What to Do When Myeloma Relapses: A Complete Guide to Every Treatment Option in Your Playbook
Relapse Management Guide · Distinguishing Biochemical vs. Clinical Relapse, Prior-Exposures Regimen Selection, and Next-Generation Immunotherapies
Medical Disclaimer: The following content is compiled based on the latest authoritative guidelines at home and abroad. It is for reference only for patients and their families and cannot replace the professional medical advice of the attending physician. Please be sure to follow the doctor's advice for the treatment plan.
Foreword: Key Takeaways
"My M-protein has started rising again—does this mean I need to start chemotherapy immediately?" "I progressed on Revlimid (lenalidomide) maintenance—what are my next options?" "When should we consider CAR-T cells, bispecific antibodies, or precision-targeted drugs?"
Disease relapse in multiple myeloma is an anticipated transition in long-term disease management rather than a failure of therapy. In 2026, the therapeutic landscape for relapsed/refractory multiple myeloma (RRMM) offers an expansive armamentarium of targeted options:
- Distinguish "Biochemical Relapse" from "Clinical Relapse": A slow, isolated rise in laboratory markers in an asymptomatic patient does not always require immediate therapy. Close observation every 2 to 3 months avoids overtreatment and preserves future drug classes.
- Mandatory Immediate Treatment Triggers Exist: When M-protein doubles rapidly within 2 months, high-risk cytogenetics evolve, or CRAB organ damage threatens, therapy must be instituted immediately.
- Refractory-Stratified Sequencing: Modern treatment selection is strictly guided by the patient's prior drug exposures:
- Lenalidomide-refractory: Prioritize anti-CD38/carfilzomib triplets (Dara-Kd, Isa-Kd), pomalidomide combinations (Isa-Pd, PVd), or early CAR-T (Cilta-cel).
- Bortezomib-refractory: Prioritize Dara-Rd, KRd, or Selinexor combinations (SVd).
- Triple-Class Refractory: Deploy CAR T-cell therapies, bispecific antibodies (Teclistamab, Elranatamab, Talquetamab), ADC triplets (Belantamab combinations), or BCL-2 inhibitors for t(11;14).
1. Defining Relapse: Exact Diagnostic Thresholds and Treatment Timing
Accurately distinguishing between asymptomatic serological progression and active clinical relapse is the critical first step in RRMM management.
1.1 Exact International Diagnostic Criteria
| Relapse Category | Diagnostic Definition | Mandatory Laboratory / Clinical Criteria | Plain-Language Takeaway |
|---|---|---|---|
| Clinical Relapse (Symptomatic Relapse) | Relapse characterized by new or worsening end-organ dysfunction (CRAB symptoms) directly attributable to myeloma. | • Hypercalcemia: Serum calcium > 11.0 mg/dL (> 2.75 mmol/L).<br>• Renal Insufficiency: Serum creatinine increase ≥ 2.0 mg/dL (≥ 176.8 μmol/L).<br>• Anemia: Hemoglobin drop ≥ 2.0 g/dL (≥ 20 g/L) or absolute value < 10.0 g/dL (< 100 g/L).<br>• Bone / Soft-Tissue Lesions: New osteolytic lesions, or ≥ 50% increase (and ≥ 1 cm absolute increase) in SPD of existing lesions.<br>• Hyperviscosity: Symptomatic serum hyperviscosity syndrome. | Requires immediate systemic treatment to prevent permanent organ or skeletal damage. |
| Biochemical Relapse (Asymptomatic Relapse) | Laboratory-documented progressive disease in the complete absence of CRAB symptoms or organ damage. | Any one from nadir:<br>• Serum M-Protein: Relative rise ≥ 25% with absolute rise ≥ 0.5 g/dL (≥ 5 g/L).<br>• Urine M-Protein: Relative rise ≥ 25% with absolute rise ≥ 200 mg/24h.<br>• Serum Free Light Chains (sFLC): Relative rise ≥ 25% with absolute increase > 100 mg/L (> 10 mg/dL) in involved FLC.<br>• Bone Marrow Plasma Cells (BMPC): Relative rise ≥ 25% with absolute increase ≥ 10%. | May be safely observed if marker rise is slow and no high-risk genomic features are present. |
1.2 Observation vs. Immediate Treatment Triggers
The Rationale for Observation in Slow Biochemical Progression In patients with indolent, slowly rising M-protein (e.g., rising by 1 g/L over several months without symptoms), immediately initiating salvage chemotherapy exposes the patient to cumulative toxicities without prolonging overall survival. International consensus guidelines recommend watchful waiting with laboratory reassessment every 2 to 3 months.
Mandatory Immediate Treatment Triggers (Even Without CRAB Symptoms) Systemic therapy must be initiated promptly if any of the following aggressive progression signs occur:
- M-Protein Rapid Doubling Time: Absolute M-protein rise ≥ 5 g/L or sFLC rise ≥ 100 mg/L confirmed on two consecutive tests 2 months apart.
- High-Risk Cytogenetic Evolution: Emerging adverse clones on FISH/genomics (del(17p), TP53 mutation, t(4;14), t(14;16), t(14;20), del(1p32), or 1q21 amplification).
- Later Lines of Therapy (≥ 3): In heavily pretreated disease, the window between biochemical progression and fulminant clinical crisis is extremely narrow.
- History of Fulminant Presentation: Prior rapid-onset acute renal failure, hypercalcemic crisis, or extramedullary disease (EMD).
Literature References: IMWG Consensus Criteria for Relapse; NCCN Guidelines v5.2026; EHA-EMN Guidelines 2025
2. Refractory-Stratified Pharmacological Regimens: Phase 3 Clinical Trial Benchmarks
At relapse, selecting an optimal regimen depends on which drug classes the disease has become resistant to—most commonly lenalidomide (R) following frontline maintenance, or bortezomib (V).
2.1 Master Clinical Trial Benchmark: Relapsed/Refractory Regimens
| Regimen & Mechanism | Pivotal Phase 3 Trial | Study Population | Overall Response Rate (ORR) | Median Progression-Free Survival (PFS) | Median Overall Survival (OS) | Key Clinical Highlights & Hazard Ratios | Plain-Language Takeaway |
|---|---|---|---|---|---|---|---|
| Daratumumab + Carfilzomib + Dex (Dara-Kd) | CANDOR | 1–3 prior lines (Len-exposed/refractory) | 84.0% vs. 75.0% (Kd) | 29.0 months vs. 15.8 months | NR vs. 50.8 months | PFS HR = 0.63 (P = 0.0014). Superior PFS across both len-sensitive and len-refractory subgroups. | Premier 3-drug choice for patients progressing on Revlimid. |
| Isatuximab + Carfilzomib + Dex (Isa-Kd) | IKEMA | 1–3 prior lines (Len-exposed/refractory) | 87.0% vs. 83.0% (Kd) | 35.7 months vs. 19.15 months | NR vs. NR (HR = 0.78) | PFS HR = 0.53 (P = 0.0007). 10⁻⁵ MRD-negativity rate reached 29.6% vs. 13.0%. | Outstanding disease control approaching 3 years median PFS in len-resistant disease. |
| Isatuximab + Pomalidomide + Dex (Isa-Pd) | ICARIA-MM | ≥ 2 prior lines (Len & PI refractory) | 60.0% vs. 35.0% (Pd) | 11.5 months vs. 6.5 months | 24.6 months vs. 17.7 months | PFS HR = 0.60; OS HR = 0.76. Significant survival advantage in heavily pretreated dual-refractory disease. | Effective immunotherapy triplet for patients resistant to both Velcade and Revlimid. |
| Pomalidomide + Bortezomib + Dex (PVd) | OPTIMISMM | 1–3 prior lines (Len-refractory) | 82.2% vs. 50.0% (Vd) | 11.2 months vs. 7.1 months | NR vs. NR | PFS HR = 0.61 (P < 0.0001). In patients at first relapse (1 prior LOT), median PFS reached 22.0 months vs. 12.0 months. | Ideal choice for len-refractory relapse, especially in patients with renal impairment. |
| Daratumumab + Lenalidomide + Dex (Dara-Rd) | POLLUX | ≥ 1 prior line (Len-sensitive) | 92.9% vs. 76.4% (Rd) | 51.2 months vs. 21.0 months | 67.6 months vs. 51.8 months | PFS HR = 0.44; OS HR = 0.73 (P = 0.0003). Demonstrates extensive disease control in lenalidomide-sensitive relapse. | Delivers over 4 years of median PFS for patients who have not developed Revlimid resistance. |
| Carfilzomib + Lenalidomide + Dex (KRd) | ASPIRE | 1–3 prior lines (Len-sensitive) | 87.1% vs. 66.7% (Rd) | 26.3 months vs. 17.6 months | 48.3 months vs. 40.4 months | PFS HR = 0.69 (P < 0.0001). Statistically significant OS benefit of 7.9 months. | Highly potent proteasome inhibitor regimen with minimal peripheral neuropathy. |
| Selinexor + Bortezomib + Dex (SVd) | BOSTON | 1–3 prior lines | 76.4% vs. 62.3% (Vd) | 13.93 months vs. 9.46 months | NR vs. 25.0 months | Once-weekly oral Selinexor regimen (PFS HR = 0.70). In len-refractory subgroup, median OS was 26.7 vs. 18.6 months (HR = 0.53). | Convenient once-weekly oral mechanism targeting nuclear export protein XPO1. |
| Selinexor + Pomalidomide + Dex (SPd) | STOMP | ≥ 2 prior lines (PI + Len refractory) | 65.0% | 12.2 months | NR | Highly active all-oral rescue triplet for triple-class exposed disease (40–60 mg weekly Selinexor). | Completely oral rescue triplet overcoming dual and triple class resistance. |
Literature References: CANDOR (Lancet 2020), IKEMA (Lancet Oncol 2021), ICARIA-MM (Lancet 2019), POLLUX (NEJM 2016), ASPIRE (NEJM 2015), BOSTON (Lancet 2020)
3. Next-Generation Modalities: CAR-T, Bispecific Antibodies, and ADCs
In patients experiencing early relapse on lenalidomide, or those with double- and triple-class refractory disease, next-generation targeted immunotherapies provide high response rates and deep remissions.
3.1 Chimeric Antigen Receptor (CAR) T-Cell Therapies
- Ciltacabtagene Autoleucel (Cilta-cel / Carvykti):
- CARTITUDE-4 (Phase 3 in Early Relapse; 1–3 Prior Lines): Evaluated single-infusion cilta-cel vs. standard triplets (PVd or DPd) in lenalidomide-refractory patients.
- Median PFS: Not Reached vs. 11.8 months (HR = 0.29, P < 0.001), reducing progression risk by 71%.
- 30-Month Overall Survival: 76.4% vs. 63.8% (HR = 0.55, P = 0.0009).
- In patients treated at first relapse (1 prior LOT), PFS HR = 0.27.
- CARTITUDE-1 (Phase 1b/2 in Late-Line Disease; Median 6 Prior Lines):
- Overall Response Rate (ORR): 97.9% (sCR = 82.5%).
- Median Overall Survival: 60.7 months (over 5 years).
- 33% of patients remained in continuous remission for ≥ 5 years post-infusion without any maintenance therapy.
- Idecabtagene Vicleucel (Ide-cel / Abecma):
- KarMMa-3 (Phase 3 in 2–4 Prior Lines): Compared ide-cel vs. standard multi-agent regimens in triple-class exposed RRMM.
- Median PFS: 13.3 months vs. 4.4 months (HR = 0.49, P < 0.001).
- Crossover-adjusted median OS: 41.4 months vs. 23.4 months (HR = 0.72).
3.2 "Off-the-Shelf" Bispecific T-Cell Engagers (BsAbs)
Bispecific antibodies bind simultaneously to CD3 on cytotoxic T-cells and a tumor antigen on myeloma cells, creating an artificial immunological synapse that triggers direct tumor cell destruction without manufacturing delays.
- Arm 1 (CD3 Engagement): Binds to CD3 on the patient's endogenous cytotoxic T-lymphocytes.
- Arm 2 (Target Engagement): Binds specifically to BCMA (Teclistamab, Elranatamab) or GPRC5D (Talquetamab) on myeloma plasma cells.
- Effector Cytolysis: Cross-links immune cells with cancer cells, releasing perforin and granzyme B for targeted tumor lysis.
- Teclistamab (BCMA × CD3; Tecvayli):
- MajesTEC-1 (Phase 1/2): In 165 triple-class exposed patients (median 5 prior lines), ORR was 63.0% (≥ CR = 46.1%) with a median PFS of 11.4 months and median OS of 22.2 months.
- MajesTEC-3 (Phase 3 Triplet: Teclistamab + Daratumumab vs. DPd/DVd in 1–3 Prior Lines):
- Median PFS: Not Reached vs. 18.1 months (HR = 0.17, P < 0.0001), lowering progression risk by 83%.
- 36-Month PFS Rate: 83.4% vs. 29.7%; 36-Month OS Rate: 83.3% vs. 65.0% (HR = 0.46).
- Elranatamab (BCMA × CD3; Elrexfio):
- MagnetisMM-3 (Phase 2): In triple-class refractory patients, achieved an ORR of 61.0% (≥ CR = 35.0%) and median PFS of 17.2 months.
- Talquetamab (GPRC5D × CD3; Talvey):
- MonumenTAL-1 (Phase 1/2): Targets GPRC5D (independent of BCMA). Achieved an ORR of 70.0% in heavily pretreated patients, including those with prior BCMA therapy failure.
- RedirecTT-1 (Dual Targeting: Talquetamab + Teclistamab): Achieved a 79% ORR and 52% ≥ CR in challenging extramedullary disease (EMD).
3.3 Antibody-Drug Conjugates (ADCs)
- Belantamab Mafodotin (Belamaf; Blenrep):
- DREAMM-7 (Phase 3: Belamaf + Bortezomib + Dex vs. DaraVd in ≥ 1 Prior Line):
- Median PFS: 36.6 months vs. 13.4 months (HR = 0.41, 95% CI: 0.31–0.53; P < 0.001).
- 36-Month Overall Survival: 74.0% vs. 60.0% (HR = 0.58, P < 0.001).
- DREAMM-8 (Phase 3: Belamaf + Pomalidomide + Dex vs. PVd in ≥ 1 Prior Line):
- 12-Month PFS Rate: 71.0% vs. 51.0% (HR = 0.52, P < 0.001).
- In the lenalidomide-refractory cohort, median PFS was 25.0 months vs. 8.6 months (HR = 0.31).
Literature References: CARTITUDE-4 (NEJM 2023), KarMMa-3 (NEJM 2023), MajesTEC-1 (NEJM 2022), DREAMM-7 (NEJM 2024), DREAMM-8 (NEJM 2024)
4. Precision Targeted Therapy, Salvage Chemotherapy, and Second ASCT
4.1 Precision Targeted Therapy for t(11;14) Translocations
Approximately 15–20% of multiple myeloma patients harbor the chromosomal translocation t(11;14), which confers high biological dependency on the anti-apoptotic protein BCL-2.
- Venetoclax (Venclexta):
- In t(11;14)-positive RRMM, venetoclax monotherapy achieves an ORR of 40% vs. 6% in non-translocated patients.
- When combined with dexamethasone ± bortezomib/daratumumab, ORR exceeds 80–85%.
- Sonrotoclax: A next-generation, highly potent BCL-2 inhibitor that achieved an 80.6% ORR and median PFS of 13.3 months in t(11;14) RRMM.
Mandatory Infection Prophylaxis with BCL-2 Inhibitors In the phase 3 BELLINI trial, venetoclax increased infection-related mortality despite improving PFS. Patients receiving venetoclax or sonrotoclax must receive mandatory antimicrobial prophylaxis with levofloxacin, acyclovir/valacyclovir, and TMP-SMX.
4.2 Intensive Salvage Infusional Chemotherapy (Debulking)
For patients presenting with hyper-aggressive relapse, rapidly expanding extramedullary disease (EMD), or secondary plasma cell leukemia (sPCL), continuous infusional multi-agent chemotherapy is used as an emergency debulking bridge:
- DCEP: Dexamethasone, Cyclophosphamide, Etoposide, Cisplatin (ORR ~53%, median PFS ~3.8 months).
- DT-PACE / VTD-PACE: Dexamethasone, Thalidomide, Cisplatin, Doxorubicin, Cyclophosphamide, Etoposide ± Bortezomib (ORR ~73%, median PFS ~4.5–5.6 months).
Clinical Role: Response duration is short; multi-agent infusional chemotherapy should strictly be utilized as a rapid cytoreductive bridge to CAR T-cell therapy or a second transplant.
4.3 Second Autologous Stem Cell Transplantation (ASCT2) Criteria
According to international guidelines (EHA-EMN and British Society for Haematology, BSH), a second salvage autologous transplant is a valid option if the patient meets the following strict criteria:
- Achieved a Partial Response or better (≥ PR) to salvage re-induction therapy.
- Achieved a durable first progression-free survival (PFS1) after ASCT1:
- ≥ 18 months (if no maintenance therapy was given after ASCT1); OR
- ≥ 24 months (if lenalidomide maintenance was given after ASCT1).
- Has adequate pre-cryopreserved autologous stem cells (> 2.0 × 10⁶ CD34+ cells/kg) and adequate organ reserve.
Absolute Contraindication for ASCT2 Do not offer a second ASCT to patients who relapsed within < 12 months of their first transplant (PFS1 < 12 months) (GRADE 1A Evidence), as it does not provide survival benefit in early-relapsing disease.
5. 2026 RRMM Strategic Treatment Framework
Managing relapsed multiple myeloma involves moving through structured therapy lines designed to maximize disease control while preserving patient stamina:
- Tier 1: First Relapse & Early Relapse (1–3 Prior Lines):
- Lenalidomide-Refractory: Dara-Kd, Isa-Kd, PVd, or early single-infusion CAR-T (Cilta-cel).
- Lenalidomide-Sensitive: Dara-Rd, KRd, or Dara-Vd.
- Tier 2: Second to Third Relapse (2–4 Prior Lines):
- Isa-Pd, Dara-Pd, PVd, SVd, or Belantamab triplets (Bela-Pd / Bela-Vd).
- Cellular immunotherapy: Cilta-cel or Ide-cel.
- Tier 3: Triple-Class Refractory & Advanced Relapse:
- "Off-the-shelf" Bispecific antibodies (Teclistamab, Elranatamab, Talquetamab).
- Targeted precision therapy: Venetoclax or Sonrotoclax for t(11;14).
- Rescue triplets and debulking bridges: Selinexor (SPd / SKd) or DCEP infusional chemotherapy.
Conclusion: Navigating Relapse with Precision and Confidence
- Do Not Panic at Marker Fluctuations: Work with your hematologist to establish whether a marker increase reflects indolent biochemical progression or true clinical relapse.
- Select the Right Drug Class at the Right Time: If your disease progresses on lenalidomide, switch classes immediately to CD38/carfilzomib, pomalidomide, or CAR-T platforms.
- Explore Modern T-Cell Immunotherapies Early: CAR T-cell therapies (Cilta-cel) and bispecific antibodies (Teclistamab, Talquetamab) are moving into earlier lines of relapse, providing deep and durable remissions.
- Leverage Genomic Testing: Request repeat FISH and NGS profiling at relapse to identify actionable mutations such as t(11;14) or high-risk clonal evolution.
With multiple complementary drug classes and cellular platforms available in 2026, relapsed multiple myeloma is an increasingly manageable chronic condition with pathways toward prolonged disease control and excellent quality of life.
This clinical education guide is compiled by the China Myeloma Development Network (CMDN - ChinaMyeloma.org) based on peer-reviewed literature, international clinical practice guidelines, and phase 3 trial evidence. It is intended for educational purposes only and does not constitute formal medical advice. Please consult your treating hematologist or oncology team for individual clinical decision-making.
FAQs
- Does a rising M-protein mean I need to start chemotherapy immediately?
- Not necessarily. If you have slow biochemical progression without symptoms or organ damage, guidelines recommend close monitoring every 2 to 3 months to avoid premature toxicity. Treatment is started if markers double rapidly or CRAB symptoms threaten.
- What is the difference between biochemical relapse and clinical relapse?
- Biochemical relapse is an isolated increase in laboratory markers (such as M-protein or free light chains) with no organ dysfunction. Clinical relapse involves new or worsening CRAB symptoms (hypercalcemia, renal impairment, anemia, or new bone lesions) requiring immediate therapy.
- What are my options if my myeloma progressed on Revlimid (lenalidomide) maintenance?
- If your disease is lenalidomide-refractory, your team will switch to a different drug class. Leading regimens include CD38 antibody triplets with carfilzomib (Dara-Kd, Isa-Kd), pomalidomide triplets (Isa-Pd, PVd), or early CAR T-cell therapy (Cilta-cel).
- When should we consider CAR T-cell therapy or bispecific antibodies?
- CAR-T and bispecifics (such as teclistamab, elranatamab, and talquetamab) are highly effective in early relapse (1 to 3 prior lines) for lenalidomide-refractory disease and in triple-class exposed settings, delivering response rates between 60% and 100%.
- What is t(11;14) and how does targeted therapy work for it?
- The t(11;14) chromosomal translocation is found in 15% to 20% of patients and makes cancer cells dependent on the BCL-2 protein. Targeted BCL-2 inhibitors like venetoclax or sonrotoclax achieve response rates over 80% when combined with dexamethasone.
- Can I have a second autologous stem cell transplant (ASCT2) if I relapse?
- Yes, if you achieved a durable remission from your first transplant (at least 18 months without maintenance, or 24 months with lenalidomide maintenance), respond well to salvage re-induction, and have adequate stored stem cells.
Related reading
References used for this guide
- NCCN Guidelines v5.2026, Multiple Myeloma
- EHA-EMN Evidence-Based Guidelines on Multiple Myeloma
- CARTITUDE-4: Cilta-cel vs Standard Care in Lenalidomide-Refractory Multiple Myeloma
- KarMMa-3: Idecabtagene Vicleucel in Relapsed and Refractory Multiple Myeloma
- CANDOR: Daratumumab, Carfilzomib, and Dexamethasone in Relapsed/Refractory Myeloma
- IKEMA: Isatuximab, Carfilzomib, and Dexamethasone in Relapsed Multiple Myeloma
Key Active Trials for Relapsed / Refractory Multiple Myeloma
Active trials evaluating next-generation CELMoDs, antibodies, and cellular therapies for relapsed disease:
A Phase III, Randomized Study Comparing JNJ-79635322 and Teclistamab in Participants With Relapsed or Refractory Multiple Myeloma Who Have Received 1 to 3 Prior Lines of Therapy (Including an Anti-CD38 Antibody and Lenalidomide)
This study aims to evaluate the efficacy and safety of JNJ-79635322 versus teclistamab in the treatment of multiple myeloma. The trial mainly enrolls adult participants with relapsed or refractory disease who have received 1 to 3 prior lines of anti-myeloma therapy (including an anti-CD38 antibody and lenalidomide). Eligible participants will be randomized to receive subcutaneous injections of JNJ-79635322 or teclistamab. This is an international multicenter study conducted simultaneously in multiple hospitals, including the Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences.
A Randomized, Controlled, Double-Blind, Multicenter Phase III Clinical Trial Evaluating the Efficacy and Safety of SG301 Injection Combined with Pomalidomide and Dexamethasone Versus Placebo Combined with Pomalidomide and Dexamethasone in the Treatment of Relapsed/Refractory Multiple Myeloma (RRMM)
This project is a Phase III clinical trial sponsored by Hangzhou SJ Biosciences Co., Ltd. (Hangzhou Shangjian Biotechnology Co., Ltd.), primarily targeting participants with relapsed/refractory multiple myeloma (RRMM) who have received at least 1 prior line of therapy, have not previously received pomalidomide, and whose prior anti-CD38 antibody therapy was not determined to be refractory/ineffective. The treatment regimen utilizes an anti-CD38 monoclonal antibody (SG301 injection) combined with an immunomodulator (pomalidomide) and a glucocorticoid (dexamethasone), administered in 4-week (28-day) cycles until disease progression or intolerable toxicity. The trial is being conducted across a total of 78 top domestic hospitals in China, including the Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences; The First Affiliated Hospital of Soochow University; Beijing Chaoyang Hospital, Capital Medical University; The Second Affiliated Hospital, Zhejiang University School of Medicine; and Sun Yat-sen University Cancer Center, among others.
A Multicenter, Randomized, Controlled, Open-Label, Phase III Clinical Study of IBI3003 Versus Investigator's Choice of Regimen (DPd or PVd) on the Efficacy and Safety in Participants with Relapsed or Refractory Multiple Myeloma
This study is a multicenter, randomized, controlled, open-label Phase III clinical study in patients with relapsed or refractory multiple myeloma. The study aims to evaluate the efficacy and safety of IBI3003 compared with investigator's choice of regimen (DPd or PVd). The trial is open to participants aged 18 and older who meet the eligibility criteria, and is conducted across multiple hospitals including Zhongshan Hospital, Fudan University.
A Two-Stage, Randomized, Multicenter, Controlled, Open-Label, Phase III Study Comparing Iberdomide Maintenance Therapy with Lenalidomide Maintenance Therapy Following Autologous Stem Cell Transplantation (ASCT) in Participants with Newly Diagnosed Multiple Myeloma (NDMM)
This project is a Phase III clinical trial sponsored by Celgene (Bristol Myers Squibb/BMS), primarily targeting patients with newly diagnosed multiple myeloma (NDMM). Eligible patients must have received 3 to 6 cycles of prior induction therapy (including a proteasome inhibitor and an immunomodulatory drug), subsequently completed autologous stem cell transplantation (ASCT), and achieved at least a partial response (PR). Patients are randomized to receive maintenance therapy with either the investigational drug Iberdomide (a novel immunomodulatory agent administered for 21 days of each 28-day cycle) or the control drug lenalidomide (a conventional immunomodulatory agent administered continuously in 28-day cycles) until disease progression or unacceptable toxicity. The trial is conducted concurrently across 38 premier centers in China (including Hong Kong and Taiwan)—such as Peking University People's Hospital, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, The First Affiliated Hospital of Zhejiang University School of Medicine, Tongji Hospital of Tongji Medical College of Huazhong University of Science and Technology, and Qilu Hospital of Shandong University—as well as leading international medical centers across 32 countries, including the United States, the United Kingdom, France, Japan, and Australia.
for their academic support:
for myeloma patients globally