— 01 · At a Glance
What is mIBG therapy?
★ In one paragraph
I-131 mIBG is a targeted radionuclide therapy using iodine-131 bound to metaiodobenzylguanidine — a synthetic analog of the hormone noradrenaline. The molecule is taken up via the norepinephrine transporter expressed on chromaffin cells, sympathetic neurons, and certain neuroendocrine tumours. Once inside the cell, the I-131 emits beta radiation that destroys the tumour from within.
mIBG therapy has been used clinically for over four decades and is the established standard of care for malignant pheochromocytoma, paraganglioma, refractory neuroblastoma, and selected metastatic carcinoid tumours. Unlike emerging theranostics, mIBG is regulator-approved internationally and reimbursed by major Indian insurers.
The therapy is administered as a single intravenous infusion in a shielded inpatient isolation suite. Patients typically stay 3 to 5 days for radiation safety reasons before discharge. Standard adult protocol is 200 mCi (7.4 GBq) per cycle, repeated 2 to 4 times at 3 to 6 month intervals depending on response.
— 02 · Mechanism
How mIBG works.
The norepinephrine transporter (NET) is a cell surface protein that normally takes up noradrenaline from the bloodstream into sympathetic neurons and chromaffin cells. Tumours arising from these cells — pheochromocytoma, paraganglioma, neuroblastoma — retain NET expression, which makes them targetable. The therapy exploits this biology in three steps:
- Recognition. mIBG is a structural analog of noradrenaline. The norepinephrine transporter cannot distinguish it from the natural hormone and pulls it into the cell.
- Internalisation and storage. Once inside, mIBG is stored in chromaffin granules and remains within the cell for days — far longer than free circulation.
- Beta emission. The bound I-131 emits beta particles (range ~2 mm) and gamma photons. Beta radiation causes DNA double-strand breaks and apoptosis in the tumour cell and its immediate neighbours via crossfire.
Because NET is also expressed on the thyroid gland (which takes up iodine directly), patients receive potassium iodide (SSKI) for thyroid blockade starting 24 hours before therapy and continuing for 7 to 10 days afterwards. This prevents radiation damage to the thyroid.
★ The blood pressure conversation
For patients with active pheochromocytoma, mIBG release of stored catecholamines during infusion can trigger a hypertensive crisis. This is uncommon at modern dose rates and with proper pre-medication, but it is the reason mIBG infusion is given slowly (1 to 4 hours), with continuous blood pressure monitoring, and after adequate alpha-adrenergic blockade where indicated. Our protocol includes mandatory pre-medication review with the referring endocrinologist.
131I
mIBG MECHANISM
[Image: Mechanism diagram — mIBG (noradrenaline analog) entering chromaffin cell through norepinephrine transporter, accumulating in granules, with I-131 emitting beta radiation causing DNA damage. Show 2 mm crossfire radius.]
— 03 · Indications
The three indications we treat.
mIBG therapy is established standard of care across three principal indication groups. Within each, eligibility is confirmed by a diagnostic mIBG scan showing strong tracer uptake in the patient's specific disease.
Malignant pheochromocytoma
Adult · primary indication
For patients with metastatic or unresectable pheochromocytoma where surgery is not curative. Approximately 10% of pheochromocytomas are malignant (defined by metastasis, not histology alone). mIBG therapy is offered after surgical options are exhausted, with combined surgical-radionuclide planning when partial debulking is feasible.
Malignant paraganglioma
Adult · primary indication
For metastatic or unresectable paraganglioma. Roughly 15–35% of paragangliomas are malignant, with higher rates in SDHB-mutated disease. mIBG is the leading radionuclide option; for SSTR-positive paragangliomas, PRRT is an alternative. Many patients receive both lines sequentially over the disease course.
Refractory neuroblastoma
Paediatric · high-risk relapse
For relapsed or refractory high-risk neuroblastoma. High-dose protocols use 12 to 18 mCi per kilogram body weight, often combined with autologous stem cell rescue for marrow protection. Reported response rates in refractory disease are 30 to 40 percent. We administer paediatric mIBG in collaboration with the referring paediatric oncology team.
Additional indications occasionally treated: metastatic carcinoid tumour with documented mIBG-PET avidity and progression on standard somatostatin analog therapy, and medullary thyroid carcinoma in highly selected cases. Each is individually reviewed.
— 04 · Eligibility
Who is a candidate?
mIBG therapy is offered to patients meeting the following criteria, confirmed at our consultation:
- Histologically confirmed pheochromocytoma, paraganglioma, neuroblastoma, or another mIBG-responsive neuroendocrine tumour.
- Unresectable or metastatic disease — surgical resection either contraindicated, has failed, or would leave gross residual disease.
- Strong mIBG uptake on a diagnostic I-123 or I-131 mIBG scan, with uptake visibly greater than normal adrenal medullary background. Patients with weak or absent mIBG-scan uptake are unlikely to respond and we counsel against offering therapy.
- Adequate organ function: creatinine clearance >40 mL/min, haemoglobin >9 g/dL, platelets >100 × 10⁹/L, AST/ALT <3× upper limit.
- Blood pressure controlled on alpha-adrenergic blockade if patient has functional pheochromocytoma or paraganglioma producing catecholamines.
- Life expectancy >6 months and ECOG performance status 0–2 (adults), or appropriate paediatric assessment.
— 05 · Protocol
The treatment cycle.
Each mIBG cycle is administered as an inpatient procedure with strict radiation safety protocols. The standard adult cycle:
01
Pre-treatment · week before
Diagnostic mIBG scan (mandatory). Baseline bloods, renal function, thyroid function. Alpha-adrenergic blockade review with referring endocrinologist. Discontinuation of medications that interfere with mIBG uptake (tricyclic antidepressants, sympathomimetics, labetalol).
02
Thyroid blockade · 24 hours prior
Potassium iodide (SSKI) 130 mg daily started 24 hours before infusion, continued for 7–10 days post-therapy. Prevents I-131 uptake by the thyroid gland.
03
Day of therapy · isolation admit
Admission to shielded isolation suite. Slow IV infusion of 200 mCi (7.4 GBq) I-131 mIBG over 1 to 4 hours with continuous BP and cardiac monitoring. Hydration. Antiemetics.
04
Isolation stay · 3–5 days
Patient remains in shielded suite until radiation dose rate falls below regulatory threshold (typically 30 μSv/h at 1 m). Daily dose measurements. Family contact via intercom and glass window. Post-therapy whole-body scan day 3–5.
Cycle repeated 2 to 4 times at 3 to 6 month intervals, with response assessment between cycles. Interim assessment includes catecholamine biochemistry (urinary fractionated metanephrines, plasma free metanephrines), repeat mIBG scan, and structural imaging.
— 06 · Evidence
What the data shows.
mIBG therapy has four decades of clinical evidence. The pivotal Pryma et al.1 phase 2 trial (which led to FDA approval of high-specific-activity I-131 mIBG, brand name Azedra, in 2018) and earlier cohort series form the evidence base.
50–80%
Symptomatic response in malignant pheo/para
30–50%
Biochemical response (catecholamine fall)
30–40%
Objective response in refractory neuroblastoma
The Azedra (Pryma) trial
The pivotal Pryma trial1, published in JNM in 2019, enrolled 68 adults with advanced pheochromocytoma or paraganglioma who received high-specific-activity I-131 mIBG. The primary endpoint — at least 50 percent reduction in antihypertensive medication for at least 6 months — was achieved by 25 percent of patients. Tumour responses by RECIST were seen in 22 percent, with disease control (response or stable disease) in 92 percent at primary endpoint assessment.
Real-world Indian cohorts
Indian centres have reported mIBG therapy outcomes broadly consistent with international data, including from AIIMS Delhi and major theranostic centres. Symptomatic response is typically the most clinically meaningful outcome — patients with debilitating catecholamine excess often experience marked quality-of-life improvement well before structural tumour response is measurable.
— 07 · FMRI Capability
The shielded suite — why this matters.
High-dose I-131 mIBG therapy requires specialised infrastructure: a lead-shielded patient room, dedicated radiation-safe waste management, trained nursing staff, and continuous dose-rate monitoring. Only a handful of Indian hospitals have all three. Many centres that offer "mIBG therapy" can only administer low-dose protocols (under 100 mCi) on outpatient basis, which limits efficacy.
FMRI Sector 44 capability
Dedicated shielded inpatient suite.
FMRI's Department of Nuclear Medicine has a dedicated lead-shielded isolation room commissioned specifically for high-dose radioiodine therapy and high-dose mIBG. Compliant with AERB (Atomic Energy Regulatory Board, India) standards. Trained nursing staff. Continuous dose-rate monitoring. Designed to accept full-protocol 200 mCi mIBG therapy — the dose level associated with maximum response in published trials.
— 08 · Tolerability
Side effects.
Common (>20% of patients)
- Nausea and vomiting — during and shortly after infusion; pre-medication with anti-emetics.
- Fatigue — moderate, typically 1–2 weeks post-therapy.
- Transient cytopenia — haemoglobin, platelet and lymphocyte reductions; nadir at 4–6 weeks, recovery by 12 weeks.
- Sialadenitis — salivary gland inflammation from circulating I-131; usually mild.
Uncommon (1–20%)
- Thyroid dysfunction — if blockade incomplete; long-term hypothyroidism monitored.
- Bone marrow suppression — dose-limiting in heavily pre-treated patients.
- Mild hepatic enzyme elevation — transient.
Rare but serious
- Hypertensive crisis — during infusion in pheochromocytoma; mitigated by slow infusion, BP monitoring, and adequate alpha-blockade.
- Severe myelosuppression — requires growth factor support; rare with appropriate dosimetry.
- Secondary malignancy (myelodysplastic syndrome / acute leukaemia) — very rare; reported with cumulative doses.
— 09 · Pricing
Cost in India.
Indicative cycle pricing. Figures cover the radiopharmaceutical, isolation room, and standard monitoring. Diagnostic mIBG scan, additional imaging, and concomitant medication are billed separately.
| Variant |
Per cycle |
2–4 cycle course |
I-131 mIBG (adult, Indian) |
~ ₹ 3,50,000–5,00,000
~ USD 3,889–5,556 |
~ ₹ 7–20 L
~ USD 7,778–22,224 |
I-131 mIBG (adult, international) |
~ ₹ 5,40,000–7,20,000
~ USD 6,000–8,000 |
~ ₹ 10.8–28.8 L
~ USD 12,000–32,000 |
I-131 mIBG (paediatric, weight-based) |
On request
case-by-case |
Individualised
by body weight |
Diagnostic mIBG scan (123I or 131I) |
~ ₹ 18,000–25,000
~ USD 200–278 |
Single scan
before therapy |
★ Please read
Figures are indicative ranges, not quotes, presented at 1 USD = ₹ 90. They cover therapy fees only. A formal written quote is issued after pre-treatment evaluation including the diagnostic mIBG scan.
Several major Indian insurers cover mIBG therapy for the approved indications. Our coordinators help patients prepare the clinical documentation insurers require — WhatsApp us for a pre-authorisation pack.
— 10 · Availability
Next available mIBG slots.
mIBG therapy at our centre is scheduled monthly (or fortnightly when demand is high), governed by isolation suite availability. Reservations require 7 days advance notice for radiopharmaceutical procurement and pre-medication coordination.
mIBG calendar — next slots.
Frequently asked questions.
mIBG therapy is a targeted radionuclide treatment using iodine-131 bound to metaiodobenzylguanidine (mIBG), a synthetic analog of the hormone noradrenaline. The molecule is taken up via the norepinephrine transporter (NET) expressed on chromaffin cells, sympathetic neurons, and neuroendocrine tumours.
Once inside the cell, the I-131 emits beta radiation that destroys the tumour. Administered as a 1 to 4 hour IV infusion. Approved for malignant pheochromocytoma, paraganglioma, neuroblastoma, and refractory carcinoid.
For localised pheochromocytoma, surgical resection after careful alpha-adrenergic blockade is the standard first-line treatment.
For malignant or metastatic pheochromocytoma that cannot be removed, treatment options include I-131 mIBG therapy (the leading radionuclide option), targeted therapies such as sunitinib, somatostatin-receptor-targeted PRRT for SSTR-positive disease, and chemotherapy regimens such as cyclophosphamide-vincristine-dacarbazine.
For preoperative blood pressure control, alpha-adrenergic blockers are the drugs of choice — phenoxybenzamine is the classical agent, with doxazosin used commonly today.
For malignant pheochromocytoma, the leading radionuclide therapeutic is iobenguane I-131 (high-specific-activity I-131 mIBG, branded as Azedra in the US). Indian centres use both high-specific-activity and conventional I-131 mIBG.
The classic triad is paroxysmal headache, sweating (diaphoresis) and tachycardia (palpitations) — typically occurring in episodes with elevated blood pressure.
The triad is present in only a minority of patients; many pheochromocytomas present with sustained hypertension, anxiety attacks, or are detected incidentally on imaging. Diagnosis requires plasma free metanephrines or 24-hour urinary fractionated metanephrines.
Yes. While most paragangliomas are benign tumours, approximately 15 to 35 percent are malignant — defined by the presence of metastasis (not by histology alone). Malignant paragangliomas have a higher incidence in certain genetic syndromes including SDHB mutations.
Malignant paraganglioma is precisely the indication for which I-131 mIBG therapy is most commonly used, when surgery cannot remove all disease.
Localised paraganglioma is curable with complete surgical resection. Metastatic or malignant paraganglioma is typically not curable but is highly treatable — patients can live with their disease for many years with combination therapy including surgery, I-131 mIBG, PRRT (for SSTR-positive cases), targeted agents and chemotherapy.
Five-year survival in metastatic disease is approximately 50 to 80 percent depending on disease pattern and treatment response.
No. The infusion itself is not painful — it is administered through a standard IV line over 1 to 4 hours, similar to many chemotherapy infusions. Patients are awake, comfortable, and remain conscious throughout. Some experience mild nausea or warmth during infusion, both manageable.
The treatment requires hospital isolation for 3 to 5 days afterward for radiation safety reasons, not because of pain or illness.
At Theranostic Physicians, I-131 mIBG therapy is priced individually based on dose (typically 200 mCi / 7.4 GBq for high-dose adult protocols), inpatient isolation duration and patient age.
Indicative range: ₹ 3,50,000 to ₹ 5,00,000 per cycle for Indian patients; USD 6,000 to USD 8,000 for international patients. Pricing covers the radiopharmaceutical, isolation room, and standard monitoring. mIBG scan and concomitant medication billed separately.
For paediatric neuroblastoma, I-131 mIBG therapy is used in refractory or relapsed high-risk disease. Standard high-dose protocols administer 12 to 18 mCi per kilogram body weight per cycle, often combined with autologous stem cell rescue.
Reported response rates in refractory neuroblastoma are 30 to 40 percent in published cohorts. We administer paediatric mIBG therapy at FMRI in collaboration with paediatric oncology and the radiation safety team.
Most adult patients are admitted for 3 to 5 days in a shielded isolation suite. Discharge depends on the radiation dose rate falling below regulatory thresholds (typically 30 microSieverts per hour at 1 metre).
Some patients with rapid renal clearance may be discharged at 48 hours; others with slower clearance may stay up to 7 days. Family contact is restricted but visible glass viewing and intercom communication are available throughout the stay.
IS
[Image: Dr. Sen portrait]
Written & Medically Reviewed By
Dr. Ishita B. Sen
MBBS · DRM · DNB (Nuclear Medicine) · 30+ years in nuclear oncology
Director and Head, Department of Nuclear Medicine and Molecular Imaging, Fortis Memorial Research Institute. Visiting fellowships at Memorial Sloan Kettering Cancer Center, New York and University of Marburg, Germany. Past President, Association of Nuclear Medicine Physicians of India. Active interest in high-dose radioiodine and mIBG therapy programmes for adults and children.
FellowshipsMSK New York · Marburg
Past PresidentANMPI
SpecialityRadioiodine & mIBG therapy
Full profile
References & citations
- Pryma DA, Chin BB, Noto RB, et al. Efficacy and Safety of High-Specific-Activity 131I-MIBG Therapy in Patients with Advanced Pheochromocytoma or Paraganglioma. Journal of Nuclear Medicine, 2019;60(5):623–630. DOI: 10.2967/jnumed.118.217463 — the Azedra approval trial.
- Loh KC, Fitzgerald PA, Matthay KK, et al. The treatment of malignant pheochromocytoma with iodine-131 metaiodobenzylguanidine (131I-MIBG): a comprehensive review of 116 reported patients. Journal of Endocrinological Investigation, 1997;20(11):648–58.
- Matthay KK, Yanik G, Messina J, et al. Phase II study on the effect of disease sites, age, and prior therapy on response to iodine-131-metaiodobenzylguanidine therapy in refractory neuroblastoma. Journal of Clinical Oncology, 2007;25(9):1054–60.
- Carrasquillo JA, Pandit-Taskar N, Chen CC. 131I-Metaiodobenzylguanidine Therapy of Pheochromocytoma and Paraganglioma. Seminars in Nuclear Medicine, 2016;46(3):203–214.
- Wakabayashi H, Inaki A, Yoshimura K, et al. A phase I clinical trial for [131I]meta-iodobenzylguanidine therapy in patients with refractory pheochromocytoma and paraganglioma. Scientific Reports, 2019;9(1):7625.
- EANM / SNMMI Practice Guidelines for 131I-meta-iodobenzylguanidine (mIBG) therapy. European Journal of Nuclear Medicine and Molecular Imaging, 2018;45(12):2436–2457.