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ERLEADA - Effect on Prostate-Specific Antigen (PSA) Levels

Last Updated: 05/19/2025

SUMMARY

In the phase 3 SPARTAN study evaluating the efficacy and safety of ERLEADA compared to placebo in patients with high-risk non-metastatic castration-resistant prostate cancer (nmCRPC) receiving continuous androgen deprivation therapy (ADT), the median prostate-specific antigen (PSA) results were blinded and not used for treatment discontinuation. Time to PSA progression (TTPP) and PSA response rate were exploratory endpoints in the study.¹^,²
- At the final analysis for overall survival (OS), after a median follow-up of 52 months, the median TTPP was 40.5 months in the ERLEADA group vs 3.7 months in the placebo group (HR, 0.07; 95% CI, 0.060.09). This endpoint was not adjusted for multiple comparisons, and statistical significance has not been established.³
- In an exploratory analysis, ERLEADA decreased the risk of PSA progression by 94% compared with placebo (not reached [NR] vs 3.71 months; HR, 0.064; 95% CI, 0.052-0.080; P<0.0001). Confirmed PSA response (≥50% decline in PSA from baseline [PSA50]) was reported in 90% of patients in the ERLEADA group and 2% of patients in the placebo group (relative risk [RR], 40.09; 95% CI, 20.99-76.58; P<0.0001).⁴
- In a post hoc analysis, among patients in the ERLEADA group, PSA50, ≥90% PSA reduction (PSA90), and PSA ≤0.2 ng/mL was achieved in 95%, 63%, and 34% of patients, respectively, at 6 months. Among patients in the ERLEADA group who achieved PSA90 and PSA ≤0.2 ng/mL at 6 months, the HR for metastasis-free survival (MFS) was 0.41 (95% CI, 0.29-0.57) and 0.3 (95% CI, 0.19-0.47), respectively. The HR for OS in the ERLEADA group at 6 months in patients who achieved PSA90 and PSA ≤0.2 ng/mL was 0.45 (95% CI, 0.35-0.59) and 0.26 (95% CI, 0.18-0.38), respectively. These endpoints were not adjusted for multiple comparisons, and statistical significance has not been established.⁵
- Adverse events (AEs) that occurred in ≥15% of patients in the ERLEADA group included fatigue, hypertension, diarrhea, fall, nausea, arthralgia, weight decreased, back pain, and hot flush.³
In the phase 3 TITAN study evaluating the efficacy and safety of ERLEADA compared to placebo in patients with metastatic castration-sensitive prostate cancer (mCSPC) receiving continuous ADT, progression or change in PSA level was not used as the lone indicator for disease progression or treatment discontinuation. For patients who had an increasing PSA in the absence of radiographic or clinical progression, study treatment was continued. TTPP was an exploratory endpoint in the study.⁶^,⁷
- At the final analysis for OS, after a median follow-up 44.0 months, median TTPP was NR in the ERLEADA group and 12.9 months in the placebo group (HR, 0.27; 95% CI, 0.22-0.33). This endpoint was not adjusted for multiple comparisons, and statistical significance has not been established.⁸
- In an exploratory secondary analysis, OS was significantly improved in patients in the ERLEADA group with an early PSA nadir (HR, 0.66; 95% CI, 0.44-1.00). No OS improvement was observed in patients in the ERLEADA group without an early PSA nadir (HR, 1.14; 95% CI, 0.89-1.46), with a differential treatment effect between groups stratified by early PSA nadir by 6 months (P=0.03).⁹^,¹⁰
- In a post hoc analysis, 90% and 73% of patients in the ERLEADA group had an overall PSA50 and PSA90 vs 55% and 29% in the placebo group, respectively. Undetectable PSA levels were achieved by 68% and 32% of patients in the ERLEADA and placebo groups, respectively.¹¹
- Treatment-emergent AEs (TEAEs) that occurred in ≥15% of patients in the ERLEADA group were hot flush, back pain, fatigue, rash, arthralgia, and hypertension.¹²
Post hoc analyses of the SPARTAN and TITAN studies evaluating the relationship of PSA decline with health-related quality of life (HRQoL) after treatment with ERLEADA,¹³ treatment effect on best PSA decline by age group,¹⁴ and clinical outcomes based on progression status¹⁵ have been reported.
There are no published data regarding PSA flare from the SPARTAN or TITAN studies.
Post hoc analyses of PSA kinetics,¹⁶^-¹⁸ clinical outcomes in patients with PSA decline to <0.2 ng/mL,¹⁹ molecular subtypes,²⁰ subgroup analyses,²¹^,²² radiographic progression without corresponding PSA progression,²³ the effect of ultra-low PSA on clinical outcomes,²⁴ and PSA results in patients with and without baseline cardiovascular (CV) or metabolic risk factors²⁵ have been reported.
Results from retrospective real-world analyses evaluating PSA response in patients with nmCRPC²⁶^-²⁹ or mCSPC³⁰^-³² receiving ERLEADA, assessing PSA response in patients with nmCRPC or mCSPC treated with ERLEADA and stratified by race (Black and non-Black patients),³³^-³⁵ and describing PSA responses for patients receiving ERLEADA or other prostate cancer therapies³⁶^-⁴⁶ have been reported.

CLINICAL DATA

Phase 3 studies

SPARTAN Study

Smith et al (2018)¹ evaluated the efficacy and safety of ERLEADA compared to placebo in patients with high-risk nmCRPC (N=1207).

Study Design/Methods

SPARTAN (NCT01946204) was a phase 3, randomized, double-blind, placebo-controlled, multicenter study in patients with high-risk (defined as prostate-specific antigen doubling time [PSADT] ≤10 months) nmCRPC receiving either ERLEADA 240 mg orally (PO) once daily (QD; n=806) or placebo PO QD (n=401). All patients received continuous ADT with a gonadotropin-releasing hormone (GnRH) analog or surgical castration throughout the study.² The primary endpoint was MFS. Exploratory endpoints included TTPP (See Table: PCWG2 Criteria for PSA Progression) and PSA response rate.
Patients were stratified based on PSADT (≤6 months vs >6 months), use of bonesparing agents (yes vs no), and classification of local or regional nodal disease (N0 vs N1) at the time of trial entry.
PSA was assessed by a central laboratory and blinded to the patients and investigators, and PSA results were not used for treatment discontinuation.²^,⁴
PSA response was defined as a PSA50 and confirmed on a subsequent measurement ≥4 weeks later.²^,⁴

PCWG2 Criteria for PSA Progression⁴⁷

PCWG2 Criteria for PSA Progression
Decline from baseline	Record time from start of therapy to first PSA increase that is ≥25% and ≥2 ng/mL above nadir, and which is confirmed by a second value 3 or more weeks later (ie, a confirmed PSA rising trend)
No decline from baseline	PSA progression ≥25% and ≥2 ng/mL after 12 weeks
Abbreviations: PCWG2, Prostate Cancer Working Group 2; PSA, prostate-specific antigen.

Results

Patient Characteristics

Patient demographics and disease characteristics were well balanced between the 2 groups, and there were no significant differences (Table: Select Baseline Patient and Disease Characteristics Related to PSA).

Select Baseline Patient and Disease Characteristics Related to PSA¹^,⁴⁷

	ERLEADA Group (n=806)	Placebo Group (n=401)
Median PSA at study entry, ng/mL	7.78	7.96
Median PSADT, months	4.40	4.50
PSADT (n, %)
≤6 months	576 (71.5)	284 (70.8)
>6 months	230 (28.5)	117 (29.2)
Abbreviations: PSA, prostate-specific antigen; PSADT, prostate-specific antigen doubling time.

Efficacy

At the final analysis for OS, after a median follow-up of 52 months, the median TTPP was 40.5 months in the ERLEADA group vs 3.7 months in the placebo group (HR, 0.07; 95% CI, 0.060.09). This endpoint was not adjusted for multiple comparisons, and statistical significance has not been established.³
- The treatment effect of ERLEADA on OS was generally consistent across study subpopulations, including in patients who had a baseline PSA at or below the median (median OS NR in either group; HR, 0.79; 95% CI, 0.581.09) and above the median (median OS was 59.4 months in the ERLEADA group and 50.3 months in the placebo group; HR, 0.78; 95% CI, 0.611.00).
- The relative PSA response rate based on confirmed response was 40.2 with ERLEADA vs placebo (95% CI, 21-77), with 38% of patients in the ERLEADA group attaining a confirmed PSA level ≤0.2 ng/mL compared to 0 patients in the placebo group. This endpoint was not adjusted for multiple comparisons, and statistical significance has not been established.³

Exploratory and Post Hoc Analyses of PSA Response

Results from an exploratory analysis evaluating PSA from the SPARTAN study are shown in Table: PSA Response.⁴ The median TTPP was 29 days (range, 8-310 days) in the ERLEADA group. At 12 weeks following randomization, median PSA decreased by 90% in the ERLEADA group and increased by 40% in the placebo group. A PSA90 was reported in 66% of patients in the ERLEADA group and 1% of patients in the placebo group.

PSA Response¹^,⁴

Exploratory Endpoints	ERLEADA Group (n=806)	Placebo Group (n=401)	Hazard Ratio (95% CI)	P-Value
Median time to PSA progression, months	NR	3.71	0.064 (0.052-0.080)	0.0001
Patients with a PSA response (%)	90	2	40.09 (20.99-76.58)^a	0.0001
Abbreviations: CI, confidence interval; NR, not reached; PSA, prostate-specific antigen. ^aThe comparison for this exploratory endpoint was calculated as a relative risk rather than as a hazard ratio.

A post hoc analysis of the SPARTAN study assessed the relationships between PSA kinetics, outcomes, and molecular subtypes in the SPARTAN study (Table: PSA Kinetics in the SPARTAN Study).⁵
- Following ERLEADA treatment, PSA50, PSA90, and PSA ≤0.2 ng/mL were similar regardless of nodal status (N0, N1, NX) at baseline.
- PSA reductions were observed within 3 months and up to a period of 12 months of ERLEADA treatment and were similar across molecular subtypes (GC high-/low-risk and basal/luminal subtypes); see Table: PSA Kinetics in Molecular Subtypes Among Patients in the ERLEADA Group in the SPARTAN Study.
- At 6 months of ERLEADA treatment, achievement of confirmed PSA response (PSA50, PSA90, and PSA ≤0.2 ng/mL) was associated with improved TTPP, OS, and MFS (Table: Association Between Confirmed PSA Response and Outcomes at 6 Months of ERLEADA Treatment).
- Upon achievement of PSA50, PSA90, and PSA ≤0.2 ng/mL, median TTPP was prolonged from 13.9 to 55.3 months, 22.1 to 55.3 months, and 25.8 months to NR, respectively, and median OS was prolonged from 53.8 to 73.9 months, 55.3 to 73.9 months, and 59.1 to 73.9 months, respectively. In patients that reached PSA90, median MFS was prolonged from 29.1 months to 40.5 months. In patients that reached PSA ≤0.2 ng/mL, median MFS was prolonged from 30.0 months to 40.5 months.
- At 6 months, patients with a PSA reduction of 50% to <90% vs those with a PSA50 had a longer median TTPP (22.4 vs 13.9 months) and median OS (55.8 vs 53.8 months).
- Patients with PSA90 at 6 months vs those with 50% to <90% or <50% PSA reduction had the longest median TTPP (55.3 vs 22.4 or 13.9 months) and OS (73.9 vs 55.8 or 53.8 months).

PSA Kinetics in the SPARTAN Study⁵

	ERLEADA Group (n=806)	Placebo Group (n=401)
PSA at baseline, ng/mL, median (Q1-Q3)	7.78 (3.8-17.0)	7.96 (3.9-19.2)
PSA nadir, ng/mL	n=799	n=395
Median (Q1-Q3)	0.38 (0.1-1.6)	7.24 (3.5-17.6)
Maximum change in PSA from baseline, %, median (Q1-Q3)	-94 (-98 to -81)	15 (4.1-28)
Time to PSA nadir, months, median (Q1-Q3)	7.4 (4.5-11.9)	1.0 (1.0-1.8)
Time to achieve PSA response, months
≥50% PSA reduction	n=724	n=9
Median (Q1-Q3)	1.0 (1.0-1.0)	1.9 (1.8-9.2)
≥90% PSA reduction	n=498	n=0
Median (Q1-Q3)	1.9 (1.0-3.1)	NA
PSA ≤0.2 ng/mL	n=303	n=0
Median (Q1-Q3)	2.8 (1.9-4.6)	NA
Patients with confirmed PSA response by 6 months, n (%)^a
≥50% PSA reduction	723 (90)^b	6 (1.5)
≥90% PSA reduction	462 (57)^b	0
PSA ≤0.2 ng/mL	258 (32)^b	0
Patients with confirmed PSA response at 6 months, n (%)^c	n=680	n=107
≥50% PSA reduction	648 (95)	4 (3.7)
≥90% PSA reduction	428 (63)	0
PSA ≤0.2 ng/mL	233 (34)	0
Abbreviations: NA, not applicable; PSA, prostate-specific antigen; Q, quartile. ^aBest PSA response during any time in the first 6 months of initiation of ERLEADA treatment. ^bP<0.001 for ERLEADA vs placebo from the chi-squared test. ^cPSA response in patients who were alive at 6 months following initiation of treatment ± 28 days (1 ERLEADA treatment cycle).

PSA Kinetics in Molecular Subtypes Among Patients in the ERLEADA Group in the SPARTAN Study⁵

	GC High Risk (n=76)	GC Low Risk (n=78)	Basal (n=102)	Luminal (n=52)
Median PSA at baseline, ng/mL (Q1-Q3)	6.8 (4.0-17.3)	8.0 (3.9-13.5)	7.0 (3.7-13.3)	8.2 (4.8-16.8)
Median PSA nadir, ng/mL, (Q1Q3)	0.4 (0.1-1.7)	0.2 (0.1-0.9)	0.4 (0.1-1.8)	0.2 (0.03-0.8)
Median maximum change in PSA from baseline, % (Q1-Q3)	-93 (-99 to -80)	-97 (-99 to -87)	-92 (-98 to -79)	98 (-99 to -93)
Median time to PSA nadir, months, (Q1-Q3)	7.3 (4.6-9.2)	8.3 (4.6-12.9)	7.3 (4.6-10.2)	8.3 (5.6-11.1)
≥50% PSA reduction, n (%)
Overall	71 (93)	73 (94)	94 (92)	50 (96)
≤6 months	71 (93)	73 (94)	94 (92)	50 (96)
Abbreviations: GC, genomic classifier; PSA, prostate-specific antigen; Q, quartile.

Association Between Confirmed PSA Response and Outcomes at 6 Months of ERLEADA Treatment⁵^,a

	Time to PSA Progression HR (95% CI; P-Value)	MFS HR (95% CI; P-Value)	OS HR (95% CI; P-Value)
Achieved vs not achieved PSA response at 6 months^b
PSA50	0.21 (0.13-0.35; <0.001^c)	0.46 (0.22-0.94; 0.03^c)	0.5 (0.3-0.84; 0.008^c)
PSA90	0.25 (0.18-0.33; <0.001^c)	0.41 (0.29-0.57; <0.001^c)	0.45 (0.35-0.59; 0.001^c)
PSA ≤0.2 ng/mL	0.13 (0.08-0.21; <0.001^c)	0.3 (0.19-0.47; <0.001^c)	0.26 (0.18-0.38; 0.001^c)
Deep PSA decline vs PSA decline <50% at 6 months^d
50 to <90%	0.45 (0.27-0.75; 0.002^c)	0.78 (0.37-1.63; 0.50^c)	0.81 (0.47-1.37; 0.43^c)
≥90%	0.12 (0.07-0.21; <0.001^c)	0.32 (0.15-0.68; 0.003^c)	0.37 (0.22-0.63; 0.001^c)
Abbreviations: CI, confidence interval; HR, hazard ratio; MFS, metastasis-free survival; OS, overall survival; PSA, prostate-specific antigen; PSA50, ≥50% PSA reduction; PSA90, ≥90% PSA reduction. ^aPSA response achieved in patients who were alive at 6 months following the initiation of ERLEADA ± 28 days (1 treatment cycle). ^bEach row has results from an individual Cox proportional-hazards model. ^cThe endpoints were not adjusted for multiple comparisons. Therefore, the P-value displayed is nominal, and statistical significance has not been established. ^dResults from 1 model considering depth of PSA response as a category.

Additional Information

Additional information regarding the SPARTAN study, including the clinical study report, protocol, and statistical analysis plan, can be found at: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2018/Erleada_210951_toc.cfm (scroll to the “Sponsor Clinical Study Reports ARN-509-003 SPARTAN NCT # 01946204” section at the bottom of the web page).

TITAN Study

Chi et al (2019)⁶ evaluated the efficacy and safety of ERLEADA plus ADT compared to placebo plus ADT in patients with mCSPC (N=1052).

Study Design/Methods

TITAN (NCT02489318) was a phase 3, randomized, double-blind, placebo-controlled, multicenter study in patients with mCSPC receiving either ERLEADA 240 mg PO QD (n=525) or placebo PO QD (n=527). All patients received continuous ADT with a concomitant GnRH analog or had a bilateral orchiectomy.⁷ The dual primary endpoints were radiographic progression-free survival (rPFS) and OS. A select exploratory endpoint was TTPP (see Table: PCWG2 Criteria for PSA Progression above).⁴⁸
Patients were stratified based on Gleason score (≤7 vs >7) at diagnosis, region (North America and European Union vs other), and prior docetaxel use (yes vs no).
PSA was assessed by a central laboratory and blinded to the investigators during treatment cycles 1 to 4. Beginning with cycle 5 and for all subsequent cycles, PSA results were available to the investigator.⁷
Progression or change in PSA level was not used as the lone indicator for disease progression or treatment discontinuation. For patients who had an increasing PSA in the absence of radiographic or clinical progression, study treatment was continued.⁷
A prespecified subgroup analysis of rPFS and OS for patients with and without baseline PSA levels above the median was used to assess consistency of treatment effect.⁷

Results

Patient Characteristics

Patient demographic and disease characteristics were well balanced between the 2 groups, and there were no significant differences.
Median PSA levels at baseline were 5.97 µg/L (range, 0-2682 µg/L) in the ERLEADA group and 4.02 µg/L (range, 0-2229 µg/L) in the placebo group.⁴⁸

Efficacy

Subgroup analysis of rPFS favored ERLEADA across prespecified subgroups, including in patients who had a baseline PSA above the median (median rPFS could not be estimated [NE] in the ERLEADA group vs 15.4 months in the placebo group; HR, 0.51; 95% CI, 0.39-0.67).
The treatment effect on OS consistently favored ERLEADA across prespecified subgroups, including in patients who had a baseline PSA above the median (median OS NE in either group; HR, 0.68; 95% CI, 0.48-0.97).
- At the final analysis for OS, the treatment effect of ERLEADA on OS was favorable across certain prespecified subgroups, including patients who had a baseline PSA above the median (median OS: NR in the ERLEADA group vs 38.9 months in the placebo group; HR, 0.67; 95% CI, 0.520.86).⁸
Median TTPP favored the ERLEADA group (median TTPP NE in the ERLEADA group vs 12.9 months in the placebo group; HR, 0.26; 95% CI, 0.21-0.32).
- The 24-month event-free rate for TTPP was 75% in the ERLEADA group and 36% in the placebo group.⁴⁸
- PSA reached undetectable levels (PSA <0.2 ng/mL) in 68.4% and 28.7% of the patients in the ERLEADA and placebo groups, respectively.
At the final analysis for OS, the median TTPP was NR in the ERLEADA group and 12.9 months in the placebo group (HR, 0.27; 95% CI, 0.22-0.33). This endpoint was not adjusted for multiple comparisons, and statistical significance has not been established.⁸
- PSA progression occurred in 138 (26.3%) patients in the ERLEADA group and 344 (65.3%) patients in the placebo group.

Exploratory Analysis of PSA Response

An exploratory secondary analysis of the TITAN study evaluated the effect of ERLEADA on OS based on early PSA response (defined as reaching a PSA nadir of ≤0.2 ng/mL at ≤6 months of randomization. Results are summarized in Table: OS Based on Early PSA Response in the TITAN Study).⁹
- In total, 321 (61%) patients in the ERLEADA group and 125 (24%) in the placebo group achieved an early PSA nadir.
- The ERLEADA group was associated with improved OS in patients with an early PSA nadir (HR, 0.66; 95% CI, 0.44-1.00). There was no improvement in OS among those without an early PSA nadir (HR, 1.14; 95% CI, 0.89-1.46), with a differential treatment effect between groups stratified by early PSA nadir by 6 months (P=0.03)
- In the ERLEADA vs placebo group, 3-year confounder-adjusted OS was 84% (80%-88%) vs 74% (66%-82%) among 6-month PSA responders and 58% (52%-65%) vs 56% (51%-60%) among nonresponders.
- The number needed to treat (NNT) in the overall population was 7.8 (95% CI, 6-15); the NNT in patients with vs without PSA nadir by 6 months was 7.7 (95% CI, 5-36) vs 55 (95% CI, 10 to -4).

OS Based on Early PSA Response in the TITAN Study⁹

Adjusted 4-Year OS, % (95% CI)	ERLEADA Group (n=523)	Placebo Group (n=526)
PSA nadir achieved	78 (74-83)	66 (56-75)
PSA nadir not achieved	47 (40-54)	46 (41-52)
Abbreviations: CI, confidence interval; OS, overall survival; PSA, prostate-specific antigen.

Post Hoc Analyses of PSA Response

Depth of PSA reduction and long-term outcomes: the ERLEADA group demonstrated a greater improvement in magnitude of PSA response compared to the placebo group and was associated with improved long-term outcomes. The median nadir attained following ERLEADA was 0.02 ng/mL at a median of 5.6 months.¹¹
- Overall, 68% of patients achieved undetectable PSA (≤0.2 ng/mL) in the ERLEADA group compared to 32% in the placebo group, with 3-months, 6months, and 12-months data as follows: 51% vs 18%, 61% vs 21%, and 64% vs 23%, respectively.
- Overall, 90% and 73% of patients had a PSA50 and PSA90 in the ERLEADA group compared to 55% and 29% in the placebo group, with 3months, 6-months, and 12-months data as follows: 89% vs 41% and 59% vs 13%, 90% vs 49% and 68% vs 18%, and 90% vs 51% and 71% vs 22%, respectively.
- Achievement of deep PSA decline (PSA90 or PSA ≤0.2 ng/mL) at 3 months of ERLEADA initiation was associated with improved OS (HR, 0.35; 95% CI, 0.25-0.48), rPFS (HR, 0.44; 95% CI, 0.30-0.65), TTPP (HR, 0.31; 95% CI, 0.22-0.44) and time to castration resistance (HR, 0.38; 95% CI, 0.27-0.52); P≤0.0001 for all. Similar results were seen at 6 and 12 months of ERLEADA initiation.
PSA kinetics and rPFS: patients in the ERLEADA group achieved PSA50, PSA90, and PSA ≤0.2 ng/mL as early as 3 months after initiation of ERLEADA, with a median time to achieve a PSA50 response of 1 month. Patients in the ERLEADA group who achieved PSA50, PSA90, and PSA ≤0.2 ng/mL were at lower risk of radiographic progression compared to patients who did not achieve these responses (median rPFS for patients in the ERLEADA group with vs without PSA50, PSA90, and PSA ≤0.2 ng/mL: NR vs 18.3 months [HR, 0.27; 95% CI, 0.17-0.43], NR vs 28.7 months [HR, 0.46; 95% CI, 0.32-0.65], and NR vs 18.4 months [HR, 0.19; 95% CI, 0.14-0.27], respectively; all P<0.0001). At 6 months, the median rPFS was 18.3 months, 28.7 months, and NR for patients treated with ERLEADA who achieved a PSA response of <50%, 50% to <90%, and ≥90%, respectively.¹⁶
Relationship between depth of PSA decline and OS: patients in the ERLEADA group who achieved PSA50, PSA90, and PSA ≤0.2 ng/mL achieved significant improvement in OS compared with patients who did not achieve these responses (median OS for patients in the ERLEADA group with vs without PSA50, PSA90, and PSA ≤0.2 ng/mL: NR vs 35.5 months [HR, 0.38; 95% CI, 0.25-0.59], NR vs 45.2 months [HR, 0.44; 95% CI, 0.32-0.60], NR vs 30.0 months [HR, 0.17; 95% CI, 0.13-0.23]; all P<0.0001). Shorter time to undetectable PSA (≤0.2 ng/mL) correlated with longer OS time (rank correlation, rho -0.5; 95% CI, 0.6 to 0.4; P<0.05).¹⁷
Protocol-defined subgroup analysis: TTPP was prolonged in all 4 subgroups (synchronous/high-volume, synchronous/low-volume, metachronous/highvolume, metachronous/low-volume) in the ERLEADA group in analysis of efficacy and safety outcomes based on disease volume (high vs low), number of metastases (oligometastases vs polymetastases), and timing of metastasis presentation (synchronous vs metachronous). In addition, the proportion of patients with confirmed best PSA50 or PSA90 or to ≤0.2 ng/mL at any time during the study was increased, regardless of stratification.²¹^,²²
Effect of ultra-low PSA (≤0.2 ng/mL) on clinical outcomes: the percentage of patients achieving ultra-low 1 (>0.02 to ≤0.2 ng/mL) and ultra-low 2 (≤0.02 ng/mL) PSA levels with ERLEADA vs placebo by 3 months was 38% and 23% vs 15% and 5%, respectively. Compared with patients with PSA >0.2 ng/mL, OS and rPFS were significantly improved in patients with ultra-low 1 (OS: HR, 0.46; 95% CI, 0.31-0.67; nominal P<0.001; rPFS: HR, 0.54; 95% CI, 0.35-0.83; nominal P=0.005) and ultra-low 2 (OS: HR, 0.24; 95% CI, 0.13-0.43; nominal P<0.001; rPFS: HR, 0.28; 95% CI, 0.14-0.54; nominal P<0.001) PSA at 3 months. Patients with ultra-low 2 PSA also showed significantly improved time to castration resistance (HR, 0.2; 95% CI, 0.11-0.38; nominal P<0.001) and TTPP (HR, 0.11; 95% CI, 0.04-0.27; nominal P<0.001). Compared with patients with PSA >0.2 ng/mL anytime, those achieving ultra-low 2 PSA by 3 months showed improved OS, with higher HRs observed with longer time to reach ultra-low 2 PSA (3 months: HR, 0.12 [95% CI, 0.06-0.22; nominal P<0.001]; 3-6 months: HR, 0.14 [95% CI, 0.08-0.27; nominal P<0.001]; 6 months: HR, 0.25 [95% CI, 0.17-0.36; nominal P<0.001]). These endpoints were not adjusted for multiple comparisons. Therefore, the P-values displayed are nominal, and statistical significance has not been established. The overall safety profile in patients who achieved PSA decline at 3 months of study treatment was similar to a prior post hoc PSA analysis¹¹ and the overall intent-to-treat population.²⁴
Impact of baseline CV or metabolic risk factor comorbidities: the percentage of patients achieving PSA90 or PSA <0.2 ng/mL was similar in those with and without baseline CV or metabolic risk factors or associated concomitant medications and approximately double in the ERLEADA vs placebo group. In the ERLEADA and placebo groups, respectively, 72% and 69% of patients had a baseline history of CV or metabolic risk factors and 68% and 66% of patients had CV or metabolic risk factors and concomitant medication usage. PSA90 or PSA <0.2 ng/mL was achieved as follows: with CV/metabolic risk factors (ERLEADA group: 86.2% of n=378 vs placebo group: 43.1% of n=364); with CV/metabolic risk factors and concomitant medications (ERLEADA group: 85.8% of n=358 vs placebo group: 42.1% of n=347); without CV/metabolic risk factors (ERLEADA group: 82.3% of n=146 vs placebo group: 43.6% of n=163).²⁵

Post Hoc Analyses of the SPARTAN and TITAN Studies

Treatment effect on best PSA decline by age group: treatment with ERLEADA was evaluated using descriptive statistics, Kaplan-Meier analysis, Cox proportional-hazards model, and mixed-effects model for repeated measures. Results are summarized in Table: PSA Kinetics by Age in the TITAN and SPARTAN Studies.¹⁴

PSA Kinetics by Age in the TITAN and SPARTAN Studies¹⁴

	TITAN Study (N=1052)			SPARTAN Study^a(N=1207)
Age Group, Years	<65 (n=331)	65-79 (n=628)	≥80 (n=93)	<65 (n=149)	65-79 (n=741)	≥80 (n=317)
Median (range) PSA nadir,^b ng/mL
ERLEADA group	0.04 (0-133) n=148	0.02 (0-498) n=321	0.04 (0-83.7) n=52	0.20 (0-48.9) n=106	0.32 (0-32.2) n=488	0.75 (0-150) n=205
Placebo group	0.93 (0-408) n=181	0.68 (0-1408) n=303	0.73 (0-1180) n=41	7.11 (1.5-67.2) n=43	7.18 (0.3-146) n=246	9.0 (1.0-292) n=106
Median time (range) to PSA nadir,^b months
ERLEADA group	5.6 (0.1-40.6) n=149	5.6 (0.1-47.9) n=324	6.4 (1.0-36.8) n=52	8.7 (0.9-29.5) n=106	7.4 (0.9-44.2) n=488	6.5 (0.7-29.4) n=205
Placebo group	2.8 (0.7-50.6) n=182	4.7 (0.8-50.0) n=304	3.7 (0.7-40.4) n=41	1.0 (0.9-35.7) n=43	1.0 (0.2-24.4) n=246	1.0 (0.8-8.3) n=106
Confirmed PSA decline ≥50% from baseline,^c n (%)
ERLEADA group	132 (89) n=149	292 (90) n=324	49 (94) n=52	98 (93) n=106	451 (92) n=492	175 (84) n=208
Placebo group	86 (47) n=182	180 (59) n=304	24 (59) n=41	1 (2.3) n=43	5 (2.0) n=249	3 (2.8) n=109
Median time (range) to confirmed PSA decline ≥50% from baseline,^c,d months
ERLEADA group	0.95 (0.9-8.3) n=149	0.95 (0.3-11.1) n=324	0.95 (0.9-9.2) n=52	0.95 (0.7-5.2) n=106	0.95 (0.5-10.2) n=492	0.95 (0.3-6.5) n=208
Placebo group	0.97 (0.1-30.7) n=182	0.99 (0.1-35.4) n=304	1.4 (0.9-23.5) n=41	20.3 (20.3-20.3) n=43	1.9 (1.0-11.2) n=249	1.9 (1.8-4.6) n=109
Confimed PSA decline to ≤0.2 ng/mL,^c n (%)
ERLEADA group	90 (60) n=149	231 (71) n=324	35 (67) n=52	51 (48) n=106	197 (40) n=492	55 (26) n=208
Placebo group	52 (29) n=182	101 (33) n=304	13 (32) n=41	0	0	0
Median time (range) to confirmed PSA decline of ≤0.2 ng/mL,^c,e months
ERLEADA group	1.9 (0.9-29.4) n=149	1.9 (0.1-33.2) n=324	1.9 (0.9-25.8) n=52	2.8 (0.9-14.9) n=106	2.8 (0.9-25.8) n=492	2.8 (0.3-22.1) n=208
Placebo group	1.0 (0.8-39.6) n=182	2.8 (0.7-42.0) n=304	4.7 (0.9-33.1) n=41	NA n=0	NA n=0	NA n=0
Abbreviations: NA, not available due to lack of response; PSA, prostate-specific antigen. ^aOlder patients in the SPARTAN study population had higher median PSA levels than younger patients. ^bPatients with available PSA data are included. ^cConfirmed by a subsequent measurement ≥4 weeks later. ^dAssessed in patients with achieved ≥50% PSA decline from baseline. ^eAssessed in patients with achieved PSA decline to ≤0.2 ng/mL.

Association between rapid and deep PSA decline (defined as PSA90 or to ≤0.2 ng/mL) and HRQoL after ERLEADA treatment: In both studies, PSA decline correlated with improved HRQoL at 3 and 6 months (Table: HRQoL Measures of Patients With PSA Decline in the SPARTAN and TITAN Studies).¹³^,⁴⁹

HRQoL Measures of Patients With PSA Declinein the SPARTAN and TITAN Studies¹³^,⁴⁹

HRQoL Measures	PSA Decline (≤0.2 ng/mL)		PSA Decline (≥90%)
	3 Months	6 Months	3 Months	6 Months
	HR (95% CI); Events/N
SPARTAN Study
Median time to worsening in FACT-P total score^a	33.2 months 0.83 (0.62-1.10); 64/119	NR 0.80 (0.57-1.11); 55/127	29.7 months 0.84 (0.66-1.07); 142/264	44.2 months 1.01 (0.72-1.41); 113/238
Median time to worsening in FACT-P physical wellbeing subscale score^b	55.2 months 0.70 (0.51-0.94); 55/119	NR 0.60 (0.42-0.84); 50/137	51.6 months 0.67 (0.52-0.86); 122/259	55.2 months 0.72 (0.52-0.99); 99/245
TITAN Study
Median time to worsening in FACT-P total score^a	44.2 months 0.54 (0.38-0.76); 54/127	NR 0.65 (0.42-1.01); 49/121	27.6 months 0.99 (0.69-1.41); 78/150	44.2 months 0.82 (0.51-1.30); 58/135
Median time to worsening in FACT-P physical wellbeing subscale score^b	29.5 months 0.63 (0.45-0.89); 65/128	42.3 months 0.66 (0.43-1.03); 48/112	20.3 months 0.82 (0.58-1.15); 82/148	40.8 months 0.60 (0.38-0.96); 56/127
Median time to BPI-SF worst pain intensity progression^c	NR 0.70 (0.49-1.00); 58/169	NR 0.53 (0.34-0.81); 44/173	NR 0.67 (0.47-0.95); 70/205	NR 0.59 (0.38-0.94); 55/203
Median time to BFI worst fatigue intensity progression^d	NR 0.76 (0.53-1.10); 56/212	NR 0.97 (0.63-1.49); 59/224	NR 0.88 (0.61-1.29); 69/243	NR 0.98 (0.61-1.56); 67/257
Abbreviations: BFI, Brief Fatigue Inventory; BPI-SF, Brief Pain Inventory-Short Form; CI, confidence interval; FACT-P, Functional Assessment of Cancer Therapy-Prostate; HR, hazard ratio; HRQoL, health-related quality of life; NR, not reached; PSA, prostate-specific antigen. ^aFACT-P total, ≥10 points. ^bPhysical wellbeing, ≥3 points. ^cBPI-SF worst pain, ≥30% increases. ^dBFI worst fatigue, ≥2 points.

Retrospective analysis: evaluated patients in the ERLEADA vs placebo groups to characterize patients who experienced radiographic progression without prior or concurrent PSA progression (R-PD) and compared with patients who experienced PSA progression without prior radiographic progression (PSA-PD).¹⁵
- TITAN: 12.4% of patients (n=130 [ERLEADA group, n=64; placebo group, n=66]) were R-PD and 41.2% of patients (n=433 [ERLEADA group, n=125; placebo group, n=308]) were PSA-PD.
- SPARTAN: 10.4% of patients (n=125 [ERLEADA group, n=95; placebo group, n=30]) were R-PD and 45.4% of patients (n=548 [ERLEADA group, n=224; placebo group, n=324]) were PSA-PD.
- In the ERLEADA vs placebo group, median time to radiographic progression was delayed in R-PD patients (TITAN: 11 vs 3.6 months; HR, 0.51; 95% CI, 0.36–0.73; P=0.0003; SPARTAN: 11 vs 3.7 months; HR, 0.17; 95% CI, 0.1–0.28; P<0.0001).
- In addition, in the ERLEADA vs placebo group, median TTPP was delayed in PSA-PD patients (TITAN: HR, 0.61; 95% CI, 0.49–0.75; P<0.0001; SPARTAN: HR, 0.22; 95% CI, 0.18–0.27; P<0.0001).
- Median OS was shorter in patients with R-PD vs PSA-PD in both studies.
  - TITAN: 22.9 months [95% CI, 20.2-30.9] vs 37.4 months [95% CI, 33.7-40.3]; HR, 1.56; 95% CI, 1.22-1.99; P=0.0004.
  - SPARTAN: 49.8 months [95% CI, 38.6–60.5] vs 53.7 months [95% CI, 50.3–57.8]; HR, 1.23; 95% CI, 0.94–1.62; P=0.1289.

Literature Search

A literature search of MEDLINE^®, Embase^®, BIOSIS Previews^®, and Derwent Drug File (and/or other resources, including internal/external databases) was conducted on 24 April 2025. Summarized in this response are relevant data limited to the phase 3 SPARTAN and TITAN studies in patients with nmCRPC and mCSPC, respectively.

References

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