The potential of (177Lu)-PSMA-617 in the first-line combination therapy with enzalutamide for metastatic castration-resistant prostate cancer: clinical insights from the ENZA-p trial
Editorial Commentary

The potential of (177Lu)-PSMA-617 in the first-line combination therapy with enzalutamide for metastatic castration-resistant prostate cancer: clinical insights from the ENZA-p trial

Renning Zheng1,2, Stephen J. Freedland1,3,4, Anthony T. Nguyen4,5,6

1Department of Urology, Cedars-Sinai Medical Center, Los Angeles, CA, USA; 2Tsinghua Medicine, Tsinghua University, Beijing, China; 3Department of Surgery, Section of Urology, Durham VA Health Care System, Durham, NC, USA; 4Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA; 5Department of Radiation Oncology, Cedars-Sinai Medical Center, Los Angeles, CA, USA; 6Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA

Correspondence to: Anthony T. Nguyen, MD, PhD. Assistant Professor, Department of Radiation Oncology, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Assistant Professor, Department of Biomedical Sciences, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Suite AC1010, Los Angeles, CA, 90048, USA; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Email: Anthony.Nguyen@cshs.org.

Comment on: Emmett L, Subramaniam S, Crumbaker M, et al. Overall survival and quality of life with [177Lu]Lu-PSMA-617 plus enzalutamide versus enzalutamide alone in metastatic castration-resistant prostate cancer (ENZA-p): secondary outcomes from a multicentre, open-label, randomised, phase 2 trial. Lancet Oncol 2025;26:291-9.

Keywords: (Lutetium-177)-prostate-specific membrane antigen-617 [(177Lu)-PSMA-617]; enzalutamide; combination therapy; metastatic castration-resistant prostate cancer (mCRPC); ENZA-p

Submitted Jun 16, 2025. Accepted for publication Aug 14, 2025. Published online Oct 23, 2025.

doi: 10.21037/cco-25-65

The past decade has been defined by the development and approval of several novel therapies for metastatic castration-resistant prostate cancer (mCRPC). To date, androgen receptor pathway inhibitors (ARPI), such as abiraterone and enzalutamide, and taxane-based chemotherapies remain the most frequently used first-line (1L) treatments for mCRPC. New therapies, including prostate-specific membrane antigen (PSMA)-targeted radioligand therapy (RLT) with Lutetium-177 (177Lu)-PSMA-617, have further demonstrated significant benefit in mCRPC, leading to its approval by the United States Food and Drug Administration (U.S. FDA) (1). However, the optimal treatment sequence after 1L therapy and the potential benefits of combination therapies remain unclear.

Recently, Emmett et al. reported key secondary outcomes, including overall survival (OS) and quality of life (QoL), from the ENZA-p trial, a multicenter, randomized phase II study comparing enzalutamide with or without (177Lu)-PSMA-617 in patients with ARPI- and chemotherapy-naïve mCRPC (2). Eligible participants had a positive PSMA positron emission tomography/computed tomography (PET/CT) scan, at least 2 risk factors for early progression on enzalutamide, and no prior treatment with docetaxel or an ARPI. The addition of (177Lu)-PSMA-617 to enzalutamide significantly improved OS compared to enzalutamide alone [median 34 vs. 26 months; hazard ratio (HR) =0.55, 95% confidence interval (CI): 0.36–0.84; P=0.005]. Additionally, QoL deterioration-free survival was also significantly prolonged in the combination group (median 10.6 vs. 3.4 months; HR =0.51, 95% CI: 0.36–0.72; P<0.001). As previously reported, prostate-specific antigen progression-free survival (PSA-PFS) was also significantly improved with combination therapy (median 13.0 vs. 7.8 months; HR =0.43, 95% CI: 0.29–0.63; P<0.0001) (3). Rates of grade 3 or higher adverse events were comparable between groups. Limitations of the study included its modest sample size (n=83 for the combination group; n=79 for the enzalutamide group) and generalizability to patients who have received prior ARPI or docetaxel. Put together, these findings demonstrate that the combination of 1L (177Lu)-PSMA-617 and enzalutamide for mCRPC is both safe and effective, warranting evaluation in a phase III trial.

ENZA-p builds upon a body of recent trials that have evaluated RLT for mCRPC following 1L treatment (Table 1). The VISION trial was the first phase III study for (177Lu)-PSMA-617, demonstrating its efficacy as a third-line (3L) therapy after prior treatment with both ARPI and taxanes (4). Another phase III trial, PSMAfore established the efficacy of (177Lu)-PSMA-617 as a second-line (2L) treatment among mCRPC patients who had received only one ARPI without previous taxane (5). Additionally, the phase II TheraP trial also supported the efficacy of (177Lu)-PSMA-617 as a 2L treatment following 1L docetaxel (6,7). Yet, real-world evidence suggests the benefit of RLT in later-stage mCRPC may be limited (8). Indeed, in the PSMAfore and TheraP trials, (177Lu)-PSMA-617 did not improve OS as a 2L treatment relative to the comparator arm, though this may be confounded by either a high degree of cross-over (PSMAfore) or use of an active control arm (TheraP) (5,7). Although the VISION trial did demonstrate an OS benefit of (177Lu)-PSMA-617 in the 3L setting, the limited life expectancy at that stage only translated into a modest 4-month OS improvement (4). Furthermore, several recent trials, such as UpFrontPSMA and PSMAddition have begun evaluating the use of RLT in metastatic hormonal-sensitive prostate cancer (mHSPC) (9,10), with a recent press release for PSMAddition saying that (177Lu)-PSMA-617 in combination with standard of care (SoC) improved radiographic progression-free survival (rPFS) vs. SoC alone in mHSPC (11). Additional trials, including BULLSEYE and PSMA-DC, are currently underway in earlier stages, such as oligometastatic prostate cancer (12,13). These ongoing trials will test the hypothesis that earlier use of RLT, either in the 1L setting of mCRPC or in earlier stages of prostate cancer, may improve oncologic outcomes compared to later lines of use.

Table 1

Important clinical trials for (177Lu)-PSMA-617 in metastatic castration-resistant prostate cancer

Clinical trial (phase) Prior therapies for mCRPC Treatment comparisons Dose Results
VISION (4) (III) (NCT03511664) ≥ 1 ARPI + 1–2 taxane (177Lu)-PSMA-617 + SoC vs. SoC alone† 4–6‡ rPFS: median 8.7 vs. 3.4 months, HR =0.40 (95% CI: 0.29–0.57), P<0.001
OS: median 15.3 vs. 11.3 months, HR =0.62 (95% CI: 0.52–0.74), P<0.001
PSMAfore (5) (III) (NCT04689828) 1 ARPI, previous taxane not allowed (177Lu)-PSMA-617 vs. ARPI change 6 rPFS: median 11.6 vs. 5.6 months; HR =0.49 (95% CI: 0.39–0.61)
OS: median 23.7 vs. 23.8 months; HR =0.98 (95% CI: 0.75–1.28); P=0.44
TheraP (6,7) (II) (NCT03392428) 1 docetaxel, previous ARPI allowed (177Lu)-PSMA-617 vs. cabazitaxel ≤6§ PSA50%RR: 66% vs. 37%; difference 29% (95% CI: 16–42%); P<0.0001
PFS: median both 5.1 months; HR =0.63 (95% CI: 0.46–0.85); P=0.003
OS: median 16.4 vs. 19.4 months; HR =0.97 (95% CI: 0.70–1.35); P=0.99
ENZA-p (2,3) (II) (NCT04419402) None (177Lu)-PSMA-617 + enzalutamide vs. enzalutamide alone 2/4 PSA-PFS: median 13.0 vs. 7.8 months; HR =0.43 (95% CI: 0.29–0.63); P<0.0001
OS: median 34 vs. 26 months; HR =0.55 (95% CI: 0.36–0.84); P=0.005

†, SoC included ARPI but not taxane. ‡, standard protocol included 4 doses, and up to 2 additional doses could be administered in patients who had evidence of response. §, 177Lu retention was assessed after each dose, and treatment was suspended if SPECT-CT showed very low or no uptake at sites of metastatic diseases. , standard protocol included 2 doses, and an additional 2 doses could be administered in patients with persistent PSMA PET-CT-positive diseases after the first 2 doses. ARPI, androgen receptor pathway inhibitors; CI, confidence interval; HR, hazard ratio; mCRPC, metastatic castration-resistant prostate cancer; OS, overall survival; PET-CT, positron emission tomography-computed tomography; PFS, progression-free survival; PSA, prostate-specific antigen; PSA50%RR, PSA decline ≥50% response rate; PSMA, prostate-specific membrane antigen; rPFS, radiographic progression-free survival; SoC, standard of care; SPECT-CT, single photon emission computed tomography-computed tomography.

RLT now becomes the third class of therapeutics to demonstrate survival benefit when combined with ARPI in 1L mCRPC, following poly ADP-ribose polymerase (PARP) inhibitors (14-16), and Radium-223 (17). The biological rationale for such combination strategies lies in the synergistic effects observed with androgen receptor blockade, including activation of the PARP pathway (18), upregulation of PSMA expression (19,20), and enhanced sensitivity to DNA damage induced by Radium-223 (21). Importantly, in addition to their efficacy, current ARPI-based combination regimens have shown similar adverse event profiles to ARPI monotherapy (3,14-17). Given that ARPI is the dominant choice for 1L mCRPC treatment (22), the combination of superior efficacy with comparable safety and tolerability suggests that ARPI-based combination therapies might represent the next standard of care for mCRPC. However, the expanding use of ARPI in earlier disease stages further complicates the selection of ARPI-based combinations in mCRPC (23,24). Nonetheless, several trials are now evaluating combinations building upon ARPI in mHSPC patients, such as PSMAddition [ARPI + (177Lu)-PSMA-617] (10), TALAPRO-3 (enzalutamide + talazoparib) (25), and AMPLITUDE (abiraterone + niraparib) (26). It is possible that ARPI-based combination therapies will supplant ARPI monotherapy as the treatment of choice for earlier stages of prostate cancer.

An important feature of the ENZA-p trial was its adaptive dosing strategy for (177Lu)-PSMA-617, in which only patients with persistent PSMA expression, determined by PSMA PET-CT after the initial 2 doses, received the additional 2 doses (2,3). Similar adaptive approaches have been used in previous clinical trials of (177Lu)-PSMA-617. In the VISION trial, only patients with evidence of response to the first 4 doses of (177Lu)-PSMA-617 received 2 additional doses (4). Meanwhile, the TheraP trial required participants to undergo SPECT-CT imaging after each dose to evaluate 177Lu retention, with treatment discontinued for patients showing very low or no uptake at the metastatic sites (6,7). Notably, while the VISION trial relied solely on standard radiographic assessments to evaluate response, both the ENZA-p and TheraP trials incorporated biomarker-based evaluations to improve accuracy. In support of this strategy, a previous study validated the accuracy of 177Lu retention in predicting treatment outcomes after the initial 2 doses of (177Lu)-PSMA-617 (27). As such, an adaptive dosing strategy based on the early treatment response, ideally using biomarkers such as PSMA expression or 177Lu retention, could serve as a valuable tool in clinical decision-making. For patients with a favorable early response, a treatment break might be safe to mitigate the impact of side effects and allow them to conserve the doses for future treatment upon disease progression. Conversely, patients with early signs of disease progression could promptly switch to alternative therapies, thereby improving both prognosis and cost-effectiveness. Further studies are needed to determine the optimal adaptive dosing strategies for guiding clinical practice.

An important inclusion criterion for the ENZA-p trial was the presence of at least 2 out of 9 predefined risk factors for early progression on enzalutamide [serum lactate dehydrogenase ≥ institutional upper limit of normal (IULN), alkaline phosphatase ≥ IULN, albumin <35 g/L, de novo metastatic disease at initial diagnosis (based on conventional imaging), <3 years from initial diagnosis to randomization, >5 bone metastases or visceral metastases (based on conventional imaging), PSA doubling time <84 days, pain requiring opiates for >14 days, or previous treatment with abiraterone acetate]. These risk factors were adapted from a validated prognostic model for enzalutamide and a prior study with similar criteria (28,29). Although this requirement limits the eligibility of the combination therapy to a specific subset of mCRPC patients, it effectively identifies those at higher risk of early progression on enzalutamide alone, and therefore more likely to need treatment beyond enzalutamide alone. This approach represents a tradeoff between narrowing the eligible population and identifying the subset that stands the most to benefit. While the exact improvement in prognosis from this strategy cannot be quantified, the prior prognostic model incorporating 11 risk factors found that 56% of participants had more than 3 risk factors (28), suggesting that the ENZA-p criterion of at least 2 risk factors is not overly restrictive and is unlikely to exclude a substantial proportion of eligible patients. As such, this strategy is likely to yield a net clinical benefit. While the ENZA-p trial focused on predictors of early progression on enzalutamide, multiple studies have also identified prognostic indicators specific to (177Lu)-PSMA-617 (30-32). If improvements in outcomes and adverse event profiles are confirmed in future prospective studies, adaptive dosing strategies could be integrated into clinical practice for precision mCRPC management, with potential future incorporation of biomarker-based selection and sequencing strategies.

In summary, the phase II ENZA-p trial was the first clinical trial to evaluate the potential of (177Lu)-PSMA-617 as part of 1L combination therapy for mCRPC, which demonstrated that combination therapy with enzalutamide significantly improved PFS, OS, and QoL compared to enzalutamide alone. Additionally, the use of an adaptive dosing strategy and the inclusion criterion based on risk factors for early progression on enzalutamide may enhance the clinical utility and personalization of radioligand treatment. These findings highlight the promise of this combination approach and support the need for a phase III trial to validate its benefits in a broader patient population.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Chinese Clinical Oncology. The article has undergone external peer review.

Peer Review File: Available at https://cco.amegroups.com/article/view/10.21037/cco-25-65/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://cco.amegroups.com/article/view/10.21037/cco-25-65/coif). S.J.F. reports consultancy to Astellas, Pfizer, Astra Zeneca, Merck, Novartis, Bayer, Janssen, Tolmar, Eli Lilly, Sumitomo, and Sanofi; and being speaker for Pfizer and Astellas. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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Cite this article as: Zheng R, Freedland SJ, Nguyen AT. The potential of (177Lu)-PSMA-617 in the first-line combination therapy with enzalutamide for metastatic castration-resistant prostate cancer: clinical insights from the ENZA-p trial. Chin Clin Oncol 2025;14(5):63. doi: 10.21037/cco-25-65

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