e20717 Background: Amivantamab, a bispecific EGFR/MET antibody, is approved for EGFR exon 20 insertion-mutant non-small cell lung cancer (NSCLC). However, real-world data evaluating it as monotherapy beyond exon 20 variants remain limited, as most retrospective series include combination therapy or heterogeneous settings. In clinical practice, some patients may receive monotherapy due to toxicity concerns, comorbidities, prior treatment tolerance, or physician/patient preference. We evaluated clinical outcomes of amivantamab monotherapy in a real-world cohort of patients with EGFR-mutant NSCLC. Methods: We conducted an IRB-approved retrospective review (Pro2025-0001) of patients with advanced EGFR-mutant NSCLC treated with amivantamab monotherapy in the second line or later between June 2021 and September 2024. Patients were categorized as classical (exon 19 deletion or L858R), atypical (eg, exon 18 or G719X), or exon 20 insertion (ex20ins), and unspecified variants. Analyses evaluated progression-free survival (PFS), overall response rate (ORR), disease control rate (DCR), time to next treatment (TTNT), overall survival (OS), and safety. Radiographic response was assessed by investigator review using RECIST v1.1. Time-to-event outcomes were censored at last assessment on or before September 30, 2024. Confidence intervals (CIs) were calculated using exact binomial methods for proportions and Kaplan-Meier methods for time-to-event endpoints. Results: Twenty-two patients met inclusion criteria; median age was 67.5 years (range, 42-82), and patients were heavily pretreated (median prior therapies, 2). Baseline CNS metastases were present in 36%. Mutation subgroups included 13 classical, 5 atypical, and 3 exon 20 insertions, and 1 unclassified variant. Twenty patients were evaluable for response. ORR was 25.0% (95% CI, 8.7-49.1) and DCR was 60.0% (95% CI, 36.1-80.9). ORR/DCR were 25%/75% in classical EGFR (3/12), 40%/40% in atypical EGFR (2/5), and 0%/33% in ex20ins (0/3), though subgroup estimates were limited by small sample size. Median PFS was 4.2 months (95% CI, 1.35-7.29). Median TTNT was 5.2 months. Median OS was 10.7 months (95% CI, 2.9-31.3) from amivantamab initiation and 35.4 months (95% CI, 25.8-74.0) from initial diagnosis. Median follow-up was 27.8 months. Grade ≥3 treatment-related adverse events occurred in 2 patients, including hyponatremia, peripheral edema, and infusion reaction. Intracranial progression occurred in 7 of 11 patients with evaluable CNS imaging (64%). Conclusions: In this heavily pretreated real-world cohort, amivantamab monotherapy demonstrated meaningful antitumor activity across diverse EGFR mutation subtypes, with outcomes comparable to prior trials and real-world experiences. These findings support consideration of amivantamab monotherapy beyond exon 20 insertions and warrant prospective evaluation in defined clinical settings.

Summary of PK data for EZH2 inhibitors used in KARPAS-422 and HT1376 xeograft mmouse models

Tulmimetostat increases PRC2-repressed gene expression in ARID1A mutant bladder cancer cells. (

Table with antibody source information including RRID if available

TPS2665 Background: TROP2 is a type I transmembrane glycoprotein involved in cell proliferation, migration, and survival, that is upregulated in and is associated with poor prognosis in patients (pts) with several malignancies including urothelial carcinoma, non-small cell lung cancer, gastric cancer and breast cancer. TROP2 antibody drug conjugates (ADCs) have demonstrated clinical efficacy and are approved for metastatic breast cancer and epidermal growth factor receptor-mutated non-small cell lung cancer. ASP2998 is a dual-payload (topoisomerase I inhibitor plus stimulator of interferon genes [STING] agonist) immunostimulatory ADC targeting TROP2. ASP2998 monotherapy has shown preclinical antitumor activity in a syngeneic mouse model bearing human TROP2-expressing tumors that was superior to single-payload topoisomerase I inhibitor TROP2 ADCs. Methods: This first-in-human, multicenter, open-label, phase 1b/2 dose escalation (DESC) and expansion (DEXP) study, is evaluating the safety, tolerability, recommended phase 2 dose (RP2D) and/or maximum tolerated dose (MTD), preliminary antitumor activity, and pharmacokinetic profile of ASP2998 in pts with locally advanced unresectable or metastatic solid tumors. Initial DESC of ASP2998 includes 6 dose levels (n≥3 per dose level) to determine the RP2D and/or MTD. Eligible pts (aged ≥18 years) include those with urothelial carcinoma, non-small cell lung cancer, gastric/gastroesophageal junction cancer, or locally confirmed human epidermal growth factor receptor 2-negative breast cancer, who have progressed on, are ineligible for, or have refused all available standard therapies per investigator’s decision. At DEXP, multiple dose levels of ASP2998 may be evaluated based on the totality of data to optimize dosage in at least one tumor type (n≤40 per dose level per tumor type). Eligible DEXP pts with non-small cell lung include those who have received ≤3 prior lines of therapy and known programmed death-ligand 1 status, without actionable oncogenic alterations, who have progressed on or after platinum-based chemotherapy and/or checkpoint inhibitors. Eligible DEXP pts with urothelial carcinoma include those who have received ≤3 prior lines of therapy and progressed on or after enfortumab vedotin plus pembrolizumab. Prior exposure to TROP2, STING agonists or topoisomerase I inhibitor-directed therapy is permitted at DESC but not DEXP. Tumor-specific backfill pts can be enrolled in the DESC cohorts at dose levels that are deemed safe and tolerable, and will be counted towards the corresponding tumor-specific DEXP cohorts. Recruitment is ongoing with 196 planned pts (36 in DESC; 160 in DEXP). ClinicalTrials.Gov Identifier: NCT07287995. Clinical trial information: NCT07287995 .

In cancer patients tulmimetostat plasma exposure levels correlate with PRC2 target gene expression changes in peripheral blood.

Summary of cell viability data for bladder cancer cells treated with tulmimetostat

Context Patients from historically marginalized racial and ethnic groups are often underrepresented in symptom management research, but little is known about how to improve inclusivity and reach of these studies. Objectives This mixed-methods study aimed to: 1) establish the feasibility and acceptability of study procedures for assessing symptoms and shared decision-making (SDM) among Black patients with advanced lung cancer; and 2) elicit participants’ suggestions for improving study procedures. Methods Black patients with advanced lung cancer were recruited from three thoracic oncology clinics. Participants completed a baseline survey (T0), optional audio-recording of a routine oncology outpatient appointment, follow-up surveys one week (T1) and one month (T2) postappointment, and a semistructured exit interview examining experiences in the study and suggestions for improving future research. At each timepoint, participants completed the Treatment Acceptability and Preferences Questionnaire (TAPQ). Results We approached 69 potentially eligible patients, 40 (58%) completed the eligibility screener, 35 (88%) were eligible, 30 (86%) consented, and 27 (90%) were retained through T2, exceeding our a priori thresholds of ≥70% enrollment and retention through T2. Participants rated study procedures as acceptable (TAPQ scores ≥3) in 88% of observations, exceeding our a priori threshold of ≥70%. Qualitative analysis identified three categories of themes: participants’ motivation for participating, their overall experiences in the study, and recommendations for future research. Conclusion Research practices common in communication, palliative, and SDM studies were acceptable to most participants. Opportunities to improve were also identified. Findings can inform best practices in conducting inclusive palliative care and communication research.

Table with cell line information including source and RRID

BACKGROUND:Ifinatamab deruxtecan is a novel B7-H3-directed antibody-drug conjugate that leverages the clinically validated deruxtecan technology. We report dose-escalation results from a trial of ifinatamab deruxtecan in patients with solid tumours. METHODS:In this two-part, multicentre, open-label, first-in-human, phase 1/2 study of ifinatamab deruxtecan conducted at clinics in ten hospitals and cancer centres in the USA and Japan, we recruited patients aged 18 years or older who had advanced treatment-refractory solid tumours (small-cell lung cancer, oesophageal squamous cell carcinoma, castration-resistant prostate cancer, squamous non-small-cell lung cancer, head and neck squamous cell carcinoma, bladder cancer, sarcoma, endometrial cancer, melanoma, or breast cancer), and Eastern Cooperative Oncology Group performance status of 0 or 1. Patients received ifinatamab deruxtecan at doses of 0·8-16·0 mg/kg intravenously every 3 weeks. The primary outcome of dose escalation was the safety profile, which was evaluated in patients who received one or more dose of ifinatamab deruxtecan. Antitumour activity (per Response Evaluation Criteria in Solid Tumours version 1.1; secondary outcome) was evaluated in patients receiving ifinatamab deruxtecan at doses of 4·8 mg/kg or higher. The data cutoff was Jan 31, 2023. This trial is registered with ClinicalTrials.gov (NCT04145622) and is ongoing. FINDINGS:Between Oct 25, 2019, and July 13, 2022, 97 patients were enrolled and treated. 77 (79%) patients were male and 20 (21%) were female, 56 (58%) patients were White, and 31 (32%) were Asian. Three patients (3%) had dose-limiting toxicities; however, on the basis of protocol-defined criteria, the maximum tolerated dose was not reached. The most common grade 3 or worse treatment-emergent adverse events (TEAEs) were anaemia (17 [18%] patients), neutropenia (four [4%]), lymphocyte count decreased (three [3%]), and neutrophil count decreased (three [3%]). Serious TEAEs occurred in 31 (32%) patients. TEAEs associated with death were reported in five patients (5%; pneumonia, pneumonia aspiration, COVID-19 pneumonia, interstitial lung disease, and one death of undesignated cause); death due to interstitial lung disease was considered related to study medication by the investigator. After a median follow-up of 8·6 months (IQR 4·1-12·9), the confirmed objective response rate across tumour types was 34% (95% CI 23-47; 24 of 70 evaluable patients). INTERPRETATION:The maximum tolerated dose was not reached with ifinatamab deruxtecan; however, one death due to treatment-related interstitial lung disease highlights the importance of prompt evaluation and careful management of patients who develop interstitial lung disease. Promising antitumour activity was observed across various solid tumours. These findings support further evaluation of ifinatamab deruxtecan in randomised controlled trials. FUNDING:Funding for this study was provided by Daiichi Sankyo Company (Daiichi Sankyo) and Merck Sharp & Dohme, a subsidiary of Merck, Rahway, NJ, USA.

Cancer classification traditionally focuses on tissue of origin and histology appearance. Traditional “hard” classification for a specific diagnostic class yields binary yes/no class prediction. However, newer therapeutic approaches have demonstrated that tumors overlap biologically and may respond to a specific therapeutic approach regardless of traditional histological classifications. Instead of histological classification, we propose the use of a “Functional classification” based on machine learning models, leveraging high-dimensional RNA expression data. This approach identifies not only the predicted diagnostic class with the highest probability, but also the second, third, and other possible diagnostic classes. RNA from various types of cancers was sequenced and quantified using next generation sequencing. We used these RNA expression profiles in several functional classification models trained on 3484 tumors across 25 cancer types and tested these models using 1716 tumors. The Extreme Gradient Boosting Classifier showed the greatest accuracy, followed by the Multi-Layer Perceptron and random forest models. We demonstrate that using RNA profiling and machine learning achieve high accuracy in both hard and functional classifications of tumors. However, significantly better accuracy in classification was achieved using functional classification reflecting biological overlapping between tumors. Functional classification shows proximity between tumors and enables exploring treatments used in other close diagnostic class.

List of 365 genes (used in main Fig. 7F) that are induced in patient’s whole blood upon treatment with tulmimetostat

e20127 Background: Tarlatamab, a Delta-like ligand 3 (DLL3)-targeting Bispecific T-cell Engager (BiTE), has shown significant efficacy in heavily pretreated SCLC, leading to its recent approval. However, real-world data on its use, particularly in the rare cohort of patients with extrapulmonary small cell carcinoma (EPSCC), are limited. We report our single-institution experience with tarlatamab in patients with both pulmonary and extrapulmonary SCC. Methods: We conducted a retrospective review of all adult patients with advanced SCLC or EPSCC who received at least one dose of tarlatamab at our center between May 16, 2024, and September 30, 2025. The primary endpoints were Overall Response Rate (ORR), Progression-Free Survival (PFS), and Overall Survival (OS). Safety, including rates of Cytokine Release Syndrome (CRS) and Immune effector Cell-Associated Neurotoxicity Syndrome (ICANS), was a key secondary endpoint. Survival was estimated using the Kaplan-Meier method. Results: A total of 24 patients were included, with a median age of 67 years (range, 55-85). The cohort comprised 19 (79%) patients with SCLC and 5 (21%) with EPSCC (prostate, cervix, GEJ). Patients were heavily pretreated, with a median of 2 prior lines of therapy (range, 1-3). At tarlatamab initiation, 8 (33%) patients had brain metastases and 82% had an ECOG performance status of 0-1. With a median follow-up of 7.5 months, the ORR for the entire cohort was 20.8% (5/24), including 5 partial responses (PR). The median PFS was 4.0 months (95% CI, 1.8 to 5.7). The median OS from the start of tarlatamab was not reached, with a 6-month OS rate of 55%. CRS of any grade occurred in 14 patients (58%), with Grade ≥3 in 2 patients (8%). ICANS of any grade occurred in 7 patients (29%), with Grade ≥3 in 1 patient (4%). Tocilizumab was administered to 12 patients (50%) for management of toxicity. Conclusions: In this real-world cohort, tarlatamab demonstrated meaningful clinical activity and a manageable safety profile. The observed efficacy and toxicity rates are consistent with those reported in the pivotal DeLLphi-301 trial, supporting its use outside of a clinical trial setting. These findings provide valuable insights into the application of tarlatamab across the broader spectrum of DLL3-expressing neuroendocrine malignancies. Baseline characteristics and key toxicities. Characteristic All Patients (N=24) Median age, years (range) 67 (55-85) Female, n (%) 14 (58) Primary Site, n (%) Lung (SCLC) 19 (79) Extrapulmonary (EPSCC) 5 (21) Median prior lines of therapy (range)* 2 (1-3) Brain metastases at baseline, n (%) 8 (33) Cytokine Release Syndrome (Any Grade), n (%) 14 (58) Immune Effector Cell-Associated Neurotoxicity Syndrome (Any Grade), n (%) 7 (29) Tocilizumab Use, n (%) 12 (50) Data for prior lines of therapy were available for 23 patients.

Tulmimetostat treatment results in greater PRC2 target gene expression induction in phenotypically sensitive ARID1A LOF cell lines

List of gene names corresponding to 132 tulmimetostat upregulated genes in responder versus non responder cell lines

3010 Background: Most pts with newly diagnosed extensive-stage small cell lung cancer (ES-SCLC) relapse after initial response to standard of care (SOC; platinum/etoposide + anti–programmed death-ligand 1 [PD-L1] therapy); novel combination strategies are needed. This Phase Ib/II study (NCT05142696) assessed [ 177 Lu]Lu-DOTA-TATE ( 177 Lu-DOTATATE) – a radioligand therapy with high affinity for somatostatin receptor 2 (SSTR2; a poor prognostic biomarker expressed in ~50% of SCLC tumors) – plus SOC. Here, we report Phase Ib data (cutoff 20 Nov 2025). Methods: Phase Ib was a dosage escalation study to determine the recommended dosage (RD) of 177 Lu-DOTATATE – alongside carboplatin AUC 5 + etoposide 100 mg/m 2 + anti–programmed cell death protein 1 (PD-1)/PD-L1 therapy (pre/post protocol amendment: tislelizumab 200 mg/atezolizumab 1200 mg, respectively) Q3W in the induction phase, and alongside anti–PD-1/PD-L1 therapy Q3W in the maintenance phase – in pts aged ≥18 y with newly diagnosed SSTR+ (by PET/CT) ES-SCLC. Cohorts of 3–6 pts were enrolled to increasing dosage levels (DLs) of 177 Lu-DOTATATE (backfill allowed to ≤10 pts); escalation was guided by dosage-limiting toxicity (DLT) rate (Bayesian Optimal Interval design) and other safety data. The primary endpoint was DLTs ( 177 Lu-DOTATATE–related adverse events within the 42-day DLT period). Results: Of 57 pts screened, 29 received treatment (median [range] age 62 [43–73] y; white 89.7%; male 44.8%; ECOG PS 0/1/2 37.9%/58.6%/3.4%; smoking history 100%; bone/brain/liver metastases 51.7%/13.8%/48.3%); 93.1% completed the induction phase (DL1 [3.7 GBq] 9/9; DL2a [5.55 GBq] 11/11; DL3a [7.4 GBq] 7/9). Median treatment duration between first/last dosage and cutoff was 14.2/9.4 months. For 177 Lu-DOTATATE, median (range) number of doses was 4.0 (1.0–7.0), duration was 4.1 (1–6) months, and cumulative activity was 22.7 (7.1–44.4) GBq. There were no DLTs in 17 evaluable pts. The table reports safety and preliminary efficacy data. Conclusions: The observed safety profile was consistent with expected toxicity; the RD for Phase II was 7.4 GBq. Clinical trial information: NCT05142696 . Safety and preliminary efficacy (N=29). AEs, % Any: all grades; Grade ≥3 100; 100 Treatment related 100 177 Lu-DOTATATE related 86.2* Serious 72.4 † Leading to discontinuation 24.1 ‡ Deaths due to AEs, n 2 § Confirmed best overall response, % 82.8 ¶ 6-month duration of response rate, % 28.5 (95% CI 11.8, 47.7) 6-month progression-free survival rate, % 36.1 (95% CI 19.0, 53.6) *Most commonly reported: thrombocytopenia (58.6) and anemia (44.8). † 66.7 DL1, 63.6 DL2a, 88.9 DL3a. ‡ 33.3 DL1, 27.3 DL2a, 11.1 DL3a. § DL1: cardiac failure, large intestinal hemorrhage (on-treatment death); not treatment related. ¶ 100 DL1, 90.9 DL2a, 55.6 DL3a. AE, adverse event; CI, confidence interval; DL, dosage level.

4201 Background: Pancreatic ductal adenocarcinoma (PDAC) is resistant to immune checkpoint inhibitors, in part due to a cold tumor immune microenvironment (TME). BXCL701 (‘701) is a small molecule inhibitor of dipeptidyl peptidases 4, 8, 9 and fibroblast activation protein. We have shown that combinations of ‘701 and anti-PD1 antibodies lead to tumor regression in murine PDAC models due to 1) activation of the inflammasome and expression of CXCL9 to attract and activate CXCR3+ lymphocytes, 2) tumor invasion of CD8+ T cells and other effector cells, 3) induction of adaptive immunity, and 4) reduced fibrosis in the PDAC TME. We sought to evaluate the efficacy of this combination in patients (pts) with previously-treated advanced PDAC. Methods: In this phase II clinical trial (NCT05558982), pts with second-line advanced PDAC received ‘701 at a 0.2 mg PO BID dose on days 1-7 and then 0.3 mg BID on days 8-14 during cycle 1 (21 days) followed by 0.3 mg BID on days 1-14 every 21 days in all subsequent cycles, administered with pembrolizumab 200 mg IV every 21 days (all cycles). The primary objective was to determine the 18-week progression-free survival rate (PFS 18weeks ) in pts with advanced PDAC treated in the second-line setting. We estimated that the historical second-line PFS 18weeks is 30% or less; using a Simon’s two-stage (minimax) design, a type I error rate of 0.05 and a power of 80%, if the true rate is 50%, we would need 19 pts in stage 1 and 20 pts in stage 2 (a total of 39 evaluable). Seven of 19 evaluable pts would need to be progression-free at 18 weeks to trigger stage 2. Results: Twenty-one pts were enrolled. Four out of 18 evaluable pts (22%) were alive and progression-free at 18 weeks. Three had partial responses (PR, 17%), and 4 had stable disease (SD, 22%), for a disease control rate of 39%. One responder had MSI-H PDAC, while the other 2 had MSS disease. Median follow-up was 4.5 months. Median PFS was 2.3 months (95% CI 1.6 – 5.3), and median overall survival was not reached (NR, 95% CI 4.5 – NR). Three pts (14%) had PFS exceeding 6 months (2 PR, 1 SD). No new safety signals have been identified. Baseline and on-treatment tumor biopsies will be analyzed to understand the mechanisms underlying therapeutic benefit and to examine the characteristics of responders vs. non-responders. Conclusions: ‘701 plus pembrolizumab in second-line advanced PDAC did not reach the preliminary efficacy endpoint to trigger the second stage. However, there were encouraging signs as this combination induced objective responses in 2 MSS pts, and PFS exceeded 6 months in 3 pts. Ongoing correlative studies should elucidate predictive markers of efficacy and resistance to this novel immunotherapy combination. Clinical trial information: NCT05558982 .

Abstract Background: Brain metastasis (BM) is prevalent in extensive-stage small-cell lung cancer (ES-SCLC) and also a common cause for treatment failure. BM remains as an unmet need with limited treatment options available such as palliative radiotherapy. ZL-1310 is a novel antibody-drug conjugate (ADC) that employs the TMALIN® (Tumor Microenvironment Activable LINker-payload) platform, an anti-DLL3 monoclonal antibody linked to a topoisomerase I inhibitor payload via a protease-cleavable linker. ZL-1310 has demonstrated encouraging systemic efficacy in heavily pre-treated ES-SCLC. We report the initial intracranial efficacy of ZL-1310 from a phase 1 study. Methods: This multi-country Phase 1 study (NCT06179069) enrolled adults with ES-SCLC who have progressed following ≥1 platinum-based chemotherapy. Those with stable or asymptomatic BM are eligible (including those with no prior brain radiotherapy). ZL-1310 is given intravenously every 3 weeks until disease progression or unacceptable toxicity. Systemic efficacy was assessed by investigators using Response Evaluation Criteria in Solid Tumors (RECIST) v1.1. Intracranial efficacy was assessed by blinded independent radiologists using Modified Criteria for Radiographic Response Assessment in NeuroOncology (mRANO). Results: As of 1 Aug 2025, 104 pts received ZL-1310 across 6 dose levels (0.8-2.8 mg/kg). The median age was 65 years (range: 36, 80); 42.3% of pts were female, and 28.8% were Asian. Fifty-four (51.9%) had 1 prior line and the remaining 50 (48.1%) had 2 or more lines of prior therapies. A total of 94 (90.4%) received a prior anti-PDL1, 13 (12.5%) had prior lurbinectedin, and 10 (9.6%) had prior DLL3-targeted therapy. Brain metastases were present in 33 (31.7%) pts (including 11 pts with untreated BM) at baseline. Independently reviewed intracranial efficacy results were available for 24 pts, including 15 pretreated with radiation and 9 untreated. Confirmed intracranial response was 58.3% (14/24, 95% CI: 36.6, 77.9%), including 5 CR and 9 PR. The intracranial response rate in pts without prior brain radiation was 66.7% (6/9) and 53.3% (8/15) in pts with prior brain radiation. Intracranial disease control rate was 95.8% (23/24). The median time to onset of intracranial response was 5.6 weeks (min 5.1, max 8.7 weeks). Of the 33 pts with BM and systemic efficacy evaluable, confirmed ORR was 61%, including 1 confirmed CR. Grade ≥3 treatment-related adverse events were reported for 22/104 (21.2%) pts overall and 5/39 (12.8%) pts in the 1.6 mg/kg dose level; those reported in ≥2 pts at the 1.6 mg/kg dose level included anemia and neutropenia (2 pts each). Independent mRANO evaluation is ongoing and updated data will be provided. Conclusions: ZL-1310 is well tolerated and demonstrated encouraging systemic efficacy in heavily pretreated ES-SCLC with BM. The preliminary independent assessment also showed ZL-1310 has high intracranial efficacy including in patients with untreated BM. Citation Format: Pedro Rocha, Manish Patel, Yi-Long Wu, Jun Zhao, Grace Dy, María Eugenia Olmedo García, Qiming Wang, Valentina Gambardella, Oscar Juan-Vidal, Afshin Dowlati, David Vicente Baz, Alexander Spira, Anne C. Chiang, Yingying Du, Martin Gutierrez, Xiaorong Dong, Jie Hu, Mariam Alexander, Haiyong Wang, Wenxiu Yao, Liza Villaruz, Zhen Wang, Pingkuan Zhang, Renke Zhou, Xiao Wang, Luis Paz-Ares. Intracranial activity of ZL-1310, a DLL3-targeted ADC, in patients with previously treated extensive-stage small cell lung cancer and baseline brain metastasis: Analysis of a phase 1 trial [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2026; Part 2 (Late-Breaking, Clinical Trial, and Invited Abstracts); 2026 Apr 17-22; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2026;86(8_Suppl):Abstract nr CT193.

1652 Background: Socio-economic Status (SES) indicators create barriers to access Phase 1 clinical trial (Ph1) enrollment, particularly for underrepresented minorities (URM). However, it remains unclear whether they directly affect enrollment after screening, or represent upstream barriers. We evaluated whether SES indicators impacted the enrollment rate in Ph1. Methods: All patients were screened for Ph1 at Hackensack University Medical Center (2014-2025). Patient ZIP codes were linked to the U.S. Census data (ACS 2018-2022) to derive neighborhood-level SES indicators: median household income (MHI), educational attainment (Bachelor), poverty rate (PR), unemployment rate (UR), and median home value (MHV). SES indicators were compared to national and state census benchmarks. The primary outcome was enrollment rate by SES indicators. We performed univariate analyses (Mann-Whitney U tests, chi-square), stratified analyses by race/ethnicity and gender, temporal trend analysis, and multivariable logistic regression. Results: A total of 1,316 patients were screened for 140 Ph1. Demographics were non-Hispanic White (NHW) 66.2%, Hispanic 19.0%, African American/Black (AA) 7.8%, Asian 6.5%. No SES variable predicted enrollment: median income (enrolled $62,646 vs not-enrolled $61,820, p=0.450), education (38.3% vs 37.9%, p=0.598), poverty (12.9% vs 12.3%, p=0.416), unemployment (6.1% vs 6.0%, p=0.422), home value ($277,461 vs $275,697, p=0.605). SES quartile analysis showed no enrollment gradient (Q1=61.7%, Q2=58.1%, Q3=60.5%, Q4=63.8%; p=0.491). Findings were consistent across all racial/ethnic groups (all p>0.05), see Table 1, gender (all p>0.05), age groups <65 and ≥65 years (all p>0.05), and time periods 2014-2019 vs 2020-2025. When compared to their respective racial/ethnic groups U.S. Census averages, it demonstrated atypical SES profiles: Hispanic patients had higher education (36.6% vs 20.6%), AA showed higher SES across all indicators, and Asians showed lower SES, suggesting regional selection bias in who reaches Ph1 screening. Conclusions: When patients reach Ph1 screening, SES indicators do not predict enrollment, demonstrating that equitable enrollment practices can be achieved at screening. Although there were no visible SES-related barriers at the enrollment point, disparities exist among groups likely suggesting referral patterns prior to screening. Future research should examine how to improve access to Ph1 in URM and upstream inequities. SES analysis stratified by race/ethnicity. Race SES Variable p-value NHW MHI 0.4476 NHW Education 0.4585 NHW PR 0.7483 NHW UR 0.6957 NHW MHV 0.4982 Hispanic MHI 0.8270 Hispanic Education 0.4104 Hispanic PR 0.0646 Hispanic UR 0.2401 Hispanic MHV 0.9677 AA MHI 0.9569 AA Education 0.7355 AA PR 0.9112 AA UR 0.3962 AA MHV 0.3076 Asian MHI 0.2037 Asian Education 0.3200 Asian PR 0.2067 Asian UR 0.0867 Asian MHV 0.1677