6077 Background: The phase III VELIA trial (NCT02470585) demonstrated statistically significant improvement in PFS per investigator (INV) for V added to CP and continued as maintenance (CPV-V) vs. CP alone in pts with newly diagnosed HGSC in the BRCA mutated ( BRCAm), homologous recombination deficient (HRD), and whole populations. Here we present pre-specified analyses of PFS per BICR. Methods: Pts with Stage III-IV HGSC received V or Placebo (PL) with CP (6 cycles) and as maintenance (30 additional cycles). Primary analysis of PFS by INV compared CPV-V to CP alone in the BRCAm, HRD, and whole populations. Exploratory analyses of PFS in BRCA wildtype (wt) and non-HRD HGSC were performed. Radiologic tumor assessments were also prospectively submitted to an independent central reviewer for blinded assessment per RECIST v 1.1. PFS per BICR and rates of concordance between INV and BICR for determination of disease progression were analyzed. Safety data from the primary analysis were previously reported. Results: 1140 total pts were enrolled (CPV-V 382; CP 375). In the whole population, 26% of HGSCs were BRCAm and 55% were HRD. Concordance rates between INV and BICR were 68-85% by arm for each population. Analyses of PFS per BICR and per INV were consistent (Table). PFS was prolonged in the CPV-V vs. CP arm in all primary and exploratory populations assessed. Conclusions: Analyses of PFS per BICR supported the primary analysis of PFS per INV in the BRCAm, HRD, and whole populations, as well as exploratory BRCAwt and non-HRD populations. Median PFS per BICR was longer compared to PFS per INV assessments in all populations and in both arms. These findings support the reliability of PFS by INV in ovarian cancer trials. Alternate strategies like audits may be appropriate to support PFS by INV with less time and expense than full BICR. Clinical trial information: NCT02470585. [Table: see text]

519 Background: HRD status is significantly associated with a higher rate of response to neoadjuvant platinum-based therapy and improved PFS following adjuvant doxorubicin and cyclophosphamide (AC) in TNBC. We assessed the prognostic and predictive role of the HRD assay for platinum and PARP inhibitor response in BrighTNess. Methods: 634 stage II-III TNBC pts were randomized 2:1:1 to: Arm A: Paclitaxel (T) q wk x 12 + carboplatin (P) (AUC 6) q3 wk x 4 + veliparib (TPV) - > AC q2-3 wk x 4; Arm B: T + P + placebo (TP) - > AC; or Arm C: T + dual placebo (T) - > AC. HRD status was defined as HRD+ (HRD score ≥ 42 or a tumor BRCA1/2 mutation) or HRD- (HRD score < 42 and no tumor BRCA1/2 mutation). An exploratory HRD threshold of ≥ 33 vs < 33 was also assessed. Results: HRD status was available for 438 pts. HRD data by arm for pCR for the 42 and 33 cut-offs are shown. Within each arm using the 42 and 33 cut-offs, respectively, ORs for pCR by HRD status (HRD+/HRD-) were 2.85 (p = 0.0005) and 3.10 (p = 0.004) for Arm A, 1.55 (p = 0.30) and 2.28 (p = 0.10) for Arm B and 2.13 (p = 0.13) and 1.52 (0.48) for Arm C. Comparing between arms using the 42 threshold, ORs for pCR (Arm A/Arm B, Arm A/Arm C, Arm B/Arm C) in the HRD+ group were 1.04, 3.02 and 2.90 and were not statistically significantly different than in the HRD- group (0.57 [p = 0.23], 2.26 [p = 0.60] and 4.0 [p = 0.61]). Similar results were observed with the 33 cut-off. Conclusions: In BrighTNess, higher rates of pCR were observed in HRD+ pts across all treatment arms. However, pts treated with P had higher rates of pCR in both HRD+ and HRD- subsets. The exploratory HRD threshold of 33 appeared to provide greater sensitivity to identify responders with the addition of P + V. Receipt of AC in all pts may have contributed to the lack of interaction observed between HRD status and P +/- V treatment. Clinical trial information: NCT02032277.Arm pCR HRD+ ≥ 42 pCR HRD- < 42 pCR HRD+ ≥ 33 pCR HRD- < 33 TPV-AC (A) n = 213 87/141 (61.7%) 26/72 (36.1%) 93/153 (60.8%) 20/60 (33.3%) TP-AC (B) n = 116 51/84 (60.7%); p = 0.88# 16/32 (50%); p = 0.18# 57/92 (62%); p = 0.89# 10/24 (41.4%); p = 0.61# T-AC (C) n = 109 24/69 (34.8%); p = 0.0003‡ 8/40 (20%); p = 0.08‡ 25/79 (31.6%); p = < 0.0001‡ 7/30 (23.3%); p = 0.46‡ # = for TPV-AC vs TP-AC; ‡ = for TPV-AC vs T-AC