Gordon Brown, DO1; Raoul S. Concepcion, MD2; Celestia Higano, MD3; Bassem Elmankabadi, MD4; Ben Chien, PhD4; Yisheng Lee, MD4; Yuhua Li, PhD4; Andrew Guarino, PhD4; William Miller, PhD4; Jagdish Parasrampuria, PhD4; Mathieu Boudreau, PhD4; Martha Hernandez-Illas, MD5; Connor Peterson, MD4
1Department of Urology, Jefferson Health, Sewell, New Jersey, USA
2 Department of Urology, US Urology Partners, Nashville, Tennessee, USA
3 Department of Medical Oncology, Madrona Oncology and University of British Columbia, Vancouver, BC, Canada
4 Foresee Pharmaceuticals Co, Newark, Delaware, USA
5 QPS Holdings LLC, Newark, Delaware, USA
KEYWORDS:
Prostatic neoplasms; leuprolide; testosterone; prostate-specific antigen
Abstract
Background: We sought to determine the safety, efficacy, and pharmacokinetic profile of a 3-month depot formulation of leuprolide mesylate 21 mg for up to 6 months of treatment in patients with advanced prostate cancer.
Methods: Patients with prostate cancer who were candidates for androgen-deprivation therapy received 2 subcutaneous injections of leuprolide mesylate 21 mg 3 months apart. The study’s co–primary end points were the percentage of patients with a serum testosterone level lower than 1.7 nmol/L (50 ng/dL) at day 28 and a serum testosterone level lower than 1.7 nmol/L (50 ng/dL) sustained at every visit from days 28 to 168. The secondary end points included changes in prostate-specific antigen and luteinizing hormone levels and testosterone levels lower than 0.7 nmol/L (20 ng/dL). Safety, tolerability, and pharmacokinetic parameters were also assessed.
Results: A total of 144 patients were enrolled in the study. Following the first dose of leuprolide mesylate 21 mg, 98% (95% CI, 95.0%-99.8%) of participants had castration-level testosterone (<1.7 nmol/L [<50 ng/dL]) on day 28. On days 42 through 168, 98% (95% CI, 93.0%-99.0%) of patients had sustained castration-level testosterone (<1.7 nmol/L [<50 ng/dL]). The percentage of participants with serum testosterone suppression (<0.7 nmol/L [<20 ng/dL]) was 72.0% on day 28 and 96.4% on day 168. The majority of adverse events were mild to moderate and most commonly included hot flushes (24.3%) and hypertension (11.1%). Effects on QT corrected intervals were comparable to other gonadotropin-releasing hormone agonists.
Conclusions: Leuprolide mesylate 21 mg administered at 3-month intervals suppressed and maintained serum testosterone at castration levels (<1.7 nmol/L [<50 ng/dL]) while demonstrating an acceptable safety profile.
In 1941, Huggins and Hodges1,2 established prostate cancer as an endocrine-responsive disease. The use of androgen-deprivation therapy (ADT) to lower testosterone to a castration level (<1.7 nmol/L [<50 ng/dL]) has been shown to improve oncologic outcomes in patients with localized prostate cancer receiving radiation therapy as primary treatment. Since then, ADT has been the backbone of therapy for advanced disease. Newer and more sensitive assays suggest that a serum testosterone level lower than 0.7 nmol/L (20 ng/dL) may, in fact, be the new standard.3,4
Chronic administration of a gonadotropin-releasing hormone (GnRH) agonist downregulates GnRH receptors in the pituitary gland, resulting in the complete suppression of luteinizing hormone (LH), follicle-stimulating hormone, and gonadal steroids after an initial stimulatory phase. Among currently available GnRH agonists, the administration of leuprolide acetate has shown satisfactory efficacy with manageable side effects.1,5
Leuprolide acetate is the synthetic analogue of naturally occurring GnRH. Chemically modified on residues 6 and 10, leuprolide acetate possesses a higher binding affinity to androgen receptors and is more stable than naturally occurring GnRH.6 Within 1 month of treatment, patients with prostate cancer receiving leuprolide acetate showed clinically significant suppression of serum testosterone levels, similar to surgical castration.
Foresee Pharmaceuticals previously developed an FP-001 42-mg (Camcevi) 6-month depot formulation, a mesylate salt of leuprolide that has been approved by the US Food and Drug Administration for the treatment of advanced prostate cancer. The drug under investigation in the current study, FP-001 21 mg, is a depot formulation of leuprolide mesylate intended for the treatment of advanced prostate cancer, with biological activity comparable to Eligard (leuprolide acetate) 22.5 mg.7
Leuprolide mesylate 21 mg was designed to be delivered at a controlled rate over a 3-month period. The FP-001 21-mg formulation uses the same solvent, N-methyl-2-pyrrolidone, as Eligard but has a different polymer system—poly(D,L-lactide–co-glycolide)—to achieve sustained release of leuprolide. Leuprolide mesylate 21 mg is supplied as a single sterile, filled syringe that is ready to use and does not require mixing before subcutaneous injection.
This multinational, multicenter, open-label, single-arm study assessed the safety, efficacy, and pharmacokinetic characteristics of FP-001 21 mg in male participants with prostate cancer who were candidates for ADT. The study was conducted following good clinical practice requirements. Local ethics approval and written informed consent from participants were obtained in accordance with the ethical principles stated in the Declaration of Helsinki.
This study enrolled patients with advanced prostate cancer who were hormone therapy–naive candidates for continuous ADT. Patients were required to have a morning serum testosterone level above 5.2 nmol/L (150 ng/dL) at screening, adequate organ function, an ECOG-ACRIN performance score of at least 2, and a life expectancy of at least 18 months. Key exclusion criteria included concomitant use of chemotherapy (or chemotherapy within the past 8 weeks), immunotherapy, cryotherapy, radiation therapy, or antiandrogen therapy for the treatment of prostate cancer; clinical evidence or risk of urinary obstruction or spinal cord compression; clinically significant abnormal electrocardiogram (ECG) or clinically significant cardiovascular disease; use of 5-α reductase inhibitor within the past 6 months; the history or presence of insulin-dependent diabetes (type 1; the presence of well-controlled type 2 diabetes was allowed if only oral hypoglycemic agents were required); use of systemic corticosteroids at a dose greater than 10 mg/d; or any contraindication to the use of an LH-releasing hormone analogue.
The study lasted 28 weeks, including a 4-week screening period. Participants were treated with 2 separate doses of FP-001 21 mg by subcutaneous injection 12 weeks apart, at day 0 and day 84. All participants were followed for safety, efficacy, and pharmacokinetic assessments through day 168 (ie, 24 weeks after starting FP-001). Testosterone levels were collected throughout the study, including at screening and days 0 (before and after their index dose), 1, 2, 3, 7, 14, 21, 28, 42, 56, 77, 84 (pre-dose and post-dose), 85, 86, 87, 98, 112, 126, 140, 161, and 168. To evaluate whether testosterone levels remained in the castration range beyond day 168, pharmacokinetic and pharmacodynamic assessments were performed on day 182 for the first 30 patients enrolled in the study.
The co–primary end points for the study were the percentage of participants with castration levels of testosterone (<1.7 nmol/L [<50 ng/dL]) on day 28 following administration of FP-001 21 mg and the percentage of participants with sustained castration levels of testosterone maintained from day 28 through day 168. The secondary efficacy end points included the changes in testosterone and LH levels from before the second injection of FP-001 21 mg through 14 days after the second injection (to assess acute-on-chronic effect surge), the overall change in LH and prostate-specific antigen (PSA) levels, the percentage of patients with PSA relapse by day 168 (ie, an increase in serum PSA >50% PSA nadir by day 168), and the percentage of patients with serum testosterone suppression levels lower than 0.7 nmol/L (20 ng/dL) on days 28 and 168 and sustained from days 28 through 168.
Safety assessments in this study included monitoring for adverse events (AEs) and serious AEs by taking vital signs; performing a physical examination and a 12-lead ECG; examining local injection site reactions; and assessing bone pain, urinary signs and symptoms, and laboratory values.
In a subset of 30 participants, the serum pharmacokinetic profile of leuprolide was determined from baseline to day 182 (ie, for 14 weeks following the second injection of FP-001 21 mg). The pharmacokinetic parameters of leuprolide were determined during the study period, including maximum concentration (Cmax), time to Cmax, concentration at weeks 4 and 12, area under the curve for weeks 0 through 4 and weeks 0 through 12, and average concentration from weeks 0 through 12 after each dose. Serum testosterone levels were measured to determine the pharmacodynamic effect of FP-001 21 mg.
The intention-to-treat population was defined as any participant who received at least 1 dose of FP-001 21 mg; this population was used in the efficacy analyses. Any participant receiving a dose of FP-001 21 mg was included in the safety analysis.
Continuous variables were presented as mean, median, SD, and 95% CI values for descriptive statistics. Categorical variables were presented as frequencies and percentages. Changes from baseline were evaluated with a paired t test or Wilcoxon signed rank test for continuous variables at a significance level of .05. For primary end points, the percentage of participants with a serum testosterone value lower than 1.7 nmol/L (50 ng/dL) on days 28 and 168 was analyzed using a standard largesample approximation to a binomial distribution. The percentage of participants with serum testosterone values below 1.7 nmol/L (50 ng/dL) from day 28 through day 168 was analyzed using the Kaplan-Meier approach. A participant with a testosterone level of at least 1.7 nmol/L (50 ng/dL) between days 28 and 168 was considered to have experienced an event. The change from baseline was evaluated by paired t test. If the data strongly indicated a violation of the standard assumption (P < .05 for the test of normality), the Wilcoxon signed rank test was applied for analysis. Unless otherwise specified, all statistical assessments were 2 sided and evaluated at a significance level of .05. The baseline value was defined as the last value collected before the start of the first dose of study drug administration unless otherwise specified. A nominal visit was used to analyze the efficacy and safety end points.
A total of 144 participants were enrolled in this study. Of the 144 enrolled participants, 15 (10.4%) participants did not complete the study (see Figure 1). Baseline demographics and characteristics of disease severity are summarized in Table 1. All 144 enrolled participants were included in the intention-to-treat analysis.
Following the first dose of FP-001 21 mg, the percentage of participants with castration levels of testosterone (<1.7 nmol/L [<50 ng/dL]) on day 28 was 98% (95% CI, 95.0%-99.8%). Two participants did not reach a testosterone level lower than 1.7 nmol/L (50 ng/dL) by day 28, but both participants’ serum testosterone levels were lower than 1.7 nmol/L (50 ng/dL) on day 56, and their serum testosterone levels remained lower than 1.7 nmol/L (50 ng/dL) until the end of the study.
Figure 1. CONSORT flowchart for the study
The percentage of participants with serum testosterone suppressed to castration levels (<1.7 nmol/L [<50 ng/dL]) was 100% (95% CI, 97.2%-100%) at day 168. In addition, of the 29 participants with evaluable data in the subset followed through day 182, all 29 (100% [95% CI, 88.1%-100%]) maintained castration levels of testosterone. The percentage of participants with sustained testosterone suppression (<1.7 nmol/L <50 ng/dL] each month) was 98% (95% CI, 93.0%-99.0%) from day 28 through day 168 (see Figure 2).
Only 1 participant had serum testosterone levels above 1.7 nmol/L (50 ng/dL) after having previously attained castration levels during the study. He was observed with a serum testosterone level of 11.7 nmol/L (338 ng/dL) at 4 hours after dose administration on day 84, but the level fell to 0.3 nmol/L (9.49 ng/dL) on day 85.
Figure 2. Line graph showing mean serum testosterone levels over time in the intention-totreat population SI conversion factor: To convert ng/dL to nmol/L, multiply by 0.0347.
The median PSA level at baseline was 8.2 ng/mL (range, 0.08-698.5 ng/mL), and the mean (SD) PSA level at baseline was 34.2 (109.7) ng/mL. The administration of FP-001 21 mg resulted in a statistically significant reduction in serum PSA levels after the first injection, and the PSA-lowering effect of FP-001 21 mg was sustained until the end of the study. Median PSA level decreased to 4.02 ng/mL (range, 0.02-205.20 ng/mL), and mean (SD) PSA levels decreased to 9.3 (20.9) ng/mL on day 28. On day 84, median PSA further decreased to 0.84 ng/mL (range, 0.02-37.60 ng/mL) while mean (SD) PSA decreased to 1.9 (4.1) ng/mL. The lowered values were maintained on day 168, with a median PSA of 0.5 ng/mL (range, 0.02-11.70 ng/mL) and a mean (SD) PSA of 1.2 (2.0) ng/mL (see Figure 3).
Two participants had an increase in PSA levels during the treatment period, despite sustained castration levels of testosterone (ie, they became castration resistant). The first participant (cancer stage III, T3N0M0) had a baseline PSA level of 18.3 ng/mL (baseline testosterone, 18.3 nmol/L [527 ng/dL]), a PSA level of 1.6 ng/mL on day 84 (testosterone, 0.5 nmol/L [15.2 ng/dL]), and a PSA level of 2.48 ng/mL on day 168 (testosterone, 0.5 nmol/L [15.8 ng/dL]). The second participant (stage IIA disease, T2NxM0) had a baseline PSA level of 1.23 ng/mL (baseline testosterone, 16.7 nmol/L [481 ng/dL]), a PSA level of 0.23 ng/mL on day 84 (testosterone, 0.5 nmol/L [13.4 ng/dL]), and a PSA level of 0.53 ng/mL on day 168 (testosterone, 0.4 nmol/L [12.2 ng/dL]).
The median LH level at baseline was 2.5 IU/L (range, 0.6-18.1 IU/L), and the mean (SD) LH level at baseline was 3.3 (2.7) IU/L. A rapid increase in serum LH levels was observed on day 1, with a median level of 13.9 IU/L (range, 1.6-29.3 IU/L) and a mean (SD) level of 14.1 (5.7) IU/L after the first dose of FP-001 on day 0. The rise in LH levels on day 2 fell over time and reached a nadir on day 42 (median, 0.06 IU/L; mean [SD], 0.08 [0.04] IU/L), which persisted on day 84 (median, 0.05 IU/L; mean [SD], 0.08 [0.19] IU/L). The rise in LH levels after the second dose of FP-001 21 mg on day 84 started to decline on day 86 and approached a nadir by day 98 (median, 0.05 IU/L; mean [SD], 0.08 [0.15] IU/L). The lower LH level was maintained to day 168 (median, 0.05 IU/L; mean [SD], 0.08 [0.17] IU/L) (see Figure 4).
Figure 3. Line graph showing mean prostate-specific antigen (PSA) levels over time in the intention-totreat population SI conversion factor: To convert ng/mL to µg/L, multiply by 1.
Leuprolide mesylate 21 mg given on days 0 and 84 significantly reduced serum LH levels on day 168 compared with baseline. With each dose, LH transiently increased, followed by a rapid decline, consistent with the biology of GnRH agonists.
The percentage of participants with serum testosterone levels lower than 0.7 nmol/L (20 ng/dL) was 72.0% on day 28 and 96.4% on day 168. Of the participants with serum testosterone lower than 0.7 nmol/L (20 ng/dL) at day 28, 63% maintained this serum testosterone level through day 168.
A total of 217 AEs in 90 participants (62.5%) were reported, with at least 1 treatment-emergent AE (Table 2). When analyzed by relationship to FP-001 21 mg, 88 AEs in 53 participants (36.81%) were judged by an investigator to be drug related. The most common (≥5%) treatment-emergent AEs observed were hot flushes (24.3%), followed by hypertension (11.1%), injection-site reactions (9.7%), and weight gain (7.6%). When analyzing the severity of all observed AEs during the study period, 95.9% of treatment-emergent AEs were grade 1 (mild) or grade 2 (moderate) in severity. Nine grade 3 (severe) AEs were observed in 7 participants, and 10 serious AEs were observed in 9 participants (6.3%), none of which were considered drug related. No life-threatening AEs or deaths were reported during the study period. One participant experienced a grade 3 AE (stroke), which led to premature trial discontinuation.
Figure 4. Line graph showing mean luteinizing hormone (LH) levels over time in the intention-to-treat population
Results of physical examination and vital sign assessments revealed no clinically significant changes at the end of the study. Regarding safety assessments, 1 participant was noted to have clinically significant elevations in aspartate aminotransferase (AST) (116 U/L) and alanine aminotransferase (ALT) (145 U/L) at the end of the study. These abnormalities were assessed by the investigator as possibly related to FP-001 21 mg. Across all participants, the mean changes in ALT and AST from baseline to the end of the study were 5.4 U/L and 3.2 U/L, respectively. There was a slight decrease in serum bilirubin (−0.14 mg/dL) from baseline to the end of the study. Only 1 participant with a normal ALT level at baseline had an abnormal ALT level at the end of the study, while 4 participants with normal AST levels at baseline had abnormal AST levels at the end of the study.
At day 168, most changes in ECG parameters were not statistically significant compared with the baseline values, with the exception of decreases in heart rate and increases in R-R, QT, and QT corrected (QTcF) intervals and in the QRS complex.
Additional pharmacokinetic and ECG analyses showed that the standard clinical dose of FP-001 21 mg reduced testosterone to castration levels with no meaningful change in ECG, except for the expected increase in the QTcF interval. The observed increase in QTcF interval was consistent with the known effect of similar sex hormone preparations on QT interval. In the central tendency analysis, the peak increase in change in QTcF was 15.9 milliseconds at 4 hours after the dose administered on day 84. The simplified models showed the expected negative relationship between change in QTcF and concentrations of testosterone and leuprolide.
Although minimal and clinically insignificant effects of FP-001 21 mg on heart rate, PR interval, and QRS complex were observed during the study period, the PR interval increased to above 200 milliseconds, with at least a 25% increase, in as many as 3.6% of patients on day 28 after FP-001 21 mg administration. This result could indicate an effect of leuprolide or reduced testosterone on atrioventricular conduction. There were no instances of seconddegree atrioventricular block in this study, though testosterone administration was associated with either no change in PR interval or a modest increase of 6 milliseconds, as previously reported. Although unlikely, a small, infrequent direct effect of leuprolide on PR interval cannot be excluded.
All 144 participants who had FP-001 21 mg administered had grade 0 to grade 1 skin irritation at the injection site. No participants had moderate local injection-site intolerance. Some abnormal findings were noted, however, including subcutaneous hemorrhage, ecchymosis, nodules, and induration.
No statistically significant change was observed in bone pain assessments from day 0 to day 168. According to the quality-of-life assessment, 2 separate doses of FP-001 21 mg did not cause additional urinary discomfort during the study period.
The formulation of FP-001 21 mg resulted in a 2-phase leuprolide concentration vs time profile characterized by a distinctive burst and a plateau phase. After dosing, an initial rapid increase of serum leuprolide concentration was observed, followed by a rapid decline over the first 3 days after the dose. After an initial burst phase characterized by high mean serum leuprolide concentrations (>34 ng/mL), leuprolide levels remained relatively constant over the majority of each 12-week (3-month) dosing interval. Leuprolide appeared to be released continuously by the third day after dosing, with steady serum concentrations (plateau phase) through the 12-week dosing interval (mean concentration range, 0.2-1.6 ng/mL). The Cmax concentration of serum leuprolide was between 37.7 ng/mL and 43.4 ng/mL and reached a maximum level approximately 2 to 4 hours after the first and second injections of FP-001 21 mg. The mean concentration range of leuprolide declined to a week 12 concentration of 0.3 ng/mL to 0.4 ng/mL.
Serum leuprolide concentrations and the associated pharmacokinetics following the first and second doses of FP-001 21 mg were similar, suggesting a lack of clinically significant accumulation with repeated dosing 12 weeks apart (Table 3).
This trial demonstrated that the first injection of FP-001 21 mg was effective in achieving castration levels of testosterone (<1.7 nmol/L [<50 ng/dL]) by day 28 in 98% of participants and that a subsequent dose, administered approximately 3 months later, successfully suppressed serum testosterone to castration levels in 100% of participants at day 168. Using a more stringent criterion for testosterone suppression,8 96% of the patients had serum testosterone levels lower than 0.7 nmol/L (20 ng/dL) at the end of the study. Although 1 participant exhibited serum testosterone levels above 1.7 nmol/L (50 ng/dL) after achieving the castration level of testosterone on day 28, no participants exhibited an elevation of serum testosterone above 1.7 nmol/L (50 ng/dL) by day 168.
Overall, the incidence of drug-related AEs after the administration of FP-001 21 mg in the present study was comparable to the incidence of drug-related AEs for similarly approved GnRH analogues, with hot flushes being the most frequently reported AE. The administration of FP-001 furthermore did not cause any additional unexpected AEs for this class of drug administered in this patient population. Regarding pharmacokinetics, administration of FP-001 21 mg resulted in a multiphasic leuprolide concentration vs time profile characterized by a distinctive burst phase and a plateau phase. The initial acute increase of FP-001 concentration, followed by the rapid decline to a steady-state level, was similar to the release pattern seen with the other leuprolide depot formulations.
Adequate reconstitution of GnRH analogues is essential for the administration of products that require premixing to safeguard optimal and effective treatment of patients with prostate cancer. Because preparation errors associated with a lack of drug efficacy have been reported, including an increase in testosterone levels above the castration level and an increase in PSA levels,7 eliminating the need to mix FP-001 saves time in the clinic and could reduce a potential source of iatrogenic therapeutic inefficiency. Leuprolide mesylate 21 mg was developed as a filled, ready-to-use syringe that does not require reconstitution before subcutaneous injection and therefore has an advantage over other depot formulations.
Leuprolide mesylate 21 mg achieved the therapeutic goal of suppressing serum testosterone to less than 1.7 nmol/L (50 ng/dL) in 98% of participants on day 28. Serum testosterone levels lower than 1.7 nmol/L (50 ng/dL) were maintained in 98% of participants from day 28 through day 168. Two separate doses of FP-001 21 mg administered 12 weeks apart demonstrated similar safety and pharmacokinetic profiles compared with marketed products for the treatment of advanced prostate cancer, with the associated advantage of eliminating the need for manual reconstitution.
Two sequential doses of FP-001 21 mg 12 weeks apart effectively reduced serum testosterone levels below 1.7 nmol/L (50 ng/dL) in more than 98% of study participants on day 28, a level that 98% of participants maintained from days 28 through 168. There was no observed acute-on-chronic surge effect after the second injection during the study period. In addition, administration of FP-001 21 mg effectively reduced serum PSA levels. The administration of 2 doses of FP-001 21 mg 12 weeks apart demonstrated a safe and tolerable profile during the study period. Whether achieving testosterone levels lower than 0.7 nmol/L (20 ng/dL) is clinically significant remains to be determined.
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Published: October 5, 2025.
Conflict of Interest Disclosures: Bassem Elmankabadi, Ben Chien, Yisheng Lee, Yuhua Li, Andrew Guarino, William Miller, Jagdish Parasrampuria, Mathieu Boudreau, and Connor Peterson are employees of Foresee Pharmaceuticals. Martha Hernandez-Illas is an employee of QPS Holdings LLC.
Funding/Support: This study was funded by Foresee Pharmaceuticals Co, Ltd (Taipei City, Taiwan). In collaboration with the investigators and authors of this study, the funder contributed to the study design. The clinical research organization (QPS Holdings LLC) conducted the clinical trial in collaboration with primary investigators in protocol implementation, data collection, data analysis, and data interpretation. Foresee funded editorial assistance for the writing of the report.
Author Contributions: All authors had full access to the trial data. All authors were involved in developing and approving the manuscript.
Data Availability Statement: Data presented in this article have been submitted to the US Food and Drug Administration and European Medicines Agency as part of a New Drug Application. The data presented in this article are not available anywhere else.
Acknowledgments: Foresee Pharmaceuticals is the marketing authorization holder.
Citation: Brown G, Concepcion RS, Higano C, et al. An open-label, single-arm study of the efficacy, safety, and pharmacokinetics of leuprolide mesylate injectable suspension in patients with prostate cancer. Rev Urol. 2025;24(3):e51-e62.
Corresponding author: Connor Peterson, MD, Foresee Pharmaceuticals Co, 550 S College Ave, Suite 107, Newark, DE 19713 (connor.peterson@foreseepharma.com)
