Actinium Pharmaceuticals, Inc.
For the period ended Jun 30, 2026. Filed Aug 7, 2026.
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A company's report for each of its first three quarters. The financial statements are not audited. It shows how the business has moved since the last annual report, and what management says changed.
Jun 30, 2026 · Filed Aug 7, 2026
ATNM$1.43+10.0%Stored close · as of Nov 6, 2026
What changed in Management’s Discussion and Analysis?
Read the current filingPrevious report: 10-Q
Period ended 2026-03-31; filed 2026-05-08.
0001213900-26-053980
Item 2. Management’s Discussion and Analysis of Financial Condition and Results of OperationsCurrent report: 10-Q
Period ended 2026-06-30; filed 2026-08-07.
0001213900-26-086769
Item 2. Management’s Discussion and Analysis of Financial Condition and Results of OperationsThe baseline is this issuer’s latest earlier reporting period of the same form that was filed before the current report. A previous 10-Q is a different quarter, not a year-over-year comparison. Amendments are excluded.
Compared 133 previous paragraphs and 208 current paragraphs.
70 unchanged; 35 reworded; 98 added; 28 removed; 0 previous and 5 current paragraphs rearranged.
Tables are not compared: 51 previous and 52 current tables excluded. Dates, whitespace, punctuation and numbering changes are ignored; changes to financial figures remain significant.
A changed paragraph is not evidence that risk increased or decreased. An unchanged paragraph does not establish that risk stayed the same.
Added paragraphs (98)
Current report
Market Opportunity
Current report
ATNM-400 Is Designed to Address Large, Treatment Resistant Patient Populations Across Prostate, Lung and Breast Cancer - Indications in Which Approved Targeted Therapies Generated More Than $30 Billion in Worldwide Sales in 2025
Current report
We are developing ATNM-400 as a mutation- and pathway-agnostic radiotherapeutic - as a monotherapy or in combination with standard of care - for large, treatment resistant solid tumor populations, with initial focus on prostate cancer, non-small cell lung cancer (NSCLC) and breast cancer. These diseases have been selected for initial clinical development driven by a common scientific and commercial rationale. Each disease represents a large, well-established market due to targeted agents and yet a major underserved opportunity once their resistance to these therapies develops. The antigen targeted by ATNM-400 is expressed in all these disease areas and its expression further increases in many cases as the existing therapies fail. Several of these therapies have blockbuster sales generated by treating a large number of patients. ATNM-400 target expression is reported in a majority of prostate cancer, NSCLC and breast cancer tumors based on immunohistochemistry datasets, which we estimate corresponds to an addressable population of well over 350,000 patients per year in the United States across these three indications and considerably more worldwide. We believe this addressable population may expand as we evaluate ATNM-400 in additional indications and treatment settings.
Current report
Prostate cancer is the most frequently diagnosed cancer in men in the United States. According to the American Cancer Society, approximately 333,830 men in the United States were estimated to be diagnosed with prostate cancer in 2026, representing approximately 30% of all cancer diagnoses in men. While localized prostate cancer is frequently curable, metastatic disease is not: approximately 5% to 7% of patients present with metastatic disease at initial diagnosis, and approximately 20% to 30% of patients initially diagnosed with localized disease subsequently progress to metastatic disease, for which available therapies slow, but do not cure, disease progression.
Current report
Because prostate cancer cells rely on androgens for growth, most patients receive androgen receptor pathway inhibitor (ARPI) therapy, including enzalutamide (Xtandi®), apalutamide (Erleada®) and darolutamide (Nubeqa®), which generated more than $6.3 billion, $3.6 billion and $2.7 billion in worldwide sales, respectively, in 2025. We estimate that up to approximately 50,000 to 60,000 men in the United States progress following ARPI therapy each year. Collectively, ARPIs generated more than $12 billion in worldwide sales in 2025.
Current report
Since the March 2022 approval of the PSMA-directed radioligand therapy Pluvicto® (with active ingredient Lu177-PSMA-617), targeted radiotherapy has become a prominent component of the metastatic castration-resistant prostate cancer (mCRPC) treatment paradigm. Pluvicto®, marketed by Novartis, generated approximately $2.0 billion in worldwide sales in 2025, and its addressable population has expanded from approximately 44,000 patients toward approximately 86,500 patients with successive label expansions into earlier lines of therapy. More than 30 PSMA-targeted radiotherapies are currently in various stages of development. Notwithstanding this activity, we believe a significant unmet need remains: we estimate that approximately 30% of patients with mCRPC have low or no PSMA expression and are therefore poorly served by PSMA-directed radioligand therapies, and re-treatment with PSMA-directed agents may be limited by reduced PSMA surface expression and increased tumor heterogeneity following initial PSMA-targeted therapy. In addition, because PSMA is expressed in the salivary glands, PSMA-directed radiotherapies are associated with xerostomia, a quality-of-life limitation that is particularly relevant for Ac-225-based PSMA agents.
Current report
Because ATNM-400 is directed against a novel, non-PSMA antigen and acts independently of both androgen receptor (AR) signaling and PSMA expression, we believe it is positioned to address the full metastatic castration-resistant prostate cancer (mCRPC) treatment continuum. This includes patients whose disease has progressed on androgen receptor pathway inhibitors (ARPIs), as well as patients with PSMA-low or PSMA-negative tumors, for whom there are very limited commercially available targeted radiotherapy options. Together, these patient populations represent a combined opportunity that we estimate exceeds 100,000 patients annually in the United States and may be addressable with ATNM-400 as either a monotherapy or in combination with existing standards of care.
Current report
Non-Small Cell Lung Cancer
Current report
Lung cancer is the leading cause of cancer death worldwide. Approximately 229,410 new cases of lung cancer were estimated to be diagnosed in the United States in 2026, and NSCLC accounts for approximately 85% of the more than two million lung cancer cases diagnosed globally each year. Approximately 70% are either diagnosed with advanced/metastatic disease or progress to advanced metastatic disease. NSCLC is a large and heterogeneous market in which no single mutation dominates. EGFR and KRAS mutations together account for approximately 50% to 60% of NSCLC cases, and existing therapies are segmented by mutation subtype and ultimately limited by acquired resistance.
Current report
Beyond EGFR and KRAS Driver Mutations the NSCLC Market is Fragmented
Current report
Source: Adapted from Fregni M, et al. Int J Mol Sci. 2022;23:7213, based on Skoulidis F and Heymach JV. Nat Rev Cancer. 2019;19:495–509
Current report
Current targeted therapies illustrate both the scale of the market and the treatment resistant- unmet need. In EGFR-mutant NSCLC, nearly all patients receive osimertinib (Tagrisso®) as first-line therapy; osimertinib generated approximately $7.3 billion in worldwide sales in 2025. Disease progression on osimertinib is common and the resistance mechanisms are highly heterogeneous; in the second-line setting, amivantamab (Rybrevant®) plus chemotherapy became a National Comprehensive Cancer Network (NCCN)- preferred regimen following its September 2024 approval, and datopotamab deruxtecan (Datroway®, a TROP-2 antibody-drug conjugate) received accelerated approval in patients with prior platinum chemotherapy in June 2025, yet a significant unmet need remains for durable options beyond chemotherapy. Separately, the KRAS-inhibitor class in NSCLC, led by sotorasib (Lumakras®) and adagrasib (Krazati®), is conservatively projected to exceed $3 billion in peak sales by 2032.
Current report
We believe ATNM-400 is well suited to this fragmented market. Based on prior immunohistochemistry studies, the antigen targeted by ATNM-400 is expressed in approximately 98% of NSCLC tumors, is highly expressed in approximately 70%, is conserved across EGFR-, KRAS- and other driver-defined subgroups, and is further increased in tumors that have become resistant to EGFR, KRAS and immune-checkpoint therapies. Because ATNM-400 addresses NSCLC as a broad, target-defined population rather than as another mutation-specific therapy for a single molecular subset, we believe its mutation-agnostic profile positions it to participate in these large, established markets as a backbone therapy - enhancing the standard of care in combination while also reaching the broader NSCLC population beyond any single mutation.
Current report
Breast cancer is the most frequently diagnosed cancer among women in the United States. The National Cancer Institute’s Surveillance, Epidemiology, and End Results (SEER) Program estimates that approximately 321,910 women will be diagnosed with invasive breast cancer in 2026. Approximately 200,000 women were living with metastatic breast cancer in the United States in 2025, a figure expected to grow to approximately 250,000 by 2030.
Current report
Hormone receptor-positive, HER2 negative (HR+/HER2−) breast cancer is the largest molecular subtype, accounting for approximately 70% of newly diagnosed cases. Endocrine therapy is the backbone of treatment, with endocrine therapy plus a CDK4/6 inhibitor preferred for most patients in the first-line metastatic setting. Approximately half of patients experience disease progression or death within two years, and the substantial majority progress within five years. Following progression, treatment is guided by prior therapy and biomarkers such as ESR1, PIK3CA, AKT1, PTEN, and germline BRCA1/2 alterations. Patients with ESR1-mutated disease may receive elacestrant, imlunestrant, or vepdegestrant, which was approved in May 2026 as the first proteolysis-targeting chimera in oncology. Gedatolisib-based therapy provides another pathway-targeted option for patients with PIK3CA-wild-type disease, while trastuzumab deruxtecan is approved following endocrine therapy for HR+, HER2 low or HER2 ultralow disease. Although post-endocrine options have expanded, these approvals were based on progression-free survival benefits generally measured in months. Median PFS across approved second-line regimens ranges from approximately four to thirteen months, and substantially all patients ultimately progress. In later lines, datopotamab deruxtecan is approved following endocrine-based therapy and chemotherapy, while sacituzumab govitecan is approved following endocrine therapy and at least two additional metastatic systemic regimens. Despite these advances, substantial need remains for therapies that overcome resistance and provide more durable disease control across successive lines of treatment.
Current report
HER2 positive (HER2+) breast cancer accounts for approximately 15% of breast cancers. Although HER2 directed therapies have substantially improved outcomes, metastatic disease generally remains incurable, and resistance develops across successive regimens. Central nervous system progression is a major unmet need, with up to 50% of patients developing brain metastases during the course of disease. Trastuzumab deruxtecan plus pertuzumab was approved in December 2025 as a first-line treatment for unresectable or metastatic HER2+ breast cancer. Taxane chemotherapy with trastuzumab and pertuzumab remains an option for selected patients. Trastuzumab deruxtecan plus pertuzumab achieved a median PFS of 40.7 months, compared with 26.9 months for the taxane-based regimen. Nevertheless, approximately 30% of patients experienced progression or death within two years, and half were expected to do so within approximately three and a half years. For patients with HR+, HER2+ disease controlled after induction therapy, palbociclib with trastuzumab, endocrine therapy, and optional pertuzumab was approved in June 2026 as maintenance treatment. Following progression, treatment depends on prior HER2 directed therapy and the presence or risk of central nervous system disease. Trastuzumab deruxtecan remains an established second-line option after first-line taxane, trastuzumab, and pertuzumab. However, the optimal sequence after progression on a first-line trastuzumab deruxtecan-containing regimen has not been established. Later-line options include tucatinib with trastuzumab and capecitabine, particularly for patients with brain metastases, and other HER2 directed regimens. New agents are needed that remain active following resistance to HER2 directed antibody-drug conjugates and across successive lines of treatment.
Current report
Triple-negative breast cancer (TNBC), defined by the absence of estrogen receptor, progesterone receptor, and HER2 overexpression or amplification, accounts for approximately 10% to 15% of breast cancers. TNBC is more aggressive than HR+ breast cancer, carries a higher risk of early distal recurrence, and lacks endocrine and HER2 directed treatment options. First-line treatment is informed by PD-L1 expression and germline BRCA1/2 mutation status. For patients with PD-L1-positive disease, immune-checkpoint inhibition combined with systemic therapy is a common strategy. In June 2026, sacituzumab govitecan was approved with pembrolizumab for PD-L1-positive unresectable locally advanced or metastatic TNBC and as monotherapy for patients who are not candidates for PD-1- or PD-L1-directed therapy. Datopotamab deruxtecan was also approved in May 2026 for patients who are not candidates for checkpoint inhibition. Despite these advances, more than half of patients are expected to experience progression or death within one year of starting first-line treatment. With TROP-2-directed antibody-drug conjugates now used in the first-line setting, no prospectively validated preferred sequence has been established after progression. Subsequent treatment may include chemotherapy, PARP inhibition for eligible patients with germline BRCA1/2 mutations, or clinical trials. This sequencing gap and the biological heterogeneity of TNBC support the need for therapies with mechanisms distinct from TROP-2-directed cytotoxic delivery.
Current report
The antigen targeted by ATNM-400 is expressed across multiple breast cancer subtypes, including HR+/HER2−, HER2+ (including HR+ and HR-), and triple-negative disease. Based on our preclinical findings, target expression is also retained or increased in tumor models that have developed resistance to selected standard therapies. We believe ATNM-400’s target-driven, subtype-agnostic profile could position it to address treatment-resistant breast cancer populations as either a monotherapy or in combination with established standards of care.
Current report
ATNM-400 Positioned to Address HR+/HER2-, HER2+ and TNBC Breast Cancer Subtypes After Resistance to Standard of Care
Current report
Source: American Cancer Society, Cancer Facts & Figures 2026 (Atlanta: American Cancer Society, 2026), estimated new cases of invasive breast cancer in U.S. women, 2026. Subtype distribution derived from age-adjusted incidence rates for 2019–2023, National Cancer Institute, SEER Cancer Stat Facts: Female Breast Cancer Subtypes.
Current report
ATNM-400 Preclinical Data in Large Solid Tumor Indications
Current report
ATNM-400 in Prostate Cancer
Current report
ATNM-400 is a first-in-class Ac-225 antibody radioconjugate directed against a novel, non-PSMA antigen implicated in aggressive prostate cancer biology and overexpressed as tumors progress and develop resistance to standard-of-care therapies. Because ATNM-400 acts independently of both androgen-receptor signaling and PSMA expression, we believe it has the potential to address patients across the metastatic castration-resistant prostate cancer, or mCRPC, treatment continuum.
Current report
Key Findings and Therapeutic Positioning in Metastatic Castration-Resistant Prostate Cancer
Current report
We believe these findings support the potential development of ATNM-400 as a monotherapy or in combination with ARPIs across a broad mCRPC population, including patients with ARPI-resistant, PSMA-low or PSMA-negative disease, as well as patients with PSMA-high disease who may benefit from a differentiated safety profile.
Current report
Supporting Data in Metastatic Resistant Prostate Cancer Models
Current report
ATNM-400 had robust efficacy in prostate cancer xenograft mouse models with high, low and no PSMA and was superior to 177-Lu-PSMA-617 in all the models and to 225Ac-PSMA-617 in the Low-PSMA model. ATNM-400 had comparable efficacy to 225Ac-PSMA-617 in the High-PSMA model. Given that 30% mCRPC patients have low or no PSMA expression and up to 70% of patients do not respond to Pluvicto® and nearly all patients progress on Pluvicto® in <12 months, our data in 177-Lu-PSMA-617, the active ingredient in Pluvicto®, suggests that ATNM-400 has the potential to treat a broader population of mCRPC patients.
Current report
ATNM-400 Demonstrated Robust Efficacy After 177Lu-PSMA-617 Failure in Prostate Cancer Model
Current report
Beyond tumor growth inhibition, ATNM-400 conferred a survival benefit relative to PSMA-directed radioligand therapy. In preclinical prostate cancer models, animals treated with ATNM-400 survived longer than those treated with 177Lu-PSMA-617, consistent with the greater and more durable tumor control described above and achieved it at approximately one-thousandth of the administered radioactivity.
Current report
ATNM-400 Improved Survival vs 177Lu-PSMA-617 in Prostate Cancer Model
Current report
ATNM-400 demonstrated activity in prostate cancer cells and tumors resistant to all three approved androgen-receptor pathway inhibitors (ARPIs) - enzalutamide, apalutamide, and darolutamide. Across these studies, ATNM-400 delivered tumor control as either a single-bolus or repeat-dose regimen with a consistent safety profile and minimal off-target toxicity, which we believe indicates dosing flexibility and a wide therapeutic window.
Current report
In an ARPI-resistant model, ATNM-400 as a monotherapy and in combination with enzalutamide produced greater tumor growth inhibition and prolonged survival than enzalutamide alone that correlated well with overall survival. In the combination arm, 40% of the mice had complete cures that were durable up to 100 days post- treatment. The latter can be explained by mechanistic synergy since it has been published that enzalutamide resistance increases ATNM-400 target expression in prostate cancer models and in tumor biopsies from mCRPC patients.
Current report
ATNM-400 Monotherapy Demonstrated Superiority to Enzalutamide in ARPI-resistant Prostate Cancer Model and Had Complete Cures with Combination Activity
Current report
ATNM-400 Showed Survival Benefit vs Enzalutamide
Current report
Monotherapy and Combination
Current report
Following disease progression on enzalutamide, ATNM-400 produced continued tumor growth inhibition, supporting its potential to treat patients who have exhausted ARPIs.
Current report
ATNM-400 Displayed Strong Efficacy After Enzalutamide Failure
Current report
In data presented at the Society of Nuclear Medicine and Molecular Imaging (SNMMI) 2026 Annual Meeting in June 2026, as a monotherapy in the ARPI-resistant 22Rv1 model, ATNM-400 achieved 94% tumor growth inhibition, compared with 32% for apalutamide and 5% for darolutamide, and in combination with either apalutamide or darolutamide achieved 107% tumor growth inhibition (representing tumor regression), with durable complete responses in a majority of treated animals.
Current report
ATNM-400 Monotherapy Had Strong Tumor Growth Inhibition in the ARPI-Resistant 22Rv1 Prostate Cancer Model Resistant to Darolutamide and Apalutamide
Current report
ATNM-400 Combination with Darolutamide or Apalutamide Demonstrated Strong Tumor Growth Inhibition and Achieved Complete Responses (CRs) in the ARPI-Resistant 22Rv1 Prostate Cancer Model
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Removed paragraphs (28)
Previous report
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.
Previous report
ATNM-400 Tumor Growth Inhibition vs 177Lu-PSMA-617 and 225Ac-PSMA-617
Previous report
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.
Previous report
EGFR-Mutant NSCLC
Previous report
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.
Previous report
ATNM-400 achieved the highest tumor growth inhi bition(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.
Previous report
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.
Previous report
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.
Previous report
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.
Previous report
MCF7 (HR+) Breast Cancer
Previous report
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:
Previous report
In Prostate Cancer
Previous report
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.
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DU145: Low Target Expression and PSMA Negative
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In Lung Cancer
Previous report
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.
Previous report
**ATNM-400 Combination With Osimertinib vs Osimertinib Combination With Chemo In
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NCI-H1975 EGFR-m Lung Cancer
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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.
Previous report
In Breast Cancer
Previous report
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).
Previous report
Actimab-A Combinations with Revumenib and Azacitidine Upregulate Myeloid Differentiation Gene Signature in AML
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The facility has been designed for clinical stage supply of radiolabeled therapeutic drug product production.
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Results of Operations
Previous report
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.
Previous report
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.
Previous report
Net loss
Previous report
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.
Reworded paragraphs (35)
Previous wording
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.
Current wording
Since our inception, we have focused on developing innovative and differentiated radiotherapies. Our pipeline of both early and later stage development programs is a testimony to our approach in three areas with: (1) two novel solid tumor product candidates, ATNM-400 and Actimab-A, with pan-tumor potential, (2) Actimab-A, which is also being developed as a therapeutic backbone for acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) in partnership with the National Cancer Institute (NCI), and (3) two targeted conditioning agents, Iomab-B for bone marrow transplant and Iomab-ACT for cell & gene therapies. Our solid tumor asset, ATNM-400, targets a novel antigen distinct from PSMA, with demonstrated preclinical activity across metastatic castration-resistant prostate cancer (mCRPC), non-small cell lung cancer (NSCLC), and breast cancer. Actimab-A targets myeloid derived suppressor cells (MDSCs) and is being studied in multiple solid tumors in combination with immune checkpoint inhibitors where MDSCs are known to act as an efficacy deterrent for these agents. Our hematology franchise includes: Actimab-A, a CD33-targeted therapy; as well as, Iomab-B and Iomab-ACT which are CD45-targeting conditioning agents. Both Actimab-A and Iomab-B are Phase 2/3 ready assets and are supported by extensive validation in over 15 clinical trials in which more than 500 patients were treated. We have several ongoing clinical studies across our pipeline. We expect to report data from ongoing company- and investigator-sponsored clinical studies for ATNM-400, Actimab-A for MDSC’s and Iomab-ACT in 4Q:2026 and over the course of 2027.
Previous wording
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.
Current wording
ATNM-400 is our lead solid tumor program, representing a first-in-class Ac-225 antibody radioconjugate targeting a novel, undisclosed antigen with expression across multiple solid tumor types. The ATNM-400 target is implicated in disease biology during tumor progression and is also overexpressed when tumors become resistant to many approved therapies in multiple solid tumors. We are developing ATNM-400 as a potential pan-cancer, biology-driven therapy - alone or in combination with standard-of-care agents - for large, treatment resistant-solid tumor populations across prostate, NSCLC, breast cancer and potentially other sizable cancer indications.
Previous wording
Our preclinical translational data demonstrated that ATNM-400 is superior to:
Current wording
Our translational data demonstrated that ATNM-400 is superior to the active ingredients in the many of the most commonly prescribed approved therapies in prostate cancer, NSCLC and breast cancer when tested in a wide variety of preclinical models:
Previous wording
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.
Current wording
These preclinical translational data show that ATNM-400 works well as monotherapy but is even better in combination in resistant settings where the target is overexpressed as part of the resistance mechanism of several of the approved standard-of-care drugs. Evidence of ATNM-400 target expression has been observed ranging from 60%-80% of mCRPC, >90% of NSCLC, and 50-70% of breast cancer patient tumors, representing a significant addressable population of well over a hundred thousand patients in the United States based on existing datasets. We believe this number may expand as we continue our work to demonstrate the potential of ATNM-400 in various additional disease and treatment settings.
Previous wording
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.
Current wording
In addition, we have developed a theranostic strategy utilizing Zr-89 as a companion imaging agent to enable patient selection and tumor visualization. We believe this approach allows for non-invasive assessment of target expression and drug biodistribution prior to therapeutic administration, potentially enhancing the therapeutic index by selecting patients most likely to respond.
Previous wording
Our preclinical development program has generated encouraging efficacy and mechanism-of-action data across multiple indication-specific animal models:
Current wording
Our preclinical development program has generated encouraging efficacy and mechanism-of-action data across multiple indication-specific animal models of solid tumors including prostate cancer, NSCLC and breast cancer:
Previous wording
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.
Current wording
ATNM-400 Demonstrated Robust Tumor Growth Inhibition and was Superior to PSMA-Targeted Agents Across PSMA-High (C4-2), PSMA-Low (22Rv1) and PSMA-Negative (DU145) Prostate Cancer Models
Previous wording
ATNM-400 retained anti-tumor activity in prostate cancer models following progression on 177Lu-PSMA-617 and enzalutamide.
Current wording
ATNM-400 retained anti-tumor activity in prostate cancer models after tumors had progressed on 177Lu-PSMA-617. Following tumor progression on 177Lu-PSMA-617, ATNM-400 produced continued tumor growth inhibition, supporting its potential to treat patients who have exhausted PSMA-directed radioligand therapy.
Previous wording
ATNM-400 vs Standard of Care Therapies in EGFR-mutant NSCLC
Current wording
ATNM-400 vs Standard of Care Therapies Across EGFR- and KRAS-Mutant NSCLC Models
Previous wording
Osimertinib upregulated the ATNM-400 target in NCI-H1975 cells, enhancing ATNM-400 cytotoxicity when dosed in combination.
Current wording
Osimertinib treatment increased ATNM-400 target expression both in vitro and in vivo, which we believe provides a mechanistic rationale for why the combination of osimertinib with ATNM-400 works even better than ATNM-400 monotherapy alone. Furthermore, in vitro studies also demonstrated that Osimertinib upregulated the ATNM-400 target in NCI-H1975 cells, enhancing ATNM-400 cytotoxicity when dosed in combination.
Previous wording
ATNM-400 vs Dato-DXd or Izalontamab Brengitecan
Current wording
ATNM-400 Demonstrated Superior Tumor Growth Inhibition Compared to Dato-DXd or Izalontamab Brengitecan in EGFR-mutant NSCLC Model
Previous wording
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.”
Current wording
Actimab-A (lintuzumab-Ac-225) is a CD33-targeted actinium-225 radioconjugate that we are developing to enhance checkpoint inhibitor efficacy by depleting immunosuppressive CD33+ myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment. MDSCs are a heterogeneous population of immature myeloid cells that accumulate in solid tumors and suppress anti-tumor T-cell responses, representing a well-validated mechanism of resistance to PD-1/PD-L1 checkpoint inhibitors. By selectively eliminating these suppressive cells with targeted alpha-particle therapy, Actimab-A is designed to dismantle this barrier and restore an environment in which checkpoint blockade can drive meaningful Tcell–mediated tumor killing. This positions Actimab-A as a differentiated immunomodulatory approach intended to expand the population of patients who benefit from checkpoint inhibitors, including those with tumors historically considered immunologically “cold.”
Previous wording
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.
Current wording
Our preclinical studies have suggested that Actimab-A: (1) selectively homes to tumor-resident CD33+ MDSCs in vivo; (2) are cytotoxic to patient-derived MDSCs ex vivo; and (3) rescue T-cell proliferation and anti-tumor immune responses ex vivo following MDSC depletion. We believe these data provide mechanistic support for combining Actimab-A with PD-1 inhibitors to overcome MDSC-mediated resistance.
Previous wording
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*.*
Current wording
Actimab-A (Lintuzumab-Ac225) was shown to deplete MDSCs in our studies. Actimab-A was also shown to restore T-cell proliferation in a dose dependent manner*.*
Previous wording
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.
Current wording
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.
Previous wording
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.
Current wording
We have discussed with the Food and Drug Administration (FDA) and believe we are aligned on a Phase 2/3 trial design to evaluate Actimab-A plus CLAG-M in R/R AML patients eligible for first or second salvage therapy. We are actively seeking a strategic partner to execute this trial. We believe the trial design allows for enrollment of a broad R/R AML population while enriching for patients most likely to benefit based on Phase 1b results.
Previous wording
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:
Current wording
Actimab-A Development Programs: Beyond R/R AML, we are developing Actimab-A in conjunction with the National Cancer Institute, or NCI across multiple AML and MDS treatment settings and exploring its potential in additional areas:
Previous wording
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.
Current wording
The programs are supported by our Cooperative Research and Development Agreement (CRADA) with the NCI, which enables cost-effective clinical development while retaining commercial rights to Actimab-A.
Previous wording
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:
Current wording
On April 21, 2026, preclinical translational data with Actimab-A were presented at the AACR Annual Meeting in San Diego, California. The presentation highlighted the following:
Previous wording
Transc riptional Reprogramming as a Key Mechanism for Actimab-A Combination Activity
Current wording
Transcriptional Reprogramming as a Key Mechanism for Actimab-A Combination Activity
Previous wording
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.
Current wording
Iomab-B has been evaluated in over 500 patients across multiple clinical trials, including the Phase 3 SIERRA trial in R/R AML patients. The SIERRA trial demonstrated that Iomab-B enabled successful donor cell engraftment in elderly R/R AML patients who would otherwise be ineligible for conventional conditioning. The study met the primary endpoint of durable complete remission (dCR). While the study did not meet the secondary endpoint of OS due to the cross-over of two-thirds of the patients from the control arm to the Iomab-B arm, it provided important insights into optimal patient selection and trial design for future development.
Previous wording
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.
Current wording
We have also established an end-to-end supply chain spanning isotope production through patient administration. Our clinical development infrastructure supports company-sponsored clinical development activities conducted in the United States and selected international jurisdictions through relationships with isotope suppliers, contract development and manufacturing organizations and specialized radiopharmaceutical logistics providers. We maintain supply agreements with multiple redundant isotope suppliers, relationships with multiple contract manufacturing organizations, and a distribution network to approximately 50 leading cancer centers amassed via the execution of several Phase 1 – 3 clinical trials. This supply chain infrastructure provides geographic coverage across major metropolitan areas, minimizes risk of supply disruption, and positions us to reliably serve patient demand at clinical scale.
Previous wording
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 ofour 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:
Current wording
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:
Previous wording
We have established partnerships with multiple contract manufacturing organizations providing geographic redundancy and production flexibility:
Current wording
We have established partnerships with multiple contract manufacturing organizations providing geographic redundancy and production flexibility to support company-sponsored clinical development activities in the United States and selected international jurisdictions. These partnerships, together with relationships with specialized isotope suppliers and radiopharmaceutical logistics providers, support investigational product manufacturing, distribution and clinical supply while providing operational redundancy and continuity of supply as the Company expands its internal manufacturing capabilities:
Previous wording
Our manufacturing and supply chain capabilities position us to serve patient populations at clinical and commercial scale while maintaining the flexib ility to respond to changing demand and expand into new geographic markets.
Current wording
Our manufacturing and supply chain capabilities position us to support ongoing clinical development activities conducted in multiple jurisdictions and future commercial operations while maintaining flexibility to respond to changing demand.
Previous wording
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.
Current wording
As of August 6, 2026, we had 27 full-time employees, 13 of whom have Ph.D. or M.D. degrees and 23 of whom are engaged in research and development and clinical development activities. We believe that we have been successful to date in attracting skilled and experienced personnel despite the competitive hiring environment in the industry. Our employees are not covered by a collective bargaining agreement, and we believe that our relationship with our employees is excellent. We continue to engage external consultants on an as-needed basis to supplement existing staff.
Previous 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.
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 the rest of the world. The $35 million upfront payment was initially recorded as Long-term license revenue - deferred due to uncertainty regarding Immedica’s ability to obtain regulatory approval of the product by the European Medicines Agency. Subsequently, Immedica notified us that it would not pursue regulatory approval of Iomab-B in the licensed territories. In the current period, based on the facts and circumstances, we concluded that Immedica’s right to asserting a claim related to the $35 million had expired. Accordingly, the condition previously constraining recognition of the $35 million upfront payment no longer existed and that the non-refundable payment was no longer subject to a significant reversal. Therefore, we recognized the previously deferred $35 million upfront payment as revenue in June 2026.
Previous wording
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.
Current wording
Research and development expenses, net of reimbursements, of $5.4 million for the three months ended June 30, 2026 increased by $0.5 million from $4.9 million for the three months ended June 30, 2025, primarily due to increased preclinical expenses of $0.3 million, increased Chemistry, manufacturing and controls, or CMC, expenses and clinical expenses of $0.6 million, partially offset by lower compensation expense of $0.4 million due to lower headcount. In the second quarter of 2025, we conducted a workforce optimization that reduced our headcount by approximately fourteen percent and announced a strategic pipeline prioritization which resulted in additional departures in 2025.
Previous wording
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.
Current wording
Other income is comprised of net interest income in both reporting periods. The amount for the three months ended June 30, 2026 of $0.3 million decreased from $0.6 million for the three months ended June 30, 2025 primarily due to a lower average cash balance during the three months ended June 30, 2026 compared to the prior-year period.
Previous wording
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.
Current wording
On March 31, 2025, our Board of Directors approved the cancellation of certain stock options to purchase an aggregate of 4.9 million shares of common stock held by certain current employees and directors that were initially granted under our Amended and Restated 2013 Stock Plan and our 2019 Stock Plan. The cancellation of these stock options resulted in the recording of $8.7 million in non-cash stock compensation expense for the six months ended June 30, 2025, $2.1 million in Research and development expense and $6.6 million in General and administrative expense.
Previous wording
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.
Current wording
General and administrative expense of $3.8 million for the six months ended June 30, 2026 decreased by $7.8 million from $11.6 million for the six months ended June 30, 2025. Lower non-cash stock-based compensation expense of $6.9 million for the six months ended June 30, 2026 compared with the same period in 2025 was primarily driven by the cancellation of stock options in March 2025, discussed above. In addition, in comparison to the prior-year period, compensation expense decreased $0.9 million due to lower headcount.
Previous wording
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.
Current wording
Net cash used in operating activities for the six months ended June 30, 2026 was $11.0 million, a decrease of $2.0 million from $13.0 million in the prior-year period, primarily resulting from lower compensation expense as a result of lower headcount for the six months ended June 30, 2026 compared to the prior-year period.
Previous wording
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.
Current wording
Cash used in investing activities for the six months ended June 30, 2026 was $0.5 million related to the construction of modular removable manufacturing improvements within our leased manufacturing facility. There was no cash used in investing activities for the six months ended June 30, 2025.
Previous wording
Cash used in financing activities for the three months ended March 31, 2026 and March 31, 2025 was $3 thousand and $2 thousand, respectively.
Current wording
Cash used in financing activities for the six months ended June 30, 2026 and June 30, 2025 was $5 thousand and $5 thousand, respectively.
Previous wording
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.
Current wording
In August 2020, we entered into the Capital on Demand™ Sales Agreement with JonesTrading Institutional Services LLC, or JonesTrading, pursuant to which we are able to sell, from time to time, through or to JonesTrading, up to an aggregate of $200 million of our common stock. On June 28, 2022, we entered into an Amended and Restated Capital on Demand™ Sales Agreement, or the A&R Sales Agreement, with JonesTrading and B. Riley Securities, Inc. (“B. Riley”). The A&R Sales Agreement modifies the original Capital on Demand™ Sales Agreement to include B. Riley as an additional sales agent thereunder. Shares of common stock were offered pursuant to a shelf registration statement on Form S-3 (File No. 333-242322) filed with the SEC on August 7, 2020 (the “Prior Shelf Registration Statement”). On August 11, 2023, we filed a registration statement on Form S-3 (File No. 333-273911), which was amended on February 2, 2024, and declared effective on February 5, 2024, to replace the Prior Shelf Registration Statement, including a base prospectus which covers the offering, issuance and sale of up to $500 million of common stock, preferred stock, warrants, units and/or subscription rights; and a sales agreement prospectus covering the offering, issuance and sale of up to a maximum aggregate offering price of $200 million of common stock that may be issued and sold under the A&R Sales Agreement. There was no sale of shares of common stock during the six months ended June 30, 2026 and 2025, respectively.
Rearranged current paragraphs (5)
Current report — wording carried from elsewhere
The following table sets forth, for the periods indicated, data derived from our statements of operations:
Current report — wording carried from elsewhere
We recorded no commercial revenue for the six months ended June 30, 2026 and June 30, 2025, respectively.
Current report — wording carried from elsewhere
Research and development expense, net of reimbursements
Current report — wording carried from elsewhere
Research and development expenses, net of reimbursements, of $9.6 million for the six months ended June 30, 2026 decreased by $3.0 million from $12.6 million for the six months ended June 30, 2025. The cancellation of stock options in March 2025 described above resulted in lower non-cash stock-based compensation expense of $2.1 million for the six months ended June 30, 2026 compared with the six months ended June 30, 2025. In addition, there was lower compensation cost of $0.9 million due to lower headcount.
Current report — wording carried from elsewhere
Other income is comprised of net interest income in both reporting periods. The amount for the six months ended June 30, 2026 of $0.7 million decreased from $1.3 million for the six months ended June 30, 2025 primarily due to a lower average cash balance during the six months ended June 30, 2026 compared to the prior-year period.