Full-Life Technologies has received United States Food and Drug Administration clearance for its Investigational New Drug application for [225Ac]Ac-FL-261, allowing the privately held radiopharmaceutical company to begin a first-in-human Phase 1 study in patients with c-MET-expressing non-squamous non-small cell lung cancer. The program has also received Australian Human Research Ethics Committee approval and completed the country’s Clinical Trial Notification process, enabling development across both the United States and Australia.
FL-261 combines a molecule designed to recognize the c-MET protein with actinium-225, a highly energetic alpha-emitting radionuclide intended to deliver short-range radiation directly to targeted tumor cells. The planned Phase 1 study will primarily examine safety and tolerability while also evaluating pharmacokinetics and preliminary antitumor activity.
IND clearance is permission to conduct clinical research, not validation that FL-261 selectively delivers a therapeutically useful radiation dose in humans or that it can shrink lung tumors. The program has so far been supported largely by preclinical data, making the upcoming study the first opportunity to determine whether its targeting, biodistribution and dosimetry behave as expected in patients.
The program is nevertheless strategically important because c-MET could broaden targeted alpha therapy into tumor types beyond the prostate cancer and neuroendocrine settings that have dominated much of the radiopharmaceutical industry’s commercial attention.
Why is c-MET an attractive but complicated target for radiopharmaceutical therapy?
c-MET is a receptor tyrosine kinase activated by hepatocyte growth factor and involved in cell proliferation, survival, motility and tissue repair. Abnormal activation of the pathway can contribute to tumor growth, invasion and treatment resistance, making c-MET an established target in oncology drug development.
Certain non-small cell lung cancers contain MET exon 14 skipping mutations or MET amplification and can be treated with small-molecule inhibitors targeting the pathway. FL-261 is conceptually different because it does not need to inhibit the intracellular signaling machinery in the same manner. Its targeting molecule is intended to recognize c-MET expressed on tumor cells and use that protein as an address for radioactive payload delivery.
That potentially broadens the relevant biology from particular genomic alterations to c-MET protein expression, depending on the final patient-selection strategy. A tumor does not necessarily need to be driven exclusively by MET signaling for a radioligand to use the receptor as a docking point, provided expression is sufficiently strong and accessible.
The complication is that c-MET is not restricted entirely to malignant tissue. Normal epithelial and other tissues can express the receptor, creating the possibility of radiation exposure outside the tumor if the conjugate binds or persists where it should not.
Target density, internalization, circulation time and clearance therefore become critical. A useful radiopharmaceutical needs to accumulate enough radioactivity in tumors to generate a therapeutic effect while clearing rapidly from normal tissues to limit toxicity.
Why does actinium-225 generate so much interest in targeted cancer therapy?
Actinium-225 undergoes radioactive decay that releases alpha particles. These particles carry substantially greater energy over a much shorter path length than beta radiation, allowing them to produce dense DNA damage within a relatively small radius.
That physical profile is attractive for cancer because a targeting ligand can theoretically transport the radionuclide to malignant cells and deliver lethal radiation while limiting exposure to surrounding tissue. Alpha particles may also be effective against small clusters of cancer cells and microscopic metastases if sufficient target binding occurs.
The same potency creates risk. Radiation delivered to normal organs can be damaging, and some daughter isotopes generated during actinium decay may redistribute away from the original targeting molecule. Kidney, bone marrow, salivary gland and other toxicities can become relevant depending on the pharmacology of a particular radioconjugate.
Phase 1 development therefore requires detailed dosimetry rather than simply escalating a conventional milligram dose. Investigators need to understand where radioactivity travels, how long it remains in different organs and how absorbed radiation dose changes with increasing activity.
The therapeutic window may vary from patient to patient because target expression, tumor burden, renal function and prior therapies can affect biodistribution. Individual imaging could eventually become important in selecting patients and planning treatment.
How could FL-261 become a theranostic platform rather than only one therapeutic drug?
Full-Life Technologies describes FL-261 as a c-MET-targeted theranostic program. Theranostics pair diagnostic molecular imaging with a therapeutic agent directed against the same biological target, allowing physicians to visualize target expression before committing a patient to radioactive therapy.
That concept has become one of the most powerful features of modern radiopharmaceutical oncology. Instead of relying only on archived tumor tissue or a biopsy from one location, whole-body imaging can potentially show whether target expression exists across multiple tumors and metastatic sites.
For c-MET, an imaging companion could help answer whether a patient has sufficient accessible target to justify alpha therapy. It could also reveal heterogeneity, where some lesions express c-MET strongly while others do not.
Imaging may additionally assist dose planning and early pharmacology studies. Understanding whole-body distribution before or alongside therapeutic dosing can help investigators estimate which organs receive radiation and identify unexpected off-target uptake.
The eventual regulatory pathway could become more complicated if Full-Life develops separate diagnostic and therapeutic products. Manufacturing, radioactive isotope selection, imaging validation and treatment claims each require appropriate evidence.
Yet the commercial logic is compelling. A successful imaging agent can function as a patient-selection tool, while the therapeutic version captures the treatment value in those selected patients.
Why is non-squamous non-small cell lung cancer an important first test for FL-261?
Non-small cell lung cancer is one of the world’s largest oncology markets and includes several molecularly defined subgroups. Targeted medicines against EGFR, ALK, ROS1, RET, MET and other alterations have transformed treatment for selected patients, but resistance and disease progression remain common.
c-MET has particular relevance because it can function both as a primary oncogenic driver and as a resistance mechanism after other targeted therapies. That provides several possible development paths if a c-MET-directed radiopharmaceutical demonstrates convincing tumor targeting.
Full-Life’s first study is not intended to establish a place within those treatment algorithms. Phase 1 will initially determine whether patients with c-MET-expressing tumors can receive FL-261 safely and whether radiation reaches the intended lesions at biologically useful levels.
Early antitumor responses could provide important proof of concept, particularly if observed across several prior treatment backgrounds. Small uncontrolled dose-escalation cohorts, however, cannot establish that the therapy is superior to existing targeted drugs, antibody-drug conjugates or chemotherapy.
The company may eventually need to define c-MET positivity more precisely. Protein-expression thresholds, genomic alterations or imaging uptake could each become part of patient selection, and the optimal biomarker may differ from those used for conventional MET inhibitors.
Could isotope supply become as important as clinical efficacy for Full-Life Technologies?
Radiopharmaceutical manufacturing creates logistical challenges not encountered with most conventional pharmaceuticals because the active isotope is continuously decaying. Manufacturing, quality testing, transport and clinical administration therefore operate within tight time windows.
Actinium-225 adds another constraint because global supply remains limited relative to the volume that would be required if multiple targeted alpha therapies reach large oncology populations. Developers have consequently been investing in supply agreements, isotope-production technology and dedicated manufacturing facilities.
Full-Life Technologies signed an actinium-225 supply agreement with Eckert & Ziegler and is simultaneously building its own capabilities. The company raised approximately $150 million in equity and debt financing in May 2026, with part of the proceeds intended to support GMP-grade actinium-225 manufacturing at its facility in Belgium.
Vertical integration could become a significant competitive advantage if the clinical pipeline works. A company capable of controlling isotope supply, radiolabeling, drug manufacturing and logistics may be less vulnerable to shortages and better positioned to supply multinational clinical trials.
The opposite is also true. Building isotope infrastructure consumes substantial capital before commercial demand is proven, and manufacturing radioactive medicines requires highly specialized quality systems and regulatory oversight.
Full-Life is therefore making an infrastructure bet alongside a drug-development bet. The return on that investment depends on several pipeline assets succeeding rather than FL-261 alone.
How does FL-261 fit into Full-Life Technologies’ wider radiopharmaceutical portfolio?
FL-261 emerged from Full-Life’s UniRDC discovery platform, which is intended to combine targeting vectors with therapeutic radionuclides while optimizing tumor uptake and systemic clearance. The company is using the same platform to build radiopharmaceuticals against several oncology targets.
Its most advanced program, [225Ac]Ac-FL-020, targets prostate-specific membrane antigen and is already in Phase 1 development for metastatic castration-resistant prostate cancer. The FDA has granted Fast Track designation to that program.
Full-Life expects to have multiple differentiated clinical-stage assets and has been presenting translational and clinical data across major oncology and nuclear-medicine meetings. This gives the company an opportunity to learn about actinium manufacturing, dosimetry and patient management through more than one candidate.
That platform approach matters because radiopharmaceutical development has significant fixed infrastructure requirements. Manufacturing facilities, isotope logistics, radiation safety systems and specialized clinical operations become economically more attractive when they support several drugs.
FL-261 may consequently serve as a test of whether Full-Life can translate its expertise beyond a validated radiopharmaceutical target such as PSMA into a less established one such as c-MET.
If it succeeds, the company could pursue other c-MET-expressing solid tumors rather than limiting development to lung cancer. That expansion would require separate clinical evidence and should not be assumed from preclinical activity.
What should investors and oncology researchers look for in the first FL-261 human data?
The first question is biodistribution. Investigators need to show that FL-261 reaches c-MET-expressing tumors with sufficient selectivity and does not produce excessive retention in normal organs.
The second is dosimetry. Knowing where the radioconjugate travels is not enough; researchers need to estimate the absorbed radiation dose in tumors and dose-limiting organs to identify a practical therapeutic range.
Safety will determine whether escalation can continue. Bone-marrow suppression, renal effects and other organ-specific toxicities will be particularly important, along with adverse events associated with the targeting component itself.
Preliminary tumor responses will attract attention but should be interpreted according to dose and patient selection. A response in one heavily pretreated patient can confirm biological plausibility without establishing a reliable response rate.
The clearest early validation would combine favorable tumor uptake, manageable normal-organ dosimetry, predictable pharmacokinetics and objective antitumor activity that increases or becomes more consistent at biologically active doses.
Full-Life Technologies has now removed the regulatory barrier preventing that experiment from beginning in the United States and Australia. FL-261 therefore moves from an attractive c-MET and actinium-225 hypothesis into the stage where radiopharmaceutical programs are actually differentiated: not by how powerful alpha particles are in theory, but by whether the targeting chemistry can place enough radiation in human tumors while keeping it away from healthy tissue.
