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Anti-CD38 monoclonal antibodies have consistently shown increased efficacy when added to standard of care for patients with multiple myeloma. We aimed to assess the efficacy of isatuximab in addition to lenalidomide, bortezomib, and dexamethasone in patients with newly diagnosed transplantation-eligible multiple myeloma.This open-label, multicentre, randomised, active-controlled, phase 3 trial was done at 67 academic and oncology practice centres in Germany. This study is ongoing and divided into two parts; herein, we report results from part 1. Eligible patients were aged 18-70 years; had a confirmed diagnosis of untreated multiple myeloma requiring systemic treatment and a WHO performance status of 0-2; and were eligible for induction therapy, high-dose melphalan and autologous haematopoietic stem-cell transplantation, and maintenance treatment. Patients were randomly assigned (1:1) to receive three 42-day cycles of induction therapy either with isatuximab plus lenalidomide, bortezomib, and dexamethasone (isatuximab group) or lenalidomide, bortezomib, and dexamethasone alone (control group) using a web-based system and permuted blocks. Patients in both groups received lenalidomide (25 mg orally on days 1-14 and 22-35), bortezomib (1·3 mg/mBetween Oct 23, 2018, and Sep 22, 2020, 660 patients were included in the ITT analysis (331 in the isatuximab group and 329 in the control group). 654 (99%) patients were White, two were African, one was Arabic, and three were Asian. 250 (38%) were women and 410 (62%) were men. The median age was 59 years (IQR 54-64). MRD negativity after induction therapy was reached in 166 (50%) patients in the isatuximab group versus 117 (36%) in the control group (OR 1·82 [95% CI 1·33-2·48]; p=0·00017). Median follow-up time from start to end of induction therapy was 125 days (IQR 125-131) versus 125 days (125-132). At least one grade 3 or 4 adverse event occurred in 208 (63%) of 330 patients versus 199 (61%) of 328 patients. Neutropenia of grade 3 or 4 occurred in 77 (23%) versus 23 (7%) patients and infections of grade 3 or 4 occurred in 40 (12%) versus 32 (10%) patients. Among 12 deaths during induction therapy, one death due to septic shock in the isatuximab group and four deaths (one cardiac decompensation, one hepatic and renal failure, one cardiac arrest, and one drug-induced enteritis) in the control group were considered treatment-related.Addition of isatuximab to lenalidomide, bortezomib, and dexamethasone for induction therapy improved rates of MRD negativity with no new safety signals in patients with newly diagnosed transplantation-eligible multiple myeloma.Sanofi and Bristol Myers Squibb (Celgene).

BACKGROUND: Elotuzumab plus lenalidomide and dexamethasone has shown improved progression-free and overall survival versus lenalidomide and dexamethasone in patients with relapsed or refractory multiple myeloma. We aimed to assess these regimens in patients with newly diagnosed multiple myeloma who are ineligible for haematopoietic stem-cell transplantation (HSCT). METHODS: ELOQUENT-1 is an open-label, multicentre, randomised, phase 3 trial conducted at 185 hospitals, oncology practices, and research centres in 19 countries. Eligible patients were aged 18 years or older with newly diagnosed, untreated, symptomatic myeloma and not candidates for high-dose therapy plus HSCT, and an Eastern Cooperative Oncology Group (ECOG) performance status of 2 or lower. Patients were randomly assigned (1:1) to receive elotuzumab plus lenalidomide and dexamethasone or lenalidomide and dexamethasone using an interactive voice response system, stratified by the International Staging System (ISS; stage I-II vs III), age (

Mass spectrometry (MS) is a promising tool for monitoring monoclonal protein in plasma cell dyscrasias. We included 480 transplant-eligible newly-diagnosed multiple myeloma (MM) patients from the GMMG-MM5 trial (EudraCT No. 2010-019173-16) and performed a retrospective MS analysis at baseline (480 patients) and at the pre-defined, consecutive time points after induction (444 patients), prior to maintenance (305 patients) and after one year of maintenance (227 patients). We found that MS negativity was significantly associated with improved progression-free survival (PFS) even in patients with complete response (CR) at all investigated follow-up time points. The prognostic impact was independent of established risk factors, such as the revised International Staging System. Combining MS and baseline cytogenetics improved the prediction of outcome: MS-positive patients with high-risk cytogenetics had a dismal PFS of 1.9 years (95% confidence interval [CI]: 1.6–2.3 years) from the start of maintenance. Testing the value of sequential MS prior to and after one year of maintenance, patients converting from MS positivity to negativity had an excellent PFS (median not reached) while patients converting from MS negativity to positivity progressed early (median 0.6 years, 95% CI: 0.3-not reached). Among patients with sustained MS positivity, the baseline high-risk cytogenetic status had a significant impact and defined a group with poor PFS. Combining minimal residual disease (MRD) in the bone marrow and MS allowed the identification of double negative patients with a favorable PFS (median 3.33 years, 95% CI: 3.08-not reached) and no overall survival events. Our study provides strong evidence that MS is superior to conventional response monitoring, highlighting the potential of MS to become a new standard. Our data indicate that MS should be performed sequentially and combined with baseline disease features and MRD to improve its clinical value.Clinical Trials Register: EudraCT No. 2010-019173-16

To investigate cytogenetic evolution after upfront autologous stem cell transplantation for newly diagnosed myeloma we retrospectively analyzed fluorescence in situ hybridization results of 128 patients with paired bone marrow samples from the time of primary diagnosis and at relapse. High-risk cytogenetic abnormalities (deletion 17p and/or gain 1q21) occurred more frequently after relapse (odds ratio: 6.33; 95% confidence interval: 1.86–33.42; P

Infection with the human immunodeficiency virus type 1 (HIV-1) requires the presence of a CD4 receptor and a chemokine receptor, principally chemokine receptor 5 (CCR5). Homozygosity for a 32-bp deletion in the CCR5 allele provides resistance against HIV-1 acquisition. We transplanted stem cells from a donor who was homozygous for CCR5 delta32 in a patient with acute myeloid leukemia and HIV-1 infection. The patient remained without viral rebound 20 months after transplantation and discontinuation of antiretroviral therapy. This outcome demonstrates the critical role CCR5 plays in maintaining HIV-1 infection.

Background: CD38 is a type II transmembrane glycoprotein that is expressed at high levels on multiple myeloma cells. MOR202 is a HuCAL-derived, human, IgG1 anti-CD38 monoclonal antibody showing effective antibody-dependent cell-mediated cytotoxicity (ADCC), antibody-dependent cell-mediated phagocytosis (ADCP), and high activity in preclinical models of multiple myeloma. Patients and Methods: Here we reportinterimsafety and preliminary efficacy data from this ongoing, multicenter, MOR202 dose-escalation, phase I/IIa study in patients with relapsed or refractory disease who had failed ≥2 prior therapies for multiple myeloma, including an immunomodulatory drug and a proteasome inhibitor. The objectives are to evaluate the safety, maximum tolerated dose (MTD)/recommended dose and preliminary efficacy of MOR202 when administered as monotherapy or in combination with dexamethasone (DEX); pomalidomide (POM) + DEX; and lenalidomide (LEN) + DEX. Patients received MOR202 as a 2-hour intravenous infusion every 2 weeks (q2w; dose levels 0.01-16 mg/kg), 4 mg/kg weekly (q1w) and 4, 8 and 16 mg/kg q1w + DEX. The combination cohorts receiving MOR202 8 mg/kg with LEN + DEX and POM + DEX have been opened, and the 16 mg/kg q1w with LEN + DEX or POM + DEX, as well as confirmation cohorts, are planned. Results: As of 26 June 2015, 44 patients have been treated; 31 and 13 patients in the q2w and q1w dose levels, respectively. Median age was 69 years (range 44-80); median number of prior therapy lines was 4 (2-11). The MTD has not been reached. The most common treatment-emergent adverse events (TEAEs) at any grade were anemia (15 patients, 34%), fatigue (14 patients, 32%), infusion-related reactions (IRRs) and leukopenia (13 patients, 30% each), lymphopenia and nausea (11 patients, 25% each). Grade ≥3 TEAEs were reported for 28 patients (64%); the most common included lymphopenia (8 patients, 18%), leukopenia (5 patients, 11%) and hypertension (4 patients, 9%). IRRs arose mainly during the first infusion; all were grade 1-2 except for one patient (grade 3); no IRRs occurred in patients receiving MOR202 in combination with DEX. Infections were commonly reported (26 patients, 59%) but in the majority of the cases were not considered to be treatment-related. There have been no treatment-related deaths. Pharmacokinetic (PK) data demonstrated a significant target-mediated drug disposition effect for most patients treated q2w. By contrast, patients treated q1w (4 or 8 mg/kg) showed constant or slightly accumulating MOR202 trough levels, suggesting the potential for full target occupancy at 16 mg/kg. Long-lasting tumor control has already been observed in early monotherapy cohorts, including one partial response and one very good partial response in the weekly cohorts; efficacy analyses are ongoing. First data from the dose escalation of the weekly cohorts with DEX and the combination cohorts with LEN + DEX and POM + DEX will be presented. Conclusions: At doses up to 16 mg/kg,MOR202 was safe and well tolerated. Encouraging preliminary activity of MOR202 was observed, especially with the weekly regimen. PK data show the potential for full target occupancy in patients receiving MOR202 16 mg/kg q1w. This dosing schedule of MOR202 is currently being tested in combination with DEX, LEN + DEX, and POM + DEX. Disclosures Raab: MorphoSys: Research Funding; Novartis: Consultancy, Research Funding, Speakers Bureau; Celgene: Consultancy; BMS: Consultancy. Goldschmidt:Chugai: Honoraria, Research Funding, Speakers Bureau; Onyx: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Millenium: Honoraria, Research Funding, Speakers Bureau; Janssen-Cilag: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Bristol-Myers Squibb: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Takeda: Consultancy, Membership on an entity's Board of Directors or advisory committees; Amgen: Consultancy, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau. Einsele:Janssen: Consultancy, Honoraria, Research Funding, Speakers Bureau; Novartis: Consultancy, Honoraria, Research Funding, Speakers Bureau; Amgen/Onyx: Consultancy, Honoraria, Research Funding, Speakers Bureau; Celgene: Consultancy, Honoraria, Research Funding, Speakers Bureau. Ferstl:Bristol-Myers Squibb: Other: Advisory board; Novartis: Other: Case report presentation. Weisel:Celgene: Consultancy, Honoraria, Other: Travel Support, Research Funding; Amgen: Consultancy, Honoraria, Other: Travel Support; Novartis: Other: Travel Support; Janssen Pharmaceuticals: Consultancy, Honoraria, Other: Travel Support, Research Funding; BMS: Consultancy, Honoraria, Other: Travel Support; Onyx: Consultancy, Honoraria; Noxxon: Consultancy. Klöpfer:MorphoSys: Employment. Weinelt:MorphoSys: Employment. Härtle:MorphoSys: Employment.

Background Pomalidomide (POM) in a 1-arm phase-1/-2 study and a randomized 4-arm phase-2 study in MPN-associated myelofibrosis improved anemia. Pomalidomide was evaluated at doses of 0.5 and 2.0 mg/d. Aims To evaluate efficacy of POM alone at two different doses and combined with prednisolone (PRED) in patients with MPN-associated myelofibrosis and cytopenia (ClinicalTrials.gov No. NCT00949364). Methods Main inclusion criteria were RBC-transfusion-dependence or hemoglobin Results 38 patients were treated in cohort-1 and 58 in cohort-2 (N=27, PRED-mo-4; N=31; PRED-mo-7). Median follow-up was 30 mo in cohort-1 and 10 mo in cohort-2. Median age was 72 y (range, 49-85 y). 34% were female, 72% had primary MF. Disease-stage at study-entry (DIPSS) was high-risk, 24%, intermediate-2 risk, 65% and intermediate-1 risk 12%; JAK2V617Fand MPLW515L were detected in 58% and 6% of patients; 76% of patients were RBC- and 17% platelet-transfusion-dependent. There were no significant differences in pretreatment characteristics between cohort-1 and cohort-2 or between the 2 arms of cohort-2. Median durations of POM treatment were 12, 8, and 4 mo, respectively. PRED was added in cohort-1 and in the PRED-month-4 as well as PRED-month-7 arms of cohort-2 in 50%, 59% and 26% of patients. Response-rates were: 34% (95%-CI, 21-50%), 19% (95%-CI, 8-37%) and 16% (95%-CI, 7-33%), respectively; p=0.086. Responses occurred after 6 mo (range, 1-15 mo), 7 mo (range, 1-12 mo) and 4 mo (range, 3-7 mo). Anemia responses were observed more frequently in cohort-1 (29% [95%-CI, 17-45%]) compared to cohort-2 (14% [95%-CI, 7-25%]; p=0.059). Platelet response in patients with platelets100/nL were achieved in 56% (95%-CI, 27-81%) and 25% (95%-CI, 9-53%; p=0.20). 13 patients (12 high risk) experienced blastic transformation; 4 patients developed solid neoplasms. Conclusions Response rate to POM at a dose of 2mg/d was higher compared to 0.5 mg/d. Early addition of PRED at 4 mo compared to 7 mo was associated with longer treatment duration. Disclosures: Schlenk: Novartis: Research Funding; Amgen: Research Funding; Chugai: Research Funding; Pfizer: Honoraria, Research Funding; Celgene: Honoraria, Research Funding; Ambit: Honoraria. Off Label Use: Pomalidomide in Myelofibrosis. Reiter:Sanofi: Honoraria. Gattermann:Celgene: Honoraria, Research Funding; Novartis: Honoraria, Research Funding. Hochhaus:Novartis: Consultancy, Honoraria, Research Funding, Travel Other; BMS: Consultancy, Honoraria, Research Funding; ARIAD: Consultancy, Honoraria; Pfizer: Consultancy. Platzbecker:Celgene: Honoraria, Research Funding; Novartis: Honoraria, Research Funding. Heidel:Novartis Inc.: Research Funding; Novartis Inc.: Honoraria.

Background In recent phase-I/II studies, pomalidomide (POM) has shown activity in myelofibrosis (MF) patients (pts) with anemia and/or thrombocytopenia. In the first cohort of the German multicenter MPNSG 01-09 phase-II trial, 38 MF pts were treated with POM 2 mg QD +/- prednisolone (PRED); 34% responded according to IWG-MRT criteria or became RBC-transfusion independent (Schlenk et al., ASH 2012). Additional 58 MF pts were treated in the second study cohort with POM 0.5 mg QD +/- PRED. Main inclusion criteria were age >50y, RBC-transfusion-dependency or Hb Aims To explore the presence of copy number alterations (CNAs), uniparental disomies (UPDs) and MPN-related gene mutations in the 01-09 study cohort and to correlate genetic parameters with treatment response. Methods Affymetrix 6.0 SNP arrays were used for genome-wide screening of CNAs and UPDs in 91% (87/96) of pts. Frequently mutated genes were analyzed in all pts using PCR-based techniques and sequence analysis of coding exons: JAK2 V617F, MPL W515L, ASXL1 (exon 12), EZH2 (exon 2-20), IDH1/2 (exons 4), SRSF2 (exon 1-2), and TP53(exon 4-10). Results In total, 78 CNAs were identified by SNP array analysis. The overall frequency of CNAs was 52% (45/87 pts); 24% (21 pts) showed ≥2 CNAs, while 7% (6 pts) had a complex genotype defined by ≥3 genomic aberrations. Recurrent large (>5 Mb) gains were trisomy 8 (7%; n=6), gain 1q, and trisomy 9 (5% each; n=4), whereas recurrent large losses were identified in 20q (11%; n=10), 5q (8%; n=7), 13q (7%; n=6), 7q/7 (6%; n=5), and 12p/12 (2%; n=2). Moreover, 20% (17/87) of pts showed 19 informative micro-deletions ( Large UPDs (>10 Mb) affecting a terminal end of the chromosome were present in 32% (28/87) of pts. The most frequent UPDs occurred in 9p including JAK2 (17%; n=15). Other recurrent UPDs mapped to 1p (5%; n=4), 4q, and 7q (2% each; n=2). UPDs in 9p were associated with JAK2 V617F in all pts, whereas 75% (3/4) of pts with UPD in 1p were MPLW515L mutated. Mutations in JAK2 (V617F) and MPL (W515L) were present in 55% (53/96) and 6% (6/96) of pts, respectively. The mutation frequencies for the remaining genes were 30% (ASXL1; n=29/96), 9% (SRSF2; n=9/96), 5% (EZH2; n=5/96), 2% (TP53; n=2/96), and 1% (IDH2; n=1/96). Taken together, at least one mutation was found in 79% (76/96) of pts, whereas 21% (20/96) of pts lacked any of these mutations; 28% (27/96) of pts showed ≥2 concurrent mutations. To evaluate genetic differences and predictive factors, pts were separated into a responder (R, n=23) and a non-responder (Non-R, n=73) group. Regarding DIPSS, Non-R pts were not associated with higher risk compared to R pts: 27% (20/73) high risk vs. 17% (4/23) (p=0.334), 61% (44/73) intermediate-II risk vs. 79% (18/23), and 12% (9/73) intermediate-I vs. 4% (1/23) (p=0.275). However, the overall frequency of CNAs was in trend higher in the Non-R group: 56% vs. 39% (p=0.159). Since the total number of genomic losses was similarly distributed (27% vs. 29%), the difference was mainly due to the higher frequency of large genomic gains/trisomies: 4% (R) vs. 22% (Non-R) (p=0.083). UPDs were similar frequent in R and Non-R pts (26% vs. 34%) (p=0.466). The total number of gene mutations was not different between both groups (n=25 in 23 R pts vs. n=77 in 73 Non-R pts) (p=0.475). However, genetic alterations being associated with unfavourable outcome were enriched in the Non-R group: ASXL1 mutation (39% vs. 22%), EZH2 mutation (5% vs. 0%), loss in 5q (30% vs. 4%), trisomy 8 (9% vs. 0%), 12p / ETV6 deletion (6% vs. 0%), 17p deletion / TP53 mutation (3% vs. 0%), and complex genotype (7% vs. 0%). Taken together, adverse genetic alterations were significantly more frequent in Non-R pts compared to R pts: 48% (35/73) vs. 22% (5/23) (p=0.026). Of note, adverse genetic alterations indicated high risk according to DIPSS in no more than 50% (12/24) of the pts. Conclusion Our study on a well-defined patient cohort with advanced MF revealed a high frequency of genetic alterations reflecting the molecular complexity of the disease. Pts with adverse genetic alterations identified by SNP-array and mutation analyses were not sufficiently represented by DIPSS and showed inferior response to POM +/- PRED. Disclosures: Reiter: Sanofi: Honoraria. Gattermann:Celgene: Honoraria, Research Funding; Novartis: Honoraria, Research Funding. Platzbecker:Celgene: Honoraria, Research Funding; Novartis: Honoraria, Research Funding. Hochhaus:Novartis: Consultancy, Honoraria, Research Funding, Travel Other; BMS: Consultancy, Honoraria, Research Funding; Pfizer: Consultancy, Honoraria; Ariad: Consultancy, Honoraria. Schlenk:Amgen: Research Funding; Pfizer: Research Funding; Novartis: Research Funding; Chugai: Research Funding; Ambit: Honoraria.

Abstract 3866 Poster Board III-802 Bortezomib (Velcade®) retreatment has been shown to be active and well tolerated in patients with relapsed multiple myeloma (MM) in a number of retrospective studies and a small prospective phase 4 study (EVEREST). This large, prospective, international, multi-center, open-label phase 2 study was conducted to confirm the efficacy and safety of retreatment with bortezomib in MM patients who had previously responded (at least partial response [PR]) to bortezomib-based therapy as their most recent prior treatment. Patients had to have previously tolerated bortezomib 1.0 or 1.3 mg/m2 alone or in combination and have had a treatment-free interval (TFI; time from last dose of initial bortezomib treatment to first dose of bortezomib retreatment) of ≥6 months. Additional eligibility criteria included progressive disease or relapse from complete response (CR) by EBMT criteria, no MM therapy (except maintenance with dexamethasone, thalidomide, or interferon) since the last dose of initial bortezomib treatment, KPS ≥60, and adequate renal, hepatic, and hematologic function; patients with grade ≥2 peripheral neuropathy or neuropathic pain (as defined by NCI CTCAE v3.0) were excluded. Patients received bortezomib at the last tolerated dose (1.0 or 1.3 mg/m2) during initial treatment on days 1, 4, 8, and 11 for up to eight 21-day cycles, either alone or in combination with dexamethasone at the investigator's discretion. Response was assessed by EBMT criteria every 6 weeks during treatment and then every 2 months until disease progression. Adverse events (AEs) were graded according to NCI CTCAE v3.0. A total of 130 patients received at least 1 dose of bortezomib retreatment and were included in the safety population. Patients had a median age of 67 years, 57% were male, and 16% had KPS '70%. Median time from diagnosis of MM was 4.5 years (range 0–14 years); median number of prior therapies was 2; 15, 80, 23, and 12 patients had received 1, 2, 3, and ≥4 prior lines of therapy (excluding initial bortezomib therapy). Best response by EBMT criteria to initial bortezomib treatment was CR in 26% and PR in 74% of patients; median time to progression and TFI after initial bortezomib treatment were 17.9 months and 14.3 months, respectively. Last tolerated dose of previous bortezomib therapy was 1.3 mg/m2 and 1.0 mg/m2 for 62% and 29% of patients, respectively; 9% received another dose. Patients received a median 7.0 (range 1–8) cycles of bortezomib retreatment (23% of patients completed all 8 cycles); 72% of patients received concomitant dexamethasone. A total of 126 patients were evaluable for response. In the 126 response-evaluable patients, the overall response rate (ORR; CR+PR) by best confirmed response (EBMT criteria) was 40%; in addition, 18% of patients achieved minimal response (MR), to give a CR+PR+MR rate of 58%. After a planned secondary efficacy analysis, the ORR (CR+PR) by single best response was 55% (75% ≥MR). Median time to best confirmed response (≥MR) was 2.9 months; time to first response was 1.5 months. Analysis of ORR by patient subgroups showed comparable results in patients who did versus did not receive concomitant dexamethasone (42% vs 32%), in those who received ≤1.0 mg/m2 vs 1.3 mg/m2 bortezomib (35% vs 41%), and in those aged ≤65 years vs >65 years (45% vs 36%). ORR was 67%, 39%, 33%, and 25% in patients who had received 1, 2, 3, and ≥4 prior lines of therapy (excluding initial bortezomib), respectively. Analysis of best confirmed responses according to response to initial bortezomib showed that 63% and 52% of patients who achieved a CR or PR, respectively, to initial bortezomib treatment responded to retreatment. Most (98%) patients experienced a treatment-emergent AE; 60% experienced a grade 3/4 AE, and 32% experienced a serious AE; there were 8 deaths, 2 of which (due to sepsis and stroke) were possibly treatment-related. The most common grade 3/4 AEs were thrombocytopenia (35%), neutropenia (7%), diarrhea (7%), and pneumonia (5%). AEs leading to dose reductions or discontinuations were reported for 22% and 12% of patients, respectively. The incidence of neuropathy was 39%, including 9% grade 3; 4% of patients discontinued treatment due to PN; 61% of neuropathy events resolved or improved within a median 1.3 months. These results confirm that bortezomib retreatment is a well-tolerated, feasible, and active therapeutic option for heavily pretreated MM patients without evidence of cumulative toxicity. Disclosures: Petrucci: Janssen-Cilag: Honoraria; Celgene: Honoraria. Dimopoulos:Ortho-Biotech: Consultancy, Honoraria; Millennium Pharmaceuticals, Inc.: Honoraria. Drach:Janssen-Cilag: Consultancy, Honoraria; Amgen: Honoraria; Celgene: Honoraria. Blade:Janssen-Cilag: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Honoraria; Johnson and Johnson: Honoraria; Celgene: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding.

Abstract 2293 Poster Board II-270 Introduction: Although modern chemotherapy regimens achieve a high cure rate in primary Hodgkin's disease and relapsed patients can be salvaged by high dose chemotherapy with autologous stem cell transplantation there remains a subgroup of patients with early relapse despite high dose chemotherapy. The prognosis of these patients is dismal with further chemotherapy. Allogeneic transplantation has the potential to exert an alloimmune response against lymphoma cells and has therefor been offered to patients with relapsed or refractory Hodgkin's disease, in particular when a matched sibling donor was available. However only limited information on the feasability of allogeneic transplantion from an unrelated donor is available. Methods: We performed a retrospective analysis of allogeneic transplants for Hodgkins disease within the German Cooperative Transplantation Study Group. 18 centres have provided data on patient and donor characteristics, transplant procedure and outcome. Survival data were analysed by Kaplan-Meier and tested for differences by log rank test. Cumulative incidences for relapse, non-relapse mortality and graft-versus-host-disease were calculated in a competing risk model. Results: 79 patients with a median age of 30 years (range 14-59) were included. 65 (82%) patients had failed a previous autologous transplantation 582 days (median) before allotransplantation. Disease status at transplantation was CR in 17.6%, PR in 54.0%, stable disease in 9.5%, PD in 12.2%, and untreated relapse in 6.8%. Donors were matched related in 33%, mismatched related in 5%, matched unrelated in 42% and mismatched unrelated in 20%. With a median follow up of 19 months for surviving patients the median overall survival (OS) after allotransplant was 42 months with a 2 year survival of 51%. Non-relapse mortality was 21.1% after 12 and 24 months. The median progression-free survival was 14.6 months with a 2 year PFS of 42.0%. Patients relapsing after an autologous transplantation had a significantly better OS (median 53.7 vs 8.4 months, p=0.029) and PFS (22.0 vs 7.5 months, p=0.039) than patients without a prior autograft. No significant difference was seen for OS or PFS regarding the use of related or unrelated donors or disease status at transplant. Conclusions: Allogenic transplantation is a feasible option for high-risk patients with relapsed or refractory Hodgkins disease in particular after failing an autograft. Non-relapse mortality appears to be acceptable in view of the intensive prior treatment. Probabilities for overall survival and progression-free survival were similar after transplantation from a related or unrelated donor. Further optimisation strategies have to focus on on efforts to reduce the high relapse-rate after transplantation, thereby potentially increasing overall and progression free survival. Disclosures: No relevant conflicts of interest to declare.