative DU145 models, supporting a profile differentiated from existing PSMA-targeted agents that predominantly act in PSMA-high disease. Importantly, ATNM-400 also demonstrated strong and durable combination activity with enzalutamide, with superior monotherapy efficacy compared to enzalutamide and 177Lu-PSMA-617 shown in ARPI-resistant prostate cancer models. We believe this superior combination activity is mechanistically supported by our observation that enzalutamide resistance increases ATNM-400 target expression in both prostate cancer models and mCRPC patient samples.

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

ATNM-400 outperformed 177Lu-PSMA-617 (the active ingredient in Pluvicto^®) and 225Ac-PSMA-617 in the PSMA-low, ARPI-resistant 22Rv1 prostate cancer model, demonstrating PSMA independent durable activity.

ATNM-400 Tumor Growth Inhibition vs 177Lu-PSMA-617

ATNM-400 Survival Benefit vs 177Lu-PSMA-617

ATNM-400 Tumor Growth Inhibition vs 177Lu-PSMA-617 and 225Ac-PSMA-617

Survival benefit and greater tumor inhibition shown in models with ATNM-400 monotherapy and the combination of ATNM-400 + enzalutamide versus enzalutamide alone in ARPI-resistant 22Rv1 prostate cancer model.

ATNM-400 Tumor Growth Inhibition vs Enzalutamide Monotherapy and Combination

ATNM-400 Survival Benefit vs Enzalutamide Monotherapy and Combination

ATNM-400 retained anti-tumor activity in prostate cancer models following progression on 177Lu-PSMA-617 and enzalutamide.

ATNM-400 After 177Lu-PSMA-617-Failure

ATNM-400 After Enzalutamide Failure

EGFR-Mutant NSCLC

ATNM-400 demonstrated greater tumor growth inhibition than several marketed and late-stage development drugs in various settings. Specifically, ATNM-400 demonstrated 3-5 fold greater tumor growth inhibition compared to approved EGFR-targeted therapies including osimertinib (first-line), datopotamab deruxtecan (second-line), and amivantamab (third-line) in NCI-H1975 human lung cancer models harboring L858R and T790M EGFR mutations. In combination with osimertinib, ATNM-400 achieved 100% complete responses with durable efficacy extending throughout the preclinical study period. In head-to-head preclinical comparisons, ATNM-400 monotherapy, and ATNM-400 in combination with osimertinib, exceeded the tumor growth inhibition achieved by osimertinib plus chemotherapy, and ATNM-400 monotherapy exceeded Dato-DXd (a TROP-2 antibody-drug conjugate) and izalontamab brengitecan (a HER3-EGFR bispecific antibody-drug conjugate in development) in the same EGFR-mutant NSCLC model. We believe we have established mechanistic support for ATNM-400 combinations with EGFR inhibitors, demonstrating that osimertinib treatment increases ATNM-400 target expression both in vitro and in vivo. We believe this mechanistic synergy, combined with clinical data showing improved outcomes when osimertinib is combined with external beam radiotherapy, supports ATNM-400 development across multiple EGFR-mutant NSCLC treatment settings.

ATNM-400 achieved the highest tumor growth inhibition (71%) versus approved targeted agents osimertinib (EGFR inhibitor), Dato-DXd (datopotamab deruxtecan, TROP-2 ADC )and amivantamab (EGFR-cMET ADC) in the NCI-H1975 EGFR-mutant NSCLC model. ATNM-400 + osimertinib combination achieved tumor shrinkage with 107% TGI and 100% of mice having complete cures in EGFR-mutant NSCLC model.

ATNM-400 vs Osimertinib or Dato-DXd or Amivantamab

ATNM-400 Combination with Osimertinib

Osimertinib upregulated the ATNM-400 target in NCI-H1975 cells, enhancing ATNM-400 cytotoxicity when dosed in combination.

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

In preclinical EGFR-mutant NSCLC models, ATNM-400 demonstrated superior tumor growth inhibition compared to the leading approved therapy in each line of treatment - Tagrisso® (osimertinib), Rybrevant® (amivantamab), and Datroway® (datopotamab deruxtecan) - and showed combination activity with osimertinib exceeding the current first-line standard of care. With no targeted radiotherapy currently approved or in late-stage development for EGFR-mutant NSCLC, these data position ATNM-400 as a potentially first-in-class radiotherapeutic with applicability across multiple lines of therapy in one of the largest precision-oncology markets.

ATNM-400 vs Standard of Care Therapies in EGFR-mutant NSCLC

Breast Cancer

ATNM-400 demonstrated robust anti-tumor activity and tumor regression as monotherapy and in combination with trastuzumab in preclinical breast cancer models, including trastuzumab-resistant BT474-Clone5 model, HR+ breast cancer MCF-7 model and triple-negative breast cancer (TNBC) MDA-MB-468 model. In the trastuzumab-resistant setting, we observed increased expression of both the survival pathway marker p-AKT and the ATNM-400 target, with ATNM-400 treatment inducing DNA double-strand breaks as measured by p-H2AX staining. ATNM-400 achieved 66% tumor growth inhibition as monotherapy and 103% tumor growth inhibition (representing tumor regression) in trastuzumab-resistant preclinical models. In the trastuzumab-resistant BT474-Clone5 model, ATNM-400 anti-tumor activity was comparable to trastuzumab deruxtecan (T-DXd), and ATNM-400 sustained tumor growth inhibition following trastuzumab failure compared with control and T-DXd. The ATNM-400 target is overexpressed in breast cancer, including tumors resistant to endocrine therapies such as tamoxifen and HER2-targeted therapies, as well as in TNBC. Resistance to HER2-targeted and endocrine therapies along with the limited treatment options for triple-negative breast cancer (TNBC) represent areas of significant unmet medical need that are potentially addressable with ATNM-400.

ATNM-400 drove tumor regression both alone and in combination with trastuzumab in the trastuzumab-resistant BT474-Clone5 breast cancer model, yielding 95% and 101% TGI, respectively. ATNM-400 caused tumor regression (103% TGI) as monotherapy in the MDA-MB-468 TNBC model. ATNM-400 also caused dose-dependent tumor growth inhibition in the MCF-7 HR+ breast cancer model.

Trastuzumab-Resistant Model BT474-Clone5

MDA-MB-468 (TNBC) Breast Cancer Model

MCF7 (HR+) Breast Cancer

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.

On April 21, 2026, preclinical data with ATNM-400 were presented at the American Association for Cancer Research ("AACR") Annual Meeting in San Diego, California. The data further demonstrated pan-tumor efficacy across prostate, lung, and breast cancer models. The ATNM-400 presentation highlighted the following:

In Prostate Cancer

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ATNM-400 demonstrated PSMA independent in vivo efficacy across prostate cancer models with low, medium, and high PSMA expression, including PSMA-negative models, supporting potential applicability across a broader patient population than PSMA-targeted therapies, which require PSMA expression for activity.

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ATNM-400 showed superior anti-tumor efficacy versus vehicle control, unconjugated antibody, and 177Lu-PSMA-617 (active ingredient in Pluvicto®) in both PSMA-high / ATNM-400 target-high (C4-2) and PSMA-low / ATNM-400 target-moderate (22Rv1) expressing models. This data may support the potential to address both 1) patients who relapse on, and 2) patients who are unlikely to respond to PSMA-targeted radioligand therapy.

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Activity in low ATNM-400 target expression and PSMA-negative (DU145) models supported a differentiated profile, suggesting ATNM-400 could address mCRPC patients who are ineligible for or have progressed on PSMA-targeted radioligand therapy due to low or absent PSMA expression, a population with no currently approved targeted radiotherapy option. Furthermore, the potency of an Ac-225 alpha therapy is demonstrated by activity even in the low ATNM-400 target expression DU145 model.

ATNM-400 demonstrated PSMA independent activity across 22Rv1 (target-moderate/ PSMA-low), C4-2 (target-high/PSMA-high), and DU145 (target-low/PSMA-low) prostate cancer models.

22Rv1: Moderate Target Expression and Low PSMA

C4-2: High Target and High PSMA Expression

DU145: Low Target Expression and PSMA Negative

In Lung Cancer

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The preclinical NCI-H1975 EGFR-mutant NSCLC model, a clinically relevant model of osimertinib-resistant disease, showed that ATNM-400 as monotherapy, or in combination with osimertinib, exceeded the tumor growth inhibition of osimertinib plus chemotherapy, the current standard of care in post-osimertinib progression. These results extend prior data demonstrating 100% complete tumor regression with the ATNM-400 plus osimertinib combination.

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ATNM-400 monotherapy demonstrated greater anti-tumor activity than Dato-DXd (TROP-2 ADC approved in EGFR-mutant lung cancer), the EGFR-cMET bispecific antibody amivantamab (Rybrevant®), and izalontamab brengitecan (HER3-EGFR bispecific ADC in development for EGFR-mutant lung cancer).

ATNM-400 monotherapy (80% TGI) and ATNM-400 + osimertinib combination (89% TGI) exceeded standard-of-care osimertinib plus chemo combination (49% TGI) in the NCI-H1975 EGFR-mutant NSCLC model.

ATNM-400 Combination With Osimertinib vs Osimertinib Combination With Chemo In
NCI-H1975 EGFR-m Lung Cancer

ATNM-400 achieved higher tumor growth inhibition (80%) versus approved agent Dato-DXd (TROP-2 ADC) and izalontamab brengitecan (HER3-EGFR ADC) in the NCI-H1975 EGFR-mutant NSCLC model.

ATNM-400 vs Dato-DXd or Izalontamab Brengitecan

In Breast Cancer

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Head-to-head data in the preclinical BT474 Clone5 trastuzumab-resistant HER2+ breast cancer model, a clinically relevant model of the post-trastuzumab setting where treatment options are limited, demonstrated that ATNM-400 achieved anti-tumor activity comparable to the approved HER2-ADC trastuzumab deruxtecan (Enhertu®), as monotherapy and in combination. We believe this positions ATNM-400 as a potential alternative for patients who cannot tolerate HER2-ADCs due to interstitial lung disease, a known class-related toxicity.

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In the post-trastuzumab failure setting, ATNM-400 produced durable tumor growth inhibition after treatment discontinuation, exceeding both vehicle control and trastuzumab deruxtecan (Enhertu®) in the preclinical BT474 Clone5 trastuzumab-resistant HER2+ breast cancer model, supporting the potential for less frequent dosing and more durable disease control.

ATNM-400 monotherapy (57% TGI) and combination with trastuzumab (100% TGI) showed anti-tumor effect in trastuzumab resistant BT474 Clone5 breast cancer model and was comparable to HER2-DXd (111% TGI). ATNM-400 was better at controlling post-trastuzumab failure (93% TGI) versus HER2-DXd (64% TGI).

BT474 Clone5 BC Head-On

BT474 Clone5 BC Post-Trastuzumab Failure

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 T cell-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 home to tumor-resident CD33+ MDSCs in vivo; (2) be 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 was shown to deplete MDSCs in our studies. Actimab-A was also shown to restore T cell proliferation in a dose dependent manner.

MDSC Depletion	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.

Actimab-A in combination with CLAG-M for R/R AML: 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 currently 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 NCI across multiple AML and MDS treatment settings and exploring its potential in additional areas:

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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.

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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.

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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.

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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 National Cancer Institute, which enables cost-effective clinical development while retaining commercial rights to Actinium.

On April 21, 2026, preclinical translational data with Actimab-A (lintuzumab-Ac225) 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

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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.

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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.

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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

Actimab-A Combinations with Revumenib and Azacitidine Upregulate Myeloid Differentiation Gene Signature in AML

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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.

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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:

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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.

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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.

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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 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:

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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.

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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.

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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.

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. 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.

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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.

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

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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.

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

The facility has been designed for clinical stage supply of radiolabeled therapeutic drug product production.

External Manufacturing Partnerships

We have established partnerships with multiple contract manufacturing organizations providing geographic redundancy and production flexibility:

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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 serve patient populations at clinical and commercial scale while maintaining the flexibility to respond to changing demand and expand into new geographic markets.

Human Capital

As of May 7, 2026, we had 25 full-time employees, 12 of whom have Ph.D. or M.D. degrees and 21 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 temporarily supplement existing staff.

Results of Operations

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

		For the Three Months Ended March 31,
(in thousands)		2026				2025
Revenue:
Revenue		$	-			$	-
Other revenue			-				-
Total revenue			-				-
Operating expenses:
Research and development, net of reimbursements			4,201				7,700
General and administrative			1,702				8,938
Total operating expenses			5,903				16,638
Other income:
Interest income - net			381				700
Total other income			381				700
Net loss		$	(5,522	)		$	(15,938	)

Revenue

We recorded no commercial revenue for the three months ended March 31, 2026 and March 31, 2025, respectively.

Other revenue

The National Institutes of Health awarded us a Small Business Technology Transfer cost reimbursable grant to support a clinical collaboration with Memorial Sloan Kettering Cancer Center, or MSK, to study Iomab-ACT, our CD45-targeting Antibody Radio-Conjugate, for targeted conditioning to achieve lymphodepletion prior to administration of a CD19-targeted CAR T-cell therapy developed at MSK. There was no other revenue recognized for the three months ended March 31, 2026 and March 31, 2025, respectively.

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 rest of the world.

Our contract liabilities are recorded within Other revenue deferred - current liability or Long-term license revenue deferred in our condensed consolidated balance sheets depending on the short-term or long-term nature of the payments to be recognized. Our contract liabilities primarily consist of advanced payments from licensees. There was no Other revenue deferred-current liability at March 31, 2026 and December 31, 2025. Long-term license revenue deferred was $35 million at March 31, 2026 and December 31, 2025, resulting from the receipt from Immedica; this deferred revenue will be recognized upon the European Union's regulatory approval of Iomab-B or provision of definitive feedback that Iomab-B will not receive approval in the European Union.

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. Such cancellations were subject to the consent of the applicable holders of the stock options. The cancellation of these stock options resulted in the recording of $8.7 million in non-cash stock compensation expense for the three months ended March 31, 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 $4.2 million for the three months ended March 31, 2026 decreased by $3.5 million from $7.7 million for the three months ended March 31, 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 three months ended March 31, 2026 compared with the three months ended March 31, 2025. In addition, there was a decline in outside CRO services and other preclinical R&D expenses of $1.0 million and lower compensation 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 $1.7 million for the three months ended March 31, 2026 decreased by $7.2 million from $8.9 million for the three months ended March 31, 2025. The cancellation of stock options in March 2025 described above resulted in lower non-cash stock-based compensation expense of $6.6 million for the three months ended March 31, 2026 compared with the three months ended March 31, 2025. In addition, in comparison to the prior-year period, compensation decreased $0.3 million due to lower headcount and consulting and legal fees decreased $0.2 million as the company further rationalized efforts.

Other income

Other income is comprised of net interest income in both reporting periods. The amount for the three months ended March 31, 2026 of $0.4 million decreased from $0.7 million for the three months ended March 31, 2025 primarily due to a lower average cash balance during the three months ended March 31, 2026 compared to the prior-year period.

Net loss

Net loss of $5.5 million for the three months ended March 31, 2026 decreased by $10.4 million from $15.9 million for the three months ended March 31, 2025 due to lower research and development expenses and lower general and administrative expenses, partially offset by lower other income.

Liquidity and Capital Resources

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

		For the Three Months Ended March 31,
(in thousands)		2026				2025
Cash used in operating activities		$	(5,870	)		$	(7,574	)
Cash used in investing activities			(2	)			-
Cash used in financing activities			(3	)			(2	)
Effect of foreign currency rates on cash			11				-
Net change in cash, cash equivalents and restricted cash		$	(5,864	)		$	(7,576	)

Net cash used in operating activities for the three months ended March 31, 2026 was $5.9 million, a decrease of $1.7 million from $7.6 million in the prior-year period, primarily resulting from a lower net loss for the three months ended March 31, 2026 compared to the prior-year period.

Cash used in investing activities for the three months ended March 31, 2026 was $2 thousand. There was no cash used in investing activities for the three months ended March 31, 2025.

Cash used in financing activities for the three months ended March 31, 2026 and March 31, 2025 was $3 thousand and $2 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 three months ended March 31, 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.

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.

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.