Actinium Pharmaceuticals, Inc.

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Actinium Pharmaceuticals, Inc. is a pioneer in the development of targeted radiotherapies intended to meaningfully improve outcomes for patients with advanced cancers. Our goal is to create a specialty radiopharmaceutical company with capabilities across radioisotope production, final drug product manufacturing, preclinical research and development (“R&D”) and clinical development. We are deploying our technologies, capabilities and intellectual property with approximately 240 issued and pending patents worldwide, to develop next-generation radiotherapies. We are focused on developing highly differentiated and innovative first-in-class product candidates. Our current pipeline of clinical and preclinical stage targeted radiotherapy product candidates are directed against validated cancer targets for indications in hematology, solid tumors and conditioning for cell and gene therapies, which we believe have high unmet needs that are not addressed by currently available treatment options.

Current wording

Actinium Pharmaceuticals, Inc. is a pioneer in the development of differentiated, targeted radiotherapies intended to meaningfully improve outcomes for patients with advanced cancers. We are focused on developing highly innovative, first-in-class product candidates. To support our objective of achieving industry leading, cost-effective product development to maximize value creation from our innovative pipeline, we are working to expand the scope of our capabilities to include radioisotope production of Ac-225 via collaborations for our Ac-225 technology and in-house manufacturing of pipeline candidates to support clinical trials. We are deploying our technologies, capabilities and intellectual property with approximately 250 issued and pending patents worldwide, to develop next-generation radiotherapies focused on solid tumors, hematology and conditioning for cellular therapies.

Previous wording

We are advancing two clinical stage product candidates and one preclinical stage product candidate that are directed against validated cancer targets. Actimab-A is our most advanced clinical-stage product candidate that we are actively developing and is intended to address the significant unmet medical needs of patients with myeloid malignancies, including acute myeloid leukemia (“AML”) and myelodysplastic syndromes (“MDS”). We are also evaluating Actimab-A’s potential to synergize with PD-1 immune checkpoint inhibitors (“ICIs”) in solid tumor indications through the depletion of immune cells known as myeloid derived suppressor cells (“MDSCs”). We recently announced our ATNM-400 program, a novel preclinical, non-prostate specific-membrane antigen (“non-PSMA”) targeting, first-in-class radiotherapy utilizing the Actinium-225 (“Ac-225”) radioisotope payload intended for patients with prostate cancer directed against a novel radiotherapy target and thereby differentiated from Lu-177-PSMA-617, the active agent used in Pluvicto®, a blockbuster approved prostate cancer radiotherapy and the majority of radiotherapies in development for prostate cancer. Iomab-ACT is a next-generation targeted conditioning agent we are developing with the intent to improve patient access to, and outcomes with, cellular therapies such as CAR-T for various blood cancer indications and gene therapies for non-malignant hematologic disorders such as sickle cell disease (“SCD”).

Current wording

We are advancing clinical stage and preclinical stage targeted radiotherapy candidates directed against validated cancer targets for indications in solid tumors, hematology and conditioning for cell and gene therapies that we believe have high unmet needs not addressed by currently available treatment options. Recently prioritized as our lead program, ATNM-400, is a highly innovative, first-in-class, and pan-tumor Actinium-225 (“Ac-225”) alpha-emitter targeted radiotherapy candidate with preclinical data in prostate cancer, non-small cell lung cancer (“NSCLC”) and breast cancer. We believe ATNM-400 has the potential to address critical gaps across multiple treatment settings in each of these targeted indications and can therefore address large patient populations. Actimab-A is our most advanced clinical-stage product candidate, which utilizes an antibody linked to Ac-225 to target CD33, a cell surface protein that Actimab-A is designed to target, that is expressed ubiquitously in acute myeloid leukemia (“AML”) and myelodysplastic syndromes (“MDS”) and on myeloid derived suppressor cells (“MDSC”). We are evaluating Actimab-A’s potential to synergize with immune checkpoint inhibitors (“ICIs”) such as programmed cell death 1 (“PD-1) inhibitors in solid tumors by depleting MDSC immune cells. Iomab-ACT is our next-generation targeted conditioning agent we are developing with the intent to improve patient access to, and outcomes with, cellular therapies such as CAR-T for various blood cancer indications and gene therapies for non-malignant hematologic disorders such as sickle cell disease (“SCD”).

Previous wording

We currently intend to commit a significant portion of our current and future resources to the development and advancement of our targeted radiotherapy solid tumor pipeline candidates as well as solid tumor focused R&D efforts. In the first quarter of 2025, we announced ATNM-400, our first solid tumor focused program, which we are developing for prostate cancer. In addition, we announced our solid tumor initiative with Actimab-A in combination with PD-1 immune checkpoint inhibitors for head and neck squamous cell carcinoma (“HNSCC”) and non-small cell lung cancer (“NSCLC”). We believe solid tumors represent large addressable markets and there remains high unmet needs in several indications that are not addressed by currently available therapies. We will continue to advance Actimab-A in a focused manner as a therapeutic for hematology indications including supporting our CRADA with the NCI and Iomab-ACT as a targeted conditioning agent for cell and gene therapies while simultaneously seeking strategic development partners or collaborators for these programs. There have been significant changes in senior leadership at the United States Food & Drug Administration (“FDA”) and other government agencies including the Center for Biologics Evaluation and Research (“CBER”). We believe these changes could impact the FDA’s approach toward approving therapies in part based on their perception of value and their cost benefit profile. There have also been funding cuts to healthcare spending and at governmental healthcare agencies such as the National Institutes of Health (“NIH”) and National Cancer Institute (“NCI”). We have a Cooperative Research and Development Agreement (“CRADA”) with the NCI for the development of Actimab-A, and while currently not the case, in the future there could be funding cuts to the NCI may cause delays, and/or pauses or termination of clinical trials under our CRADA. As previously announced, we are actively seeking a strategic partner for Iomab-B in the U.S. As part of our strategic pipeline prioritization, we may seek to partner, divest, spin-out, or out-license Iomab-B, Actimab-A and Iomab-ACT individually or collectively for all non-solid tumor indications. We believe, in aggregate, the clinical data from these hematology and cellular therapy focused programs is supportive of a partnering approach, which if successful, may yield greater value as the Company focuses on its solid tumor development efforts utilizing existing resources.

Current wording

In addition to prioritized development efforts described above, we plan to continue to advance Actimab-A in a focused manner as a therapeutic for select hematology indications including supporting our Cooperative Research and Development Agreement (“CRADA”) with the National Cancer Institute (“NCI”). Actimab-A has the potential to address the significant unmet medical needs of patients across multiple solid tumor indications and with high-risk blood cancers including AML and MDS which are highly sensitive and susceptible to radiation. We also plan to support Iomab-ACT as a targeted conditioning agent for cell and gene therapies while simultaneously seeking strategic development partners or collaborators for these programs. We are actively seeking a strategic partner for Iomab-B, our CD45 targeted conditioning agent for bone marrow transplant (“BMT”) in the U.S. and we may seek to partner, divest, spin-out, or out-license Iomab-B, Actimab-A, and Iomab-ACT individually or collectively for all non-solid tumor indications. We believe, in the aggregate, the clinical data from these hematology and cellular therapy focused programs is supportive of a partnering approach, which if successful, may yield greater value as the Company focuses on its solid tumor development efforts utilizing existing resources.

Previous wording

ATNM-400 is a novel antibody radioconjugate designed to deliver the potent alpha-emitter Ac-225 to prostate cancer cells by targeting a non-PSMA, disease-driving protein overexpressed in advanced and treatment-resistant disease. Unlike PSMA-targeted agents that primarily serve as imaging and targeting tools, the ATNM-400 target is directly implicated in tumor progression, survival signaling, and resistance to AR inhibition. This target is markedly overexpressed in advanced, treatment-refractory prostate cancer and is associated with faster progression to castration resistance and poorer overall survival in metastatic castrate resistant prostate cancer (“mCRPC”).

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ATNM-400 for Metastatic Castrate-Resistant Prostate Cancer

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ATNM-400 Market Opportunity in Prostate Cancer

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ATNM-400 Market Opportunity

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Approximately 313,780 men in the United States are expected to be diagnosed with prostate cancer in 2025, accounting for approximately 30% of all cancer diagnoses in men according to the American Cancer Society. Prostate cancer is by far the most diagnosed cancer in men in the United States and is the same in 118 of 185 countries. Of those diagnosed with prostate cancer, approximately 5-7% exhibited metastatic disease at initial diagnosis, and among those exhibiting localized prostate cancer, approximately 20-30% will progress to metastatic disease. A majority of metastatic prostate cancer patients receive hormone therapy such as ARPI therapy, as prostate cancer cells rely on androgen hormones for growth. In the U.S., approximately 40,000–60,000 mCRPC patients annually progress after ARPI therapy, which as a class generated sales of greater than $10 billion in 2024 including Xtandi® (>$5.9 billion) Erleada® (>$2.9 billion), and Nubeqa® (>$1.7 billion), highlighting a significant unmet need. Unlike localized diseased, there are currently no known cures for metastatic prostate cancer – there are only treatments to slow the progression of disease.

Current wording

Prostate cancer is by far the most diagnosed cancer in men in the United States and is the same in 118 of 185 countries. Of those diagnosed with prostate cancer, approximately 5-7% exhibited metastatic disease at initial diagnosis, and among those exhibiting localized prostate cancer, approximately 20-30% will progress to metastatic disease. A majority of metastatic prostate cancer patients receive hormone therapy such as ARPI therapy, as prostate cancer cells rely on androgen hormones for growth. Unlike localized disease, there are currently no known cures for metastatic prostate cancer – there are only treatments to slow the progression of disease.

Previous wording

With the approval of the targeted radiotherapy Pluvicto® (lutetium Lu 177 vipivotide tetraxetan; active agent: Lu-177-PSMA-617) for post-taxane mCRPC in March 2022, targeted-radiotherapy has become a prominent component of the metastatic prostate cancer treatment paradigm. Pluvicto®, marketed globally by Novartis, generated approximately $1.39 billion in sales in 2024 and approximately $825M in the first half of 2025. In March 2025, the total addressable market for Pluvicto® essentially doubled to approximately 44,000 patients with its approval in mCRPC after treatment with ARPI therapy and prior to taxane. Subsequently, in June 2025, Novartis announced that Pluvicto® reached the primary endpoint in the Phase 3 PSMAddition study in metastatic hormone sensitive prostate cancer (“mHSPC”) and expects to file an FDA submission in the second half of 2025. An approval would add approximately 42,500 additional patients to the addressable market for Pluvicto®.

Current wording

With the approval of Pluvicto® for patients with mCRPC post-taxane therapy and post ARPI therapy and prior to taxane therapy, targeted-radiotherapy has become a prominent component of the metastatic prostate cancer treatment paradigm. Pluvicto® generated sales of approximately $1.4 billion in the first nine months of 2025. In June 2025, Novartis announced expects to file an FDA submission in the second half of 2025 for Pluvicto® in metastatic hormone sensitive prostate cancer (“mHSPC”), that could add approximately 42,500 additional patients to the addressable market for Pluvicto®. With approximately one-third of patients not responding to PSMA-directed radiotherapy and that virtually all patients will progress on PSMA-directed radiotherapy within 12 months, we believe this demonstrates the high unmet need for a non-PSMA prostate cancer therapy such as ATNM-400.

Previous wording

With the only approved targeted radiotherapy moving up in the prostate cancer treatment paradigm and very few differentiated products in clinical development, a significant opportunity exists in the post-Pluvicto® setting. Currently, over 20 PSMA-targeted radiotherapies are in various stages of development, of which few offer a substantial efficacy advantage compared to Pluvicto®. Re-treatment with PSMA-targeting agents has not yet been supported substantially in clinical trials and could be less effective than targeting a different antigen due to potential reduction of PSMA surface expression as well as increased tumor heterogeneity following initial PSMA-targeted therapy.

Current wording

With the only approved targeted radiotherapy in prostate cancer moving up in the treatment paradigm with very few differentiated products in clinical development, we believe there is a significant potential market opportunity for ATNM-400. Currently, over 30 PSMA-targeted radiotherapies are in various stages of development, of which few offer a substantial efficacy advantage compared to Pluvicto®. Re-treatment with PSMA-targeting agents has not yet been supported substantially in controlled clinical trials and could be less effective than targeting a different antigen due to potential reduction of PSMA surface expression as well as increased tumor heterogeneity following initial PSMA-targeted therapy.

Previous wording

ATNM-400 targets a non-PSMA tumor antigen that is implicated in disease progression, shorter time to hormone therapy resistance such as ARPI therapy and poorer survival outcomes. We have demonstrated that ATNM-400’s differentiated target is expressed and druggable following ARPI therapy and PSMA radiotherapy. We believe ATNM-400 can therefore target a significant subset of the mCRPC patient population with aggressive disease who progressed on second generation ARPIs or have had no response to or progressed on Lu-177 labelled PSMA-targeted therapy. ATNM-400 utilizes the alpha-particle emitter Ac-225, which is more potent than Lu-177, and due to Ac-225’s short path length, could result in fewer off-target effects. As ATNM-400 does not target PSMA, xerostomia or dry mouth, which can be a significant quality of life issue for patients with metastatic prostate cancer receiving PSMA-targeted radiotherapies as PSMA is expressed on salivary glands, would not be expected. Additionally, the antigen targeted by ATNM-400 is implicated in a pathway leading to ARPI-resistance in mCRPC patients; therefore, along with the tumor suppressing ability of Ac-225, ATNM-400 displays a compelling mechanism for synergy with ARPIs. As a result, we believe ATNM-400 has the potential to address critical gaps in prostate cancer treatment as a monotherapy or in combination or sequenced with other therapeutic modalities.

Current wording

We have demonstrated that ATNM-400’s differentiated target is expressed and druggable following ARPI therapy and PSMA radiotherapy. We believe ATNM-400 can therefore target a significant subset of the mCRPC patient population with aggressive disease who progressed on second generation ARPIs or have had no response to or progressed on Lu-177 labelled PSMA-targeted therapy. As ATNM-400 does not target PSMA, xerostomia or dry mouth, which can be a significant quality of life issue for patients with metastatic prostate cancer receiving PSMA-targeted radiotherapies as PSMA is expressed on salivary glands, would not be expected. Additionally, the antigen targeted by ATNM-400 is implicated in a pathway leading to ARPI-resistance in mCRPC patients and expression increases post-ARPI treatment; therefore, along with the tumor suppressing ability of Ac-225, ATNM-400 displays a compelling mechanism for synergy with ARPIs. This mechanistic synergy is supported by the complete tumor regression in 40 percent of tumor bearing animals treated with the combination of ATNM-400 and the ARPI enzalutamide. As a result, we believe ATNM-400 has the potential to address critical gaps in prostate cancer treatment as a monotherapy or in combination or sequenced with other therapeutic modalities.

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Actimab-A Solid Tumor Program: Potential Pan Solid Tumor Therapy in Combination with PD-1 Checkpoint Inhibitors Including KEYTRUDA® and OPDIVO® by Depleting Myeloid Derived Suppressor Cells

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Potential Pan Solid Tumor Therapy in Combination with PD-1 Checkpoint Inhibitors Including KEYTRUDA® and OPDIVO® by Depleting Myeloid Derived Suppressor Cells

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Given the significant number of patients treated with PD-1 ICIs, there is extensive data in the medical literature on outcomes in these patients. PD-1 ICIs have significantly improved patient outcomes across several solid tumor indications, however, not all patients have robust or durable responses. Multiple therapeutic modalities have been studied in combination with PD-1 ICIs in attempt to improve patient outcomes, but few combinations have produced a sufficient clinical benefit or have been approved. To our knowledge, our Actimab-A solid tumor program is the only CD33 targeted radiotherapy being evaluated in combination with PD-1 ICIs. The rationale for studying Actimab-A in combination with either KEYTRUDA® or OPDIVO® is based on the premise that depleting MDSCs with Actimab-A may improve the efficacy of these drugs.

Current wording

Immunotherapy is the leading class of oncology therapies with PD-1 checkpoint inhibitors generating global sales of over $40 billion in 2024. PD-1 inhibitors have significantly improved patient outcomes across several solid tumor indications, however, not all patients have robust or durable responses, and the benefit of PD-1 inhibitors has not been realized in several cancer indications. As a result, there are extensive efforts to improve outcomes for these patients with multiple therapeutic modalities studied in combination with PD-1 inhibitors in attempt to improve patient outcomes. However, few combinations have produced a sufficient clinical benefit or have been approved. To our knowledge, our Actimab-A solid tumor program is the only CD33 targeted radiotherapy being evaluated in combination with PD-1 inhibitors. The rationale for studying Actimab-A in combination with the PD-1 inhibitors is based on the premise that depleting MDSCs, which express CD33, with Actimab-A may work synergistically and therefore improve the efficacy of drugs such KEYTRUDA® (Merck) or OPDIVO® (Bristol Myers Squibb).

Previous wording

MDSCs are immune-suppressive cells that help tumors evade immune detection and promote disease progression. They are overexpressed in the tumor microenvironment in several different solid tumors and associated with poor outcomes. They work by multiple mechanisms but most relevant to PD-1 inhibitors which work by keeping T-cells active is that MDSCs prevent T-cells from recognizing and attacking cancer cells.

Current wording

MDSCs are immune-suppressive cells that help tumors evade immune detection and promote disease progression. They are overexpressed in the tumor microenvironment in several different solid tumors and associated with poor outcomes. PD-1 inhibitors work by binding and blocking PD-1, allowing T-cells to resume their anti-tumor activity. MDSCs function as a resistance mechanism by preventing T-cells from recognizing and attacking tumors, which we believe supports our strategy for using Actimab-A to deplete MDSCs to reenable PD-1 inhibitors to work after patients stop responding to or in indications where PD-1 inhibitors have had limited clinical success.

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Potential Mechanistic Synergy of Actimab-A with PD-1 ICI’s

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Potential Mechanistic Synergy of Actimab-A with PD-1 Inhibitors

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Studies have shown that MDSCs are overexpressed in patients with cancers. For instance, a study by Bronte et al., in patients with NSCLC receiving ICIs evaluated the role of immune cells on patient outcomes. In this study, MDSCs were the only immune cell subtype to show a statistically significant association with tumor response. The median level of MDSCs was determined to be 1.9% with patients above that level being classified as “High-MDSC” and patients below that level being classified as “Low-MDSC”. In this study, only Low-MDSC patients had a clinical response, with no responses observed in High-MDSC patients and over 80% of High-MDSC patients having progressive disease. In addition, Low-MDSC patients had a statistically significantly improvement in progression-free survival (“PFS”) of 8.39 months compared to 1.94 months in High-MDSC patients and OS of 15.15 months compared to 3.03 months in High-MDSC patients.

Current wording

Clinical and preclinical studies, including studies we have conducted, have shown that MDSCs are overexpressed in patients with cancers. For instance, a study by Bronte et al., in patients with NSCLC receiving PD-1 inhibitors evaluated the role of immune cells on patient outcomes. In this study, MDSCs were the only immune cell subtype to show a statistically significant association with tumor response. The median level of MDSCs was determined to be 1.9percent with patients above that level being classified as “High-MDSC” and patients below that level being classified as “Low-MDSC”. In this study, only Low-MDSC patients had a clinical response, with no responses observed in High-MDSC patients and over 80percent of High-MDSC patients having progressive disease. In addition, Low-MDSC patients had a statistically significantly improvement in PFS of 8.39 months compared to 1.94 months in High-MDSC patients and OS of 15.15 months compared to 3.03 months in High-MDSC patients.

Previous wording

We believe there is strong scientific rationale supporting the potential for Actimab-A to deplete CD33 expressing MDSCs and hence improve patient outcomes with PD-1 ICIs such as KEYTRUDA® and OPDIVO®. Our Actimab-A solid tumor program is expected to be comprised of several controlled, head-to-head clinical trials that will evaluate the combination of Actimab-A with KEYTRUDA® versus KEYTRUDA® alone, and Actimab-A with OPDIVO® versus OPDIVO® alone. The initial tumors that are being targeted are HSNCC and NSCLC with a separate trial for each indication.

Current wording

We believe there is strong scientific and clinical rationale supporting the potential for Actimab-A to deplete CD33 expressing MDSCs and hence improve patient outcomes with PD-1 ICIs such as KEYTRUDA® and OPDIVO®. Our Actimab-A MDSC solid tumor program is expected to initially evaluate the combination of Actimab-A with KEYTRUDA® or OPDIVO®in a basket trial in patients with head and neck squamous cell carcinoma (“HNSCC”), NSCLC, Glioblastoma Multiforme (“GBM”) and colorectal cancer that are PD-1 inhibitor naïve.

Previous wording

The patient population for these trials will be adults with PD-L1 expression and locally advanced metastatic HNSCC or NSCLC randomized to either Actimab-A alone or Actimab-A with a specific checkpoint inhibitor. The objective of each trial would be to evaluate the safety and tolerability as well as following endpoints including ORR, PFS and OS. Further, the following biomarker data would be collected including the pattern of depletion of CD33+ MDSCs and T-cell activity in peripheral blood. We are advancing these trials and expect initial proof of concept data in the first half of 2026.

Current wording

The objective of this trial would be to evaluate the safety and tolerability as well as following endpoints including ORR, PFS and OS. Further, the following biomarker data would be collected including the pattern of depletion of CD33-positive MDSCs and T-cell activity in peripheral blood. We are completing a regulatory submission to advance this trial and expect initial proof of concept data in the first half of 2026.

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Actimab-A: Mutation Agnostic Mechanism of Action with Backbone Therapy Potential in Myeloid Malignancies including AML and high-risk MDS

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Mutation Agnostic Mechanism of Action with Backbone Therapy Potential in Mutation Rich, Highly Radiosensitive Myeloid Malignancies such as AML

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Actimab-A is being developed as a targeted radiotherapeutic to leverage the Ac-225 isotope payload directed against CD33, a target expressed ubiquitously in patients with AML, MDS and other myeloid malignancies. We are attempting to leverage the mutation-agnostic ability of Ac-225 to establish Actimab-A as a backbone therapy in myeloid malignancies, which are extremely heterogenous and radiosensitive, as a single agent or in combinations with chemotherapy, targeted agents, cellular therapy and immunotherapy. Actimab-A has been studied in over 150 patients as a single agent and in combination with other modalities. This clinical experience is informing our current clinical development strategy for Actimab-A. We plan to initiate a Phase 2/3 trial with Actimab-A in combination with the chemotherapy regimen CLAG-M in patients with r/r AML based on promising results with this combination in a Phase 1b trial. In addition to our internal development efforts, we entered into a Cooperative Research and Development Agreement (“CRADA”) with the National Cancer Institute (“NCI”) in February 2023 for the development of Actimab-A for AML and other myeloid malignancies. The first Actimab-A trial initiated under the CRADA is being conducted in patients with frontline AML in combination with Venetoclax, an oral Bcl-2 inhibitor and ASTX-727, an oral hypomethylating agent (“HMA”) developed by Taiho Oncology, an Otsuka Holdings company. To date, there has been broad interest from investigators through the NCI CRADA to study Actimab-A in a variety of hematology indications that we believe may support our partnering efforts given the potential to expand the addressable market opportunity for Actimab-A.

Current wording

We are developing Actimab-A to leverage the mutation-agnostic mechanism of Ac-225 and ubiquitous expression of CD33 in AML. We believe Actimab-A has the potential become a backbone therapy in AML, which is extremely heterogenous and radiosensitive, either as a single agent or in combinations with chemotherapy, targeted agents, cellular therapy and immunotherapy.

Previous wording

Our development strategy is to exploit these properties of Actimab-A to address the unmet needs of patients with myeloid malignancies across the treatment journey including the frontline, relapsed/refractory and maintenance settings. To accomplish this, we are leveraging our clinical development experience, clinical data and preclinical work supporting Actimab-A’s mutation agnostic capabilities.

Current wording

Our development strategy is to exploit these properties of Actimab-A to address the unmet needs of patients with myeloid malignancies across the treatment journey including the frontline, relapsed/refractory and maintenance settings. To accomplish this, we are leveraging our clinical development experience, clinical data and preclinical work supporting Actimab-A’s mutation agnostic capabilities across multiple treatment settings including currently planned trials in r/r AML in combination with chemotherapy CLAG-M and frontline AML in combination with Venetoclax and hypomethylating agents We are evaluating multiple studies leveraging Actimab-A’s mutation agnostic profile in AML including trials under our CRADA.

Previous wording

We have aligned with the FDA on a randomized pivotal Phase 2/3 trial to compare Actimab-A + CLAG-M to CLAG-M alone in patients with r/r AML. Based on our interactions with the FDA, this trial will first complete a Phase 2 portion where the Actimab-A dose will be optimized in combination with CLAG-M. Once the optimized Actimab-A dose is determined, we expect the trial will advance to the Phase 3 portion of the study, which may reduce time and resources required compared to separate Phase 2 and Phase 3 studies.

Current wording

Based on our interactions with the FDA, this trial will first complete a Phase 2 portion where the Actimab-A dose will be optimized in combination with CLAG-M. Once we have the Phase 2 results, we will meet with FDA to determine the optimized Actimab-A dose and obtain feedback on our Phase 3 protocol. We expect this interim analysis and meeting with FDA will allow for an operationally seamless transition to the Phase 3 portion of the study, which may reduce time and resources required compared to separate Phase 2 and Phase 3 studies.

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The primary endpoint of the Phase 3 trial will be Overall Survival. Event-Free Survival (“EFS”) and other efficacy measures as well as safety also being evaluated. We are actively seeking potential strategic partners or collaborators to advance this trial.

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We expect the primary endpoint of the Phase 3 trial will be OS. Event-Free Survival (“EFS”) and other efficacy measures as well as safety will also be evaluated. We are actively seeking potential strategic partners or collaborators to advance this trial.

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In 2023, we entered into a CRADA with NCI to develop Actimab-A for the treatment of patients with AML and other hematologic malignancies. The NCI will serve as the regulatory sponsor for any clinical trials mutually approved by both parties to study Actimab-A. The CRADA will provide support for and may accelerate the development of Actimab-A alone or in combination with chemotherapy, immunotherapy, targeted agents and other novel combinations. The CRADA studies will be overseen by the NCI in collaboration with Actinium’s clinical development team, where we have the right to review and approve all protocols and have full rights to all data. The NCI CRADA provides for us to supply Actimab-A and for NCI to cover all clinical trial execution and development expenses, which we believe will be a cost-efficient approach as opposed to a Company sponsored trial and may therefore spare our balance sheet. The NCI Cancer Therapy Evaluation Program (“CTEP”), which sponsors approximately two thirds of all combination cancer studies, will accept Letters of Intent (“LOIs”) or concepts for Phase 1, 2 or 3 studies of Actimab-A in AML and other hematological malignancies.

Current wording

In 2023, we entered into a CRADA with NCI to develop Actimab-A for the treatment of patients with AML and other hematologic malignancies. The NCI will serve as the regulatory sponsor for any clinical trials mutually approved by both parties to study Actimab-A. The CRADA will provide support for and may accelerate the development of Actimab-A alone or in combination with chemotherapy, immunotherapy, targeted agents and other novel combinations. The CRADA studies will be overseen by the NCI in collaboration with Actinium’s clinical development team, where we have the right to review and approve all protocols and have full rights to all data. Under the NCI CRADA, we will supply Actimab-A and NCI will cover all clinical trial execution and development expenses, which we believe will be a cost-efficient approach as opposed to a Company sponsored trial. The NCI Cancer Therapy Evaluation Program (“CTEP”), which sponsors approximately two thirds of all combination cancer studies, will accept Letters of Intent (“LOIs”) or concepts for Phase 1, 2 or 3 studies of Actimab-A in AML and other hematological malignancies such as high-risk myelodysplastic syndromes (“MDS”).

Previous wording

Additional clinical trial concepts for Actimab-A have been submitted through our CRADA. We believe this supports the differentiated profile of Actimab-A for hematologic and solid tumor indications and presents an opportunity to expand Actimab-A’s addressable market for a potential partner or collaborator.

Current wording

Additional clinical trial concepts for Actimab-A have been submitted through our CRADA. We believe this supports the differentiated profile of Actimab-A for hematologic and solid tumor indications and presents an opportunity to expand Actimab-A’s addressable market for a potential partner or collaborator. However, as a result of the recent government shutdown that began on October 1, 2025 and ended on November 12, 2025, we expect to experience delays to our current and planned trials under the CRADA. See Risk Factors – “Disruptions at the FDA, the SEC and other government agencies or comparable regulatory authorities caused by the government shutdown, funding shortages or global health concerns, in addition to substantial uncertainty regarding the new Administration’s initiatives and how these might impact the FDA, its implementation of laws, regulations, policies and guidance, and its personnel, could hinder government agencies’ ability to hire and retain key leadership and other personnel, or otherwise prevent new products and services from being developed or commercialized in a timely manner, or otherwise prevent those agencies from performing normal business functions on which our business operations rely, including timely reviews, which could negatively impact our business.”

Previous wording

On April 27, 2025, we presented data at the AACR annual meeting preclinical data demonstrating that the combination of Actimab-A with standard of care targeted AML therapies including menin and FLT3 inhibitors and the HMA azacitidine resulted in significant antileukemic activity in AML cells lines with FLT3, NPM1, KMT2A and TP53 mutations. Additionally, in animal models, Actimab-A significantly enhanced tumor growth inhibition, prolonged the duration of response and survival when combined with the menin inhibitor revumenib, and potentiated AML cell killing in combination with the FLT3 inhibitor gilteritinib and HMA azacitidine. We expect to present additional data supporting Actimab-A’s mutation agnostic capabilities and backbone potential at future scientific and medical conferences. In addition, we will continue to explore potential clinical trials under our CRADA with NCI, investigator-initiated trials or under our sponsorship.

Current wording

We presented preclinical data in April 2025 at the AACR annual meeting demonstrating that the combination of Actimab-A with standard of care targeted AML therapies including menin and FLT3 inhibitors and the HMA azacitidine resulted in statistically significant antileukemic activity in AML cells lines with FLT3, NPM1, KMT2A and TP53 mutations. Additionally, in animal models, Actimab-A showed statistically significant enhanced tumor growth inhibition, prolonged the duration of response and survival when combined with the menin inhibitor revumenib, and potentiated AML cell killing in combination with the FLT3 inhibitor gilteritinib and HMA azacitidine. We expect to present additional data supporting Actimab-A’s mutation agnostic capabilities and backbone potential at future scientific and medical conferences. In addition, we will continue to explore potential clinical trials under our CRADA with NCI, investigator-initiated trials or under our sponsorship.

Previous wording

Iomab-ACT is our next-generation targeted conditioning agent directed against CD45, a target expressed widely across the hematopoietic system including normal nucleated immune cells such as lymphocytes that are relevant to this program and uses the Iodine-131(“I-131”) radioisotope payload. We are developing Iomab-ACT as conditioning for cell and gene therapies in both malignant and non-malignant hematologic indications. Iomab-ACT utilizes non-myeloablative doses of I-131, to not fully deplete the patient’s bone marrow and immune system with the goal of improving patient access and outcomes for potentially curative cell and gene therapies by replacing the need for the non-targeted, chemotherapy-based conditioning regimens that are currently used. Iomab-ACT is currently being studied in three clinical trials. These trials include Iomab-ACT with a commercial CAR-T therapy, Iomab-ACT prior to allogeneic bone marrow transplant for patients with SCD, which could potentially inform a trial design with gene therapy for SCD, and Iomab-ACT with a novel investigational CD19 CAR-T therapy. In May 2025, we announced that the first patient was enrolled in the Iomab-ACT commercial CAR-T trial at the University of Texas Southwest Medical Center (“UTSW”).

Current wording

Iomab-ACT is our next-generation targeted conditioning agent directed against CD45, a target expressed widely across the hematopoietic system including normal nucleated immune cells such as lymphocytes that are relevant to this program and uses the Iodine-131(“I-131”) radioisotope payload. We are developing Iomab-ACT to condition or prepare patients’ immune system to enable cell and gene therapies in both malignant and non-malignant hematologic indications. Iomab-ACT utilizes non-myeloablative doses of I-131, to not fully deplete the patient’s bone marrow and immune system with the goal of improving patient access and outcomes for potentially curative cell and gene therapies by replacing the need for the non-targeted, chemotherapy-based conditioning regimens currently used, which are associated with toxicities that limit patient access. As an example, in order to receive gene therapy, SCD patients receive Busulfan, a chemotherapy associated with infertility, that can therefore require patients to undertake fertility counseling. Iomab-ACT is currently being studied in three clinical trials. These trials include Iomab-ACT with a commercial CAR-T therapy, Iomab-ACT prior to allogeneic bone marrow transplant for patients with SCD, which could potentially inform a trial design with gene therapy for SCD, and Iomab-ACT with a novel investigational CD19 CAR-T therapy. We expect initial clinical data from the Iomab-ACT commercial CAR-T therapy and SCD trials in the first half of 2026.

Previous wording

In February 2023, Actinium announced that the SIERRA trial met the primary endpoint with statistical significance, as 22% of patients (13/76) on the Iomab-B arm achieved durable Complete Remission (“dCR”) compared to 0% of patients (0/77) on the control arm resulting in a p-value of <0.0001. The SIERRA trial met the secondary endpoint of Event-Free Survival (“EFS”) with a 78% reduction in the probability of an event (Hazard Ratio=0.22, p<0.0001 for both per protocol and ITT basis). EFS at 180 days for the Iomab-B arm was 28% compared to 0.2% for the control arm. In the SIERRA trial, an event was defined as one of the following: a patient not achieving CR/CRp or crossing over, patient not receiving BMT, a patient relapsing or death. The SIERRA trial did not, however, meet the secondary endpoint in achieving a statistically significant improvement in OS in the intent to treat (“ITT”) population.

Current wording

We previously advanced our targeted conditioning program Iomab-B through the Phase 3 Study of Iomab-B in Elderly Relapsed and Refractory AML (“SIERRA”) trial, a 153 patient, randomized multi-center trial conducted in the United States and Canada. Iomab-B is comprised of the anti-CD45 monoclonal antibody apamistamab with myeloablative doses of I-131 intended to enable patient access to BMT, the only potentially curative treatment option for patients with r/r AML. The SIERRA trial met the primary endpoint with statistical significance, as 22% of patients (13/76) on the Iomab-B arm achieved durable Complete Remission (“dCR”) compared to 0% of patients (0/77) on the control arm resulting in a p-value of <0.0001. The SIERRA trial met the secondary endpoint of Event-Free Survival (“EFS”) with a 78% reduction in the probability of an event (Hazard Ratio=0.22, p<0.0001 for both per protocol and ITT basis). EFS at 180 days for the Iomab-B arm was 28% compared to 0.2% for the control arm. In the SIERRA trial, an event was defined as one of the following: a patient not achieving CR/CRp or crossing over, patient not receiving BMT, a patient relapsing or death. The SIERRA trial did not, however, meet the secondary endpoint in achieving a statistically significant improvement in OS in the intent to treat (“ITT”) population.

Previous wording

On August 5, 2024, Actinium announced that it concluded both its clinical and Chemistry, Manufacturing and Controls (“CMC”) interactions with the FDA regarding the BLA pathway for Iomab-B based on the SIERRA trial results. As previously disclosed, we had received positive feedback from the FDA regarding our CMC package for Iomab-B and were also assigned a BLA number. However, in the third quarter of 2024, the FDA provided definitive feedback that the SIERRA trial alone is not adequate to support a BLA filing for Iomab-B, despite (a) the SIERRA trial meeting the primary endpoint of dCR with statistical significance (p-value<0.0001) and other positive secondary endpoints including Event Free Survival (“EFS”) and safety, and (b) our presentation of several additional analyses from the SIERRA study, including long-term follow-up demonstrating a trend towards improved overall survival and evidence of survival benefit in patients with high-risk TP53 mutations, to support Iomab-B’s impact on overall survival. The FDA indicated that demonstrating an overall survival benefit in a randomized head-to-head trial is necessary and has advised us to conduct a study to evaluate allogeneic BMT using Iomab-B plus a reduced intensity conditioning regimen of fludarabine and total body irradiation (“Flu/TBI”) versus allogeneic BMT using reduced intensity conditioning comprised of cyclophosphamide plus Flu/TBI. This proposed additional study differs from the SIERRA trial, which allowed physician’s choice of salvage chemotherapies and heterogenous conditioning regimens in the control arm. Additionally, the proposed new study will not allow patients to cross over from the control arm, which was allowed in the SIERRA trial and confounded the overall survival analysis in the ITT patient population, as nearly 60% of patients crossed over from the control arm.

Current wording

On August 5, 2024, Actinium announced that it concluded both its clinical and Chemistry, Manufacturing and Controls (“CMC”) interactions with the FDA regarding the BLA pathway for Iomab-B based on the SIERRA trial results. As previously disclosed, we had received what we believe to be positive feedback from the FDA regarding our CMC package for Iomab-B and were also assigned a BLA number. However, in the third quarter of 2024, the FDA provided definitive feedback that the SIERRA trial alone is not adequate to support a BLA filing for Iomab-B, despite (a) the SIERRA trial meeting the primary endpoint of dCR with statistical significance (p-value<0.0001) and other positive secondary endpoints including Event Free Survival (“EFS”) and safety, and (b) our presentation of several additional analyses from the SIERRA study, including long-term follow-up demonstrating a trend towards improved OS and evidence of survival benefit in patients with high-risk TP53 mutations, to support Iomab-B’s impact on OS. The FDA indicated that demonstrating an OS benefit in a randomized head-to-head trial is necessary and has advised us to conduct a study to evaluate allogeneic BMT using Iomab-B plus a reduced intensity conditioning regimen of fludarabine and total body irradiation (“Flu/TBI”) versus allogeneic BMT using reduced intensity conditioning comprised of cyclophosphamide plus Flu/TBI. This proposed additional study differs from the SIERRA trial, which allowed physician’s choice of salvage chemotherapies and heterogenous conditioning regimens in the control arm. Additionally, the proposed new study will not allow patients to cross over from the control arm, which was allowed in the SIERRA trial and confounded the OS analysis in the ITT patient population, as nearly 60% of patients crossed over from the control arm.

Previous wording

Actinium continued interactions with the FDA in 2024 to further discuss the specifics of the additional head-to-head clinical trial required by the FDA, including the patient population, which the FDA had suggested could include all adult r/r AML patients. The FDA also requires that a Phase 2 dose optimization trial demonstrating safety and efficacy be completed to calculate the dose of Iomab-B based on absorbed dose by the bone marrow, rather than the maximum tolerable dose of 24 Gy of radiation to the liver as was done in the SIERRA trial based on several interactions we had with the FDA before starting the SIERRA trial. In the second quarter of 2025, Actinium conducted another meeting with the FDA. Based on this meeting, Actinium has reached agreement with the FDA on a Phase 2/3 clinical trial protocol and has been authorized by FDA to initiate the Phase 2 portion of the trial. We are actively seeking a strategic partner for Iomab-B in the U.S. to execute the Phase 2/3 clinical trial. This planned study will be conducted to establish dose optimization and evaluate allogeneic BMT using Iomab-B plus a reduced intensity conditioning regimen of Flu/TBI versus allogeneic BMT using reduced intensity conditioning comprised of cyclophosphamide plus Flu/TBI. The study population will be all adult patients aged 18 and above with active AML with blasts counts between 5 and 20 percent. This is a broader patient population than the patients enrolled on the SIERRA trial, which only enrolled patients aged 55 and above and with blast counts that exceeded 20 percent.

Current wording

Actinium continued interactions with the FDA in 2024 and 2025 to further discuss the specifics of the additional head-to-head clinical trial required by the FDA. Based on these interactions, Actinium has reached agreement with the Agency on a Phase 2 clinical trial protocol and has been authorized by FDA to initiate the Phase 2 portion of the trial. We are actively seeking a strategic partner for Iomab-B in the U.S. to execute the Phase 2/3 clinical trial. This planned study will consist of a Phase 2 dose optimization portion to demonstrate safety and efficacy with the dose of Iomab-B based on absorbed dose by the bone marrow, rather than the maximum tolerable dose of 24 Gy of radiation to the liver as was done in the SIERRA trial based on several interactions we had with the FDA before starting the SIERRA trial. Once what the FDA considers adequate safety data to establish a treatment plan for the Phase 3 protocol is gathered, a meeting with the FDA will be necessary to gain approval to proceed to the Phase 3 portion of this planned trial. The optimized dose established in the Phase 2 portion is then expected to be studied in the randomized Phase 3 portion to evaluate allogeneic BMT using Iomab-B plus a reduced intensity conditioning regimen of Flu/TBI versus allogeneic BMT using reduced intensity conditioning comprised of cyclophosphamide plus Flu/TBI. The study population will be all adult patients age 18 and above with active AML with blasts counts between 5 and 20 percent. This is a broader patient population than the patients enrolled on the SIERRA trial, which only enrolled patients aged 55 and above and with blast counts that exceeded 20 percent.

Previous wording

Our R&D capabilities have the potential to yield differentiated, high-value targeted radiotherapy programs that demonstrate our experience across multiple validated cancer targets and isotopes and cover broad areas of focus leveraging our clinical development experience across hematology, targeted conditioning, solid tumors, and next-generation radiotherapies. We have internal R&D capabilities with our research laboratory capable of executing in vitro and in vivo experiments and translational research. We are working on several preclinical programs which include novel approaches to validated cancer targets, as well as novel targets that we believe show immense potential for radiotherapeutic approaches. Preclinical pharmacology studies with our targeted radiotherapeutics, such as HER2, CD33 and CD38, have shown strong improvement in tumor growth inhibition in various preclinical tumor models.

Current wording

Our R&D capabilities, we believe, have the potential to yield differentiated, high-value targeted radiotherapy programs that demonstrate our experience across multiple validated cancer targets and isotopes and cover broad areas of focus leveraging our clinical development experience across hematology, targeted conditioning, solid tumors, and next-generation radiotherapies. We have internal R&D capabilities with our research laboratory capable of executing in vitro and in vivo experiments and translational research. We are working on several preclinical programs which include novel approaches to validated cancer targets, as well as novel targets that we believe show immense potential for radiotherapeutic approaches. Preclinical pharmacology studies with our targeted radiotherapeutics, such as HER2, CD33 and CD38, have shown improved tumor growth inhibition in various preclinical tumor models.

Previous wording

We seek to expand our capabilities and technologies across therapeutic modalities, linker technologies and in vivo cancer models, and build visibility through presentations at key conferences and publications in journals of high impact. Our R&D efforts are centered on the advancement of key programs with a robust “fast-to-clinic” approach. Underpinning our development programs is our expanded patent portfolio of approximately 240 issued patents and pending patent applications worldwide.

Current wording

We seek to expand our capabilities and technologies across therapeutic modalities, linker technologies and in vivo cancer models, and build visibility through presentations at key conferences and publications in journals of high impact. Our R&D efforts are centered on the advancement of key programs with a robust “fast-to-clinic” approach. Underpinning our development programs is our expanded patent portfolio of approximately 250 issued patents and pending patent applications worldwide.

Previous wording

We plan to establish our own manufacturing capabilities and intend to commence the build-out of a facility in the second half of 2025. We believe that having in-house manufacturing will provide enhanced control, flexibility and scalability to serve our current and planned clinical trials and R&D efforts as well as potential future activity.

Current wording

We plan to establish our own manufacturing capabilities and intend to commence the build-out of a facility that will be capable of supplying final drug product for our current and planned clinical trials. We believe that having in-house manufacturing will provide enhanced control, flexibility and scalability to serve our current and planned clinical trials and R&D efforts as well as potential future activity.

Previous wording

As of August 2025, our patent portfolio is comprised of approximately 240 issued patents and pending patent applications worldwide, which we believe constitutes a valuable business asset. Our IP includes 48 patent families, including key patents that relate primarily to our radiotherapeutic candidates. Our patent portfolio includes 20 issued patents and 51 pending patent applications in the U.S., and 173 that are issued or pending internationally. The effective lives of the issued patents in our portfolio, or patents that may issue from the pending applications in our portfolio, ranges from expirations between 2026 and 2046.

Current wording

As of November 2025, our patent portfolio is comprised of approximately 250 issued patents and pending patent applications worldwide, which we believe constitutes a valuable business asset. Our IP includes 48 patent families, including key patents that relate primarily to our radiotherapeutic candidates. Our patent portfolio includes 22 issued patents and 51 pending patent applications in the U.S., and 180 that are issued or pending internationally. The effective lives of the issued patents in our portfolio, or patents that may issue from the pending applications in our portfolio, ranges from expirations between 2026 and 2046.

Previous wording

As of August 8, 2025, we had 27 full-time employees, 12 of whom have Ph.D. or M.D. degrees and 20 of whom are engaged in research and development and clinical development activities. In the second quarter of 2025, we conducted a workforce optimization aligned with our strategic pipeline prioritization that reduced our headcount by approximately fourteen percent. Also in the second quarter of 2025, Dr. Avinash Desai resigned from his position as Chief Medical Officer. There were no disagreements with the Company that contributed to Dr. Desai’s resignation. We do not expect the aforementioned workforce optimization or departures to have a material impact on our operations or ability to execute our operating plan. We believe that we have been successful to date in attracting skilled and experienced personnel despite the competitive hiring marketing 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.

Current wording

As of November 13, 2025, we had 25 full-time employees, 12 of whom have Ph.D. or M.D. degrees and 20 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 marketing 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.

Previous wording

Stock option expense for the three months ended March 31, 2025 and March 31, 2024, respectively and stock option expense for the three months and six months ended June 30,2025 and June 30,2024, respectively, is presented below:

Current wording

Stock option expense for the three months ended March 31, 2025 and March 31, 2024, respectively, three months ended June 30, 2025 and June 30, 2025, respectively and stock option expense for the three months and nine months ended September 30,2025 and September 30,2024, respectively, is presented below:

Previous wording

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 June 30, 2025 and 2024, respectively.

Current wording

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. We recognized other revenue during the three months ended September 30, 2025 of $0.1 million. There was no other revenue recognized for the three months ended September 30, 2024.

Previous wording

As noted above, 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.

Current wording

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.

Previous wording

As noted above, the cancellation of stock options in March 2025 resulted in a significant decrease in non-cash stock compensation expense for the three months ended June 30, 2025. During the three months ended June 30, 2025 and June 30, 2024, total non-cash stock-based compensation expense, including stock option compensation expense, was $0.2 million and $1.4 million, respectively.** **

Current wording

As noted above, the cancellation of stock options in March 2025 resulted in a significant decrease in non-cash stock compensation expense for the three months ended September 30, 2025. During the three months ended September 30, 2025 and September 30, 2024, total non-cash stock-based compensation expense, including stock option compensation expense, was $0.1 million and $1.3 million, respectively.** **

Previous wording

Research and development expenses of $4.9 million for the three months ended June 30, 2025 decreased by $3.9 million from $8.8 million for the three months ended June 30, 2024. The decrease was primarily a result of lower compensation of $1.6 million due to lower headcount and lower non-cash stock-based compensation expense of $0.3 million due to the cancellation of stock options in March 2025. In the second quarter of 2025, we conducted a workforce optimization that reduced our headcount by approximately fourteen percent. In addition, there was a decline in Chemistry, manufacturing and controls, or CMC, expenses and clinical expenses of $1.4 million due to lower activity related to Iomab-B and preclinical expenses decreased $0.7 million.

Current wording

Research and development expenses of $4.2 million for the three months ended September 30, 2025 decreased by $5.6 million from $9.8 million for the three months ended September 30, 2024. The decrease was primarily a result of a decline in outside CRO services and other preclinical R&D expenses of $4.3 million, lower compensation of $1.5 million due to lower headcount and lower non-cash stock-based compensation expense of $0.2 million due to the cancellation of stock options in March 2025. 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.

Previous wording

General and administrative expense of $2.6 million for the three months ended June 30, 2025 decreased by $1.0 million from $3.6 million for the three months ended June 30, 2024. The cancellation of stock options in March 2025 described above resulted in lower non-cash stock-based compensation expense of $0.9 million for the three months ended June 30, 2025 compared with the three months ended June 30, 2024.

Current wording

General and administrative expense of $1.5 million for the three months ended September 30, 2025 decreased by $1.3 million from $2.8 million for the three months ended September 30, 2024. The cancellation of stock options in March 2025 described above resulted in lower non-cash stock-based compensation expense of $1.0 million for the three months ended September 30, 2025 compared with the three months ended September 30, 2024. In addition, compensation decreased $0.2 million due to lower headcount due to recent workforce optimization aligned with our strategic pipeline prioritization that reduced our headcount by approximately 14 percent.

Previous wording

Other income is comprised of net interest income in both reporting periods. The amount for the three months ended June 30, 2025 of $0.6 million decreased from $1.1 million for the three months ended June 30, 2024 primarily due to a lower average cash balance during the respective time periods.

Current wording

Other income is comprised of net interest income in both reporting periods. The amount for the three months ended September 30, 2025 of $0.6 million decreased from $1.0 million for the three months ended September 30, 2024 primarily due to a lower average cash balance during the respective time periods.