PSMA targeted Therapy: From molecular mechanisms to clinical breakthroughs in castration-resistant prostate cancer.

336 Background: Salvage radiation therapy (sRT) is standard of care for biochemically recurrent prostate cancer following radical prostatectomy (RP). In this setting, prostate specific membrane antigen (PSMA) PET/CT has superior sensitivity and specificity for identifying recurrent disease, especially at low prostate specific antigen (PSA) levels, and can guide target volume delineation for sRT. We set out to identify how PSMA PET/CT guidance impacts long term clinical outcomes following sRT. Methods: We retrospectively screened five prospective PSMA PET/CT studies conducted at the University of California, Los Angeles between 2016 and 2021 for patients who had a prior RP, were restaged with a PSMA PET/CT at their first biochemical recurrence (PSA >0.2 ng/mL), subsequently received sRT, and had at least 24 months of follow up from the start of sRT. Progression-free survival (PFS), freedom from distant progression, and overall survival (OS) were calculated from the start of sRT using the Kaplan-Meier method. Cox regression was used to calculate adjusted hazard ratios (aHRs) for PFS, adjusting for androgen deprivation therapy (ADT), age, pre-sRT PSA level, and use of whole pelvis radiotherapy (WPRT). Results: 113 patients who received sRT between December 2016 and March 2021 met inclusion criteria. Median PSA at PSMA PET/CT was 0.4 ng/mL (IQR, 0.3-1). Median time from RP was 19.9 mo. (IQR, 5.6-51.8 mo). On PSMA PET/CT, 19 patients (17%) were staged TrN0M0, 35 (31%) N1/M1a, 13 (12%) M1b-c, and 46 (41%) T0N0M0 (no visible disease). 76 (67%) received ADT and 70 (62%) received WPRT. Median follow-up was 59.4 mo. (interquartile range [IQR], 47.4-69.5 mo.). 57 (50%) had documented progression. Median PFS was 49.2 mo. (95% confidence interval [CI], 24.1-74.3 mo.). Median freedom from distant progression was 76.4 mo. (95% CI, 62.9-89.9 mo.). Median OS was not reached. The five-year OS rate was 97.1% (95% CI, 94.1-100%). T0N0M0 patients had the most favorable PFS (aHR relative to M1b-c cohort, 0.25) followed by TrN0M0 and N1/M1a patients (aHR relative to M1b-c cohort, 0.39 for both). Pre-radiotherapy PSA was not associated with PFS (aHR, 1.0; p =0.98). WPRT was significantly associated with improved PFS in TrN0M0 patients (aHR, 0.12; p =0.035) but not in T0N0M0 patients (aHR, 0.87; p =0.8). Among T0 N1/M1 patients, prostate bed irradiation was significantly associated with improved PFS (aHR, 0.25; p =0.005). Among T0N0M0 and TrN0M0 patients, ADT was not associated with improved PFS ( p >0.05 for both). Among N1/M1 patients, ADT was significantly associated with improved PFS (aHR, 0.37; p =0.02). Conclusions: PSMA PET/CT-guided sRT was associated with favorable long-term clinical outcomes. Exploratory analyses suggest a benefit for WPRT following a positive PSMA PET/CT and for ADT for N1 or M1 disease. Further prospective data are needed to confirm these findings.

DETECTION OF MICROMETASTATIC PROSTATE CANCER CELLS IN THE LYMPH NODES BY REVERSE TRANSCRIPTASE POLYMERASE CHAIN REACTION IS PREDICTIVE OF BIOCHEMICAL RECURRENCE IN PATHOLOGICAL STAGE T2 PROSTATE CANCER.

The Promise of Circulating Tumor Cells in Metastatic CRPC

Docetaxel treatment prolongs survival of patients with castration-resistant prostate cancer (CRPCa); however, the overall survival advantage still remains low. Antibody-drug conjugates (ADCs) have proven to be a viable approach for targeting cytotoxic agents to tumor cells to increase efficacy and minimize negative side effects. Prostate-specific membrane antigen (PSMA) is expressed by CRPCa cells and neovasculature surrounding non-prostatic solid tumors, and is currently under investigation as a therapeutic target. The objective of our studies was to evaluate the efficacy of an investigational agent, PSMA ADC, consisting of a fully human anti-PSMA antibody linked to monomethylauristatin E (MMAE) to inhibit CRPCa in a preclinical setting. LuCaP 96CR, a model of CRPCa, was used in our study. Animals bearing subcutaneous LuCaP 96CR were treated for four weeks, once weekly with PSMA-ADC or with PSMA antibody and free MMAE. PSMA ADC significantly decreased tumor volumes in the high-PSMA expressing LuCaP 96CR. Tumor volume (TV) of the ADC treated groups were only 10-14% of TV in the control group and only 2-3% at the time of sacrifice. The inhibition of tumor growth was more pronounced with the PSMA ADC treatment than with the unconjugated antibody and free MMAE. The inhibitory effects lasted for six weeks after cessation of the treatment when the animals were sacrificed. Importantly, no significant negative side effects were associated with the PSMA ADC treatment. The effects of PSMA ADC on additional xenografts with moderate and low PSMA expression, including those derived from soft tissue and bone metastases, are currently under investigation. We also performed a gene expression analysis of 24 LuCaP xenografts that reflect the highly diverse and heterogeneous nature of PCa in patients. This analysis revealed associations between the expression of PSMA and a number of genes involved in glutamate and glutamate decarboxylase pathways (i.e., glutamate dehydrogenase (GLUD1 and GLUD2; and GAD1 respectively) suggesting potential pathways associated with PSMA function. In summary PSMA ADC possesses potent antitumor activity in the LuCaP 96CR model with no significant negative side effects. Furthermore, correlates of PSMA expression may suggest a biological role of PSMA within the tumor environment influencing survival, proliferation and migration of tumor cells by alterations in the glutamatergic pathway. Evaluation of PSMA ADC efficacy in additional clinically relevant LuCaP models is ongoing, as well as investigation of the biology of PSMA in CRPCa. Citation Format: Vincent A. DiPippo, Holly M. Nguyen, Robert L. Vessella, Ilsa M. Coleman, Peter S. Nelson, William C. Olson, Eva Corey. In vivo efficacy of PSMA ADC in castration-resistant prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 2133. doi:10.1158/1538-7445.AM2013-2133

Background and objectiveBiochemical recurrence (BCR) of prostate cancer (PCa) after curative radiotherapy (RT) is defined according to the Phoenix criteria, which is a prostate-specific antigen (PSA) rise of ≥2.0 ng/ml above the PSA nadir. Prostate-specific membrane antigen (PSMA)-based positron emission tomography/computed tomography (PET/CT) can identify PCa recurrences at very low PSA values. Our aim was to investigate the detection rate and extent of PCa recurrences using PSMA PET/CT after curative RT among patients with a PSA rise of ≥2.0 ng/ml above the nadir (Phoenix positive, Ph+) and patients not reaching this threshold (Phoenix negative, Ph−) and to compare therapeutic management and clinical outcomes in terms of time to androgen deprivation therapy (ADT) and castration-resistance PCa (CRPC), as well as overall survival. MethodsWe conducted a retrospective analysis of the Prostate Cancer Network Amsterdam (2015–2023) cohort of 568 patients who received curative-intent RT for PCa. Data on PSMA PET/CT outcomes, therapeutic management, and clinical follow-up were collected, including (re)initiation of ADT, progression to CRPC, and survival. Results were compared between groups using logistic regression and survival analyses. Key findings and limitationsThe study cohort comprised 222 patients (39.1%) classified as Ph− and 346 (60.9%) classified as Ph+. PSMA-avid lesions were detected in 170 Ph− patients (76.6%) and 322 (93.1%) Ph+ patients. In these groups, 75.9% of Ph− patients and 45.0% of Ph+ patients were eligible for local salvage therapy (odds ratio [OR 3.84]; p < 0.001). Distant metastases were less frequent in the Ph− group (n = 37, 21.8%) than in the Ph+ group (n = 157, 48.8%; OR 0.29; p < 0.001). Survival analyses revealed longer times to ADT (re)initiation and progression to CRPC, as well as lower overall mortality, in the Ph− group (log-rank p < 0.001). The retrospective study design is the main limitation. Conclusions and clinical implicationsFor patients with PCa recurrence, PSMA PET/CT can detect this recurrence in the majority of cases not meeting the Phoenix criteria for BCR. Early imaging detects recurrences at a less advanced disease stage, allowing potential salvage treatments. In addition, early PSMA PET/CT is associated with longer times to ADT (re)initiation and progression to CRPC, as well as longer overall survival. These positive clinical implications warrant confirmation of our results in prospective studies to reduce potential leadtime bias. Patient summaryWe investigated early use of a special type of scan called PSMA PET (prostate-specific membrane antigen positron emission tomography) in patients with suspicion of recurrence of their prostate cancer after radiotherapy. Early scans can detect recurrence before the cancer progresses to a more advanced stage.

83 Background: The abundant expression of prostate-specific membrane antigen (PSMA) on prostate cancer cells provides a rationale for antibody therapy. PSMA antibody drug conjugate (ADC) is a fully human antibody to PSMA linked to the microtubule disrupting agent monomethyl auristatin E (MMAE). It binds PSMA and is internalized and cleaved by lysosomal enzymes releasing free MMAE causing cell cycle arrest and apoptosis. We enrolled 70 patients (pts) in a phase II trial of PSMA ADC in taxane-refractory metastatic castration-resistant prostate cancer (mCRPC). Methods: Pts with progressive mCRPC following taxane and ECOG PS 0 or 1 were eligible. PSMA ADC was administered Q3 week IV for up to eight cycles. Safety, tumor response by prostate-specific antigen (PSA), circulating tumor cells (CTC), imaging, biomarkers and clinical progression were assessed. Dosing was initiated at 2.5 mg/kg and adjustment for tolerability was allowed. Results: Thirty five pts began treatment at 2.5 mg/kg. Due to neutropenia, the remaining 35 pts began at 2.3 mg/kg. All pts received prior docetaxel and abiraterone and/or enzalutamide. Forty one percent also received cabazitaxel. Adverse events (AEs) were consistent with what was seen in phase I; most common significant AEs were neutropenia (grade 4, 6.7% and 11.4% at 2.3 and 2.5 mg/kg, respectively) and peripheral neuropathy (grade 3 or higher, 6.7% (2.3) and 5.7% (2.5)). Two pts at 2.5 mg/kg died of sepsis. 43% of pts at 2.3 and 37% of pts at 2.5 had declines in CTC from 5 or more to less than 5 cells/7.5 ml blood and 57.1% (2.3) and 74.1% (2.5) had 50% or more CTC declines; 26.1% (2.3) and 16.1% (2.5) had PSA declines of 30% or more thus far. PSA and CTC responses were associated with higher PSMA expression on CTC and lower neuroendocrine (NE) markers. The CTC conversion rate (5 or more to less than 5) was approximately 80% in pts with low NE markers. Prior cabazitaxel or abiraterone and/or enzalutamide did not appear to affect response. Centralized assessments of images by RECIST of all pts are currently planned and will be presented. Conclusions: PSMA ADC at 2.3 mg/kg was generally well tolerated in pts with progressive mCRPC previously treated with taxane. Anti-tumor activity, CTC and PSA reductions were observed at 2.3 and 2.5 mg/kg. Updated safety, tumor response and radiographic assessments from the full cohorts of 2.3 and 2.5 mg/kg will be presented. Testing in taxane naïve pts is also ongoing. Clinical trial information: NCT01695044.

Invited Commentary: Changing Landscape of Imaging in Recurrent Prostate Cancer.

Introduction: Recent approvals of new prostate cancer (PCa) drugs and a growing number of pipeline agents have created opportunities for designing rational drug combinations. Potent antiandrogens such as enzalutamide and abiraterone affect expression of numerous androgen-regulated molecules, including PSMA, a well-characterized cell-surface target for PCa therapy. Methods: Cytotoxicity and the kinetics of antigen expression were evaluated in PCa cell lines (LNCaP, C4-2 and 22Rv1) that vary according to androgen dependence and level of PSMA expression. Expression of PSMA and prostate-specific antigen (PSA) was evaluated over time in cells cultured in enzalutamide or abiraterone. Reversibility was examined following drug washout. Cells were tested for susceptibility to antiandrogens used alone and in combination with PSMA ADC, which is a fully human PSMA monoclonal antibody conjugated to the microtubule disrupting agent monomethyl auristatin E (MMAE). Potential drug synergy or antagonism was evaluated using the Combination Index and Bliss independence methods. Results: In androgen-dependent LNCaP cells, enzalutamide and abiraterone exerted antiproliferative effects that were accompanied by a 2- to 3-fold increase in PSMA expression and a decrease in PSA expression. PSMA expression reached maximum levels after four weeks’ culture in enzalutamide and returned to baseline levels within days following enzalutamide removal. In androgen-independent C4-2 cells, enzalutamide and abiraterone increased PSMA expression in the absence of any significant anti-proliferative effect. PSMA ADC exhibited synergistic antitumor activity with both enzalutamide and abiraterone in LNCaP and C4-2 cells. Lesser effects were observed using 22Rv1 cells, an androgen-independent cell line with low basal expression of PSMA. Conclusions: Enzalutamide and abiraterone significantly and reversibly augmented PSMA expression and potentiated the activity of PSMA ADC in androgen-dependent and -independent PCa cell lines in vitro. In androgen-independent cells, the effects on PSMA expression and PSMA ADC activity were uncoupled from any anti-proliferative effect of the antiandrogens. The findings support clinical exploration of regimens that combine potent antiandrogens and PSMA-targeted therapies. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):A262. Citation Format: Jose D. Murga, Wells W. Magargal, Sameer M. Moorji, Vincent A. DiPippo, William C. Olson. Antiandrogen modulation of prostate-specific membrane antigen (PSMA): Dynamics and synergy with PSMA-targeted therapy. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr A262.

TPS5122 Background: Up to half of patients (pts) whose prostate cancer (PC) has been treated with radiotherapy (RT) or radical prostatectomy (RP) as primary therapy will develop biochemical recurrence (BCR), defined as a prostate-specific antigen (PSA) increase without evidence of metastases on conventional imaging (e.g., CT/MRI). Compared with conventional imaging, prostate-specific membrane antigen (PSMA) positron emission tomography/computed tomography (PET/CT) is a more precise imaging method that may detect small PC lesions in pts with BCR. Effective treatment is needed for pts with BCR at high risk of metastatic progression, and who have lesions identified by PSMA PET/CT, to delay progression. Darolutamide (DARO) is a structurally distinct and highly potent androgen receptor inhibitor with low blood–brain barrier penetration and limited potential for drug–drug interactions. In ARAMIS (phase 3; NCT02200614), DARO significantly improved metastasis-free survival (MFS) and reduced risk of death in pts with nonmetastatic castration-resistant prostate cancer (nmCRPC). ARASTEP (NCT05794906) is evaluating whether DARO plus androgen-deprivation therapy (ADT) improves radiological progression-free survival (rPFS) by PSMA PET/CT vs placebo (PBO) plus ADT in pts with BCR following primary therapy and PSMA PET/CT-positive lesions. Methods: ARASTEP is a global, phase 3, double-blind, placebo-controlled study in which ~750 pts from 192 sites will be randomized to receive oral DARO 600 mg twice daily or PBO, both with ADT, for 24 months. Eligible pts have PC previously treated with primary RT or RP followed by adjuvant RT (ART) or salvage RT (SRT) or RP alone if unfit for ART/SRT, ECOG PS 0/1, serum testosterone &gt;150 ng/dL, and high-risk BCR. High-risk BCR is defined as PSA doubling time (PSADT) &lt;12 months, PSA ≥0.2 ng/mL above the nadir after primary RP followed by ART or SRT or ≥2 ng/mL after primary RT only, and ≥1 PSMA PET/CT-positive lesion with no evidence of metastasis on conventional imaging. Image-guided RT (IGRT) or surgery of baseline (BL) PSMA PET lesions assessed by blinded independent central review (BICR) is allowed ≤12 weeks from randomization. Stratification factors are PSADT (&lt;6 vs ≥6–&lt;12 months), intent to treat BL PSMA PET/CT lesions by BICR with IGRT/surgery (Yes vs No), and distant ± locoregional vs locoregional-only metastases. The primary endpoint is rPFS by PSMA PET/CT assessed by BICR. Secondary endpoints are MFS by BICR, time to CRPC, time to first subsequent systemic antineoplastic therapy, time to locoregional progression by PSMA PET/CT, time to first symptomatic skeletal event, overall survival, PSA &lt;0.2 ng/mL at 12 months, time to deterioration in FACT-P score, safety, and time to symptomatic progression. Enrollment for ARASTEP began in April 2023. Currently 18 patients have been enrolled. Clinical trial information: NCT05794906 .

Upregulation of prostate-specific membrane antigen after androgen-deprivation therapy

266 Background: Prostate-specific membrane antigen (PSMA) is expressed ubiquitously in prostate adenocarcinoma, and the intensity of expression increases with disease aggressiveness. Exploiting PSMA for therapy could potentially be aided by a minimally invasive means for measuring PSMA on tumor cells. Here we describe the development and characteristics of a novel assay for quantitating PSMA on canonical and non-canonical circulating tumor cells (CTCs). Methods: The PSMA CTC test was developed using LNCaP (high PSMA), 22Rv1 (low PSMA) and PC3 (no PSMA) cells spiked into normal blood. Nucleated blood cells were plated onto glass slides and subjected to immunofluorescent staining followed by CTC identification using the Pyxis Scanning Platform at Epic Sciences. The four-color assay evaluated PSMA expression on individual CTCs, identified as cells which are cytokeratin+, CD45-, and with an intact DAPI nucleus. Multiple antibody clones and assay conditions were evaluated, and the final PSMA CTC test has high specificity and sensitivity. Acceptance criteria included signal intensities in LNCaP versus PC3, subcellular localization of PSMA, and potential interference by a PSMA-targeted therapy. Clinical feasibility of the optimized assay was assessed on samples from CRPC patients. Results: The average PSMA signal intensity for LNCaP was 20-fold higher than that for PC3 and 10-fold higher than the minimum cutoff. PSMA displayed a predominantly membrane-localized pattern of staining that was distinct from cytokeratin. Assay performance was unaffected by the presence of PSMA ADC, a PSMA-targeted antibody-drug conjugate that is in phase II clinical testing. In feasibility tests on patient samples, the assay demonstrated utility in detecting and quantitating PSMA on individual and clustered CTCs as well as on apoptotic, cytokeratin-negative, and small cytokeratin-positive CTC candidates. Conclusions: PSMA expression was successfully detected and quantitated on diverse types of circulating cells present in the blood of patients with CRPC. Assay performance was unaffected by the presence of a PSMA-targeted therapeutic agent. PSMA CTC data are being collected in the ongoing phase II study of PSMA ADC for comparison with treatment outcomes.

Prostate-specific membrane antigen (PSMA), a type II transmembrane glycoprotein folate receptor, is highly expressed in metastatic castrate-resistant prostate cancer (CRPC) and expression increases following androgen deprivation therapy. TD001 is a novel antibody-drug conjugate (ADC) composed of a deimmunized anti-PSMA IgG1 monoclonal antibody (HuJ591), conjugated to a highly stable, protease-cleavable proprietary Topo I inhibitor exatecan linker-payload (LD038), with a drug-to-antibody ratio (DAR) of 8. Free payload and total ADC were evaluated in mouse plasma, tumor, and liver, after TD001 10 mg/kg IV (which has potent antitumor activity in vivo) in 2 human CRPC cell line-derived xenograft (CDX) models, LNCaP-abl (high PSMA expression ∼104 ligands/cell) and 22Rv1 (intermediate/heterogeneous PSMA ∼102-104 ligands/cell) in castrated NRG/NSG mice. The TD001 PK profile was characterized across a wide temporal span post treatment, in LNCaP-abl (5 min to 10 days) and 22Rv1 (2 h to 6 days). The PK/PD profile of a range of doses (3-20 mg/kg) was characterized in both models. Dose proportional free exatecan concentrations were observed in tumor and plasma, and a consistently high tumor/plasma (T/P) ratio (∼70-100 fold) was seen in both tumor models across the range of TD001 doses tested. Potent tumor growth inhibition (TGI) was dose dependent up to 20 mg/kg. PK/PD and the high therapeutic index with different dosing schedules are presented separately. Free exatecan was detected in tumors 5 min post treatment in LNCaP-abl. Free exatecan concentrations were approximately 80x higher in tumor compared to plasma 2 h post treatment, and at least 100x higher from 6 h to 6 days post treatment, showing rapid and high distribution of TD001 to the targeted tumor tissue regardless of PSMA expression levels. The concentration of total ADC (assuming constant DAR 8) was ∼200 µg/mL (5 min post treatment), remained high for up to 6 days post treatment, while decreasing gradually from 24 h allowing for prolonged tumor exposure to TD001. The high and prolonged T/P ratio supports the excellent therapeutic index observed in TGI studies in both CDX castrated mice models, with TGI &amp;gt;90% and good tolerance (described separately). Of note, exatecan plasma levels rapidly declined under 0.5 ng/mL (from 24 h) and were under the limit of quantification (0.1 ng/mL) 10 days post treatment, preventing systemic toxicity. No free exatecan accumulation was observed after repeat dosing (described separately). TD001 effectively and preferentially delivers the potent exatecan payload to tumor tissue, with minimal systemic exposure, contributing to an excellent therapeutic index and strong antitumor activity in multiple CRPC models with high or intermediate PSMA expression. Our preclinical PK data support clinical development of TD001 in PSMA-expressing CRPC patients. Citation Format: Lavinia Morosi, Daniela Impellizzieri, Roberta Frapolli, Elisa Storelli, Atik Balla, Carlo V. Catapano, Jemila Houacine, Esteban Cvitkovic, Maurizio D’Incalci. Optimal free exatecan payload tumor/plasma ratio of TD001, a new ADC against PSMA, in CRPC CDX mouse models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 318.

Prostate-specific membrane antigen (PSMA) tracers have increased sensitivity in the detection of prostate cancer, compared with conventional imaging. We assessed the management impact of 18F-DCFPyL PSMA PET/CT in patients with prostate-specific antigen (PSA) recurrence after radical prostatectomy (RP) and report early biochemical response in patients who underwent radiation treatment. Methods: One hundred patients were enrolled into a prospective study, with a prior RP for prostate cancer, a PSA of 0.2-2.0 ng/mL, and no prior treatment. All patients underwent diagnostic CT and PSMA PET/CT, and management intent was completed at 3 time points (original, post-CT, and post-PSMA) and compared. Patients who underwent radiotherapy with 6-mo PSA response data are presented. Results: Ninety-eight patients are reported, with a median PSA of 0.32 ng/mL (95% CI, 0.28-0.36), pT3a/b disease in 71.4%, and an International Society of Urological Pathology grade group of at least 3 in 59.2%. PSMA PET/CT detected disease in 46.9% of patients, compared with 15.5% using diagnostic CT (PSMA PET, 29.2% local recurrence and 29.6% pelvic nodal disease). A major change in management intent was higher after PSMA than after CT (12.5% vs. 3.2%, P = 0.010), as was a moderate change in intent (31.3% vs. 13.7%, P = 0.001). The most common change was an increase in the recommendation for elective pelvic radiation (from 15.6% to 33.3%), nodal boost (from 0% to 22.9%), and use of concurrent androgen deprivation therapy (ADT) (from 22.9% to 41.7%) from original to post-PSMA intent because of detection of nodal disease. Eighty-six patients underwent 18F-DCFPyL-guided radiotherapy. Fifty-five of 86 patients either did not receive ADT or recovered after ADT, with an 18-mo PSA response from 0.32 to 0.02 ng/mL; 94.5% of patients had a PSA of no more than 0.20 ng/mL, and 74.5% had a PSA of no more than 0.03 ng/mL. Conclusion: 18F-DCFPyL PET/CT has a significant impact on management intent in patients being considered for salvage radiotherapy after RP with PSA recurrence. Increased detection of disease, particularly in the pelvic lymph nodes, resulted in increased pelvic irradiation and concurrent ADT use. Early results in patients who are staged with 18F-DCFPyL PET/CT show a favorable PSA response.

Nadir Prostate-specific Antigen as an Independent Predictor of Survival Outcomes: A Post Hoc Analysis of the PROSPER Randomized Clinical Trial.

18F-PSMA-1007 PET/CT Detects Micrometastases in a Patient With Biochemically Recurrent Prostate Cancer.