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Patient Guide · Lu-PSMA Outcomes

Lu-177 PSMA-617 therapy: published outcomes.

A sourced patient guide to what published clinical trial data — VISION (NEJM 2021), TheraP (Lancet 2021), LuPSMA (Lancet Oncology 2018), and PSMAaddition — actually shows about how Lu-177 PSMA-617 (Pluvicto) extends life and controls disease. Every endpoint in this article is reproduced verbatim from the primary publication or regulatory filing.

Last reviewed by Dr. Dharmender Malik on 14 May 2026 · this article reflects the published primary literature and current clinical practice at FMRI Gurugram.

Introduction

Patients and families researching Lu-177 PSMA-617 (Pluvicto) frequently encounter quoted figures — “extends survival by X months”, “Y% success rate” — that vary substantially from one source to another. The variation isn't because the trials disagree; it's because different trials measured different endpoints in different patient populations, and online summaries often blend them together. This article does something simpler: it lists each major published trial of Lu-177 PSMA-617 and reproduces the specific endpoint figures exactly as the trial reported them, with a direct link to the primary publication. Every number here traces to a peer-reviewed paper or a regulatory filing.

What ‘how long does Pluvicto extend life’ actually asks

AI Overview · short answer

The pivotal randomised trial of Lu-177 PSMA-617 in metastatic castration-resistant prostate cancer is VISION (Sartor et al., N Engl J Med 2021). VISION randomised 831 patients with PSMA-positive mCRPC progressing after at least one androgen-receptor pathway inhibitor and one taxane to Lu-177 PSMA-617 plus standard of care versus standard of care alone. Median radiographic progression-free survival was 8.7 months in the Lu-177 PSMA-617 arm versus 3.4 months in the control arm (hazard ratio 0.40, 99.2% CI 0.29-0.57, p<0.001). Median overall survival was 15.3 months versus 11.3 months (hazard ratio 0.62, 95% CI 0.52-0.74, p<0.001)[1]. These are the endpoint figures referenced by the FDA Pluvicto label and by Novartis[2]. A randomised comparison versus cabazitaxel (TheraP, Hofman et al., Lancet 2021) showed PSA50 response of 66% with Lu-177 PSMA-617 versus 37% with cabazitaxel[3]. Individual patient outcomes vary with eligibility, prior treatment, disease biology, and tolerability.

The phrasing matters. Several different things get asked, often interchangeably, that have meaningfully different answers in the trial data:

  • Overall survival (OS) — how long, on average, patients lived from the point of randomisation. This is the headline endpoint most patients mean when they ask “how long does it extend life”.
  • Radiographic progression-free survival (rPFS) — how long, on average, before imaging showed disease progression. A measure of disease control, not survival.
  • PSA50 response — the proportion of patients whose PSA fell by at least 50%. A measure of biochemical response, not survival.
  • Objective response rate (ORR) — the proportion with measurable tumour shrinkage on imaging (per RECIST criteria).
  • Time to symptomatic skeletal event — how long before a fracture, spinal cord compression, or palliative bone radiation was required.

Each of these endpoints has been published with specific figures in specific trials. The remainder of this article walks through them trial by trial, with citation[4].

VISION (Sartor et al., NEJM 2021) — the pivotal randomised trial

VISION is the trial that supports the FDA and EMA approval of Lu-177 PSMA-617 (branded as Pluvicto). It randomised 831 patients with PSMA-positive metastatic castration-resistant prostate cancer (mCRPC) who had progressed after at least one androgen-receptor pathway inhibitor (ARPI) and at least one taxane-based chemotherapy. Randomisation was 2:1 to Lu-177 PSMA-617 plus standard of care versus standard of care alone[1].

Endpoint Lu-177 PSMA-617 + SoC Standard of care alone Statistical comparison
Median rPFS 8.7 months 3.4 months HR 0.40, 99.2% CI 0.29-0.57, p<0.001
Median overall survival 15.3 months 11.3 months HR 0.62, 95% CI 0.52-0.74, p<0.001
PSA50 response 46% 7.1% Difference 38.9 percentage points
Confirmed objective response (in patients with measurable disease) 30.3% 1.7%
Time to first symptomatic skeletal event or death 11.5 months 6.8 months HR 0.50, 95% CI 0.40-0.62

VISION was the first randomised trial to establish overall-survival benefit of a PSMA-targeted radioligand therapy in mCRPC. The trial design and patient population are critical context: these were heavily pre-treated patients who had already progressed on prior ARPI and taxane therapy[1].

TheraP (Hofman et al., Lancet 2021) — vs cabazitaxel

TheraP randomised 200 patients with mCRPC who had progressed after docetaxel to Lu-177 PSMA-617 versus cabazitaxel (the standard second-line chemotherapy after docetaxel). This was a direct head-to-head trial — unlike VISION, where the comparator was standard of care alone[3].

Endpoint Lu-177 PSMA-617 Cabazitaxel Statistical comparison
PSA50 response 66% 37% Difference 29 percentage points, 95% CI 16-42, p<0.0001
Median rPFS (HR comparison) HR 0.63, 95% CI 0.46-0.86 (favouring Lu-177 PSMA-617)
Pain response 60% 43%
Grade 3-4 adverse events 33% 53% Lower with Lu-177 PSMA-617

The TheraP overall-survival update (Hofman et al., Lancet Oncol 2024) reported median OS was numerically similar between the two arms (19.1 months Lu-177 PSMA-617 vs 19.6 months cabazitaxel), but with very different toxicity profiles and quality-of-life outcomes favouring Lu-177 PSMA-617[5]. The trial therefore established Lu-177 PSMA-617 as a substantively different — and for many patients more tolerable — second-line option after docetaxel.

LuPSMA (Hofman et al., Lancet Oncology 2018) — single-arm phase II

The LuPSMA phase II single-arm trial preceded VISION and TheraP. It enrolled 30 patients with progressive mCRPC after standard therapies, and reported the first prospective dataset on Lu-177 PSMA-617[6]:

  • PSA50 response: 57%
  • Median PSA-progression-free survival: 7.6 months
  • Median overall survival: 13.5 months
  • Pain response in two-thirds of evaluable patients
  • Generally well-tolerated; common adverse events were transient xerostomia, fatigue, and mild marrow effects

The LuPSMA trial was hypothesis-generating and built the case for the larger randomised trials. The 13.5-month overall survival in this single-arm study should not be directly compared to VISION's 15.3 months, as the patient populations and trial designs differed materially.

PSMAaddition (Novartis 2024) — earlier-setting data

PSMAaddition is a phase III randomised trial of Lu-177 PSMA-617 plus standard of care versus standard of care alone in patients with metastatic hormone-sensitive prostate cancer (mHSPC) — an earlier disease setting than VISION (which enrolled castration-resistant disease). In December 2024, Novartis announced that PSMAaddition met its primary endpoint of radiographic progression-free survival[7]:

  • Statistically significant and clinically meaningful improvement in rPFS in the Lu-177 PSMA-617 plus SoC arm versus SoC alone
  • Overall survival data not yet mature at the time of the rPFS readout
  • Full results expected at a future medical congress (publication pending at the time of this article)

This data is important context for two reasons: first, it confirms that Lu-177 PSMA-617 has activity in earlier disease settings (not only in heavily pre-treated mCRPC); and second, it signals that the regulatory and treatment landscape for Lu-PSMA therapy is still evolving. Final PSMAaddition publication should be referenced when it becomes available[7].

What ‘success rate’ actually means in published data

“Success rate” is a non-clinical phrase that can refer to several different trial endpoints depending on context. When patients ask about Pluvicto success rate, the published data points that are typically being referenced are:

  • PSA50 response rate — the proportion of patients whose PSA falls by at least 50% from baseline. In VISION: 46% with Lu-177 PSMA-617 vs 7.1% with SoC. In TheraP: 66% with Lu-177 PSMA-617 vs 37% with cabazitaxel[1][3].
  • Objective response rate (ORR) per RECIST criteria — the proportion with measurable tumour shrinkage. In VISION: 30.3% confirmed ORR in measurable-disease patients[1].
  • Imaging response by PSMA PET re-staging — disease distribution and avidity decrease on follow-up Ga-68 PSMA-11 PET-CT scans. Reported across multiple cohort studies including Indian institutional series[8].
  • Pain and quality-of-life improvement — patient-reported outcomes documented in both VISION and TheraP, with favourable directional change relative to comparator arms[9].

None of these is a “cure rate”, and none should be reported as one. Lu-177 PSMA-617 is a disease-control therapy that meaningfully extends time without progression and time alive, with durable symptomatic and biochemical responses in a majority of properly selected patients[10].

Why individual prognosis differs from trial medians

Published trial endpoints are medians and proportions across a study population. For an individual patient, several factors meaningfully shift the prognostic picture[11]:

  • PSMA SUVmean on baseline Ga-68 PSMA PET-CT — higher PSMA expression is associated with better response. The VISION trial documented this as a prespecified subgroup analysis[12].
  • Burden and pattern of disease — extensive marrow disease, visceral involvement, or large-volume liver disease are associated with poorer outcomes.
  • Prior treatment history — patients earlier in the treatment course generally do better; the VISION population was specifically heavily pre-treated.
  • Baseline biochemistry — baseline LDH, alkaline phosphatase, haemoglobin, and PSA kinetics all carry independent prognostic information.
  • Concomitant FDG-PET-positive PSMA-negative disease — a discordant pattern signalling neuroendocrine differentiation predicts poorer response[13].
  • Tolerability and ability to complete the prescribed course — patients who complete more cycles generally do better, though this is partly a reflection of underlying disease biology.

For most patients, a personalised expected-outcome discussion considers all of these factors together — not a single headline figure from a trial.

How the Pluvicto mechanism of action produces these outcomes

The mechanism of Lu-177 PSMA-617 explains why response is closely related to PSMA expression on imaging. PSMA-617 is a small-molecule PSMA-binding ligand chemically attached (via a DOTA chelator) to Lutetium-177, a beta-emitting radionuclide. When injected intravenously, the radioligand circulates briefly, binds to PSMA on the surface of prostate cancer cells, and is internalised. Lu-177 then decays over approximately 6.65 days, emitting beta radiation that deposits energy over a short range (mean 0.7 mm) into the surrounding tumour cells[14].

Because the radiation is targeted by the radioligand and short-range, surrounding non-PSMA-expressing tissues receive much less of the dose. This is what allows Lu-177 PSMA-617 to deliver meaningful tumour-absorbed dose while sparing most of the body — and is why response correlates with the intensity of PSMA expression on the baseline Ga-68 PSMA-11 PET-CT eligibility scan[15].

The FDA Pluvicto label and eligibility criteria

FDA approval of Pluvicto (Lu-177 vipivotide tetraxetan, the formal name for Lu-177 PSMA-617) was granted on 23 March 2022 for the treatment of adult patients with PSMA-positive metastatic castration-resistant prostate cancer who have been treated with ARPI and taxane-based chemotherapy[2]. In March 2025, the FDA expanded the Pluvicto label to include patients eligible for taxane chemotherapy who had progressed after ARPI therapy — based on the PSMAfore trial[16].

The PSMA PET-CT eligibility criteria — derived from VISION — require at least one PSMA-positive metastatic lesion with SUVmax greater than the SUVmax of the liver parenchyma, and the absence of large measurable non-PSMA-avid disease above defined size thresholds. These criteria are followed at experienced Indian centres including FMRI Gurugram, and have been described in detail in our companion article on PSMA expression in prostate cancer[17].

Limits of published data

Several appropriate caveats apply when interpreting any published Lu-177 PSMA-617 outcome figure[18]:

  • Trial populations are defined by eligibility criteria, particularly PSMA expression on PET imaging. Patients outside these criteria may experience meaningfully different outcomes.
  • Improvements observed in randomised trials are over a comparator arm; the comparator was not the same across trials, which limits direct cross-trial comparison.
  • Median survival is the survival time at which 50% of patients have died — half of patients survive longer, half shorter. The variance around the median is wide.
  • Trial follow-up is finite. Longer-term outcomes for any individual patient may differ from the median follow-up reported in a publication.
  • Most published cohorts are from Western academic centres. Indian institutional experience, while consistent with international data, is published in fewer randomised settings and largely in cohort form[8].
  • The treatment landscape continues to evolve. PSMAaddition, PSMAfore, and ongoing trials continue to refine where Lu-177 PSMA-617 fits in the treatment pathway[7][16].

The bottom line

  • VISION (Sartor et al., NEJM 2021) is the pivotal randomised trial of Lu-177 PSMA-617 in heavily pre-treated mCRPC. Median rPFS was 8.7 months vs 3.4 months SoC (HR 0.40), median OS 15.3 months vs 11.3 months (HR 0.62)[1].
  • TheraP (Hofman et al., Lancet 2021) randomised post-docetaxel mCRPC patients to Lu-177 PSMA-617 vs cabazitaxel and reported PSA50 response of 66% vs 37% with substantially lower Grade 3-4 toxicity[3].
  • LuPSMA (Hofman et al., Lancet Oncol 2018) was the single-arm phase II trial that established the early signal — PSA50 57%, median OS 13.5 months[6].
  • PSMAaddition (Novartis press release, December 2024) reported that Lu-177 PSMA-617 plus SoC met its primary endpoint of rPFS improvement in hormone-sensitive metastatic disease (an earlier setting than VISION)[7].
  • “Success rate” in a clinical sense refers most often to PSA50 response (46% in VISION, 66% in TheraP) and objective response rate (30.3% in VISION measurable-disease subset) — these are response measures, not cure rates[1][3].
  • Individual prognosis differs from trial medians based on PSMA SUVmean on baseline PET, disease burden, prior treatment history, baseline biochemistry, and tolerability — a personalised expected-outcomes discussion is appropriate for every patient.
  • The FDA Pluvicto label (March 2022, expanded March 2025) defines current eligibility, which is updated as PSMAaddition and PSMAfore data mature[2][16].
Important

This article reproduces specific endpoint figures from peer-reviewed publications and regulatory filings as published. Individual patient outcomes vary based on eligibility, prior treatment history, disease biology, and tolerability. Trial endpoints describe study populations, not individuals — and should not be quoted as guarantees or predictions for any specific patient.

“The question is not what number to put on a brochure; it is which trial endpoint best matches the question this specific patient is actually asking. VISION's 15.3 months overall survival is the right answer for a specific population in a specific trial. For an individual patient in front of us at clinic, the answer is built from their imaging, their prior therapy history, their biochemistry, and their tolerance — and it is framed as a range, not a number.”

Dr. Ishita B. Sen, MD · Director & Chief, Nuclear Medicine, FMRI

Personalised outcomes discussion · Lu-177 PSMA at FMRI

At FMRI Gurugram, every Lu-177 PSMA-617 candidacy review includes a personalised outcomes discussion — reviewing your Ga-68 PSMA PET-CT (eligibility and SUVmean), prior treatment history, baseline biochemistry, and disease distribution against the published trial data. Expected response and survival are framed as ranges derived from your specific clinical picture, not from a single headline figure.

Request outcomes review · WhatsApp +91 8800 988936
For patients & referring clinicians

Frequently asked questions

Q01 How long does Pluvicto extend life?

In the VISION randomised trial (Sartor et al., NEJM 2021) — the pivotal trial supporting FDA approval — median overall survival was 15.3 months in the Lu-177 PSMA-617 plus standard-of-care arm versus 11.3 months in the standard-of-care alone arm (hazard ratio 0.62, 95% CI 0.52-0.74, p<0.001). This is a 4-month improvement in median survival across the trial population [1]. Individual patient survival varies based on PSMA expression, disease burden, prior therapy, and tolerability — and should not be quoted as a guarantee.

Q02 What is the Pluvicto success rate?

“Success rate” can mean several different endpoints. In the VISION trial, PSA50 response (PSA fall ≥50%) was 46% with Lu-177 PSMA-617 vs 7.1% with standard of care; confirmed objective response on imaging (RECIST) was 30.3% in measurable-disease patients [1]. In the TheraP head-to-head trial vs cabazitaxel, PSA50 response was 66% with Lu-177 PSMA-617 vs 37% with cabazitaxel [3]. These are response measures, not cure rates.

Q03 What is the VISION trial?

VISION (Sartor et al., New England Journal of Medicine, 2021) is the phase III randomised trial that established Lu-177 PSMA-617 as a treatment for metastatic castration-resistant prostate cancer (mCRPC). 831 patients with PSMA-positive mCRPC who had progressed after at least one ARPI and one taxane were randomised 2:1 to Lu-177 PSMA-617 plus standard of care versus standard of care alone. VISION supported FDA approval of Pluvicto in March 2022 [1][2].

Q04 What is rPFS and why does it matter?

rPFS (radiographic progression-free survival) is the median time from randomisation to imaging evidence of disease progression. In VISION, median rPFS was 8.7 months with Lu-177 PSMA-617 vs 3.4 months with standard of care (HR 0.40, p<0.001). rPFS is a measure of disease control — how long the therapy holds disease back — and is one of the regulatory primary endpoints for prostate cancer trials [1].

Q05 How does the TheraP trial compare to VISION?

TheraP (Hofman et al., Lancet 2021) randomised 200 mCRPC patients who had progressed after docetaxel to Lu-177 PSMA-617 vs cabazitaxel — a head-to-head comparison. VISION compared Lu-177 PSMA-617 plus SoC vs SoC alone. The trials therefore answer different questions: VISION established benefit vs continued standard care; TheraP established Lu-177 PSMA-617 as a tolerability-favoured alternative to second-line chemotherapy [3][5].

Q06 Why is the TheraP overall survival similar between arms?

The TheraP final overall-survival update (Lancet Oncol 2024) reported median OS of 19.1 months for Lu-177 PSMA-617 vs 19.6 months for cabazitaxel — numerically similar. This means that, in this specific post-docetaxel mCRPC population, both options provided broadly similar overall survival but with very different toxicity profiles and quality-of-life outcomes favouring Lu-177 PSMA-617. The choice between them is therefore tolerability- and quality-of-life-driven [5].

Q07 What does the LuPSMA single-arm trial show?

The LuPSMA phase II single-arm trial (Hofman et al., Lancet Oncology 2018) enrolled 30 patients with progressive mCRPC. PSA50 response was 57%, median PSA-PFS 7.6 months, and median overall survival 13.5 months [6]. It was the trial that built the case for the larger randomised studies (VISION and TheraP).

Q08 What is the PSMAaddition trial?

PSMAaddition is a phase III randomised trial of Lu-177 PSMA-617 plus standard of care versus standard of care alone in metastatic hormone-sensitive prostate cancer (mHSPC) — an earlier setting than VISION (which was castration-resistant). In December 2024, Novartis announced that PSMAaddition met its primary endpoint of rPFS improvement; full results are expected at a future medical congress with the formal publication pending [7].

Q09 Does PSMA expression on the eligibility PET scan predict response?

Yes. The VISION trial prespecified subgroup analyses by PSMA expression on the baseline Ga-68 PSMA-11 PET-CT showed that higher PSMA SUVmean was associated with greater benefit from Lu-177 PSMA-617. This is the rationale for the eligibility criterion that all metastatic lesions must show SUVmax greater than liver SUVmax — patients without sufficient PSMA expression are unlikely to derive meaningful benefit [12].

Q10 How is Pluvicto's mechanism of action linked to these outcomes?

Pluvicto consists of the PSMA-binding ligand PSMA-617 attached (via a DOTA chelator) to Lutetium-177, a beta-emitting radionuclide with a 6.65-day half-life. After IV injection, the radioligand binds PSMA on prostate cancer cells, is internalised, and Lu-177 decays delivering short-range beta radiation (mean 0.7 mm) into the tumour. Because the targeting is selective and the radiation is short-range, surrounding non-PSMA-expressing tissues receive much less dose — which is what allows the therapy to extend survival while sparing most normal tissues [14][15].

Q11 How do Indian published outcomes compare with VISION?

Published Indian institutional cohorts (AIIMS, Tata Memorial, others) have reported PSA50 response rates and survival outcomes broadly consistent with international VISION and LuPSMA data. The AIIMS New Delhi published series (Yadav et al., 2017; subsequent updates) documented similar response rates and tolerability with compounded (BRIT/imported) Lu-177 PSMA-617 preparations to those reported with branded Pluvicto in international cohorts [8].

Q12 How do I get a personalised outcomes discussion at FMRI?

At FMRI Gurugram, every Lu-177 PSMA-617 candidacy review includes a personalised outcomes discussion reviewing your Ga-68 PSMA PET-CT (eligibility and SUVmean), prior treatment history, baseline biochemistry, and disease distribution against the published trial data. Expected response and survival are framed as ranges derived from your specific clinical picture, not from a single headline figure. WhatsApp +91 8800 988936 to begin a confidential review.

Citations & references

All clinical numbers above are sourced from the primary literature listed below. Every reference links to the open journal page or the regulatory archive — open in a new tab to verify.

[1] 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. View source ↗
[2] U.S. Food and Drug Administration. FDA approves Pluvicto for metastatic castration-resistant prostate cancer (March 23, 2022). FDA News Release and Prescribing Information. View source ↗
[3] Hofman MS, Emmett L, Sandhu S, et al. [177Lu]Lu-PSMA-617 versus cabazitaxel in patients with metastatic castration-resistant prostate cancer (TheraP). Lancet. 2021;397(10276):797-804. View source ↗
[4] Scher HI, Halabi S, Tannock I, et al. Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: PCWG3 recommendations. J Clin Oncol. 2016;34(12):1402-1418. View source ↗
[5] Hofman MS, Emmett L, Sandhu S, et al. Overall survival with Lu-177 PSMA-617 versus cabazitaxel in mCRPC (TheraP) — final results. Lancet Oncol. 2024;25(1):99-107. View source ↗
[6] Hofman MS, Violet J, Hicks RJ, et al. [177Lu]-PSMA-617 radionuclide treatment in patients with metastatic castration-resistant prostate cancer (LuPSMA trial). Lancet Oncol. 2018;19(6):825-833. View source ↗
[7] Novartis. PSMAaddition Phase III data show Novartis Pluvicto delays disease progression in metastatic hormone-sensitive prostate cancer (December 2024 press release). View source ↗
[8] Yadav MP, Ballal S, Tripathi M, et al. 177Lu-DKFZ-PSMA-617 therapy in metastatic castration-resistant prostate cancer: safety, efficacy, and quality of life. Eur J Nucl Med Mol Imaging. 2017;44(1):81-91. View source ↗
[9] Sartor O, Castellano D, Herrmann K, et al. VISION final overall survival update — Lu-177 PSMA-617 in mCRPC. J Clin Oncol. 2023. View source ↗
[10] Iravani A, Violet J, Azad A, et al. Lutetium-177 PSMA therapy: practical aspects, dosimetry, and outcomes. Theranostics. 2020;10(20):8854-8866. View source ↗
[11] Heck MM, Tauber R, Schwaiger S, et al. Treatment outcome and toxicity for 177Lu-PSMA-I&T in mCRPC. Eur Urol. 2019;75(6):920-926. View source ↗
[12] Kuo PH, Benson T, Messmann R, et al. Why we did what we did: PSMA PET/CT selection criteria for the VISION trial. J Nucl Med. 2022;63(6):816-818. View source ↗
[13] Thang SP, Violet J, Sandhu S, et al. Poor Outcomes for Patients with mCRPC with Low PSMA Expression Despite High FDG Uptake on Dual-tracer PET. Eur J Nucl Med Mol Imaging. 2019;46(8):1632-1639. View source ↗
[14] Hennrich U, Eder M. 177Lu-PSMA-617 (Pluvicto): The First FDA-Approved Radiotherapeutical for Treatment of Prostate Cancer. Pharmaceuticals (Basel). 2022;15(10):1292. View source ↗
[15] European Association of Nuclear Medicine. EANM procedure guidelines for radionuclide therapy with 177Lu-labelled PSMA-ligands. Eur J Nucl Med Mol Imaging. 2019;46(12):2536-2544. View source ↗
[16] U.S. Food and Drug Administration. FDA expands Pluvicto indication to include taxane-eligible mCRPC patients (March 2025). View source ↗
[17] Calais J, Czernin J, Cao M, et al. 68Ga-PSMA-11 PET/CT mapping of prostate cancer biochemical recurrence after radical prostatectomy. J Nucl Med. 2018;59(4):576-585. View source ↗
[18] Scher HI, Halabi S, Tannock I, et al. Updated criteria for design of clinical trials in advanced prostate cancer (Prostate Cancer Working Group). J Clin Oncol. 2008;26(7):1148-1159. View source ↗
[19] Sgouros G, Bodei L, McDevitt MR, Nedrow JR. Radiopharmaceutical therapy in cancer: clinical advances and challenges. Nat Rev Drug Discov. 2020;19(9):589-608. View source ↗
[20] Basu S, Parghane RV, Banerjee S, et al. Long-term outcome of 177Lu-PSMA-617 therapy in mCRPC: Indian institutional experience. Clin Nucl Med. 2021;46(10):820-826. View source ↗
[21] Sartor O, Bono JS, Chi KN, et al. VISION trial supplementary appendix — patient population and prespecified subgroup analyses. N Engl J Med. 2021 (Supplementary Materials). View source ↗
[22] European Medicines Agency. Pluvicto Summary of Product Characteristics (EMA EPAR). View source ↗
[23] Sartor O. The PSMAfore trial: Lu-177 PSMA-617 in taxane-naive mCRPC. N Engl J Med. 2024;391(16):1500-1510. View source ↗
[24] Calais J, Gafita A, Eiber M, et al. Prospective head-to-head comparison of 68Ga-PSMA-11 PET/CT and 18F-DCFPyL PET/CT for biochemical recurrence of prostate cancer. J Nucl Med. 2018;59(11):1611-1617. View source ↗
[25] Sathekge MM, Bruchertseifer F, Vorster M, et al. 225Ac-PSMA-617 in chemotherapy-naive prostate cancer. Eur J Nucl Med Mol Imaging. 2019;46(1):129-138. View source ↗
[26] Hofman MS, Lawrentschuk N, Francis RJ, et al. Prostate-specific membrane antigen PET-CT in patients with high-risk prostate cancer before curative-intent surgery or radiotherapy (proPSMA). Lancet. 2020;395(10231):1208-1216. View source ↗
[27] NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer (current version). National Comprehensive Cancer Network. View source ↗
[28] European Association of Urology. EAU-EANM-ESTRO-ESUR-SIOG Guidelines on Prostate Cancer. View source ↗
[29] Tagawa ST, Vallabhajosula S, Christos PJ, et al. Phase I/II study of fractionated dose 177Lu-J591 for progressive mCRPC. Cancer. 2019;125(15):2561-2569. View source ↗
[30] Atomic Energy Regulatory Board (Government of India). Safety Code for Nuclear Medicine Facilities. AERB/RF-MED/SC-2 (Rev. 2). View source ↗
Dr. Ishita B. Sen
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.

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Medical disclaimer All physicians and researchers profiled on this page hold appointments at the Department of Nuclear Medicine & Molecular Imaging, Fortis Memorial Research Institute, Gurugram. Theranostic Physicians Private Limited (TPPL) is the clinical practice entity through which they consult and treat patients. Treatment outcomes vary by individual case; clinical decisions are made on the basis of complete medical records, current imaging, and a multidisciplinary review.