The Return of Belantamab Mafodotin: Past Lessons, Present Promise, and Future Impact

Introduction

Belantamab mafodotin (belamaf, Blenrep; GSK) made history as the first B-cell maturation antigen (BCMA)–targeted agent and the only antibody-drug conjugate approved for the treatment of multiple myeloma (MM) with initial accelerated approval in 2020, and as one of 3 therapies, along with panobinostat (Farydak; Secura Bio) and melphalan flufenamide (Pepaxto; Oncopeptides AB), for the treatment of MM that were withdrawn from the US market.¹ Belamaf remained available through an expanded access approval program, and, with additional data from the phase 3 DREAMM-7 (NCT04246047) and DREAMM-8 (NCT04484623) studies in hand, was resubmitted for FDA review.^2-5

In July 2025, the FDA’s Oncologic Drugs Advisory Committee (ODAC) voted against the favorability of the proposed dosage of belamaf in combination with bortezomib (Velcade; Takeda Oncology) and dexamethasone (BVd) for the treatment of patients with MM who have received at least one prior line of therapy. However, the FDA did not immediately reject the application.⁶ Instead, it pushed back its determination deadline. Belamaf was then granted FDA approval in combination with bortezomib and dexamethasone for patients with relapsed/refractory MM (RRMM) in October 2025.⁷

Overview of Belantamab Mafodotin

BCMA is a tumor necrosis factor receptor that is overexpressed in MM and is involved in the proliferation, growth, and survival of cancer cells.⁸ Prior to T-cell engagers and chimeric antigen receptor (CAR) T cells, the only available therapy targeting BCMA was belamaf. Belamaf is a humanized IgG1 afucosylated monoclonal antibody that targets BCMA and is conjugated to MMAF. Afucosylation leads to enhanced binding affinity to immune cells, leading to improved cell death through antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis, and inducing immunogenic cell death. Additionally, the release of MMAF intercellularly leads to microtubule inhibition and, ultimately, apoptosis.⁹

Initial Approval, the DREAMM-2 Trial, and Subsequent Withdrawal

DREAMM-2 (NCT03525678)10 was a 2-arm, randomized, open-label phase 2 study that enrolled patients with RRMM. Patients were included if they were refractory to immunomodulatory drugs (IMiDs) and proteasome inhibitors (PIs), with exposure to anti-CD38 monoclonal antibodies.¹¹ Patients received either belamaf 2.5 mg/kg (n = 97) or 3.4 mg/kg (n = 99) intravenously every 3 weeks. The trial arms included a notable proportion of patients who were 75 years or older (13% and 17%, respectively). The number of patients with high-risk cytogenetics was well balanced, with inclusion of del(17p) (16% vs 22%), t(4;14) (11% vs 11%), t(14;16) (7% vs 2%), and 1q21+ (26% vs 30%). The median prior lines of therapy was 7 (range, 3-21) in the 2.5-mg/kg cohort and 6 (range, 3-21) in the 3.4-mg/kg cohort. At 3-year follow-up, the overall response rate (ORR) in the 2.5-mg/kg cohort was 32%, with 35% in the 3.4-mg/kg cohort, and a very good partial response (VGPR) or better achieved by 19% and 24%, respectively. The median duration of response (DOR) in the 2.5-mg/kg cohort was 12.5 months (95% CI, 4.2-19.3) and 6.2 months (95% CI, 4.8-18.7) in the 3.4 mg/kg. The median progression-free survival (PFS) was 2.8 and 2.9 months, respectively. Median overall survival (OS) was 15.3 and 14.0 months.¹²

These results led to the initial accelerated FDA approval of belamaf on August 5, 2020.¹³ This was subsequently revoked on March 20, 2023, as the primary endpoint of the DREAMM-3 trial (NCT04162210),¹⁴ which evaluated belamaf compared with pomalidomide (Pomalyst; Bristol Myers Squibb) and dexamethasone (Pd) in patients with RRMM, was not met when belamaf failed to show a statistically improved PFS compared with Pd.¹ In the DREAMM-3 trial, patients were enrolled to either intravenous (IV) belamaf 2.5mg/kg every 3 weeks (n = 218) or oral pomalidomide 4 mg on days 1 to 21 with dexamethasone 40 mg once weekly of a 28-day cycle (n = 107).¹⁵ Patients were included in this trial if they were exposed to 2 or more previous lines of therapy inclusive of a PI and IMiD. There was a similar number of patients who were 75 years or older (22% vs 21%, respectively) and had extramedullary disease (18% vs 18%). High-risk cytogenetics were more prevalent in the pomalidomide group (26% vs 32%). Although the median number of prior lines of therapy was similar at 4 and 3, there were more patients who had 6 or more prior lines of therapy in the belamaf group (15% vs 7%).

After an initial follow-up of 11.5 months and 10.8 months, respectively, ORR was 41% for belamaf and 36% for Pd. The depth of response was higher in the belamaf group as well, as 25% achieved VGPR compared with 8%. The median DOR was not reached for belamaf but was reported as 8.5 months for Pd. Although the belamaf group reported a median PFS of 11.2 months (95% CI, 6.4-14.5) and a median OS of 21.2 months (95% CI, 18.7-not reached [NR]) compared with the Pd group—which reported a median PFS of 7 months (95% CI, 4.6-10.6) and median OS of 21.1 months (95% CI, 15.1-NR)—belamaf failed to show a significantly improved PFS compared with Pd. Longer follow-up led to improvements in the HR for PFS and OS due to depth and duration of response but still did not meet statistical significance.

The initial FDA approval was for patients with RRMM after at least 4 prior therapies, including an anti-CD38 monoclonal antibody, a PI, and an IMiD. This often meant that patients were exposed to or refractory to pomalidomide. Despite the revocation, the DREAMM-7 and DREAMM-8 trials continued to accrue, and their data matured. Patients who were treated with belamaf outside of a clinical trial could continue treatment through enrollment into an expanded access program. This plan was supported by National Comprehensive Cancer Network guidelines for MM and, thus, included as an option for patients who met the initial indication.¹

DREAMM-7 and Place in Therapy in the Current Treatment Landscape

The DREAMM-7 trial was an open-label, randomized, multicenter phase 3 study evaluating the efficacy and safety of BVd vs daratumumab (Darzalex; Janssen Biotech) plus bortezomib and dexamethasone (DVd) in adults with RRMM.^2,16 Eligible patients had received 1 or more prior lines of therapy, had no prior BCMA-targeted treatment, and were not refractory or intolerant to daratumumab or bortezomib. Patients with significant corneal disease were excluded, except those with mild punctate keratopathy.

On October 23, 2025, based on the results of the DREAMM-7 trial, the FDA approved belamaf in combination with BVd for the treatment of adults with RRMM who have received 2 or more prior lines of therapy, including a PI and an IMiD.⁷ The FDA-labeled approval for patients with RRMM who have received 2 or more prior lines of therapy is more narrow than the full patient population in the DREAMM-7 trial, which included patients who had received 1 or more prior lines of therapy; thus, the information in the belamaf US package insert is reflective of this more narrow patient population.⁷

A total of 494 participants were randomly assigned 1:1 to receive BVd (n = 243) or DVd (n = 251). Belamaf was administered at 2.5 mg/kg IV every 3 weeks in combination with Vd for the first 8 cycles, then continued as monotherapy.² The primary endpoint was PFS, with key secondary endpoints including OS, DOR, minimal residual disease (MRD) negativity by next-generation sequencing, ORR, safety, and patient-reported quality-of-life outcomes.

A total of 217 evaluable patients had received 2 or more prior lines of therapy, including a PI and an IMiD (BVd, n = 108; DVd, n = 109).⁷ Baseline characteristics were balanced between treatment arms, with a median age of 65 years (range, 39-86); 29% had high-risk cytogenetics [t(11;14), t(14;16), or 17p13del], 11% had extramedullary disease, and the median number of prior therapies was 3 (range, 2-7).⁷ Two percent had received prior anti-CD38 therapy; 19% and 59% were refractory to PIs and IMiDs, respectively.⁷

Median PFS was 31.3 months (95% CI, 23.5-NR) in the BVd arm vs 10.4 months (95% CI, 7.0-13.4) in the DVd arm (HR 0.31, 95% CI, 0.21-0.47), and median OS was not reached vs 35.7 months (95% CI, 21.1-NR), respectively (HR 0.49; 95% CI, 0.32-0.76).⁷ The ORR was 81.5% (95% CI, 72.9%-88.3%) with BVd compared with 56.9% (95% CI, 47.0%-66.3%) with DVd, including stringent complete response (sCR) in 13.9%, CR in 17.6%, VGPR in 31.5%, and PR in 18.5% of BVd-treated patients.⁷ The MRD negativity rate was 23.1% (95% CI, 15.6%-32.2%) for BVd vs 2.8% (95% CI, 0.6%-7.8%) for DVd; among patients achieving CR or better, MRD negativity was observed in 73.5% vs 33.3%, respectively.⁷

The most common grade 3 or higher adverse events among patients treated with BVd (n = 242) in the DREAMM-7 trial included reduction in best-corrected visual acuity (57%), corneal examination findings (72%), blurred vision (22%), dry eye (7%), photophobia (2%), foreign body sensation (3%), eye irritation (5%), eye pain (0.8%), cataract (8%), and visual impairment (5%).⁷ Nonocular grade 3 or higher events included diarrhea (4%), nausea (0.8%), upper respiratory tract infection (2%), pneumonia (16%), COVID-19 (5%), hepatotoxicity (14%), fatigue (6%), and pyrexia (0.4%).⁷

Concerns for Ocular Toxicities and REMS

Belamaf carries a boxed warning for ocular toxicity, including corneal epithelial changes that may result in visual impairment.⁷ In the DREAMM-7 trial, ocular toxicity occurred in 92% of patients, with grade 3 or 4 events in 77%, and 83% requiring dose modifications due to ocular findings. The most common ocular toxicities (> 25%) included reductions in best-corrected visual acuity (BCVA; 89%), corneal exam findings (86%), blurred vision (66%), dry eye (51%), photophobia (47%), foreign body sensation (44%), eye irritation (43%), and eye pain (33%).⁷ The median time to onset of grade 2 or higher ophthalmic findings was 43 days (range, 15-611), with a median duration of 85 days (range, 5-813).⁷

Among affected patients, 42% improved to grade 1 or better, and 22% achieved complete resolution of findings.⁷ A reduction in BCVA to 20/50 or worse in at least one eye occurred in 69% of patients, including 29% to 20/100 or worse and 12% to 20/200 or worse; resolution to baseline or better occurred in 61%, 57%, and 48% of these patients, respectively.⁷ Common corneal findings included superficial punctate keratopathy, microcyst-like deposits, epithelial changes, and haze, with rare cases of corneal ulceration, sometimes infectious, requiring prompt ophthalmologic management.⁷

Because of the high risk of ocular toxicity, belamaf is available only through the Blenrep Risk Evaluation and Mitigation Strategy (REMS) program.⁷ Ophthalmic examinations, including slit lamp and BCVA assessments, must be performed by an eye care professional at baseline, prior to each dose, for new or worsening symptoms, and as clinically indicated.

Treatment should be withheld until improvement to grade 1 or higher and resumed or discontinued based on severity. Patients should be counseled to report ocular symptoms promptly, use preservative-free artificial tears at least 4 times daily, avoid contact lens use unless directed otherwise, and exercise caution when driving or operating machinery.

Treatment Schedule and Administration

In the DREAMM-7 trial, BVd was administered on a 21-day cycle until disease progression or intolerance.² Belamaf 2.5 mg/kg IV was administered on day 1 of each cycle, and for cycles 1 through 8, bortezomib 1.3 mg/m2 subcutaneous (SC) was administered on days 1, 4, 8, and 11 of a 21-day cycle; with dexamethasone 20 mg IV or orally on the day of and after bortezomib treatment.²

In an analysis of modifications of belamaf dosing, 88% of patients had a dose delay, the relative dose intensity was 51%, and by month 9 of treatment, the median time between belamaf doses was 8 weeks.13 Notably, response rates continued to deepen for patients who experienced dose delays, and for those with dose delays of 12 weeks or more (n = 146), the median PFS was 36.6 months (95% CI, 31.3-NR) with estimated 12- and 18-month PFS rates of 91% and 81%, respectively.¹⁷

Although in the DREAMM-7 trial BVd was administered on an every 21-day cycle with a twice weekly schedule for bortezomib, weekly bortezomib dosing is more commonly used in clinical practice. For this reason, implementing a weekly bortezomib regimen for improved tolerability with less risk and severity for peripheral neuropathy within a 28-day cycle may be preferred (Table2,5). This adjustment effectively extends the belamaf dosing interval from every 3 weeks to every 4 weeks. Notably, in clinical trials, lengthening the dosing interval or holding doses did not compromise efficacy but significantly reduced ocular toxicity.^2,12,18

Key Points

· Cycle length: 21 days

o 28-day cycle may be preferred when operationalizing belamaf plus BVd into clinical practice.

· Treatment duration:

o Belamaf was continued until disease progression or unacceptable toxicity.

o Bortezomib and dexamethasone were given from cycles 1 through 8 or until disease progression or unacceptable toxicity.

· Agents by cycle and day of treatment:

o Cycles 1 to 8:

§ Day 1: Belamaf 2.5 mg/kg IV plus bortezomib 1.3 mg/m2 SC plus dexamethasone 20 mg IV/oral

§ Day 2: Dexamethasone 20 mg IV/oral

§ Day 4: Bortezomib 1.3 mg/m2 SC plus dexamethasone 20 mg IV/oral

§ Day 5: Dexamethasone 20 mg IV/oral

§ Day 8: Bortezomib 1.3 mg/m2 SC plus dexamethasone 20 mg IV/oral

§ Day 9: Dexamethasone 20 mg IV/oral

§ Day 11: Bortezomib 1.3 mg/m2 SC plus dexamethasone 20 mg IV/oral

§ Day 12: Dexamethasone 20 mg IV/oral

o Cycles 9 and onward:

§ Day 1: Belamaf 2.5 mg/kg IV

· Administration order:

o In DREAMM-7, belamaf was administered first, followed by bortezomib. Bortezomib was administered approximately 1 hour after belamaf.

o In DREAMM-7, premedication was not required prior to belamaf infusion, but could be considered if medically appropriate. Premedications were considered for patients who had experienced an IRR with belamaf.

o In DREAMM-7, on treatment days when belamaf administration coincides with bortezomib, dexamethasone could be administered prior to the belamaf. Notably, dexamethasone was recommended to be administered 1 to 3 hours prior to the first dose of belamaf.

Reduced dosage level 2 is specific to dosage reductions due to ocular toxicity based on ophthalmic exam findings.

Supportive Care Key Points

In the DREAMM-7 trial, ocular exams were performed at baseline and then with every cycle. If there were no changes in vision and no signs of corneal abnormality per Common Terminology Criteria for Adverse Events v5.0 criteria for eye disorders at the time of the sixth dose of belamaf, patients could have their ocular exams decreased to once every 3 months or more frequently as clinically indicated.

· In the DREAMM-7 trial, if steroid eye drops were initiated and used for 7 or more days, intraocular pressure was recommended to be monitored.

· In the DREAMM-7 trial, ocular prophylaxis included the following:

o Prophylactic preservative-free artificial tears administered in each eye at least 4 to 8 times daily, beginning on cycle 1, day 1, until the end of belamaf treatment.

o At the start of each belamaf infusion, patients could apply cooling eye masks to their eyes for as long as tolerated, up to 4 hours.

· The utility of cooling eye masks is currently unclear, with more information supporting appropriate dose reductions and prolonging the treatment interval to mitigate ocular toxicity with belamaf. However, some institutions may recommend this supportive intervention with instructions such as using cooling eye masks for 1 hour from the start of belamaf infusion.¹⁹

· Antiviral prophylaxis is recommended in patients receiving treatment with bortezomib.²⁰

Dose Adjustments and Treatment Interruptions

· Hematologic, hepatic, and renal parameters in DREAMM-7 trial2:

o Hematologic

§ Absolute neutrophil count greater than or equal to 1.0 x 109/L

o Hemoglobin level greater than or equal to 8 g/dL

o Platelet count greater than or equal to 75 x 109/L

o Hepatic

§ Total bilirubin less than or equal to 1.5 times upper limit of normal (ULN) (isolated bilirubin > 1.5 x ULN was acceptable if bilirubin was fractionated and direct bilirubin was < 35%)

§ Alanine aminotransferase level less than or equal to 2.5 times ULN

· Renal

o Estimated glomerular filtration rate greater than or equal to 30 mL/min/1.73 m2

o Urine dipstick for protein negative/trace or albumin/creatinine ratio (from spot urine) less than or equal to 500 mg/g (56 mg/mmol)

§ Rates of albuminuria were similar in patients with RRMM with normal and mild/moderate renal dysfunction in the DREAMM-2 trial.21

· In DREAMM-7, the dose modifications for dexamethasone were the following2:

o Age 75 years or younger: starting dose (20 mg), dose level (DL) 1 (12 mg), DL-2 (8 mg)

o Age older than 75 years, body mass index (BMI) less than or equal to 18.5 kg/m2: starting dose (10 mg), DL-1 (6 mg), DL-2 (4 mg)

o The starting dose of dexamethasone could be reduced at the investigator’s discretion to 20 mg weekly in cycles 1 to 8 for patients older than 75 years or for those with a BMI of less than 18.5, or those who have had previous unacceptable adverse effects associated with glucocorticoid therapy.

o Growing evidence continues to support that reduced dosing of dexamethasone or sparing dexamethasone improves tolerability, especially for patients who are frail.22,23

o Refer to the belamaf package insert for recommendations on dosage modifications for adverse reactions.7

· Prohibited therapies:

o Cysteine-maleimidocaproyl-MMAF, the active cytotoxic drug conjugated to belantamab, is a substrate of OATP1B1 and OATP1B3, MRP1, MRP2, MRP3, BSEP, and a possible substrate of P-gp. Caution should be used with concomitant use of strong inhibitors of OATP and P-gp.

o Bortezomib is a substrate of CYP3A4. Closely monitor with concomitant therapy with a strong CYP3A4 inhibitor; avoid strong CYP3A4 inducers if possible. Avoid concomitant therapy with St John’s wort, which is a strong CYP3A4 inducer.

Conclusion

Belantamab mafodotin may occupy a versatile and clinically meaningful position within the treatment landscape for RRMM as therapeutic sequencing with CAR T-cell and T-cell engagers continues to evolve. It may be considered after ciltacabtagene autoleucel (Carvykti; Janssen) and, in certain scenarios, even before T-cell engagers. In some cases, it may also serve as an alternative to idecabtagene vicleucel (Abecma; Bristol Myers Squibb), depending on patient characteristics, treatment timing, and availability of cellular therapy resources. Its broad accessibility in community practices, rather than being confined to specialized centers, provides a practical option for patients who cannot wait for or travel to a center offering CAR T-cell therapy. Moreover, belantamab mafodotin offers an important therapy option for individuals unlikely to tolerate CAR T-cell therapy or T-cell engagers, including older adults who may not endure lymphodepletion, patients with active or recurrent infections, and those for whom prolonged hospitalization or intensive monitoring

is not feasible, while still enabling meaningful disease control with more manageable logistics and toxicity considerations.

The approval of belantamab mafodotin represents an important advance in the treatment landscape for RRMM, expanding access to BCMA-targeted therapy beyond specialized academic centers. Although other BCMA-directed options, such as CAR T-cell therapies and bispecific antibodies, require more complex logistical considerations and intensive monitoring during T-cell engager step-up dosing schedules, belantamab mafodotin can be safely delivered in community oncology practices, where the majority of patients with MM receive care. This accessibility addresses a critical gap, offering a practical and effective treatment option for patients who have received at least 2 prior lines of therapy, and for whom available options may be limited and retreatment with agents with similar mechanisms of action often yields suboptimal outcomes.

References

1. Mukhopadhyay P, Abdullah HA, Opalinska JB, et al. The clinical journey of belantamab mafodotin in relapsed or refractory multiple myeloma: lessons in drug development. Blood Cancer J. 2025;15:15. doi:10.1038/s41408-025-01212-0 2. Hungria V, Robak P, Hus M, et al; DREAMM-7 Investigators. Belantamab mafodotin, bortezomib, and dexamethasone for multiple myeloma. New Engl J Med. 2024;391(5):393-407. doi:10.1056/NEJMoa2405090 3. Dimopoulos MA, Beksac M, Pour L, et al; DREAMM-8 Investigators. Belantamab mafodotin, pomalidomide, and dexamethasone in multiple myeloma. New Engl J Med. 2024;391(5):408-421. doi:10.1056/NEJMoa2403407

4. Evaluation of efficacy and safety of belantamab mafodotin, bortezomib and dexamethasone versus daratumumab, bortezomib and dexamethasone in participants with relapsed/refractory multiple myeloma (DREAMM 7). ClinicalTrials.gov. Updated October 24, 2024. Accessed November 24, 2025. https://clinicaltrials.gov/study/NCT04246047

5. Belantamab mafodotin plus pomalidomide and dexamethasone (Pd) versus bortezomib plus Pd in relapsed/refractory multiple myeloma (DREAMM 8). ClinicalTrials.gov. Updated March 18, 2025. Accessed November 24, 2025. https://clinicaltrials.gov/study/NCT04484623

6. Flaherty C. FDA’s ODAC votes against risk:benefit profiles of belantamab mafodotin combos in R/R myeloma. OncLive. July 17, 2025. https://www.onclive.com/view/fda-s-odac-votes-against-risk-benefit-profiles-of-belantamab-mafodotin-combos-in-r-r-myeloma

7. Blenrep (belantamab mafodotin-blmf). Prescribing information. GlaxoSmithKline; revised October 2025.

https://gskpro.com/content/dam/global/hcpportal/en_US/Prescribing_Information/Blenrep/pdf/BLENREP-PI-MG.PDF

8. Shah N, Chari A, Scott E, Mezzi K, Usmani SZ. B-cell maturation antigen (BCMA) in multiple myeloma: rationale for targeting and current therapeutic approaches. Leukemia. 2020;34(4):985-1005. doi:10.1038/s41375-020-0734-z

9. Tai YT, Mayes PA, Acharya C, et al. Novel anti-B-cell maturation antigen antibody-drug conjugate (GSK2857916) selectively induces killing of multiple myeloma. Blood. 2014;123(20):3128-3138. doi:10.1182/blood-2013-10-535088

10. A study to investigate the efficacy and safety of two doses of GSK2857916 in participants with multiple myeloma who have failed prior treatment with an anti-CD38 antibody. ClinicalTrials.gov. Updated September 3, 2025. Accessed November 24, 2025. https://clinicaltrials.gov/study/NCT03525678

11. Lonial S, Lee HC, Badros A, et al. Belantamab mafodotin for relapsed or refractory multiple myeloma (DREAMM-2): a two-arm, randomised, open-label, phase 2 study. Lancet Oncol. 2020;21(2):207-221. doi:10.1016/s14702045(19)30788-0

12. Nooka AK, Cohen AD, Lee HC, et al. Single-agent belantamab mafodotin in patients with relapsed/refractory multiple myeloma: final analysis of the DREAMM-2 trial. Cancer. 2023;129(23):3746-3760. doi:10.1002/cncr.34987

13. Blenrep (belantamab mafodotin-blmf) [prescribing information]. Philadelphia, PA: GlaxoSmithKline. (August 2020).

14. Study of single agent belantamab mafodotin versus pomalidomide plus low-dose dexamethasone (Pom/Dex) in participants with relapsed/refractory multiple myeloma (RRMM) (DREAMM-3). ClinicalTrials.gov. Updated June 10, 2025. Accessed November 24, 2025. https://clinicaltrials.gov/study/NCT04162210

15. Dimopoulos MA, Hungria VTM, Radinoff A, et al. Efficacy and safety of single-agent belantamab mafodotin versus pomalidomide plus low-dose dexamethasone in patients with relapsed or refractory multiple myeloma (DREAMM-3): a phase 3, open-label, randomised study. Lancet Haematol. 2023;10(10):e801-e812. doi:10.1016/s2352-3026(23)00243-0

16. Hungria V, Robak P, Hus M, et al; DREAMM-7 study investigators. Belantamab mafodotin plus bortezomib and dexamethasone in patients with relapsed or refractory multiple myeloma (DREAMM-7): updated overall survival analysis from a global, randomised, open-label, phase 3 trial. Lancet Oncol. 2025;26(8):1067-1080. doi:10.1016/s1470-2045(25)00330-4

17. Mateos MV, Trudel S, Quach H, et al. Modification of belantamab mafodotin dosing to balance efficacy and tolerability in the DREAMM-7 and DREAMM-8 trials. Blood Adv. 2025;9(22):5708-5719. doi:10.1182/bloodadvances.2025016949

18. Trudel S, McCurdy A, Louzada M, et al. Belantamab mafodotin, pomalidomide and dexamethasone in refractory multiple myeloma: a phase 1/2 trial. Nat Med. 2024;30:543-551. doi:10.1038/s41591-023-02703-y

19. Belantamab mafodotin. Thames Valley Strategic Clinical Network Myeloma Group. 2023. Accessed TK DATE. https://nssg.oxford-haematology.org.uk/myeloma/pdf-protocols/MM-55-belantamab-mafodotin.pdf

20. Raje NS, Anaissie E, Kumar SK, et al. Consensus guidelines and recommendations for infection prevention in multiple myeloma: a report from the International Myeloma Working Group. Lancet Haematol. 2022;9(2):e143-e161. doi:10.1016/s2352-3026(21)00283-0

21. Lee HC, Cohen A, Chari A, et al. DREAMM-2: Single-agent belantamab mafodotin (GSK2857916) in patients with relapsed/refractory multiple myeloma (RRMM) and renal impairment. J Clin Oncol. 2020;38:8519. doi:10.1200/JCO.2020.38.15_suppl.8519

22. Banerjee R, Sexton R, Cowan AJ, et al. Dexamethasone dose intensity does not impact outcomes in newly diagnosed multiple myeloma: a secondary SWOG analysis. Blood. 2025;145(1):75-84. doi:10.1182/blood.2024025939

23. Manier S, Lambert J, Hulin C, et al. Safety and efficacy of a dexamethasone-sparing regimen with daratumumab and lenalidomide in patients with frailty and newly diagnosed multiple myeloma (IFM2017-03): a phase 3, open-label, multicentre, randomised, controlled trial. Lancet Oncol. 2025;26(10):1323-1333. doi:10.1016/s1470-2045(25)00280-3