Last reviewed by Dr. Dharmender Malikon 13 May 2026 · this article reflects the published evidence and current clinical practice at FMRI Gurugram.
Introduction
Conventional cancer therapy is, in much of its practice, statistical. A drug works for a defined fraction of patients with a defined cancer; we give it to everyone who matches that definition and accept that some will respond and some will not. Radio-theranostics changes this logic. It begins with a diagnostic scan — using a small radioactive tracer molecule that binds to a specific receptor or marker on cancer cells. If the scan lights up, the same molecule (loaded with a therapeutic radioisotope) is delivered as treatment. If the scan does not light up, the patient is not put through a therapy that has no biological basis to work.
This is not a marketing claim. It is the operational reality of how Lu-PSMA therapy is delivered for prostate cancer, how Lu-DOTATATE is delivered for neuroendocrine tumours, and how the broader field of radio-theranostics is now expanding into kidney cancer, lung cancer, breast cancer, and beyond. This guide walks through what theranostics is, how it works, which cancers are now treated this way, and where the field is going.
The core idea: target, image, treat
Every theranostic therapy is built on the same three-step logic. First, identify a molecular target that is highly expressed on cancer cells but largely absent (or much less expressed) on normal cells. Second, design a small molecule — a peptide, an antibody fragment, or a small inhibitor — that binds tightly to that target. Third, attach two different radioisotopes to the same molecule: a "diagnostic" isotope (typically Gallium-68 or Fluorine-18) for PET imaging, and a "therapeutic" isotope (typically Lutetium-177 for beta therapy or Actinium-225 for alpha therapy) for treatment delivery.
The diagnostic version is injected, the patient is scanned, and the cancer's target expression is mapped in three dimensions across the entire body. If the target is present in adequate intensity, the therapeutic version of the same molecule is given — and it goes to exactly the same places the diagnostic version lit up. The same biology that produced the scan is what produces the treatment effect.
Lu-PSMA for prostate cancer: the breakthrough example
Prostate-specific membrane antigen (PSMA) is a protein expressed at very high levels on prostate cancer cells and at much lower levels on most normal tissues. A Ga-68 PSMA PET-CT can detect prostate cancer with sensitivity and specificity that far exceeds older imaging methods. The same PSMA-binding molecule, loaded with Lu-177, is the active ingredient of Pluvicto — the first FDA-approved radioligand therapy for metastatic castration-resistant prostate cancer.
The VISION trial demonstrated that Lu-177 PSMA, given in addition to standard care, extended median overall survival from 11.3 months to 15.3 months in patients who had progressed on prior treatment. The biology is elegant: the scan tells you who will respond, and the therapy treats them. Patients whose PSMA PET-CT does not show adequate uptake are not offered the therapy — because there is no biological reason to expect it to work.
Lu-DOTATATE for neuroendocrine tumours
Neuroendocrine tumour (NET) cells over-express somatostatin receptors (especially SSTR2). A Ga-68 DOTATATE PET-CT lights up these tumours in three dimensions. The same DOTATATE molecule, loaded with Lu-177, is the active ingredient of Lutathera — the first radioligand therapy formally approved by the FDA for NETs.
The NETTER-1 trial demonstrated that Lu-177 DOTATATE more than doubled progression-free survival compared with high-dose octreotide alone in patients with progressive mid-gut NETs. As with prostate cancer, the eligibility logic is biological: the DOTATATE PET-CT must show adequate uptake (typically Krenning score 3 or 4) before therapy is offered. Real-world experience over the past decade has extended Lutathera to pancreatic NETs, foregut NETs, and many other receptor-positive presentations.
Y-90 microspheres: a different theranostic logic
Yttrium-90 radioembolization (TARE) uses a different version of theranostic logic. The "diagnostic" step is a Tc-99m MAA scan that maps the arterial delivery of microspheres to the liver tumour and detects any shunting to the lungs or gastrointestinal tract. This pre-treatment scan determines the dose, the delivery technique, and whether the procedure should proceed at all. The "therapy" step is the delivery of Y-90-loaded microspheres along the same pathway.
Unlike Lu-PSMA and Lu-DOTATATE, Y-90 TARE is not receptor-targeted at the molecular level — its specificity comes from arterial anatomy rather than receptor binding. But the logic is the same: the diagnostic step determines whether and how to treat. This is the foundation of modern dosimetry-guided TARE.
Alpha therapy and the next generation
Lu-177 is a beta emitter — its radiation travels a few millimetres in tissue, with a useful "crossfire" effect that treats neighbouring cells. Actinium-225 is an alpha emitter, with much shorter range (40 to 100 micrometres) but much higher energy deposition per cell crossed. Ac-225 PSMA and Ac-225 DOTATATE are now being used in patients whose tumours have progressed on Lu-177 therapy, with response rates of around 50 percent reported in case series. These are not first-line therapies — they are salvage options, delivered under the Helsinki Declaration framework with written informed consent — but they represent a meaningful next step.
Terbium-161 is an investigational beta emitter with additional Auger electron emission that may produce more cellular damage at very short range. Early clinical experience is encouraging, but Tb-161 has not been shown in head-to-head trials to outperform Lu-177, and its use remains within research protocols.
Where theranostics fits in cancer care
Radio-theranostics is not a replacement for surgery, chemotherapy, or external-beam radiotherapy — it is an addition. For most cancers where it is used, it sits in the third- or fourth-line setting, after standard therapies have stopped working. Its strength is the combination of precision (delivered by the molecular targeting) and potency (delivered by the radioisotope), and its limitation is that it only works for cancers that express a suitable target.
The list of cancers being explored is expanding: FAP-targeting tracers for many solid tumours, GRPR-targeting agents for prostate and breast cancer, MIBG for paediatric neuroblastoma and adrenal tumours, kidney-cancer-specific tracers in early trials. The field is moving from individual approvals toward a broader principle: where a target exists, a theranostic pair can be developed.
For patients and referring physicians, the practical message is simple: theranostics is now a real part of cancer care, not a future possibility. If standard therapy has stopped working and the cancer expresses a suitable molecular target, theranostic options are worth exploring through a specialist nuclear medicine centre.
For patients & referring clinicians
Frequently asked questions
Q01
What is radio-theranostics?
Radio-theranostics is a class of cancer therapy in which a single targeting molecule is used both to image the cancer (with a diagnostic radioisotope, typically Ga-68 or F-18) and to treat it (with a therapeutic radioisotope, typically Lu-177 or Ac-225). The scan determines whether the patient will respond, and only patients whose scans show the target are offered the therapy.
Q02
How is theranostics different from chemotherapy?
Chemotherapy is generally given to all patients with a given cancer diagnosis, and individual response is unpredictable. Theranostic therapy is given only to patients whose diagnostic scan shows adequate target expression on the cancer cells — so the eligibility step is biological, not statistical. Theranostic therapy also delivers radiation rather than cytotoxic drugs, so the side-effect profile is different.
Q03
Is theranostics FDA approved?
Yes, for specific indications. Lu-177 PSMA (Pluvicto) is FDA-approved for metastatic castration-resistant prostate cancer after prior taxane chemotherapy. Lu-177 DOTATATE (Lutathera) is FDA-approved for gastroenteropancreatic neuroendocrine tumours. Yttrium-90 microspheres are FDA-cleared for liver tumours. Other theranostic agents (Ac-225 PSMA, Tb-161) are used in research and compassionate-use settings; they are not yet first-line FDA-approved therapies.
Q04
Which cancers can be treated with theranostics?
The strongest evidence is for metastatic castration-resistant prostate cancer (Lu-PSMA), neuroendocrine tumours (Lu-DOTATATE), and hepatocellular carcinoma and liver metastases (Y-90 microspheres). Paediatric neuroblastoma is treated with I-131 MIBG, an earlier theranostic agent. Emerging applications include kidney cancer, breast cancer, and certain head-and-neck cancers, with several trials currently in progress.
Q05
Where can I get theranostic therapy?
Theranostic therapy is delivered in specialised nuclear medicine departments that have the radiopharmacy infrastructure, isotope supply chain, dosimetry capability, and clinical experience. At FMRI Gurugram, we operate a dedicated nuclear oncology clinic that delivers Lu-PSMA, Lu-DOTATATE, Ac-225 PSMA, Y-90 TARE, and I-131 MIBG. Patients from across India and from international medical-travel routes are routinely treated. Eligibility starts with a diagnostic theranostic scan.
Q06
What does theranostic therapy cost?
Indicative pricing at FMRI Gurugram for a complete course: Lu-PSMA therapy approximately INR 12 to 18 lakh, Lu-DOTATATE therapy approximately INR 12 to 18 lakh, Y-90 TARE approximately INR 9 to 14 lakh per procedure, Ac-225 PSMA approximately INR 18 to 28 lakh. These compare favourably to US list pricing — Pluvicto alone is approximately USD 240,000 for a course in the United States. Final pricing is confirmed after the diagnostic scan and clinical evaluation.
Q07
What are the side effects of theranostic therapy?
The side effects depend on the specific therapy. Common to all radioligand therapies are fatigue, mild nausea, and transient reductions in blood counts. Lu-PSMA can cause dry mouth and dry eyes (because PSMA is also expressed at low levels in salivary and lacrimal glands). Lu-DOTATATE can cause mild abdominal symptoms during infusion. Y-90 TARE can cause post-treatment fatigue lasting a few weeks. Severe side effects are uncommon when patient selection and dosimetry are done carefully.
Citations & references
Sartor O, de Bono J, Chi KN, et al. Lutetium-177–PSMA-617 for Metastatic Castration-Resistant Prostate Cancer (VISION).
N Engl J Med. 2021;385(12):1091-1103.
ReferenceStrosberg J, El-Haddad G, Wolin E, et al. Phase 3 Trial of
177Lu-Dotatate for Midgut Neuroendocrine Tumors (NETTER-1).
N Engl J Med. 2017;376(2):125-135.
Reference
About the Author
Dr. Ishita B. Sen
MBBS · MD (Nuclear Medicine) · DNB · Post-doctoral Fellowship, Memorial Sloan Kettering Cancer Center, New York
Director and Chief of Nuclear Medicine at Fortis Memorial Research Institute. Co-founder of Theranostic Physicians Private Limited (TPPL). Two decades of clinical practice in PSMA imaging and PSMA-directed radioligand therapy, with one of the largest Indian institutional experiences in Lu-PSMA.