Background & Aim NY-ESO-1 is a cancer testis antigen with ectopic expression on multiple myeloma (MM), melanoma and sarcoma but restricted expression on normal tissues, rendering it a good candidate target for cancer immunotherapy. We recently reported a phase 1 pilot trial of multiplex CRISPR/Cas9 genome-edited NY-ESO-1 TCR cells (NYCE T cells; NCT03399448) for patients (pts) with advanced MM, synovial sarcoma and myxoid/round cell liposarcoma (MRCL) demonstrated safety and feasibility as well as persistence of T cells. Here, we characterize the phenotype and function of the ex vivo manufactured NYCE T cells from the 3 pts that were infused in the trial. Methods, Results & Conclusion The 3 infusion products (2 MM – pt #35 and Pt #7, and 1 MRCL – pt #39) were used to compare expanded T cells with either CRISPR/Cas9 editing without TCR transduction or with Mock-editing and TCR transduction from the same pt. We examined the phenotypic markers of T cell differentiation and checkpoint inhibitors by multicolor flow cytometry and assessed in vitro anti-tumor efficacy via a luciferase-based killing assay. We found heterogeneity in the composition of T cell subsets from all 3 infusion products with various CD4 and CD8 ratios, ranging from 0.12-1.1. Transduction efficiencies (determined by Vbeta8.1+ staining) varied between 1-11% and different levels of knockout efficiency in TRAC, TRBC and PDCD1 genes were observed by digital PCR. Three NYCE T cell infusion products displayed a terminally differentiated T cell phenotype similar to CRISPR/Cas9 edited counterpart. In contrast to Mock-edited T cells from the same pt, NYCE T cells exhibited lower levels of differing combinations of exhaustion-associated markers (PD1, TIM3, LAG3, EOMES and CTLA4) in both CD4+ and CD8+ T cell compartments. All 3 infusion products elicited antigen-specific killing of NY-ESO-1 expressing target cells. We demonstrate that NYCE T cells are heterogeneous in composition. Furthermore, we showed that CRISPR/Cas9 editing does not affect T cell differentiation and anti-tumor efficacy, but does reduce levels of exhaustion-associated markers expressed by the final products. This work provides an in-depth characterization of the heterogeneous product composition and function of the first multiplex CRISPR/Cas9-edited T cells tested in humans.

Introduction: Obinutuzumab (OBI) is approved for use in combination with chlorambucil for patients (pts) with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) in both frontline and relapsed/refractory (r/r) settings. OBI has been successfully evaluated as a single agent without significant loss of efficacy (Gay ND, Leuk. Lymphoma 2018). We performed an analysis of all CLL/SLL pts treated with OBI monotherapy at our institution to assess efficacy and safety in any line of therapy. Methods: We conducted a retrospective cohort study of all adult pts who received OBI monotherapy for CLL at the University of Pennsylvania between 2/2013 and 2/2019. Demographics, duration of therapy, reason for discontinuation, overall response, survival, and toxicities were examined. The primary endpoints were progression-free survival (PFS; defined as time from OBI start to disease progression or regimen change, death due to CLL or last-follow-up in remission), and overall survival using the Kaplan-Meier method. Results: We identified 40 pts with CLL/SLL for this analysis. Median age of start was 70 years, Rai stage 2 (35% >3), and ECOG performance status 1. Most pts were rituximab naïve (58%) and 20% were rituximab refractory. Frontline use was seen in 53% of pts received OBI frontline and 47% were treated for r/r disease. 9 pts were documented with progression and 4 patients met indication for subsequent therapy. At this time, 7 pts are receiving active OBI treatment. 55% of pts followed the package insert recommended schedule of OBI administration. Overall response rate was 90% (10% CR). The median PFS and OS for the entire cohort was 11.5 and 16.5 months respectively. At least 1 adverse events (AEs) occurred in 90% of pts. AEs included infusion related reactions (63%), thrombocytopenia (43%), infection (23%), neutropenia (15%), diarrhea (10%), neutropenic fever (8%). All pts with infusion reactions experienced symptoms on the first dose (92% grade 2; 8% grade 3), with 6 pts experiencing more than one infusion reaction in the first cycle. One patient stopped therapy after experiencing a severe grade 3 infusion reaction. One patient had an opportunistic infection (Rhizopus sp.). Keywords: chronic lymphocytic leukemia (CLL); obinutuzumab. Disclosures: Hughes, M: Consultant Advisory Role: AstraZeneca; Research Funding: Acerta Pharma. Schuster, S: Consultant Advisory Role: Novartis, Nordic Nanovector, Celgene, Merck, Gilead, Pfizer; JS: BMS, Seattle Genetics, KITE, Kyowa, Pharmacyclics; Honoraria: SJS: Genentech, Novartis, Nordic Nanovector, Celgene, Merck, OncLive, Dava Oncology, Physician's Education Source, LLC; Research Funding: SJS: Genentech, Novartis, Nordic Nanovector, Celgene, Merck, OncLive, Dava Oncology, Physician's Education Source, LLC. Svoboda, J: Consultant Advisory Role: BMS, Seattle Genetics, KITE, Kyowa, Pharmacyclics; Research Funding: BMS, Regeneron, Merck, Seattle Genetics, TG Therapeutics, Pharmacyclics. Landsburg, D: Consultant Advisory Role: Celgene, Curis; Research Funding: Triphase, Takeda, Curis. Stadtmauer, E: Consultant Advisory Role: Celgene, Janssen; Research Funding: Abbvie. Nasta, S: Consultant Advisory Role: Celgene; Research Funding: Pharmacyclics, Incyte, Roche, Aileron, Rafael/WF, Debiopharm, Takeda/Millenium; Other Remuneration: Merck: DSMC.

Background:Venetoclax (Ven) is a highly selective, potent, oral BCL‐2 inhibitor that induces apoptosis in malignant cells dependent on BCL‐2 for survival. Proteasome inhibitors (PIs) and dexamethasone (d) were shown to increase BCL‐2 dependence in multiple myeloma (MM) cells, and preclinical studies showed enhanced inhibition of MM tumor growth with Ven+PI compared to either alone. Moreover, d has been shown to indirectly promote BCL‐2 dependency in MM cells. Clinical trials have since demonstrated efficacy of Ven in combination with the PI bortezomib in patients (pts) with relapsed/refractory MM (RRMM).Aims:We report interim data for Ven combined with second‐generation PI carfilzomib (K) and d in pts with RRMM.Methods:In this ongoing Phase 2 study (NCT02899052), pts with RRMM (1–3 prior lines of therapy) and no prior K exposure received VenKd on 28‐day cycles in 4 dose‐finding and 1 expansion cohort: Ven 400 mg/day + K 27 mg/m2 Day 1, 2, 8, 9, 15, 16 + d 40 mg Day 1, 8, 15, 22 (Cohort 1); same regimen but with Ven 800 mg/day (Cohort 2); Ven 800 mg/day + K 70 mg/m2 Day 1, 8, 15 + d 40 mg Day 1, 8, 15, 22 (Cohort 3/expansion cohort); or Ven 800 mg + K 56 mg/m2 Day 1, 2, 8, 9, 15, 16 + d 40 mg Day 1, 2, 8, 9, 15, 16, 22, 23 (Cohort 4). Treatment continued until progressive disease or unacceptable toxicity.Results:As of the clinical data cut‐off of 1 Feb 2019, 43 pts were enrolled. Median age was 67 (range, 37–79), 26 (62%) pts had ISS II/III disease, and 8 (19%) were t (11;14)+. Median number of prior lines of therapy was 2 (range, 1–3). Forty (93%) pts received prior PI (49% refractory), 33 (77%) received prior immunomodulatory drug (IMiD, 61% refractory), and 33 (77%) received prior PI+IMiD (33% double refractory).All pts had at least 1 adverse event (AE). The most common AEs of any grade were diarrhea (65%), nausea (49%), fatigue (47%), cough (35%), insomnia, dyspnea, vomiting, upper respiratory infection (33% each), lymphopenia (28%), thrombocytopenia, and dyspepsia (26% each). Thirty‐six (84%) pts had a Grade 3/4 AE, the most common being lymphopenia (23%), pneumonia, hypertension (16% each), and hypophosphatemia (12%).The overall response rate (ORR) was 79%, complete response or better (≥CR) rate was 40%, and very good partial response or better (≥VGPR) rate was 64% for all pts (Table). Median follow‐up for 42 pts was 10.4 months (95% CI = 8.0–13.8); 15 pts had progression‐free survival (PFS) events, with median PFS yet to be achieved. Baseline bone marrow core biopsy samples from 25 pts were evaluated for BCL‐2 expression by immunohistochemistry, with high expression (≥50% of tumor cells with moderate or higher cytoplasmic staining) seen in 23 (92%) samples. Pts with high BCL‐2 expression had response rates similar to the overall study population. Other correlative biomarker analyses are ongoing.Summary/Conclusion:The combination of VenKd was found to be tolerable with no new safety signals. VenKd demonstrates promising efficacy in pts with RRMM. The study remains ongoing with an additional 60 pts with RRMM enrolling to assess efficacy and safety in a larger group of pts with similar eligibility (Cohort 6) and t (11;14)+ pts (Cohort 7).image

Background & Aim With the goal of improving consistency and success of manufacturing (MFG), we analyzed the composition of apheresis products collected from patients (pts) enrolled in clinical trials of engineered T cell immunotherapies. We previously reported in a small cohort of NHL pts, that T cell cultures manufactured from fresh APH of challenging products comprised of 3:1 monocyte to lymphocytes, exhibited impaired proliferation. Microscopic observation of poorly expanding cell cultures revealed the phagocytosis of T cell stimulating anti-CD3/ anti-CD28 Dynabeads by large cells, possibly of monocyte/myeloid origin. Proliferative capacity of the T cells was rescued if the APH was cryopreserved/thawed prior to manufacture. Substantial reduction in MDSC frequency, following cryopreservation/thaw, was demonstrated by flow cytometry. Alternatively, lymphocyte enrichment via elutriation of APH removed the larger myeloid cells. Here we expand analysis of the critical quality attributes of APH products to a larger cohort of patients with hematological malignancies (HM) as well as solid tumors (ST). Methods, Results & Conclusion We analyzed 300 APH from pts on 20 clinical trials focused on HM or ST. Frequencies of lymphocytes and myeloid populations were determined via size/volume distribution on Multisizer, lineage and MDSC immunophenotyping by FACS (CD3, CD45, CD11b, CD33, HLA-DR, CD14, CD15). Population doubling levels (PDL) during ex vivo expansion were calculated at day 9 of manufacture. We report an overall 94% MFG success rate with 5 PDL. 12/19 MFG failures did not produce an infusible dose with -1.34 PDL and occurred in HM APH. APH of MFG fails showed the presence of myeloid cells that were not removed prior to MFG. APH from NHL, MM, and synovial sarcoma demonstrated MDSCs by flow cytometry. Cryopreservation/thaw and/or elutriation of APH enriched T cells from 81 % to 94%, reduced myeloid population from 38% to 11%, and removed MDSCs. Small scale test expansions comparing various MFG processes on the same APH confirmed that cryopreservation and or elutriation increases clinical MFG success. Myeloid subsets in HM APH increase the risk of MFG failure. Mitigation strategies to remove the myeloid cells to enrich for the lymphocytes can be employed, including cryopreservation or elutriation of fresh APH prior to MFG. To increase MFG feasibility, studies are continuing to investigate the effects of prior treatment on APH and the mechanism of inhibition by MDSCs. With the goal of improving consistency and success of manufacturing (MFG), we analyzed the composition of apheresis products collected from patients (pts) enrolled in clinical trials of engineered T cell immunotherapies. We previously reported in a small cohort of NHL pts, that T cell cultures manufactured from fresh APH of challenging products comprised of 3:1 monocyte to lymphocytes, exhibited impaired proliferation. Microscopic observation of poorly expanding cell cultures revealed the phagocytosis of T cell stimulating anti-CD3/ anti-CD28 Dynabeads by large cells, possibly of monocyte/myeloid origin. Proliferative capacity of the T cells was rescued if the APH was cryopreserved/thawed prior to manufacture. Substantial reduction in MDSC frequency, following cryopreservation/thaw, was demonstrated by flow cytometry. Alternatively, lymphocyte enrichment via elutriation of APH removed the larger myeloid cells. Here we expand analysis of the critical quality attributes of APH products to a larger cohort of patients with hematological malignancies (HM) as well as solid tumors (ST). We analyzed 300 APH from pts on 20 clinical trials focused on HM or ST. Frequencies of lymphocytes and myeloid populations were determined via size/volume distribution on Multisizer, lineage and MDSC immunophenotyping by FACS (CD3, CD45, CD11b, CD33, HLA-DR, CD14, CD15). Population doubling levels (PDL) during ex vivo expansion were calculated at day 9 of manufacture.

PB CD34+ cells are routinely monitored to optimize the timing and success of CD34+ stem cell collection after G-CSF ± chemotherapy mobilization in NHL patients (pts) undergoing auto-HSCT. A threshold of ≤10 PB CD34+ cells/μl is often used to predict poor mobilization and aid the decision of whether novel therapies such as plerixafor should be included in the mobilization scheme. This analysis evaluated whether a PB threshold ≤10 cells/μl is indeed the most optimal threshold to predict mobilization failure.

Although recent studies have shown comparable survival outcomes between unrelated donor (URD) and sibling donor stem cell transplantation in the myeloablative transplant setting, little comparative data based on donor source is available in the setting of non-myeloablative/reduced intensity conditioning (RIC), where it is presumed that GvL effects must play a key role in long term survival. In this retrospective analysis, we compare the outcome of 111 patients receiving RIC followed by either matched sibling (n = 65) or unrelated donor (n = 46) peripheral blood stem cell (PBSC) transplantation for hematologic malignancies. All patients were deemed ineligible for myeloablative conditioning based on institutional standards for age, comorbid disease, and/or prior therapy. All sibling and 38 of 46 unrelated recipients received A, B, DR matched grafts. The median recipient age in both cohorts was identical; sibling 52 y (range 12–75 y) and unrelated 52 y (range 29–69 y). Conditioning regimens were primarily fludarabine/cytoxan-based in both cohorts, with URD recipients skewed toward the addition of Alemtuzumab pre-transplant (69% URD vs 25% sib), and the use of TBI 200 for 21/23 myeloma pts. The distribution of diagnoses was similar between both cohorts in patients with lymphoid malignancies (NHL, HD, CLL n = 66) 34 sib vs 32 URD, and leukemia/MDS (n = 22), 10 sib vs 12 URD; the diagnosis of myeloma (n = 23) was skewed toward sibling donors (21 vs 2 URD). Kaplan-Meier estimate of overall survival (OS) for all patients at 2 years was 31%. At a median f/u of 43 weeks in both cohorts, overall survival was nearly identical (57% sibs; 55% URD). Of note, there was no statistically significant difference in 2 year OS between sibling and URD recipients (p = 0.25), nor was there a difference in K-M estimates of OS between sibling and URD recipients when patients with lymphoid and myeloid disease were analyzed separately. Among expired patients, there was no difference in the incidence of disease-related (26/42 sibs vs 18/32 URD) or treatment-related [organ failure, infection and GvHD] (16/42 sibs vs 14/32 URD) causes of death. Furthermore, a statistically significant higher proportion of GvHD-related death among URD patients was not seen. These data support the pursuit of unrelated donors for RIC transplantation as an alternative to sibling donors without compromising overall survival.

Velafermin (CG53135-05 or recombinant human fibroblast growth factor-20) is under investigation for the prevention of oral mucositis (OM). OM is a common side effect in patients (pts) receiving high-dose chemotherapy (HDCT) with or without total body irradiation (TBI) as conditioning regimen for AHSCT. Preclinical studies have demonstrated that velafermin promotes epithelial and mesenchymal cell proliferation in vitro and that a single dose of velafermin had activities in reducing the severity and duration of OM as effective as multiple doses. Previous clinical data suggested that velafermin could be safely given at doses up to 0.2 mg/kg. The objectives of this phase II trial were to evaluate the safety and efficacy of velafermin in preventing severe OM from approximately 200 pts undergoing HDCT with or without TBI for an AHSCT in the US. Patients were equally randomized to one of four arms: placebo, or velafermin 0.03, 0.1 or 0.2 mg/kg. Pts received a single intravenous dose of velafermin or placebo 24-36 hrs after completion of the stem cell infusion and were monitored daily until they were discharged from the hospital or until neutrophil engraftment established (defined as first day of absolute neutrophil counts ≥500/μ in this study). The primary end point was the incidence of OM (World Health Organization (WHO) score of grade 3 or 4). Secondary end points included duration of severe OM, area under the curve of all OM, days with alternative nutrition, and narcotic analgesic use. Patient enrollment was completed with 212 pts randomized. Approximately 2/3 were multiple myeloma pts receiving high dose melphalan as conditioning regimen and 1/3 of them were lymphoma pts. Less than 10% of pts had TBI as part of their conditioning regimen. Preliminary blinded aggregate data from 160 pts indicated that study drug was generally well tolerated. 30% of pts did not develop any OM and 32% pts developed grade 3/4 OM with a duration of 4.8 ± 3.7 (mean ± sd) days among the pts with severe OM. Most adverse events (AE) were mild to moderate in severity with most frequent serious AEs being neutropenicfever, pneumonia and pyrexia. The trial was monitored by a Data Safety Monitoring Board (DSMB). The results of the primary end point of grade 3/4 OM from each treatment arm or placebo as well as 30-day safety information from all pts will be reported. Velafermin (CG53135-05 or recombinant human fibroblast growth factor-20) is under investigation for the prevention of oral mucositis (OM). OM is a common side effect in patients (pts) receiving high-dose chemotherapy (HDCT) with or without total body irradiation (TBI) as conditioning regimen for AHSCT. Preclinical studies have demonstrated that velafermin promotes epithelial and mesenchymal cell proliferation in vitro and that a single dose of velafermin had activities in reducing the severity and duration of OM as effective as multiple doses. Previous clinical data suggested that velafermin could be safely given at doses up to 0.2 mg/kg. The objectives of this phase II trial were to evaluate the safety and efficacy of velafermin in preventing severe OM from approximately 200 pts undergoing HDCT with or without TBI for an AHSCT in the US. Patients were equally randomized to one of four arms: placebo, or velafermin 0.03, 0.1 or 0.2 mg/kg. Pts received a single intravenous dose of velafermin or placebo 24-36 hrs after completion of the stem cell infusion and were monitored daily until they were discharged from the hospital or until neutrophil engraftment established (defined as first day of absolute neutrophil counts ≥500/μ in this study). The primary end point was the incidence of OM (World Health Organization (WHO) score of grade 3 or 4). Secondary end points included duration of severe OM, area under the curve of all OM, days with alternative nutrition, and narcotic analgesic use. Patient enrollment was completed with 212 pts randomized. Approximately 2/3 were multiple myeloma pts receiving high dose melphalan as conditioning regimen and 1/3 of them were lymphoma pts. Less than 10% of pts had TBI as part of their conditioning regimen. Preliminary blinded aggregate data from 160 pts indicated that study drug was generally well tolerated. 30% of pts did not develop any OM and 32% pts developed grade 3/4 OM with a duration of 4.8 ± 3.7 (mean ± sd) days among the pts with severe OM. Most adverse events (AE) were mild to moderate in severity with most frequent serious AEs being neutropenicfever, pneumonia and pyrexia. The trial was monitored by a Data Safety Monitoring Board (DSMB). The results of the primary end point of grade 3/4 OM from each treatment arm or placebo as well as 30-day safety information from all pts will be reported.

Introduction: Bortezomib (Bz, VELCADE®) is a novel proteasome inhibitor that has demonstrated safety and efficacy for patients (pts) with relapsed and/or refractory multiple myeloma (MM) in phase 2 and 3 trials. Bz was associated with transient, cyclical thrombocytopenia in SUMMIT (NEJM. 2003; 348:2609) and CREST (BJH. 2004; 127:165). This analysis evaluated the hematologic profiles in pts treated with Bz or high-dose dexamethasone (Dex) in APEX, the largest phase 3 MM trial in relapsed pts. (NEJM. 2005; 352:2487). Methods:669 pts with relapsed MM were randomized to Bz 1.3 mg/m2 d 1, 4, 8, 11 q3wk for 8 cycles, then 3 cycles on d 1, 8, 15, 22 q5wk, or Dex 40 mg d 1–4, 9–12, 17–20 q5wk for 4 cycles, then 5 cycles on d 1–4 q28d. Data were collected at baseline and regularly through therapy for adverse events, laboratory values, and transfusion (tf) experience.

Background: Despite the recent increase in treatment options for patients with multiple myeloma (MM), the disease remains largely incurable. Both arsenic trioxide (ATO) and melphalan have shown clinical activity in MM. Recent in vitro and in vivo studies in our laboratory have shown that arsenic trioxide sensitizes chemoresistant MM cells to melphalan-induced cytotoxicity; the addition of ascorbic acid (AA) further improves this effect. We conducted a multi-center clinical trial to evaluate the safety and efficacy of this steroid-free combination, melphalan, ATO and vitamin C (MAC), for patients with relapsed/refractory MM.

For patients (pts) with Non-Hodgkin's Lymphoma (NHL), the optimal timing and conditioning regimen intensity for transplant has not been defined. Nonmyeloablative stem cell transplants (NMT) have been reserved for those patients at high risk for treatment related morbidity and mortality (TRM) from conventional High Dose allogeneic SCT (HDT) and have been increasingly employed as salvage therapy for relapse after autotransplantation. To assess the effectiveness of this approach, we performed a retrospective analysis of 35 pts who have undergone either HDT (n=20) with a TBI-based regimen or NMT (n=15) with a fludarabine-based regimen followed by allogeneic SCT for high risk NHL. Stem cell source varied by conditioning; 13/15 of HDT pts received bone marrow (11 sib, 2 MUD), while all NMT pts received peripheral blood (11 sib, 9 MUD). NMT pts constituted a higher risk cohort based on extent of prior therapy (including 80% s/p autotransplant), chemoresistance, and age. Distribution of histology for the entire group was skewed toward aggressive histology, but equally distributed between HDT and NMT. For pts surviving >90 days, median follow up for HDT pts is 50 months (4–92 m), vs 12 months (4–45 m) for NMT pts. A comparison of overall survival (53 vs 45%), event-free survival (53 vs 48%), and progression-free survival (88 vs 64%) at 1 year demonstrated no significant differences between HDT and NMT cohorts despite the higher risk nature of the NMT group. The 100-day TRM for HDT vs NMT pts was similar (33 vs 30%, p=ns). The incidence of grade II-IV acute GvHD was not significantly different between HDT (3/13 evaluable, 23%) and NMT (7/20, 35%). Among evaluable pts, chronic GvHD was lower in the HDT group vs NMT (13 vs 50%). Among causes of death, disease-related deaths were lower in the HDT group (1/7, 14%) compared with NMT pts (5/11, 45%). This retrospective analysis demonstrates 1) NMT induces durable remissions in a significant number of poor risk pts; 2) outcomes after NMT may be comparable to HDT; 3) relapse rates are higher after NMT while TRM is higher after HDT; and 4) long term remissions suggest that NMT is associated with an important graft vs lymphoma effect.

Background: INTERCEPT Platelets (IP) are prepared with Helinx® technology (amotosalen HCl and UVA) to inactivate a broad range of viruses, bacteria, and protozoa, as well as WBCs which can cause transfusion reactions and TA-GVHD. Methods: A double-blind, parallel group Phase III trial (SPRINT) randomized patients (pts) with malignancy undergoing chemotherapy only (CTX) (19%) or SCT (78%) to treatment with IP or Reference (RP) platelet (plt) transfusions (tx) for up to 28 days. The prophylactic tx threshold, selected by the treating physician, was 10×109/L in 61% and 20×109/L in 26% of pts. Results: 645 pts were tx'ed (318 IP vs 327 RP). The primary endpoint, equivalence of IP to RP in the control of moderate and severe (WHO Grade 2 and higher) bleeding, was demonstrated. Diagnosis (dx) and anti-neoplastic regimen (SCT vs CTX) were well balanced between IP and RP. 65% of SCT were autologous (auto) and 35% were allogeneic (allo); 70% were peripheral blood (PB) and 26% bone marrow (BM). 86% of PBSCT and 18% of BMT were auto. There were significant differences in dx, plt tx threshold, duration of plt support, no. of plt and RBC tx, and incidence and duration of Grade 2 or higher bleeding among auto SCT, allo SCT, and CTX pts (all p-values < 0.01). Leukemia was more common in allo than auto SCT; lymphoma, plasma cell dyscrasia, and solid tumor were more common in auto than allo SCT; acute leukemia was the most common dx for CTX pts (p < 0.001). Pts receiving auto SCT had the lowest tx threshold, shortest duration of plt support, fewest plt and RBC tx, and the lowest incidence and duration of Grade 2 or higher bleeding. Allo SCT were on the other extreme, and CTX pts were intermediate. No difference in incidence or duration of bleeding was observed between IP and RP for SCT pts. Conclusions: Allo SCT was associated with a longer duration of plt support, more plt and RBC tx, and a higher incidence and duration of significant bleeding than auto SCT or CTX. INTERCEPT Platelets were as effective as Reference platelets in control of Grade 2 and higher bleeding regardless of dx, anti-neoplastic tx, or stem cell source. TableStudy Endpoints for SCT PatientsEndpointAuto SCTAllo SCTIP (N = 154)RP (N = 171)P ValueIP (N = 86)RP (N = 91)P ValuePlt tx threshold 10× 109/L (%)70680.2948460.82Grade 2 bleeding (% pts)46510.4473741.00Grade 3/4 bleeding (% pts)020.259101.00Days of Grade 2 bleeding1.91.40.105.04.90.83Duration plt support (d)8.87.20.0516.816.70.88No. plt tx5.73.7<0.0114.011.30.07No. RBC tx3.42.70.046.16.60.58 Open table in a new tab