scholarly journals Safety and Efficacy of Combination Maintenance Therapy with Ixazomib and Lenalidomide in Post-transplant Myeloma Patients

2022 ◽  
pp. clincanres.3420.2021
Author(s):  
Krina K. Patel ◽  
Jatin J. Shah ◽  
Lei Feng ◽  
Hans C. Lee ◽  
Elisabet E. Manasanch ◽  
...  
Keyword(s):  
Maintenance Therapy ◽  
Safety And Efficacy ◽  
Post Transplant

Maintenance Therapy with 5-Azacytidine (5-AC) after Allogeneic Stem Cell Transplantation (allo-SCT) for Acute Myelogenous Leukemia (AML) and High-Risk Myelodysplastic Syndrome (MDS): A Dose and Schedule Finding Study.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3668-3668 ◽  
Author(s):  
Andres O. Soriano ◽  
Richard Champlin ◽  
Gloria McCormick ◽  
Sergio Giralt ◽  
Peter Thall ◽  
...  
Keyword(s):  
High Risk ◽  
Maintenance Therapy ◽  
Mononuclear Cells ◽  
Methylation Status ◽  
Conditioning Regimen ◽  
Surrogate Marker ◽  
Dose Schedule ◽  
Myelogenous Leukemia ◽  
Unrelated Donor ◽  
Post Transplant

Abstract Background: Relapse is the most frequent cause of treatment failure after allo-SCT in patients (pts) with AML or MDS. Median time to relapse after reduced-intensity allo-SCT is 3–5 months, indicating that if post-transplant interventions are to be proposed, they have to be implemented early. 5-AC is a DNA hypomethylating agent that may induce leukemic cell differentiation and increased immunogenicity, therefore potentially increasing the graft-versus-leukemia effect. Furthermore, lower doses are likely to be better tolerated after allo-SCT and to be as effective as larger doses in inducing hypomethylation. We hypothesized that 5-AC after allo-SCT will result in lower relapse rates, and designed a phase I clinical trial to determine the safest dose and schedule combination of 5-AC used as maintenance therapy after allo-SCT in pts with AML or MDS. Methods: Pts with AML or high-risk MDS not in first remission are eligible. Donors are HLA-compatible related or unrelated. Conditioning regimen is gemtuzumab ozogamicin 2 mg/m2 (day -12), fludarabine, and melphalan 140 mg/m2. GVHD prophylaxis is tacrolimus and mini-methotrexate. ATG is administered to recipients of unrelated donor transplants. Three doses of 5-AC are to be studied: 8, 16, and 24 mg/m2 daily × 5 starting on day 42 post transplant. Four schedules consisting of 1, 2, 3 or 4 28-day courses of 5-AC are being explored for a total of 3×4 = 12 dose-schedule combinations. The continual reassessment method with toxicity probabilities is used to determine the safest dose schedule combination. Results: Twelve pts were evaluable. Median age was 55.5 years (range 25–66). Eight pts had AML and 4 had MDS. At the time of the transplant 4 pts were in remission and 8 had refractory disease. Donors were HLA compatible related (n=7) and unrelated (n=5). Based on the Bayesian model, 3 pts (25 %) were assigned to 8 mg/m2 × 1 cycle, 2 pts (16%) to 8 mg/m2× 2 cycles, 2 (16%) to 8 mg/m2× 3 cycles and 3 to 16 mg/m2×3 cycles. All evaluable pts have received the assigned 5AC doses, and there has been no major drug-related toxicity (at 8 or 16 mg/m2). Two pts died before receiving 5-AC due to bleeding (n=1, in CR) and bacterial sepsis (n=1) post allo-SCT. With a median follow up of 5 months (2–9) after allo-SCT, none of the pts has relapsed and no drug related induction of GVHD has been observed. All pts were 100% donor chimeras at start of 5AC. To assess the DNA hypomethylating effect of 5-AC, the methylation status of long interspersed nuclear elements (LINE) was analyzed by pyrosequencing and used as a surrogate marker of global DNA methylation in mononuclear cells of 7 patients that have completed 1 cycle at the dose of 8 mg/m2. Mean LINE methylation pretreatment was 64.9%(±5), while it was 60.7%(±2.5) by day 5 (p=0.06) (last day of 5-AC administration), returning to baseline by day 1 of the next cycle. Analysis of gene specific methylation is ongoing. Conclusions: At the dose of 8 mg/m2 5AC is well tolerated and may produce detectable levels of hypomethylation. It is unknown if this effect will translate in reduced relapse rate or if higher doses will be as well tolerated.

Low Dose Azacitidine Maintenance Therapy Following Allogeneic Stem Cell Transplantation for MDS/AML Does Not Interact with Tacrolimus Dosing or Serum Levels

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 4209-4209
Author(s):  
Hans C. Lee ◽  
Joshua Howell ◽  
Denái Milton ◽  
Sergio A Giralt ◽  
Julianne J Chen ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Transplantation ◽  
Maintenance Therapy ◽  
Research Funding ◽  
Low Dose ◽  
Serum Levels ◽  
Off Label Use ◽  
Drug Levels ◽  
Off Label ◽  
Post Transplant

Abstract Abstract 4209 Background: Recurrence of disease remains a significant cause of morbidity and mortality in patients who undergo allogeneic SCT for AML and MDS. Low-dose azacitidine is currently under investigation in the post-transplant setting with the goal of prolonging disease-free survival and decreasing relapse rates. It is unclear if there is potential pharmacologic interaction between azacitidine and dose-adjusted tacrolimus used to prevent post-transplant graft-versus-host disease (GVHD), a clinically relevant question since any resultant tacrolimus under- or over-dosing may lead to increased risk of GVHD or drug toxicity, respectively. We hypothesized that azacitidine does not significantly interact with tacrolimus levels and performed a retrospective analysis to test this hypothesis. Patients and Methods: We reviewed tacrolimus daily doses and serum drug levels of 62 AML and MDS patients who received azacitidine maintenance therapy (n=30) or no maintenance therapy (n=32) following allogeneic stem cell transplantation at MD Anderson Cancer Center between 2008–2012. Patient characteristics are summarized in the Table. Patients in the maintenance cohort received subcutaneous azacitidine at 32 mg/m2 on days 1–5 repeated every 28 days starting at a median time of post-transplant day +65 (range 43–100). Tacrolimus doses and serum levels were averaged for 28 days for each patient before and after initiation of azacitidine maintenance and at day +66 in the non-maintenance cohort. Differences between the two cohorts in their mean change of tacrolimus doses and serum drug levels were assessed using a Student's t-test. Results: Mean (SD) oral tacrolimus doses pre- and post-maintenance therapy were 2.61 (2.13) mg daily and 2.44 (2.15) mg daily in the azacitidine group and 2.54 (1.86) mg and 2.23 (1.39) mg daily in the non-azacitidine cohort. This resulted in a mean change in tacrolimus dosing of -0.17 (1.16) mg daily in the azacitidine patients and -0.31 (1.10) mg daily in the non-maintenance group (p=0.62). Mean (SD) serum tacrolimus levels pre- and post-maintenance therapy were 8.07 (1.16) ng/mL and 7.58 (2.32) ng/mL in the azacitidine group and 8.23 (1.49) ng/mL and 7.10 (1.69) ng/mL in patients on no maintenance therapy. This resulted in a mean change in serum tacrolimus levels of -0.49 (2.75) ng/mL in the azacitidine cohort and -1.13 (2.04) ng/mL in the non-maintenance group (p=0.30). Conclusion: Maintenance azacitidine therapy following allo-SCT for AML and MDS does not appear to affect concurrent tacrolimus dosing or serum drug levels. Disclosures: Off Label Use: azacitidine: off-label use as maintenance therapy following allogeneic stem cell transplant for MDS/AML. Champlin:Otsuka: Research Funding. De Lima:Celgene: Research Funding.

Impact of proteasome inhibitor vs. IMiD maintenance therapy on outcomes of patients with high-risk multiple myeloma (HRMM).

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e20557-e20557
Author(s):  
Eric Leon Tam ◽  
David Joseph Iberri ◽  
Michaela Liedtke ◽  
Lori S. Muffly ◽  
Parveen Shiraz ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
High Risk ◽  
Maintenance Therapy ◽  
Proteasome Inhibitor ◽  
Post Transplant ◽  
Risk Patients ◽  
To Receive ◽  
Standard Risk

e20557 Background: The ideal choice of maintenance therapy in patients with HRMM high-risk multiple myeloma remains unknown. We analyzed the outcomes of patients with HRMM undergoing transplant receiving different maintenance approaches. Methods: Patients with MM undergoing their first ASCT from 2012-19 within 1 year of diagnosis were identified from the prospectively maintained database of patients undergoing ASCT. HRMM was defined as having t(4;14), t(14;16), t(14;20), del17p13, or gain 1q detected on fluorescent in situ hybridization (FISH). Results: Of the 412 patients undergoing ASCT within 1 year of diagnosis, 333 had FISH data available and of these, 37% (124/333) patients had high-risk cytogenetics. Distribution of HR cytogenetics was as follows: deletion 17p: 37% (n = 46), t(4;14): 27% (n = 34), t(14;16) or t(14;20): 12% (n = 26), gain1q: 31% (n = 41). 9% (n = 12) had more than one HR abnormality. In patients with HRMM, median age at transplant was 59 years (range: 39 to 73), and 61% (n = 103) were males. 64% (n = 107) of high-risk patients received post-transplant maintenance therapy. Maintenance therapy in this group included a proteasome inhibitor (PI) in 34% (n = 29), immunomodulatory drug (IMiD) in 59% (n = 51), or both in 7% (n = 6). There was no difference in baseline characteristics of HRMM patients receiving PI vs. IMiD maintenance, except that patients with del17p were more likely to receive PI maintenance therapy (55% vs 28%, p = 0.01). (Table) After a median follow-up of 3.1 years from diagnosis, patients with HRMM had inferior PFS compared to patients with standard risk disease, with median PFS of 3 vs. 4.8 years, p < 0.001. Amongst the 86 HRMM patients receiving maintenance therapy, median PFS in patients receiving PI vs. IMiD vs. both PI + IMiD maintenance was 3 vs. 3.2 vs. 2.2 years, respectively, log-rank p = 0.7. In the sub-group of patients with 17p deletion, median PFS in the three groups was 3 vs. 2.9 vs. 2.2 years, respectively, log-rank p = 0.7. Conclusions: Patients with HRMM have inferior PFS compared to patients with standard risk disease. We observed similar outcomes in HRMM patients post-transplant regardless of the choice of maintenance therapy. [Table: see text]

scholarly journals Bortezomib, Lenalidomide and Dexamethasone (VRD) Followed By Autologous Stem Cell Transplant for Newly Diagnosed Multiple Myeloma; The Mayo Clinic Experience

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2147-2147
Author(s):  
M Hasib Sidiqi ◽  
Mohammed A Aljama ◽  
Angela Dispenzieri ◽  
Eli Muchtar ◽  
Francis K. Buadi ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Overall Survival ◽  
High Risk ◽  
Maintenance Therapy ◽  
Board Of Directors ◽  
Mayo Clinic ◽  
Research Funding ◽  
Advisory Committees ◽  
Post Transplant ◽  
Standard Risk

Abstract We retrospectively reviewed all patients receiving bortezomib, lenalidomide and dexamethasone induction followed by autologous stem cell transplantation (ASCT) within 12 months of diagnosis for multiple myeloma at the Mayo Clinic. 243 patients treated between January 2010 and April of 2017 were included in the study. Median age was 61 (interquartile range, 55-67) with 62% of patients being male. High risk cytogenetic abnormalities (HRA) were present in 34% of patients. 166 (68%) patients received some form of maintenance/other therapy post transplant (no maintenance (NM, n=77), lenalidomide maintenance (LM, n=108), bortezomib maintenance (BM, n=39) and other therapy (OT, n=19)). Overall response rate was 99% with complete response (CR) rate of 42% and 62% at day 100 and time of best response post transplant respectively. The four cohorts categorized by post transplant therapy were well matched for age, gender and ISS stage. HRA were more common amongst patients receiving bortezomib maintenance or other therapy post transplant (NM 18% vs LM 22% vs BM 68% vs OT 79%, p<0.0001). Two year and five year overall survival rates were 90% and 67% respectively with an estimated median overall survival (OS) and progression free survival (PFS) of 96 months and 28 months respectively for the whole cohort. OS was not significantly different when stratified by post-transplant therapy (Median OS 96 months for NM vs not reached for LM vs 62 months for BM vs not reached for OT, p=0.61), however post-transplant therapy was predictive of PFS (median PFS 23 months for NM vs 34 months for LM vs 28 months for BM vs 76 months for OT, p=0.01). High risk cytogenetics was associated with a worse OS but not PFS when compared to patients with standard risk (median OS: not reached for standard risk vs 60 months for HRA, p=0.0006; median PFS: 27 months for standard risk vs 22 months for HRA, p=0.70). In patients that did not receive maintenance therapy presence of HRA was a strong predictor of OS and PFS (median OS: not reached for standard risk vs 36 months for HRA, p<0.0001; median PFS: 24 months for standard risk vs 7 months for HRA, p<0.0001). Patients receiving maintenance therapy appeared to have a similar PFS and OS irrespective of cytogenetics (median OS: not reached for standard risk vs 62 months for HRA, p=0.14; median PFS: 35 months for standard risk vs 34 months for HRA, p=0.79).On multivariable analysis ISS stage III and achieving CR/stringent CR predicted PFS whilst the only independent predictors of OS were presence of HRA and achieving CR/stringent CR. The combination of bortezomib, lenalidomide and dexamethasone followed by ASCT is a highly effective regimen producing deep and durable responses in many patients. Maintenance therapy in this cohort may overcome the poor prognostic impact of high risk cytogenetic abnormalities. Table Table. Disclosures Dispenzieri: Celgene, Takeda, Prothena, Jannsen, Pfizer, Alnylam, GSK: Research Funding. Lacy:Celgene: Research Funding. Dingli:Alexion Pharmaceuticals, Inc.: Other: Participates in the International PNH Registry (for Mayo Clinic, Rochester) for Alexion Pharmaceuticals, Inc.; Millennium Takeda: Research Funding; Millennium Takeda: Research Funding; Alexion Pharmaceuticals, Inc.: Other: Participates in the International PNH Registry (for Mayo Clinic, Rochester) for Alexion Pharmaceuticals, Inc.. Kapoor:Celgene: Research Funding; Takeda: Research Funding. Kumar:KITE: Membership on an entity's Board of Directors or advisory committees, Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees, Research Funding; AbbVie: Membership on an entity's Board of Directors or advisory committees, Research Funding; Janssen: Membership on an entity's Board of Directors or advisory committees, Research Funding. Gertz:Abbvie: Consultancy; Apellis: Consultancy; annexon: Consultancy; Medscape: Consultancy; celgene: Consultancy; Prothena: Honoraria; spectrum: Consultancy, Honoraria; Amgen: Consultancy; janssen: Consultancy; Ionis: Honoraria; Teva: Consultancy; Alnylam: Honoraria; Research to Practice: Consultancy; Physicians Education Resource: Consultancy.

Compare safety and efficacy of intramuscular progesterone versus vaginal progesterone in prevention of preterm labour

2021 ◽  
Vol 8 (4) ◽  
pp. 541-547
Author(s):  
Shilpa Chaudhari ◽  
Aparajita Mishra ◽  
Kishor Hol ◽  
Shraddha Shastri
Keyword(s):  
Maintenance Therapy ◽  
Preterm Labour ◽  
Fetal Lung ◽  
Safety And Efficacy ◽  
Positive Effects ◽  
Gestational Age At Delivery ◽  
Group A ◽  
Group B ◽  
Randomize Control Study ◽  
Micronized Progesterone

Currently preterm labour is one of the most challenging problem faced by both obstetricians and perinatologists, this episode in the course of woman’s pregnancy takes a heavy tool for perinatal mortality which accounts for approximately 50-75%. The incidence of preterm labour is estimated to be 5-10% of all pregnancies. It was a prospective randomize control study. All the cases with inclusion and exclusion criteria were selected during the study period. The subjects were randomized into two groups with group A received vaginal micronized progesteron and group B intramuscular 17a hydroxyprogesteron caproate. Total of 100 cases were included in this study. All preterm pregnancy of more than 20 weeks were considered in this study. Initial nefidipine 10 mg, 4 tablets 15 min apart was given for tocolytic activity for 48 hours. Injection bethamethasone 12 mg I.M 2 doses in a duration of 24 hours apart is given for fetal lung maturity. One group will receive weekly intramuscular 17a hydroxyprogesteron (250 mg) injection while other group will receive daily micronized vaginal progesteron suppository (200mg). Subsequently compare the safety and efficacy of intramuscular progesterone versus micronized progesterone as a maintenance therapy in preventing preterm labour and analyse maternal and fetal factors.Subsequently compared the safety and efficacy of intramuscular progesterone versus micronized progesterone as a maintenance therapy in preventing preterm labour.This analysis showed that women who randomized to progesterone prophylaxis had a significantly increase in duration of pregnancy. The mean ± SD of birthweight in Group A and Group B was 2784.2 ± 490.7 gm and 2813.9 ± 363.3 gm respectively which confirmed the positive effects of progesterone on increasing infants’ weights at birth. Authors concluded that progesterone therapy had acceptable efficacy in the prevention of preterm labor in terms of prolongation of delivery and by increasing gestational age at delivery.

Maintenance Therapy with Nilotinib (Tasigna) Post Allogeneic Stem Cell Transplantation (AlloSCT) for Advanced (>CP1) Chronic Myeloid Leukemia (CML) and Ph+ Acute Lymphoblastic Leukemia (ALL)

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2011-2011
Author(s):  
Arnon Nagler ◽  
Yulia Volchek ◽  
Nira Bloom ◽  
Raz Somech ◽  
Ronit Yerushalmi ◽  
...  
Keyword(s):  
Maintenance Therapy ◽  
Disease Progression ◽  
Nk Cell ◽  
Lymphoblastic Leukemia ◽  
Chronic Gvhd ◽  
Clinical Signs ◽  
Early Death ◽  
Severe Thrombocytopenia ◽  
Tumor Mass ◽  
Post Transplant

Abstract Abstract 2011 AlloSCT is the treatment of choice in advanced CML (>CP1) and in Ph+ ALL. However, the post transplant relapse rate is high and outcome is rather poor in this setting. Nilotinib (Tasigna, Novartis Pharmaceuticals) is a very effective, second generation, novel TKI. Reduction of tumor mass pre- and maintenance therapy post alloSCT, may improve response rate and reduce transplant related toxicities (TRT) and relapses. The aim of the current study (CAMN107AIL03T) was to investigate whether nilotinib administration pre-alloSCT (400mg BID) and at escalating doses of 200–400mg BID post-alloSCT will intensify remission, reduce relapse and improve outcome without increasing TRT in pts with advanced CML and Ph+ ALL. 24 pts (M-13, F-11) participated in the study. The median age was 36 years (range, 18–58). 17 pts were with advanced CML (BC-10, AP-7) and 7 with Ph+ ALL. Cytogenetic and molecular responses were assessed by FISH and RQ-PCR (Taqman, LeukemiaNet and Eutos criteria). 5 pts harbored ABL kinas domain mutations by Sequenom assay (Y253H-2, A397P-1, E255K-1, M351T-1). 9 pts received nilotinib (400mg BID) pre-alloSCT and 6 responded (2 are too early to evaluate) (BC- CHR–2, BC - CCR-2, AP - PCR-1, AP - CHR-1). 22/24 pts underwent alloSCT (2 are pending) from an HLA-matched sibling (n=11), matched unrelated (n=8) or alternative donor (CB-2, Haplo-1). All, but one, had myeloablative conditioning (Bu/Cy or Flu/Bu-14, TBI/Cy-7). Graft versus host disease (GVHD) prophylaxis included CSA and methotrexate or MMF. 21/22 pts engrafted in median day+13 (range, 9–38) with 100% donor chimerism. TRT included mucositis in all pts, encephalitis-2, pericarditis-1, VOD-1 and infection-3. 3 pts died very early post transplant from sepsis and multi organ failure. Acute GVHD ≥ Gr II was observed in 10 pts (III-IV in 5). Chronic GVHD was observed in 15 pts (extensive – 9). Sixteen of the 22 transplanted pts received nilotinib (200mg × 2/d – 10, 300mg × 2/d – 6) starting at median day +38 (range, 30–158) post alloSCT. 6 pts did not receive nilotinib post alloSCT due to early death -3, progressive disease -1, severe pancytopenia -1, refusal -1. No pt received the planned 400mg BID dose. In 9 pts nilotinib administration was delayed due to either liver abnormalities -3, severe thrombocytopenia -3 or infection -3. Nilotinib dose had to be reduced (n=4) or stopped (n=3) due to Gr III-IV non-hematological toxicities -5 pts, mainly abnormal liver function tests -4 in combination with pruritus -1, vomiting -1 and abdominal pain -1, or hematological toxicities -2 pts. In 1 pt we observed increased levels of amylase without clinical signs of pancreatitis. QTc (470 msec) prolongation was observed in 1 pt. All, but 2 pts achieved MMR post alloSCT and 6 of them (CML) converted to CMR following nilotinib therapy. Response was durable and maintained. Only in 1 pt with disease progression kinas mutation (G205E and F359V) were detected. With a median follow up of 14.5 months (range, 0.5–36) 12 pts are alive while 12 died (Infection -5, GVHD -3, TTP-1, disease progression -3). In 2 pts disease progressed but responded to further therapy. 5 of 6 pts that did not receive nilotinib died (early death post AllSCT -3, disease progression -1, GVHD Gr IV -1). Immunological evaluation pre- and post nilotinib administration disclosed no significant change in T, B and NK cell numbers and T cell mitogenic response to PHA and anti CD3. Thymic output (TREC) and receptor repertoire (Spectrotyping) analysis indicates continuous thymopoiesis in 8/13 evaluated pts. NK cytotoxic activity against K562 increased in 9/15 evaluated pts. In conclusion, post alloSCT nilotinib maintenance therapy in extremely high risk pts with advanced CML and Ph+ ALL may prevent relapse and disease progression as 1) pts achieved MMR and 6 converted to CMR with nilotinib therapy and 2) only 5/16 pts that received nilotinib post alloSCT progressed [in 4 of them nilotinib could not be administrated as per protocol because of side effects (n=2) or low compliance (n=2)]. Although a formal maximal tolerated dose (MTD) of nilotinib post alloSCT has not been reached, it seems that administration of nilotinib early post alloSCT may be associated with increased toxicity. nilotinib administration post alloSCT does not impair immunological reconstitution, while GVHD incidence seems not to be reduced. Based on these data we would recommend nilotinib maintenance therapy post alloSCT in pts with advanced CML and Ph+ ALL. Disclosures: Nagler: Novartis: Honoraria, Research Funding. Off Label Use: Nilotinib (Tasigna) for reduction of tumor mass pre- and maintenance therapy post alloSCT in patients with CML and Ph+ ALL (novel TKI).

Outcomes for Myeloma in the Era of Lenalidomide Maintenance Are Not Different Among Ethnic Groups Following Autologous Transplant

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 3973-3973
Author(s):  
Chandra Pooja ◽  
Ajay K. Nooka ◽  
Monica S. Chatwal ◽  
Sungjin Kim ◽  
Zhengjia Chen ◽  
...  
Keyword(s):  
Overall Survival ◽  
Multivariate Analysis ◽  
Maintenance Therapy ◽  
Ethnic Groups ◽  
Research Funding ◽  
Maintenance Treatment ◽  
Post Transplant ◽  
Factors Associated ◽  
Lytic Lesions ◽  
White Patients

Abstract Background: Multiple myeloma (MM) is the most common hematological malignancy among African Americans (AA). The introduction of postransplant maintenance has had a significant improvement in progression free and overall survival for myeloma patients as demonstrated in large phase III clinical trials. However, the impact of race on the outcome of patients receiving maintenance treatment remains unknown. Methodology: We conducted a retrospective analysis of 299 consecutive patients transplanted for MM from 2005 to 2013 at the Winship Cancer Institute of Emory University. Survival analyses were estimated by Kaplan-Meier methods and univariate and multivariate analysis were performed using a cox proportional hazard model. Results: Baseline characteristics such as stage (International Staging System, ISS), presence of lytic lesions or plasmocytomas, immunoglobulin subtype, and cytogenetic risk category at presentation, were comparable between AA and white patients. Among AA, 57.1% received triple therapy with an immune modulator and a proteasome inhibitor (IMID+PI, lenalidomide (R) or thalidomide (T) and bortezomib (V) and dexamethasone), 49% received doublets (RD, TD or VD) and 29% received other bortezomib based regimens. In white patients 50.3% were treated with IMID+PI, 37% with doublets, 13.6% with received other bortezomib based regimens. Both populations had comparable ORR and >VGPR at day 100 (AA: ORR:90.74% and >VGPR:74.07% vs White ORR:90.65% and >VGPR: 77.57%, p>0.1). Of the 299 patients, 128 patients underwent maintenance treatment with lenalidomide (AA: 61 and White:67 patients) while 171 did not receive lenalidmode as they transplanted prior approval of lenalidomide maintenance. Maintenance treatments improved progression free survival in both ethnic cohorts. AA patients receiving maintenance therapy have not yet reached their median PFS with a median follow up of 8 years (60%), while median PFS was 4.8 years among those who did not receive maintenance (p=0.4). Similarly, in white patients, the PFS improved from 2.8 years without maintenance to 5.4 years with maintenance (p=0.01). Furthermore race did not affect PFS in both maintenance treated cohorts. Within the cohort of patients that did not receive maintenance therapy, we observed a trend of improvement in overall survival in AA patients ( p=0.06), which could suggest difference in the risk of the disease. However, no differences in staging or cytogenetics were identified between both ethnic groups at diagnosis that could explain this difference. Factors associated with longer PFS in univariate and multivariate analysis included AA race and immunoglobulin subtype (IgG and kappa light chain MM). In AA multivariate analysis identified the presence of lytic lesions as a factors associated with shorter PFS. In white patients, factors such as plasma cell leukemia at diagnosis were associated with worst PFS. In conclusion, race did not impact the improvement in PFS associated with post-transplant maintenance therapy. To our knowledge this preliminary analysis provides the first assessment of the influence of race in MM outcomes post-transplant during the lenalidomide maintenance era Disclosures Lonial: Millennium: The Takeda Oncology Company: Consultancy, Research Funding; Celgene: Consultancy, Research Funding; Novartis: Consultancy, Research Funding; Bristol-Myers Squibb: Consultancy, Research Funding; Onyx Pharmaceuticals: Consultancy, Research Funding.

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