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BEYOND THE DATA: A PATIENT & CARE PARTNER CONVERSATION ON MYELOMA RESEARCH FROM ASCO/EHA AUGUST 18, 2026

Thank you to our Sponsors!

Your Panel for Today’s Webinar

Terry Glassman Patient & Support Group Leader

Todd Kennedy Patient & Support Group Leader

Diane Kennedy Care Partner & Support Group Leader 3

• Phase 3 Trials in Early Relapse • High-Risk Myeloma AGENDA

• Outpatient Approaches to Bispecific Antibodies • Future Approaches to Myeloma • This JUST in! Updates since ASCO/EHA... 4

Part 1 – Phase 3 Trials in Early Relapse a. MonumenTAL-3: Talquetamab + Daratumumab +/- Pom vs SOC b. MajesTEC-9: Teclistamab monotherapy vs Triplets c. Successor-2: Mezigdomide + Carfilzomib vs Carfilzomib

Phase 3, Randomized Study of Talquetamab Plus Daratumumab ± Pomalidomide vs Daratumumab Plus Pomalidomide and Dexamethasone in Relapsed/Refractory Multiple Myeloma: MonumenTAL-3 Peter M Voorhees 1*, Roberto Mina2, Paula Rodríguez-Otero3, Wenming Chen4, María-Victoria Mateos5, Jian Li 6, Philippe Moreau7, Yael C Cohen8, Chang Ki Min9, Roman Hajek10, Jing Christine Ye11, Hila Magen12, Samuel M Rubinstein 13, Weijun Fu14, Vania Hungria15, Guldane Cengiz Seval16, Joao Samuel Farias17, Jakub Radocha18, Senem Maral 19, Mehmet Turgut 20, Youngil Koh21, Daniel O'Leary22, Jayr Schmidt Filho23, Raymond Thertulien24, Gang An25, Shang Yi Huang 26, Sebastian Grosicki27, Agata Tyczynska 28, Rahul Banerjee 29, Matthew J Pianko30, Joaquín Martínez-López 31, Pawel Steckiewicz 32, Dai Maruyama33, Kentaro Fukushima34, Albert Oriol35, Jordi Lopez Pardo36, Hartmut Goldschmidt37, Charlotte Pawlyn38, Aurore Perrot39, Elena Zamagni40, Meletios Athanasios Dimopoulos41, Leo Rasche42, Jaszianne Tolbert43, William Terry43, Christelle Courtoux43, Xiao Liu44, Sandra Y Vasey43, Kaitlyn Connors45, Mariacristina Festa46, Christoph Heuck43, Angélique Langlois43, Lisa O’Rourke43, Jiangxiu Zhou43, Xiang Qin43, Jiashen Lu44, Jue Gong43, Diego Vieyra43, Meral Beksac47 Atrium Health/Levine Cancer Institute, Wake Forest University School of Medicine, Charlotte, NC, USA; 2Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, GA, USA; Cancer Center Clínica Universidad de Navarra, Cima, Pamplona, Spain; 4Beijing Chaoyang Hospital, Capital Medical University, Chaoyang District, Beijing, China; 5Hospital Clínico Universitario de Salamanca, Servicio de Salud de Castilla y León (SACYL), Salamanca, Castile and León, Spain; 6Department of Hematology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China; 7Hematology Clinic, University Hospital Hôtel-Dieu, Nantes, France; 8Tel Aviv Sourasky (Ichilov) Medical Center, Tel Aviv Israel; Gray Faculty of Medical & Health Sciences, Tel Aviv University, Tel Aviv, Israel; 9Seoul St. Mary’s Hospital, The Catholic University of Korea, Seoul, Republic of Korea; 10Department of Hematooncology, University Hospital Ostrava, Ostrava Czech Republic; Department of Hematooncology, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic; 11MD Anderson Cancer Center, University of Texas, Houston, Texas, USA; 12Chaim Sheba Medical Center, Ramat-Gan, Israel; Sackler Faculty of Medical and Health Sciences, Tel Aviv University, Israel; 13Division of Hematology and Oncology, Department of Medicine, University of North Carolina School of Medicine, Chapel Hill, NC, USA; 14Department of Hematology, Shanghai Fourth People’s Hospital, School of Medicine, Tongji University, 200434 Shanghai, China; 15Clinica Médica São Germano, São Paulo, Brazil; 16Ankara University Faculty of Medicine, Department of Hematology and Oncology, Ankara University, Ankara, Turkey; 17Liga Paranaense de Combate ao Câncer (LPCC), Curitiba, Paraná, Brazil; 184th Department of Internal Medicine – Hematology, University Hospital Hradec Kralove, Faculty of Medicine in Hradec Kralove, Charles University, Czechia; 19Medipol Mega University Hospital, Bağcılar, İstanbul, Turkey; 20Ondokuz Mayıs University, Samsun Turkey; 21Seoul National University Hospital, Seoul National University, Jongnogu, Seoul, Republic of Korea; 22University of Minnesota, Minneapolis, MN, USA; 23A.C. Camargo Cancer Center, São Paolo, Brazil; 24Novant Health Cancer Institute, Winston Salem, NC, USA; 25Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences, Tianjin, China; 26National Taiwan University Hospital, National Taiwan University College of Medicine, Zhongzheng District, Taipei, Taiwan; 27Department of Cancer Prevention, Medical University of Silesia, Katowice, Poland; 28Medical University of Gdańsk, Department of Hematology and Transplantology, University Clinical Center Gdańsk, Department of Hematology and Transplantology, Gdańsk, Poland; 29Fred Hutchinson Cancer Center, Seattle, WA, USA; 30University of Michigan Health, Ann Arbor, MI, USA; 31Hospital Universitario 12 de Octubre, imas12/ Complutense University of Madrid/CNIO/Madrid, Spain; 32Holy Cross Cancer Center, Department of Hematology and Bone Marrow Transplantation, Kielce, Poland; 33Cancer Institute Hospital, Japanese Foundation for Cancer Research (JFCR), Kotoku, Tokyo, Japan; 34The University of Osaka Graduate School of Medicine, Suita, Japan; 35Institut Català d’Oncologia and Josep Carreras Research Institute, Hospital Germans Trias I Pujol, Badalona, Spain; 36l’Hospital de la Santa Creu i Sant Pau, Barcelona, Catalonia, Spain; 37Internal Medicine V, Hematology, Oncology and Rheumatology, GMMG Study Group, Heidelberg University Hospital and National Center for Tumor Diseases, Heidelberg, Germany; 38The Institute of Cancer Research, London, UK, and The Royal Marsden NHS Foundation Trust, London, UK; 39Universite de Toulouse, Centre Hospitalier Universitaire de Toulouse, Service Hematologie, IUCT Oncopole, Toulouse, France; 40University of Bologna, Bologna, Italy; 41National and Kapodistrian University of Athens, Athens, Greece; 42University Hospital of Würzburg, Würzburg, Germany; 43Johnson & Johnson, Spring House, PA, USA; 44Johnson & Johnson, Shanghai, China; 45Johnson & Johnson, Raritan, NJ, USA; 46Johnson & Johnson, Leiden, Netherlands; 47Istinye University, Ankara University, Ankara, Turkey 1 3

Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

https://www.congresshub.com/EHA2026/ Oncology/Talquetamab/Voorhees The QR code is intended to provide scientific information for individual reference, and the information should not be altered or reproduced in any way.

MonumenTAL-3: Phase 3 Study Design Key inclusion criteria

Primary endpoint

Tal-DP (n=287)

• Age ≥18 years

• PFS by IRC

• Measurable RRMM

Key secondary endpoints

• ≥1 prior LOT including Len and a PI • ECOG PS 0–2 Key exclusion criteria • Refractory to anti-CD38 mAb • Prior GPRC5D, Pom, or T-cell redirecting therapy within 3 months before randomization

Regimen Tal was given SC with step-up dosing at 0.01, 0.06, and 0.4 mg/kg, followed by 0.8 mg/kg

• ORRa

1:1:1 randomizati on N=864

Tal-D (n=287)

• MRD-negative CR • OS

4 Nov 2022 to 13 Mar 2025

C1–2c

• ≥CRa

Additional secondary endpoints

DPd (n=290)

C3–4

• Safety

Tal Q4W permitted with ≥VGPR at cycle 5–6

Tal Q4W required with ≥PR at cycle 7 and beyond

C5–6

C7+

Tal-DP

Q2W QW

Q2W Q2W

Q2W Q4W

Tal-Db

Q2W QW

Q2W Q2W

Q2W Q4W

• Tal: 0.8 mg/kg • Dara: 1800 mg • Pom: - Tal-DP: 2 mg daily (D1–21)d - DPd: 4 mg daily (D1–21)

ClinicalTrials.gov identifier: NCT05455320. aResponse and disease progression were assessed by a blinded IRC per IMWG criteria. bDexamethasone, acetaminophen, and diphenhydramine premedication was required for the first 2 weeks; subsequent dexamethasone was not required thereafter. cPom is given from cycle 2. dPom dose could be increased to 4 mg at the start of cycle 3 day 1 or after per the investigator's discretion. C, cycle; CR, complete response; D, day; ECOG PS, Eastern Cooperative Oncology Group performance status; IMWG, International Myeloma Working Group; IRC, independent review committee; Len, lenalidomide; MRD, measurable residual disease; ORR, overall response rate; OS, overall survival; PR, partial response; Q2W, every 2 weeks; Q4W, every 4 weeks; QW, weekly; SC, subcutaneously; VGPR, very good partial response. Mina R, et al. N Engl J Med 2026; doi: 10.1056/NEJMoa2604657. Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

MonumenTAL-3: Prior Lines of Therapy Tal-DP (n=287)

Tal-D (n=287)

DPd (n=290)

IMiD

287 (100.0)

290 (100.0)

287 (100.0)

288 (99.3)b

33 (11.5)

34 (11.8)

33 (11.4)

3 (1.0)

Any PI

132 (46.0)

121 (42.2)

118 (40.7)

Any IMiD

253 (88.2)

250 (87.1)

250 (86.2)

Len

244 (85.0)

248 (86.4)

243 (83.8)

267 (93.0)

269 (93.7)

271 (93.4)

Characteristic

Tal-DP (n=287)

Tal-D (n=287)

DPd (n=290)

Characteristic

Prior LOT, n, median (range)

2 (1–8)

2 (1–7)

2 (1–8)

Prior exposure, n (%)

Number of prior LOT, n (%) 1a

111 (38.7)

106 (36.9)

114 (39.3)

2 or 3

150 (52.3)

153 (53.3)

148 (51.0)

Anti-CD38 mAb

26 (9.1)

28 (9.8)

28 (9.7)

207 (72.1)

192 (66.9)

196 (67.6)

Prior stem cell transplantation, n (%)

• ≥1/3 of patients had only 1 prior LOT • 11–12% of patients were Dara exposed

Dara Isatuximab Refractory status, n (%)

To last prior LOT

Median of 2 prior LOT and 93.4% of patients were refractory to their last LOT All patients with only one prior LOT were required to be refractory to lenalidomide. b2 participants were not previously exposed to a PI. One of these patients was reported as a major protocol deviation and the second patient was randomized but not treated due to not meeting laboratory criteria 72 hours prior to the planned dosing. Mina R, et al. N Engl J Med 2026; doi: 10.1056/NEJMoa2604657. Adapted with permission © The New England Journal of Medicine (2026). a

Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

Tal-DP vs DPd 24-mo PFS

100

81.3 (95% Cl, 75.8–85.7) Tal-DP Median, NR

51.2 (95% Cl, 44.8–57.1) DPd Median, 24.4 months

HR for progression or death: 0.28 (95% CI, 0.20–0.40) P<0.0001

No. at risk Tal-DP 287 DPd 290

266 249

255 223

240 198

229 218 175 158 Tal-DP

18 21 Months

169 113 DPd

116 81

74 44

32 22

8 2

0 0

212 146

Surviving without progression, %

MonumenTAL-3: PFS (Primary Endpoint) Tal-D vs DPd 24-mo PFS

100

77.6 (95% Cl, 71.7–82.5)

Tal-D Median, NR 51.2 (95% Cl, 44.8–57.1) DPd Median, 24.4 months

HR for progression or death: 0.33 (95% CI, 0.24–0.46) P<0.0001

No. at risk Tal-D DPd

18 21 Months

287 290

262 249

256 223

238 198

225 175

216 207 158 146 Tal-D

159 113

98 81 DPd

62 44

30 22

8 2

0 0

Tal-DP and Tal-D significantly improved PFS vs DPd Clinical cut-off: November 3, 2025. Median follow-up of 24.6 months. The O’Brien-Fleming stopping boundary for superiority was crossed for Tal-DP and Tal-D (P<0.0001 both arms; Tal-DP boundary, P=0.0069; Tal-D boundary, P=0.0145). HR, hazard ratio. Mina R, et al. N Engl J Med 2026; doi: 10.1056/NEJMoa2604657. Adapted with permission © The New England Journal of Medicine (2026). 10 Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

MonumenTAL-3: Treatment Responsea and MRD-Negative CRb Rates OR (95% CI); all P≤0.0005 ORR: 2.27 (1.42–3.61); ≥CR: 4.93 (3.44–7.08)

OR (95% CI)

100 90 80 70 60 50 40 30 20 10 0

88.5 (254/287)

88.2 (253/287)

≥CR 71.1

45.6

53.7 ≥VGPR 85.0

17.4 13.9 3.1 Tal-DP n=287

77.6 (225/290)

≥CR 68.9

≥CR 34.5 ≥VGPR 82.8

10-5: 5.84 (3.94–8.64), P<0.0001; 10-6: 8.05 (5.15–12.57)

sCR CR VGPR PR

24.8 9.7

23.3

23.1

13.9 5.6

20.0

Tal-D n=287

DPd n=290

≥VGPR 57.6

60 MRD-negative CR rate, %

ORR, %

ORR: 2.34 (1.47–3.74); ≥CR: 4.40 (3.08– 6.28)

10-5: 4.70 (3.16–6.98), P<0.0001; 10-6: 6.64 (4.22– 10.43)

10-5 10-6

40 30 20

52.3 47.7

46.3 42.2

10 0

15.9 Tal-DP n=287

Tal-D n=287

10.0

DPd n=290

Tal-DP and Tal-D demonstrated significantly higher ORR, ≥CR, and MRD-negative CR (10-5) rates vs DPd Clinical cut-off: November 3, 2025. Median follow-up of 24.6 months. a Response and disease progression were assessed by IRC per IMWG criteria. bMRD negativity was assessed in bone marrow aspirates with genetic sequencing (clonoSEQ, Adaptive Biotechnologies). MRD-negative CR was defined as the absence of malignant cells at a sensitivity threshold of 10–5 or 10–6, achieved within 3 months prior to achieving CR/sCR or at any time after CR/sCR and before progression or subsequent therapy. DOR, duration of response; NR, not reached; OR, odds ratio; sCR, stringent complete response. Mina R, et al. N Engl J Med 2026; doi: 10.1056/NEJMoa2604657. Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

MonumenTAL-3: OS Tal-DP vs DPd

Tal-D vs DPd

24-mo OS

100

89.2 (95% Cl, 84.9–92.4) Tal-DP DPd 79.1 (95% Cl, 73.7–83.6)

HR for death: 0.47 (95% Cl, 0.30–0.73) P=0.0006 0

1 2

1 2 1 8 1 5 Months

2 4

2 7

3 0

3 3

Tal-DP 287

277

276

269

262

248

238

200

141

DPd 290

278

264

255

245

226

217

173

125

No. at risk

87.9 (95% Cl, 83.0–91.5) Tal-D DPd 79.1 (95% Cl, 73.7–83.6)

Surviving, %

24-mo OS

100

HR for death: 0.51 (95% Cl, 0.33–0.78) P=0.0015 0

1 2

1 1 21 5 Months 8

2 4

2 7

3 0

Tal-D

287

276

275

268

264

256

251

199

130

DPd

290

278

264

255

245

226

217

173

125

No. at risk

Tal-DP and Tal-D resulted in clinically meaningful OS improvement vs DPd, with >87% of patients alive at 2 years; P-values did not cross the prespecified boundary for superiority (0.0001) Clinical cut-off: November 3, 2025. Median follow-up of 24.6 months. Mina R, et al. N Engl J Med 2026; doi: 10.1056/NEJMoa2604657. Adapted with permission © The New England Journal of Medicine (2026). Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

MonumenTAL-3: Conclusions • Synergistic1 Tal-Dara based immunotherapy combinations significantly improved PFS (HR: Tal-DP, 0.28; Tal-D, 0.33), clear benefit across clinically relevant subgroups – Substantial efficacy with Tal-D alone • Clinically meaningful improvements in OS • Safety consistent with individual agents – Favorable infection profile with Tal-D – AEs of interest for Tal infrequently led to treatment discontinuation – Rates of severe neutropenia and severe infections higher in Pom-containing arms

Tal plus Dara ± Pom showed substantial efficacy, supporting new 2L+ SOCs with broad potential for use across diverse practice settings 2L+, second line and beyond; SOC, standard of care. 1. Vishwamitra D, et al. Presented at ASH; December 7–10, 2024; San Diego, CA, USA. Presented by P Voorhees at the European Hematology Association (EHA) 2026 Congress; June 11–14, 2026; Stockholm, Sweden

MajesTEC-9: A Phase 3 Randomized Study of Teclistamab Monotherapy vs Investigator’s Choice of Pomalidomide, Bortezomib, and Dexamethasone or Carfilzomib and Dexamethasone (PVd/Kd) in Patients With Relapsed Refractory Multiple Myeloma Roberto Mina,1,2 Cyrille Touzeau,3 Vania Hungria,4 Ola Landgren,5 Divaya Bhutani,6 Wenming Chen,7 Swarup Kumar,8 Chakra P. Chaulagain,9 Meletios A. Dimopoulos,10,11 Nizar J. Bahlis,12 Senem Maral,13 Niels W.C.J. van de Donk,14 Khalid Saja,15 Raphael Teipel, 16 Miki Ando,17 Dai Wang, Susan Wroblewski,19 18 20 21 Priya Shah, Katherine Chastain,18 Hang Quach Winship Cancer Institute, Emory University, Atlanta, GA, USA; 2AOU Città della Salute e della Scienza di Torino, University of Torino, Torino, Italy; 3University Hospital of Nantes, Nantes, France; Clínica Médica São Germano, São Paulo, Brazil; 5Sylvester Comprehensive Cancer Center, University of Miami, Miami, FL, USA; 6Columbia University Medical Center, New York, NY, USA; 7Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China; 8Neag Comprehensive Cancer Center, University of Connecticut Health, Farmington, CT, USA; 9Cleveland Clinic Florida, Weston, FL, USA; 10National and Kapodistrian University of Athens, School of Medicine, Athens, Greece; 11Korea University, Seoul, South Korea; 12Arnie Charbonneau Cancer Research Institute, University of Calgary, Calgary, AB, Canada; 13Istanbul Medipol University, Istanbul, Turkey; 14Amsterdam University Medical Center, Cancer Center Amsterdam Vrije Universiteit Amsterdam, Amsterdam, The Netherlands; 15Colchester Hospital, East Suffolk and North Essex NHS Foundation Trust, Colchester, UK; 16University Hospital Dresden, Technical University Dresden, Dresden, Germany; 17Juntendo University School of Medicine, Tokyo, Japan; 18Johnson & Johnson, Raritan, NJ, USA; 19Johnson & Johnson, Spring House, PA, USA; 20Johnson & Johnson, High Wycombe, UK; 21Clinical Haematology Service, St. Vincent's Hospital Melbourne, University of Melbourne, Melbourne, VIC, Australia.

https://www.congresshub.com/Oncology/AM2026 /Teclistamab/Mina-MajesTEC-9 The QR code is intended to provide scientific information for individual reference, and the information should not be altered or reproduced in any way.

1 4

Presented by R Mina at the American Society of Clinical Oncology (ASCO) Annual Meeting; May 29–June 2, 2026; Chicago, IL,

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MajesTEC-9: Phase 3 Study Design Key inclusion criteria

Tec

• RRMM • 1–3 prior LOTs including an anti-CD38 mAb and lenalidomide • ECOG PS score of 0–2

n=296 1:1 randomization N=593

Key exclusion criteria

SUDc Tec 1.5 mg/kg

28-day cycles

Tec 3 mg/kg

C1 QW D5

D12

D19

Key secondary endpoints • ≥CRb • OS • MySIm-Q total symptom score Other secondary endpoints • ORR • Safety • PK and immunogenicity Exploratory endpoints • MRD-negative ≥CR (10–5)

PVd/Kda

April 28, 2023– April 3, 2025

• Prior BCMA-directed therapy

Primary endpoint • PFS per IRCb

by investigator’s choice n=297 (69% Kd)

C2 QW D8 D15

D22

C3–C6 Q2Wd D8 D15

D22

C7+ Q4W D8 D15

D22

Tec SC Dex (pre-med)e

Monthly Tec dosing from C7 (earlier if ≥VGPR); steroid free after C1D5 Administered per the approved schedules. Kd was administered either twice weekly (20/56 mg/m2) or once weekly (20/70 mg/m2) depending on the local clinical practice. bDisease progression and response were assessed by an IRC per IMWG 2016 criteria. cPatients received SUD of 0.06 mg/kg and 0.3 mg/kg on D1 and D3, respectively. dPatients with confirmed ≥VGPR could switch to dosing Q4W earlier than C7 per investigator’s discretion. eDexamethasone, acetaminophen, and diphenhydramine pre-med was required on C1 D1, D3, and D5. C, Cycle; CR, complete response; D, Day; Dex, dexamethasone; ECOG PS, Eastern Cooperative Oncology Group performance status; IMWG, International Myeloma Working Group; IRC, independent review committee; MRD, minimal residual disease; MySIm-Q, Multiple Myeloma Symptom and Impact Questionnaire; ORR, overall response rate; PK, pharmacokinetics; pre-med, pre-medication; QW, weekly; Q2W, every 2 weeks; Q4W, every 4 weeks; SC, subcutaneous; SUD, step-up dosing; VGPR, very good partial response. a

Presented by R Mina at the American Society of Clinical Oncology (ASCO) Annual Meeting; May 29–June 2, 2026; Chicago, IL,

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MajesTEC-9: Baseline Demographic and Disease Characteristics Characteristic

Tec (n=296)

PVd/Kd (n=297)

Tec (n=296)

Characteristic

PVd/Kd (n=297)

Baseline ECOG PS score, n (%)

Age Median (range), years ≥75 years, n (%)

70 (34–85) 8 4 (28.4)

70 (36–86)

156 (52.7)

135 (45.5)

89 (30.0)

121 (40.9)

137 (46.1)

19 (6.4)

24 (8.1)

1 (0.3)

168 (56.8)

170 (57.2)

Sex, n (%) Male

150 (50.7)

153 (51.5)

Female

146 (49.3)

144 (48.5)

White

190 (64.2)

198 (66.7)

Asian

62 (20.9)

56 (18.9)

Black or African American

10 (3.4)

Othera

34 (11.5)

33 (11.1)

ISS stage, n (%) I

Race, n (%)

86 (29.1)

82 (27.6)

III

42 (14.2)

4 5 (15.2)

31/292 (10.6)

40/295 (13.6)

5 4 (18.2)

65 (21.9)

BMPCs ≥60%,b n/N (%) Soft-tissue plasmacytomas, n (%) Extramedullary plasmacytomas

19 (6.4)

22 (7.4)

Paraskeletal plasmacytomasc

43 (14.5)

52 (17.5)

High-risk cytogenetics,d n/N (%)

105/294 (35.7)

104/296 (35.1)

Balanced baseline characteristics are reflective of a RRMM population, including high-risk disease “Other” includes American Indian or Alaska Native (Tec, n=2 [0.7%]; PVd/Kd, n=0), not reported (Tec, n=18 [6.1%]; PVd/Kd, n=23 [7.7%]), unknown (Tec, n=7 [2.4%]; PVd/Kd, n=6 [2.0%]), and multiple (Tec, n=7 [2.4%]; PVd/Kd, n=4 [1.3%]). bMaximum value from bone marrow biopsy or bone marrow aspirate was selected if both results were available. cA patient may have both extramedullary and paraskeletal plasmacytomas. dPresence of ≥1 of del(17p), t(4;14), or t(14;16). BMPC, bone marrow plasma cell; ISS, International Staging System. From The New England Journal of Medicine, Touzeau C, et al., Teclistamab in Multiple Myeloma with One to Three Previous Lines of Therapy. Copyright © 2026 Massachusetts Medical Society. Adapted with permission from Massachusetts Medical Society. a

Presented by R Mina at the American Society of Clinical Oncology (ASCO)

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MajesTEC-9: Tec Significantly Improved PFS (Primary Endpoint) Estimated 18-mo PFS

Surviving without progression, %

100 80

69.8% Tec Median, NR

No. at risk Tec PVd/Kd

26.9%

20 0

PVd/Kd Median, 8.2 months

HR, 0.29 (95% CI, 0.23–0.38); P<0.0001a Median follow-up: 17.3 months 0

29 6

258

239

206

172

141

29 7

199

162

112

Months

Tec significantly improved PFS, with a 71% reduction in the risk of disease progression or death in a highly refractory population

The P value crossed the prespecified stopping boundary for superiority for the first interim analysis (P=0.0197). CI, confidence interval; NR, not reached. From The New England Journal of Medicine, Touzeau C, et al., Teclistamab in Multiple Myeloma with One to Three Previous Lines of Therapy. Copyright © 2026 Massachusetts Medical Society. Adapted with permission from Massachusetts Medical Society. a

Presented by R Mina at the American Society of Clinical Oncology (ASCO)

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MajesTEC-9: Grade ≥3 Infections Declined Over Time QW and Q2W Tec dosing Percentage of patients with any onset of ≥1 grade ≥3 infections, %

Q4W Tec dosing

Tec PVd/Kd

33.0

30 23.3

25 20

9.1

PVd/Kd (n/N)a

8.9

7.5

8.8

9.1

5 0

0 Tec (n/N)

14.7

13.9

≤6 mo 96/291 66/2 83

>6-≤12 mo 33/237 15/164

>12-≤18 mo 15/169 6/80

>18-≤24 mo 9/102 5/34

>24 mo 3/33 0/9

Grade ≥3 infections decreased from 6 months, consistent with disease control Includes patients who are in the TEAE-reporting period for the specific window. Noting that patients are counted only once in a window for any given event, regardless of the number of times they actually experienced the event within the specific time window. a

Presented by R Mina at the American Society of Clinical Oncology (ASCO) Annual Meeting; May 29–June 2, 2026; Chicago, IL,

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MajesTEC-9: Key Takeaways 1

Second positive phase 3 study wi t h Tec-based therapy showing significant PFS and OS benefit in 2L+ RRMM

Tec monotherapy significantly improved PFS (HR, 0.29) and OS (HR, 0.60) vs PVd/Kd

The safety profile of Tec was consistent wi t h the known profile

Significant PFS and OS advantage seen in MajesTEC-9, as well as MajesTEC-3,1 support Tec-based therapy as a new 2L+ SOC across practice settings 2L+, second-line or higher; HR, hazard ratio; Kd, carfilzomib and dexamethasone; OS, overall survival; PFS, progression-free survival; PVd, pomalidomide, bortezomib, and dexamethasone; RRMM, relapsed refractory multiple myeloma; SOC, standard-of-care; Tec, teclistamab. 1. Costa LJ, et al. N Engl J Med. 2026;394(8):739-752. Presented by R Mina at the American Society of Clinical Oncology (ASCO) Annual Meeting; May 29–June 2, 2026; Chicago, IL,

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SUCCESSOR-2

Mezigdomide, carfilzomib, and dexamethasone vs carfilzomib and dexamethasone in relapsed/refractory multiple myeloma: results from the phase 3 SUCCESSOR-2 trial Paul G. Richardson,1 Fredrik Schjesvold,2 Chengcheng Fu,3 Monique A. Hartley-Brown,1 Cesar Gomez,4 Donna Reece,5 Gabor Mikala,6 Omar Alkharabsheh,7 Christopher Parrish,8 Darrell White,9 Hang Quach,10 Claudio Cerchione,11 Vania Hungria,12 Amitabha Mazumder,13 Marc S. Raab,14 Albert Oriol,15 Zehua Zhou,16 Alberto Rocci,17 Brian Yu,16 Meletios Athanasios Dimopoulos18 Dana-Farber Cancer Institute, Boston, MA, USA; 2Oslo Myeloma Center, Department of Hematology, Oslo University Hospital, Oslo, Norway; 3The First Affiliated Hospital of Soochow University, Jiangsu Institute of Hematology, Suzhou, Jiangsu, China; 4Norfolk and Norwich University Hospitals NHS Foundation Trust, Norwich, UK; 5The Princess Margaret Cancer Centre, Toronto, ON, Canada; 6Semmelweis University, Budapest, Hungary; 7 USA Health Mitchell Cancer Institute, University of South Alabama, Mobile, AL, USA; 8Leeds Teaching Hospitals NHS Trust, Leeds, UK; 9Queen Elizabeth II Health Sciences Centre, Dalhousie University, Halifax, NS, Canada; 10St Vincent’s Hospital Melbourne, University of Melbourne, Melbourne, VIC, Australia; 11Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, Meldola, Italy; 12São Germano Clinic, São Paolo, Brazil; 13The Oncology Institute of Hope and Innovation, Pasadena, CA, USA;14Heidelberg University Hospital, Heidelberg, Germany; 15Catalan Institute of Oncology and Josep Carreras Institute, Hospital Germans Trias i Pujol, Badalona, Spain; 16Bristol Myers Squibb, Princeton, NJ, USA; 17 Celgene International Sàrl, a Bristol-Myers Squibb Company, Boudry, Switzerland; 18National and Kapodistrian University of Athens, Athens, Greece 1

ASCO 2026, Presentation LBA7506

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SUCCESSOR-2

CELMoD Mechanism of Action •

Mezi and iberdomide (Iber) are CELMoDs that bind cereblon uniquely and more effectively, delivering superior MM cell killing and immune stimulation, compared to IMiDs 1

IMiD

Faster and more complete target protein degradation

Ub Ub Ub Ub

Direct MM cell cytotoxicity and activity in IMiD resistance

Aiolos/ Ikaros

Cereblon (~20% in active state)

T/NK cell activation and mitigation of immune exhaustion

CELMoD Aiolos/ Ikaros

Cereblon (50%-100% in active state)

Single enantiomer/substrate preference potentially minimizing nonhematological effects

• Iber is being investigated in combination with DARA in RRMM in the EXCALIBER-RRMM trial, 2 and as maintenance therapy3 – Iber has the potential to be the first approved CELMoD with FDA Breakthrough Therapy Designation and a PDUFA date of August 17, 2026

• Mezi is being investigated in combination with PIs in two phase 3 trials: SUCCESSOR-1 and SUCCESSOR-2 4 –

Mezi and PIs demonstrated preclinical synergistic antitumor activity superior to POM + PI, 4 with phase 1/2 data of Mezi-d, MeziVd, and MeziKd yielding promising efficacy and a manageable safety profile 5,6

DARA, daratumumab; FDA, Food and Drug Administration; Mezi-d, mezigdomide and dexamethasone; MeziVd, mezigdomide, bortezomib, and dexamethasone; NK, natural killer; PDUFA, Prescription Drug User Fee Act; PI, proteasome inhibitor; POM, pomalidomide; Ub, ubiquitin.1. Watson ER, et al. Science 2022;378:549-553. 2. Lonial S, et al. Future Oncol 2025;24:1761-1769. 3. NCT05827016. 4. Dimopoulos M, et al. Clin Lymphoma Myeloma Leuk 2024;2a:S258. 5. Richardson PG, et al. N Engl J Med 2023;389:1009-1022. 6. Sandhu I, et al. Blood 2024;144:1025.

Richardson PG, et al. ASCO 2026, Presentation LBA7506

SUCCESSOR-2

SUCCESSOR-2: Study Design Stage 2 (efficacy and safety)

Stage 1 (dose optimization)a

Confirmatory analysis group (N = 479)

− Prior treatment with LEN and an anti-CD38 mAb

Randomization 3:3:3:2 (N = 235)

• Adult participants who received ≥1 prior line of antimyeloma therapy with progressive disease

MeziKd at 1.0 mg Mezi (N = 63)b MeziKd at 0.6 mg Mezi (N = 63) MeziKd at 0.3 mg Mezi (N = 64)

Selected Mezi dose

Randomization 3:2 (N = 371)

Key eligibility criteria

Kd (N = 45)b

MeziKdc 1.0 mg Mezi + QW 56 mg/m2 K (N = 225)

Kdc,d BW 56 mg/m2 or QW 70 mg/m2 K (N = 146)

Primary endpoint • PFS per IRC Key secondary endpoint • OS Selected secondary endpoints • Recommended Mezi dose (stage 1) • ORR, VGPR, CR • TTR, DoR • PFS2 • Safety

In the MeziKd arm, patients received: • Mezi 1.0 mg orally once daily on D1–21 of each 28-day cycle • Ke 56 mg/m² IV on D1, 8, and 15 in C1-12 and on D1 and 15 in C ≥ 13 • DEXc 40 mg orally/IV on D1, 8, 15, and 22

NCT05552976. aPatients enrolled in stage 1 on a dose of Mezi not chosen for stage 2 had the option to move to the selected dose if some criteria were met; bPatients from these stage 1 arms were included in the confirmatory analysis groups; cDEX dosing – MeziKd arm: 40 mg, option of 20 mg if > 75 years of age, BMI < 18.5 kg/m2, poorly controlled diabetes, or prior intolerance to steroid therapy; Kd arm: 20 mg, 10 mg option for stated criteria (BW regimen) or 40 mg, 20 mg option for stated criteria (QW regimen); dQW regimen made available July 2023; dK dose on C1D1 was 20 mg/m2. BMI, body mass index; BW, twice weekly; C, cycle; D, day; DEX, dexamethasone; DoR, duration of response; IRC, independent review committee; K, carfilzomib; OS, overall survival; PFS2, second progression-free survival; QW, weekly; TTR, time to response.

Richardson PG, et al. ASCO 2026, Presentation LBA7506

SUCCESSOR-2

SUCCESSOR-2: PFS (Primary Endpoint) Median PFS

Hazard ratio

0.9

18.0 months

HR 0.48

0.8

8.3 months

(95% CI, 0.36–0.63) P < 0.0001

Probability of PFS

1.0

0.7 0.6 0.5 0.4

MeziKd

0.3 0.2

Median follow-up: 10.6 months

0.1 0 No. at risk MeziKd Kd

288 191

250 134

197 90

133 59

81 31

15 18 Time (months) 47 15

27 8

19 3

11 1

6 0

2 0

0 0

In anti-CD38 mAb- and LEN-exposed patients who had received ≥ 1 prior LOT (range 1–9), MeziKd significantly reduced the risk of progression or death by 52% Data cutoff: January 15, 2026. In the confirmatory analysis group, defined as all patients from stages 1 and 2 randomized to 1.0 mg Mezi plus Kd or Kd. CI, confidence interval; HR, hazard ratio.

Richardson PG, et al. ASCO 2026, Presentation LBA7506

Part 1 – Phase 3 Trials in Early Relapse Discussion What do you think about all of these combinations? How do we decide between them? What is shared decision making all about?

Part 2 – High-Risk Myeloma

Updated MajesTEC-3 based on cytogenetic risk

Teclistamab Plus Daratumumab (Tec-Dara) in Patients (Pts) With Relapsed Refractory Multiple Myeloma (RRMM): Analysis of MajesTEC-3 Based on Cytogenetic and Functional Risk Rahul Banerjee,1,2 Niels WCJ van de Donk,3 Roberto Mina,4 Maria Victoria Mateos,5 Nizar J Bahlis,6 Aurore Perrot,7 Ajay K Nooka,8 Jin Lu,9 Charlotte Pawlyn,10,11 Gaston Caeiro,12 Alain Kentos,13 Vania Hungria,14 Anne K Mylin,15 Charlotte Toftmann Hansen,16 Raphael Teipel,17 Britta Besemer,18 Meletios A Dimopoulos,19,20 Elena Zamagni,21,22 Satoshi Yoshihara,23 Kihyun Kim,24 Paul Geerts,25 Elena Van Leeuwen-Segarceanu,26 Agata Tyczynska,27 Markus Hansson,28 Mark Grey,29 Surbhi Sidana,30 Paula Rodriguez-Otero,31 Joaquin Martinez-Lopez,32 Hamza Hashmi,33 Larry D Anderson Jr,34 Claudio Cerchione,35 Salomon Manier,36 Jesús San-Miguel,37 Muhamed Baljevic,38 Robin Carson,39 Weili Sun,40 Kristen Lantz,39 Anne Seifert,41 Deborah Briseno-Toomey,42 Lisa O’Rourke,39 Maria Rubin,43 Diego Vieyra,39 Lijuan Kang,39 Hongmei Xu,44 Ricardo Attar,39 Christopher Chiu,43 Luciano J Costa45 Fred Hutchinson Cancer Center, Seattle, WA, USA; 2University of Washington, Seattle, WA, USA; 3Amsterdam University Medical Center, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands; 4Winship Cancer Institute, Emory University, Atlanta, GA, USA; 5Hospital Universitario de Salamanca, Instituto de Investigación Biomédica de Salamanca, Instituto de Biología Molecular y Celular del Cáncer (Universidad de SalamancaConsejo Superior de Investigaciones Científicas), CIBERONC, Salamanca, Spain; 6Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada; 7Universite de Toulouse, Centre Hospitalier Universitaire, Service d’Hematologie, IUCT Oncopole CRCT, Toulouse, France; 8Emory University, Winship Cancer Institute, Atlanta, GA, USA; 9Peking University People’s Hospital, Peking University Institute of Hematology, National Clinical Research Center for Hematologic Disease, Beijing, China; 10The Royal Marsden NHS Foundation Trust, London, UK; 11The Institute of Cancer Research, London, UK; 12Hospital Privado Centro Medico de Córdoba SA, Córdoba, Argentina; 13Hôpital de Jolimont, Haine-Saint-Paul, Belgium; 14Clinica São Germano, São Paulo, Brazil; 15Rigshospitalet, Copenhagen, Denmark; 16Odense University Hospital, Odense, Denmark; 17 Medizinische Klinik und Poliklinik I Universitätsklinikum Carl Gustav Carus an der Technischen Universität Dresden, Dresden, Germany; 18University Tübingen, Tübingen, Germany; 19National and Kapodistrian University of Athens, School of Medicine, Athens, Greece; 20Korea University, Seoul, South Korea; 21IRCCS Azienda Ospedaliero-Universitaria di Bologna, Istituto di Ematologia “Seràgnoli,” Bologna, Italy; 22Dipartimento di Scienze Mediche e Chirurgiche, Università di Bologna, Bologna, Italy; 23Hyogo Medical University Hospital, Nishinomiya, Japan; 24Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea; 25 Isala Klinieken, Zwolle, The Netherlands; 26St Antonius Hospital Nieuwegein, Nieuwegein, The Netherlands; 27Medical University of Gdansk, University Clinical Center, Gdansk, Poland; 28Sahlgrenska University Hospital, Göteborg, Sweden; 29The Lancashire Haematology Centre, Blackpool Teaching Hospitals NHS Foundation Trust, Blackpool Victoria Hospital, Blackpool, UK; 30Stanford University School of Medicine, Palo Alto, CA, USA; 31 Cancer Center Clínica Universidad de Navarra, Pamplona, Spain; 32Hospital 12 de Octubre, i+12, Universidad Complutense, MIC, Centro Nacional de Investigaciones Oncológicas, CIBERONC, Madrid, Spain; 33Memorial Sloan Kettering Cancer Center, New York, NY, USA; 34Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, TX, USA; 35Istituto Romagnolo per lo Studio dei Tumori "Dino Amadori"-IRST IRCCS, Meldola, Italy; 36CHU Lille, University of Lille, Lille, France; 37Cancer Center Clinica Universidad de Navarra, CIMA, IDISNA, Pamplona, Spain; 38Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN, USA; 39Johnson & Johnson, Spring House, PA, USA; 40Johnson & Johnson, Los Angeles, CA, USA; 41Johnson & Johnson, High Wycombe, UK; 42Johnson & Johnson, Yorba Linda, CA, USA; 43Johnson & Johnson, Raritan, NJ, USA; 44Johnson & Johnson, Shanghai, China; 45University of Alabama at Birmingham, Birmingham, AL, USA.

https://www.congresshub.com/EHA2026/Oncology/ Teclistamab/Banerjee The QR code is intended to provide scientific information for individual reference, and the information should not be altered or reproduced in any way.

Presented by R Banerjee at the 31st European Hematology Association (EHA) Annual Meeting; June 11-14, 2026; Stockholm, Sweden

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MajesTEC-3: Phase 3 Study Design Key inclusion criteria

Tec-Dara

• RRMM • 1-3 prior LOTs including a PI and lenalidomide – Patients with only 1 prior LOT must have been lenalidomide refractory per IMWG criteria • ECOG PS score of 0-2

1:1 randomization N=587

N=291 SC dosing following Dara schedule

DPd/DVd

22 Oct 202129 Sept 2023b

Key exclusion criteria • Prior BCMA-directed therapy • Refractory to anti-CD38 mAbsa

N=296 by investigator’s choicec

Primary end point • PFS per IRC Key secondary end points • ≥CRd and ORRd • MRD negativity (10–5) • OS • MySIm-Q Total Symptom score Other secondary end points • Safety • PK and immunogenicity

Tec 1.5 mg/kg Tec 3 mg/kg Dara 1800 mg

Tec Dara Dex (pre-med)e

Cycle 1 QW D4 D8 SUDf

D1 5

D2 2

Cycle 2 QW D1 D8 5

D2 2

Cycle 3-6 Q2W D1 D8 5

D2 2

Cycle 7+ Q4W D1 D8 5

Steroid sparing after Cycle 1 Day 8, and SC dosing aligned with approved Dara schedule BCMA, B-cell maturation antigen; ≥CR, complete response or better; D, Day; Dara, daratumumab; Dex, dexamethasone; ECOG PS, Eastern Cooperative Oncology Group performance status; IMWG, International Myeloma Working Group; IRC, independent review committee; mAb, monoclonal antibody; MySIm-Q, Multiple Myeloma Symptom and Impact Questionnaire; ORR, overall response rate; PK, pharmacokinetics; pre-med, pre-medication; QW, weekly; Q2W, every 2 weeks; Q4W, every 4 weeks; SC, subcutaneous; SUD, step-up dosing; Tec, teclistamab. aPrior exposure to anti-CD38 mAbs was permitted. bDuring the COVID-19 pandemic. cDPd/DVd were administered per approved schedules. dResponse and disease progression were assessed by a blinded IRC per IMWG criteria. eDexamethasone, acetaminophen, and diphenhydramine pre-medication was required for the first 2 weeks; subsequent dexamethasone was not required thereafter. fPatients received SUD of 0.06 mg/kg and 0.3 mg/kg on Days 2 and 4, respectively. Presented by R Banerjee at the 31st European Hematology Association (EHA) Annual Meeting; June 11-14, 2026; Stockholm, Sweden

D2 2

MajesTEC-3: Subgroup Analysis Cytogenetic Risk a

Functional High Risk

Prespecified and expanded definitions

Explored in patients with 1 prior LOT only

Prespecified high risk (≥1 HRCA)

del(17p) t(4;14) t(14;16) Gain(1q21) Amp(1q21)

Expanded high risk (≥1 HRCA)

Prespecified definition

Expanded definition

Standard risk (0 HRCAs)

Expanded standard risk (0 HRCAs)

High risk (≥1 HRCA)

Expanded high risk (≥1 HRCA)

FHR definition Patients with 1 prior LOT with progressive disease within 18 months of ASCT or start of initial therapy

Number of expanded HRCAs: 0, 1, ≥2b

Endpoints: PFS and MRD-negative ≥CR rate c (10‒5 and 10‒6) ASCT, autologous stem-cell transplant; CR/sCR, complete response/stringent complete response; FISH, fluorescence in situ hybridization; NGF, next-generation flow; NGS, next-generation sequencing; aCytogenetic risk was assessed centrally with FISH or on local FISH or karyotype testing if central FISH was not available. bAlso referred to as “ultra high-risk”. cMRD-negative ≥CR refers to MRD negativity achieved within 3 months prior to achieving CR/sCR or at any time after CR/sCR and before progression or subsequent therapy. Assessed in the MRD NGS primary analysis set, defined as all randomized patients except those recruited in China (due to China instead utilizing NGF for MRD assessment). Presented by R Banerjee at the 31st European Hematology Association (EHA) Annual Meeting; June 11-14, 2026; Stockholm, Sweden

% surviving without progression

MajesTEC-3: PFS by Expandeda Cytogenetic Risk Estimated 36-mo PFS rate

100

90.1%

Tec-Dara, expanded std. risk Tec-Dara, expanded high risk

79.9%

60 40

31.9% Expanded std. risk: Tec-Dara, n=52; DPd/DVd, n=55 HR, 0.12 (95% CI, 0.04-0.30) Expanded high risk: Tec-Dara, n=169; DPd/DVd, n=180 HR, 0.18 (95% CI, 0.12-0.26)

20 0

No. at risk Tec-Dara, expanded std. risk DPd/DVd, expanded std. risk Tec-Dara, expanded high risk DPd/DVd, expanded high risk

52 55 169 180

50 51 147 153

46 46 139 129

45 39 133 110

45 34 133 95

45 32 129 84

44 32 127 71

DPd/DVd, expanded high risk

23.6%

21 24 Months 44 29 124 64

DPd/DVd, expanded std. risk

44 26 123 57

43 22 121 52

42 19 119 45

28 12 80 27

15 8 53 11

8 3 19 8

3 0 6 3

0 0 0 1

0 0

Tec-Dara maintained superior PFS vs DPd/DVd across expanded cytogenetic risk groups, consistent with the overall study effect1 Expanded standard risk: none of del(17p), t(4;14), t(14;16), amp(1q21), or gain(1q21). Expanded high risk: ≥1 of del(17p), t(4;14), t(14;16), amp(1q21), or gain(1q21). 1. Costa LJ, et al. N Engl J Med. 2026;394(8):739-752. a

Presented by R Banerjee at the 31st European Hematology Association (EHA) Annual Meeting; June 11-14, 2026; Stockholm, Sweden

MajesTEC-3: PFS by Number of Expandeda HRCAs 1 HRCA

Estimated 36-mo PFS rate

100

% surviving without progression

90.1%

100 Tec-Dara, 0 HRCAs

Tec-Dara, 1 HRCA

DPd/DVd, 0 HRCAs

Tec-Dara, n=52 DPd/DVd, n=55

HR, 0.12 (95% CI, 0.04-0.30)

Months 52 50 46 45 45 45 44 44 44 43 42 28 15 55 51 46 39 34 32 32 29 26 22 19 12 8

8 3

3 0

0 0

Tec-Dara, ≥2 HRCAs

30.7% DPd/DVd, 1 HRCA

Tec-Dara, n=105 DPd/DVd, n=111

HR, 0.19 (95% CI, 0.11-0.32)

0 3 6 9 12151821242730333639424548 No. at risk Tec-Dara DPd/DVd

76.4%

80 60

31.9%

0 3 6 9 121518212427303336394245 No. at risk Tec-Dara DPd/DVd

82.0%

Estimated 36-mo PFS rate

100

40 20

≥2 HRCAs

Estimated 36-mo PFS rate

% surviving without progression

0 HRCAs

Months 105 93 87 84 84 82 81 79 79 78 78 54 34 111 97 82 71 61 55 49 47 44 41 34 20 10

13 7

3 2

0 1

0 0

Tec-Dara, n=64 DPd/DVd, n=69

13.7%

DPd/DVd, ≥2 HRCAs

HR, 0.16 (95% CI, 0.08-0.29)

0 3 6 9 121518212427303336394245 No. at risk Tec-Dara DPd/DVd

Months 64 54 52 49 49 47 46 45 44 43 41 26 19 69 56 47 39 34 29 22 17 13 11 11 7 1

6 1

3 1

0 0

Tec-Dara consistently improved PFS vs DPd/DVd, including in patients with ultra high-risk RRMM

HRCA number is defined as the number of abnormalities present from the following: del(17p), t(4;14), t(14;16), amp(1q21), or gain(1q21).

Presented by R Banerjee at the 31st European Hematology Association (EHA) Annual Meeting; June 11-14, 2026; Stockholm, Sweden

Part 2 – High-Risk Myeloma - Discussion

Does this combination “overcome” high-risk myeloma? What does this mean for patients with highrisk disease?

Part 3 – Outpatient Approaches to Bispecific Antibodies a. Etentamig as a novel bispecific antibody b. OPTec/OPTal Trial – Outpatient Teclistamab or Talquetamab

Etentamig in patients with relapsed/refractory multiple myeloma (RRMM) with prior exposure to BCMA-targeted therapy Saurabh Chhabra,1 Emma Searle,2 Rakesh Popat,3 Hila Magen,4 Moshe E. Gatt,5 Irit Avivi,6 Muhamed Baljevic,7 Neha Korde,8 Cesar Rodriguez-Valdes,9 Eben Lichtman,10 Cyrille Touzeau,11 Xavier Leleu,12 Anders Svensson,13 Thomas Doerr,13 Jovian Yu,13 Shane Lee,13 Aarif Ahsan,13 Tanya S. Rosenberg,13 Chetasi Talati,13 Shaji Kumar14 Mayo Clinic Arizona, Phoenix, AZ, USA; 2The Christie NHS Foundation Trust, Manchester, UK; 3NIHR UCLH Clinical Research Facility, University College London Hospitals NHS Foundation Trust, London, UK; 4Hematology Chaim Sheba Medical Center, Ramat-Gan, Faculty of Medicine, Tel Aviv University, Tel-Aviv, Israel; 5Department of Hematology, Hadassah Medical Center and Hebrew University of Jerusalem, Jerusalem, Israel; 6Department of Hematology, Tel Aviv Sourasky Medical Center, Tel-Aviv, Israel; 7Vanderbilt University Medical Center, Nashville, TN, USA; 8Memorial Sloan Kettering Cancer Center, New York, NY, USA; 9 Mount Sinai, New York, NY, USA; 10UNC Lineberger Comprehensive Cancer Center, Chapel Hill, NC, USA; 11Department of Hematology, University Hospital Hôtel-Dieu, Nantes, France; 12Service d’Hématologie et Thérapie Cellulaire, CHU and CIC Inserm 1402, Poitiers Cedex, France; 13AbbVie Inc., North Chicago, IL, USA; 14Division of Hematology, Department of Internal Medicine, Mayo Clinic, Rochester, MN, USA. 1

Presented at the 2026 American Society of Clinical Oncology (ASCO) annual meeting, May 29–June 2, 2026; Chicago, IL, United States of America (DV-019198)

MONVISO (NCT05650632): multicenter, open-label, Phase 1b study Treatment arms

Arm B:

Arm A:

BCMA exposure (no SUD)

Etentamig with SUD

Key eligibility criteria

Etentamig monthly dosing

• Adults (aged ≥18 years) with RRMM; ECOG PS ≤2 Arm A Arm B Prior LoT

Arm C: Outpatient etentamig with SUD

Etentamig after prior

≥3

≥2

PI, IMiD, and anti-CD38 mAb

Required

BCMA (CAR-T and/or ADC)

Not allowed

Required

Outpatient administration

Allowed

Prior exposure to:

Cycle 1

Cycle 2+

D 1 SUD

D1 60 mg Q4W

D4 60 mg

Arm A D 601mg

Arm B

D1 60 mg Q4W

Arm D: Outpatient etentamig with SUD in US community sites Endpoints

• Primary safety: o Arm A: Grade ≥2 CRS (Cycle 1) o Arm B: CRS and ICANS • Exploratory efficacy: o ORRb o DoR and PFS

MONVISO defined the OPTIMAL ETENTAMIG INITIATION SCHEDULE to reduce CRS and enable safe outpatient administration for ALL PATIENTS

Prior BCMA CAR-T or BCMA ADC must be completed >6 months or >30 days prior to first dose of study treatment, respectively. Prior BCMA-directed therapies included CAR-T preferred terms: CAR-T cells not otherwise specified, idecabtagene vicleucel, ciltacabtagene autoleucel, or ADC preferred terms: belantamab mafodotin and belantamab. Prior BCMA bispecific or trispecific antibody therapy is not permitted. bIMWG 2016 criteria. ADC, antibody-drug conjugate; BCMA, B-cell maturation antigen; CAR-T, chimeric antigen receptor T cell; CRS, cytokine release syndrome; D, day; DoR, duration of response; ECOG PS, Eastern Cooperative Oncology Group performance status; ICANS, immune effector cell-associated neurotoxicity syndrome; IMiD, immunomodulatory drug; IMWG, International Myeloma Working Group; LoT, line of therapy; mAb, monoclonal antibody; ORR, objective response rate; PFS, progression-free survival; PI, proteasome inhibitor; Q4W, every 4 weeks; RRMM, relapsed/refractory multiple myeloma; SUD, step-up dose. a

Etentamig achieved a 64% ORR in patients whose last LoT was BCMA CAR-T Median (range) follow-upa: 14.3 (0.2–26.1) months Prior BCMA CAR-T 100 90 ORR: ORR: 80 48% 64% 70 60 50 ≥VGPR ≥CR : : 26% 46 40 43% 26 30 ≥VGPR : 20 64% 17 10 18 4 0

Any prior BCMAb

Proportion of patients, %

ORR: 46% ≥CRd: 46%

Overall (n=23)

BCMA CAR-T as last LoT (n=11)

≥VGPRc: 38%

22 16 8 Overall (n=37)

≥C R VGPR

ORR: 58%

≥CRd: 22% ≥VGPRc: 53%

≥CRd: 32%

21 5

Any BCMA-directed therapy as last LoT (n=19)

Median (range) time to first objective response e: 1.0 (0.7–4.6) months

Etentamig monotherapy led to deep responses after any prior BCMA exposure Full analysis set. bEfficacy evaluable population. c≥VGPR: VGPR+CR+sCR. d≥CR: sCR+CR. eFor patients with any prior BCMA who achieved a ≥PR (n=17). BCMA, B-cell maturation antigen; CAR-T, chimeric antigen receptor T cell; CR, complete response; LoT, line of therapy; ORR, objective response rate; PR, partial response; sCR, stringent complete response; VGPR, very good partial response. a

Arm B

Data cutoff: March 31, 2026

MONVISO (NCT05650632): multicenter, open-label, Phase 1b study Treatment arms

Arm A: Etentamig with SUD

Arm B: Etentamig after prior BCMA exposure (no SUD)

Key eligibility criteria

Etentamig monthly dosing

• Adults (aged ≥18 years) with RRMM; ECOG PS ≤1 Arm C Arm D Prior LoT

≥2

Arm C: Outpatient etentamig with SUD

1–3

Prior exposure to: PI, IMiD, and anti-CD38 mAb

Required

BCMA (CAR-T and/or ADC)

Allowedb

Outpatient administration

Required

Cycle 1

Cycle 2+

D SUD 1

D4 60 mg

D1 60 mg Q4W

D 1 SUD

D4 60 mg

D1 60 mg Q4W

Arm C

Required a

Arm D

Arm D: Outpatient etentamig with SUD in US community sites Endpoints • Primary safety: o Arm C and Arm D: Grade ≥2 CRS (Cycle 1) • Exploratory efficacy: o ORRc o DoR and PFS

MONVISO defined the optimal etentamig initiation schedule to reduce CRS and enable SAFE OUTPATIENT ADMINISTRATION for ALL PATIENTS

Prior exposure to at least one of the following drug classes (PI, IMiD, and anti-CD38 mAb) is sufficient. bPrior BCMA CAR-T or BCMA ADC must be completed >6 months or >30 days prior to first dose of study treatment, respectively. Prior BCMA-directed therapies included CAR-T preferred terms: CAR-T cells not otherwise specified, idecabtagene vicleucel, ciltacabtagene autoleucel, or ADC preferred terms: belantamab mafodotin and belantamab. Prior BCMA bispecific or trispecific antibody therapy is not permitted. cIMWG 2016 criteria. ADC, antibody-drug conjugate; BCMA, B-cell maturation antigen; CAR-T, chimeric antigen receptor T cell; CRS, cytokine release syndrome; D, day; DoR, duration of response; ECOG PS, Eastern Cooperative Oncology Group performance status; IMiD, immunomodulatory drug; IMWG, International Myeloma Working Group; LoT, line of therapy; mAb, monoclonal antibody; ORR, objective response rate; PFS, progression-free survival; PI, proteasome inhibitor; Q4W, every 4 weeks; RRMM, relapsed/refractory multiple myeloma; SUD, step-up dose. a

Prophylactic tocilizumab use with etentamig resulted in a 0% CRS incidence

Incidence of CRS (%)

100 80 60

No SUD

1 SUD

Arm B

Arm A

Arm C

30%

27%

N=23

N=60

n=16

+ Prophylactic tocilizumaba

Grade 1 Grade 2

57%

40 20

1 SUD

45 N=42

Etentamig’s safety profile can overcome bispecific antibody implementation barriers and improve accessibility across treatment settings Prophylactic tocilizumab given per investigator discretion. CRS, cytokine release syndrome; dex, dexamethasone; mod, modified; SUD, step-up dose.

Arm A data cutoff: July 12, 2024; Arm B data cutoff: March 31, 2026; Arm C data cutoff: March 31, 2026.

Outpatient etentamig initiation is feasible across treatment settings Arm C

Arm Cc

Safety

Overall (N=60)

Prophylactic tocilizumab (n=16)

CRS incidence, n (%)

16 (26.7)

Median time to CRS onset,d (range) hours

17.1 (5.9–34.9)

N/A

5.3 (3.0–24.7)

N/A

Baseline characteristics

Overall (N=60)

Prophylactic tocilizumab (n=16)

Median age, years (range)

76 (45–90)

74 (56–90)

Female, n (%)

29 (48.3)

6 (37.5)

Race,a n (%) White Black/African American Asian

49 (83.1) 9 (15.3) 1 (1.7)

14 (87.5) 2 (12.5) 0

Median time to CRS resolution,e (range) hours Rate of CRS recurrence,f n (%)

0 (0)

ECOG PS [at entry], n (%) 0 1

21 (35.0) 39 (65.0)

5 (31.3) 11 (68.8)

CRS managed outpatient, n (%)

8 (13.3)

Cytogenetic risk, n (%) High risk

Tocilizumab for CRS management,g n (%)

7 (11.7)

15 (36.6)

5 (38.5)

Dexamethasone for CRS management,g n (%)

3 (5.0)

3 (2–9)

4 (2–9)

Any grade ICANS,h n (%)

1 (1.7)

Number of prior LoT, median (range)

Rapid CRS resolution without any recurrence supports outpatient etentamig treatment Note: Percentages calculated on nonmissing values. aRace data missing for 1 patient in Arm C overall. bCytogenetic risk evaluable population. High risk: ≥1 of the following genetic abnormalities detected: t(4;14), t(14;16), or del(17p). cMedian (range) duration of follow up was 8.3 (0.7–16.9) months. dTime to onset of AE is calculated by (start date/time of AE –date/time of last previous dose). e Time to resolution of AE is calculated as (end date/time of AE – start date/time of AE). fNo CRS recurrence was observed after the Cycle 1 SUD or in any subsequent cycle. gCRS management for Cycle 1 SUD and Cycle 1 full dose. hOne Grade 2 ICANS events was reported. AE, adverse event; CRS, cytokine release syndrome; ECOG PS, Eastern Cooperative Oncology Group performance status; ICANS, immune effector cell-associated neurotoxicity syndrome; LoT, line of therapy; N/A, not applicable; SUD, step-up dose.

Arm C

Data cutoff: March 31, 2026

Conclusions Etentamig treatment after BCMA exposure led to deep and durable responses Outcomes are encouraging post-BCMA CAR-T, supporting immediate etentamig use following BCMA CAR-T therapy Prophylactic tocilizumab resulted in a 0% CRS incidence Etentamig’s optimized monthly dosing with 1 SUD and safety profile can overcome bispecific antibody implementation barriers and improve accessibility across treatment settings Convenient Q4W dosing combined with 1 SUD has been implemented across etentamig’s multiple myeloma and AL amyloidosis clinical trial programs Scan QR code to download an electronic version of this presentation: Copies of this slide deck obtained through Quick Response (QR) Code are for personal use only and may not be reproduced without permission from ASCO ® or the author of this slide deck. QR Code expiration: April 29, 2027 To submit a medical question, please visit www.abbviemedinfo.com

AL, amyloid light chain; BCMA, B-cell maturation antigen; CAR-T, chimeric antigen receptor T cell; CRS, cytokine release syndrome; Q4W, every 4 weeks; SUD, step-up-dose.

OPTec/OPTal: A Phase 2 study to evaluate outpatient (OP) step-up administration of teclistamab (Tec) or talquetamab (Tal) with prophylactic tocilizumab (prophyToci) in patients (pts) with relapsed/refractory multiple myeloma (RRMM) Peter Forsberg, MD1, David Andorsky, MD2, Robert Rifkin, MD, FACP3, Christopher Yasenchak, MD4, Mohit Narang, MD5, Jason Melear, MD6, Henning Schade, MD1, Mitul Gandhi, MD7, Gary Simmons, DO, MSHA8, Muhamed Baljevic, MD, FACP9, Habte Yimer, MD10, Kruti Patel, MD11, Amanda GillespieTwardy12, Sudhir Manda, MD13, John Renshaw, MD14, Jessica Fowler, PhD15, Thomas S. Lin, MD, PhD15, Tonya Le Blanc15, and Weiming Xu, MD, PhD16

Colorado Blood Cancer Institute, Denver, CO; 2Rocky Mountain Cancer Centers, Boulder, CO; 3UCHealth Yampa Valley Medical Center, Steamboat Springs, CO; 4Willamette Valley Cancer Institute and Research Center, Eugene, OR; 5Maryland Hematology Oncology Associates, Columbia, MD; 6Texas Oncology PA, Austin, TX; 7Virginia Cancer Specialists, Gainesville, VA; 8Virginia Oncology Associates, Norfolk, VA; 9Vanderbilt University Medical Center, Nashville, TN; 10 Texas Onc Tyler, Tyler, TX; 11OHC (Oncology Hematology Care)/US Oncology Network, Cincinnati, OH; 12Blue Ridge Cancer Care, Roanoke, VA; 13TMC Health Cancer Center, Tucson, AZ; 14Texas Oncology–San Antonio Medical Center, The US Oncology Network, San Antonio, TX; 15Johnson & Johnson US Hematology Medical Affairs, Horsham, PA; 16Sarah Cannon Research Institute, Development Innovations, Nashville, TN 1

PRESENTED BY:

Peter Forsberg, MD; OPTec/OPTal

Key Takeaways

Prophylactic tocilizumab before outpatient step-up dose (SUD) 1 of Tec or Tal reduced the cytokine release syndrome (CRS) incidence by approximately 5-fold

The addition of prophyToci had no impact on safety and efficacy

Data support administration of bispecific antibodies (bsAbs) in the community-based outpatient setting

PRESENTED BY:

Peter Forsberg, MD; OPTec/OPTal

Part 3 – Outpatient Approaches to Bispecific Antibodies - Discussion What do you think about the less frequent dosing and using prophylactic tocilizumab? Will this facilitate the use of bispecific antibodies in the community? What could this mean for patients and care partners? © 2026, International Myeloma Foundation. All rights reserved. IMF Confidential

Part 4 – Future Approaches to Myeloma

a. Arlo-cel a CAR T targeting GPRC5D b. in vivo CAR T Cell therapy and Allo CAR T

Arlocabtagene autoleucel (arlo-cel), a GPRC5D-targeted CAR T cell therapy for patients with relapsed/refractory multiple myeloma: updated phase 1 safety and efficacy results in patients with 1–3 prior regimens Susan Bal,1 Myo Htut,2 Jesus G. Berdeja3, Larry D. Anderson, Jr,4 Adriana C. Rossi,5 Tara Gregory,6 Luciano J Costa,1 Hongxiang Hu,7 Ziyan Guo,7 Jinjie Chen,7 Kristina M. Jordahl,7 Naomey Sarkis,7 Safiyyah Ziyad,7 Wei-Ming Kao,7 Allison J. Kaeding,7* Michael R. Burgess,7 Omar Nadeem8 University of Alabama at Birmingham, Birmingham, AL, USA; 2City of Hope Comprehensive Cancer Center, Duarte, CA, USA; 3GrecoHainsworth Tennessee Oncology Centers for Research, Nashville, TN, USA; 4Hematologic Malignancies and Cellular Therapy Program, Simmons Comprehensive Cancer Center, UT Southwestern Medical Center, Dallas, TX, USA; 5Icahn School of Medicine at Mount Sinai, New York, NY, USA; 6Colorado Blood Cancer Institute, Sarah Cannon Cancer Network, Denver, CO, USA; 7Bristol Myers Squibb, Princeton, NJ, USA; 8 Dana-Farber Cancer Institute, Boston, MA, USA *At time of study. 1

Patient disposition Enrolled and underwent leukapheresis (N = 31)

All-treated population (N = 31)

Patients with 1–3 prior lines of therapy

n = 19 received optional systemic bridging therapy

Median (range) follow-upb 24.0 (3.8 − 26.0) months

Efficacy-evaluable populationa (n = 24)

Patients without measurable disease after bridging therapy (n = 7)

Arlo-cel manufacturing was successful for all patients (100%); all patients received a dose of 150 106 cells Data cutoff: February 17, 2026. aEfficacy-evaluable population defined as patients who had received arlo-cel, had measurable disease at the most recent disease assessment prior to arlo-cel infusion, and had ≥ 1 post infusion disease-response assessment. bFor all-treated and efficacy-evaluable populations. arlo-cel, arlocabtagene autoleucel.

Bal S, et al. EHA 2026

Response rates ORR 94%

SD/MR

VGPR

CR/ sCR

Death

Ongoing

PD Event

Patients with response, %

100 80

61%

60 40

end of study F/U

10% 23%

20 0

≥ CR 71% 3

Time to Progression (Months)

All treatedb (N = 31)

All treated Series1 (N = 31) sCR

VGPR

18-mo DOR, % mTTR, mo (IQR)

64.6 0.99 (0.95−1.68)

MRD evaluable (n = 20) MRD-negative CR ratec • 65% (95% CI, 40.8−84.6)

Deep and durable responses were observed; 94% ORR, 71% CRR, and 65% 18−mo DOR Data cutoff: February 17, 2026. Efficacy-evaluable population defined as patients who had received arlo-cel, had measurable disease at the most recent disease assessment prior to arlo-cel infusion, and had ≥ 1 post-infusion disease-response assessment. a ORR and CRR for efficacy evaluable population (n=24) was 96% and 67%, respectively. bThe 18-month DOR and mTTR (IQR) were 57% and 0.99 (0.95−1.05) months, respectively for the efficacy evaluable population. cMRD-negative CR rate defined as the proportion of patients who achieve at least CR and MRD-negative status at a 10 -5 sensitivity level. CI, confidence interval; CR, complete response; F/U, follow-up; mDOR, median duration of response; MR, minimal response; MRD, minimal residual disease; mTTR, median time to response; NE, not evaluable; ORR, overall response rate; PD, progressive disease; PR, partial response; sCR, stringent complete response; SD, stable disease; VGPR, very good partial response.

Bal S, et al. EHA 2026

Treatment-related adverse events (TRAEs) of special interest All treated (N = 31)

TRAE, n (%)

Any grade

Grade 3/4

30 (96.8)

15 (48.4)

CRS

26 (83.9)

ICANS

3 (9.7)

HLH

Other select neurotoxicitya

2 (6.5)

OTOT event (cumulativeb)

17 (54.8)

Any TRAE TRAEs of special interest

No grade ≥3 TRAEs of special interest were reported; all CRS and ICANS resolved Data cutoff: February 17, 2026. All-treated population. Medical Dictionary for Regulatory Activities (MedDRA) version 28.1. Common Terminology Criteria for Adverse Events (CTCAE) version 5.0; CRS graded using Lee DW, et al Blood. 2014;124(2):188-95. a Includes ataxia, neurotoxicity, nystagmus, dysarthria, diplopia, dysmetria, and gait disturbance (excluding dizziness). bCumulative events include selected preferred terms from skin and subcutaneous tissue disorders and tongue conditions (within gastrointestinal disorders), as well as ad hoc preferred terms (ageusia, dysphagia, dysgeusia, and taste disorder), and excluded preferred terms include night sweats, dermal cyst, hyperhidrosis, and skin mass. CRS, cytokine release syndrome; HLH, hemophagocytic lymphohistiocytosis; ICANS, immune effector cell-associated neurotoxicity syndrome; OTOT, on-target/off-tumor; TRAE, treatment-related adverse events.

Bal S, et al. EHA 2026

Select on-target off-tumor events Patients, n (%)

Skin

N=31

With event Grade 1

8 (25.8) 6 (19.4)

Grade 2

2 (6.5)

Oral

With event Grade 1 Grade 2

Nail

With event Grade 1 Grade 2

12 (38.7) 10 (32.3) 2 (6.5)

With event Grade 1

1 (3.2) 1 (3.2)

Grade 2

Weight loss

13 (41.9) 10 (32.3) 3 (9.7)

Resolved, %a

Time to resolution (days) median (IQR)

OVERALL

88%

38% without intervention

77%

69% without intervention

92%

92% without intervention

100%

without intervention

(14−97)

(38−92)

118

(89−184)

81 -10 10

90 110 130 150

Time from onset (days)

OTOT events and weight loss were all low-grade (grade 1/2); most events resolved Data cutoff: February 17, 2026. All-treated population. Time to resolution was calculated per episode; only resolved episodes are considered. Multiple events occurring within 1 day from each other are considered as 1 episode. Medical Dictionary for Regulatory Activities (MedDRA) version 28.1. Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. a Percent resolved calculated based on patients with an event. IQR, interquartile range; OTOT, on-target/off-tumor.

Bal S, et al. EHA 2026

Conclusions • In this final analysis of Cohort C from the phase 1 study of arlo-cel in patients with 1−3 prior LoT, the safety profile was consistent with previous reports; no new safety signals were observed ― No high-grade infections, OSN, CRS, ICANs, or OTOT AEs were reported; non-hematologic TEAEs were primarily low-grade • Arlo-cel demonstrated deep and durable responses following a single infusion ― High response rates were observed; ORR 94% and CRR 71% ― 18-month PFS and OS rates were 62.6% and 100%, respectively

These results support arlo-cel as a potentially efficacious early-line treatment option for patients with RRMM

Ongoing studies

(NCT06297226)

Phase 2 study of arlo-cel in quadruple class–exposed patients and ≥ 3 prior LOT

(NCT06615479)

Phase 3 study of arlo-cel vs SOC in patients with 1–3 prior LOT, including lenalidomide

AE, adverse event; arlo-cel, arlocabtagene autoleucel; BCMA, B-cell maturation antigen; CAR, chimeric antigen receptor; CRS, cytokine release syndrome; GPRC5D, G protein–coupled receptor class C group 5 member D; ICANS, immune effector cell-associated neurotoxicity syndrome; LoT, lines of therapy; ORR, overall response rate; OS, overall survival; OTOT, on-target/off-tumor; PFS, progression-free survival; RRMM, relapse/refractory multiple myeloma; SOC, standard of care.

Bal S, et al. EHA 2026

Updated results from inMMyCAR, the ongoing first-in-human Phase 1 study of KLN-1010 in patients with relapsed and refractory MMSpencer , Sueh-Li Lim , Stephanie Talam , Phoebe Joy Ho , Andrew 1,2

3,4

Hannah Pahl5, Dharmesh Dingar6, Scott Currence6, Travis Quigley6, Simon Harrison7,8

Royal Prince Alfred Hospital, Sydney, Australia; 2University of Sydney, Sydney, Australia; 3Monash University, Australian Centre for Blood Diseases, Melbourne, Australia; 4Alfred Hospital, Malignant Haematology, Transplantation and Cellular Therapies Service, Melbourne, Australia; 5Peter MacCallum Cancer Centre, Parkville Cancer Clinical Trials Unit, Melbourne, Australia; 6Kelonia Therapeutics, Inc., Boston, MA, United States; 7Peter MacCallum Cancer Centre, Centre of Excellence for Cellular Immunotherapy, Melbourne, Australia; 8Sir Peter MacCallum Dept of Oncology, University of Melbourne, Parkville, Australia 1

Active Study Locations

• The Alfred Hospital (Australia) • City of Hope, Duarte (USA) • Emory University Hospital (USA) • Massachusetts General Hospital (USA) • Peter MacCallum Cancer Centre (Australia) • Providence Portland Medical Center (USA) • Royal Prince Alfred Hospital (Australia) • Stanford University (USA)

Study Sponsor

• Kelonia Therapeutics

Collaborations

• IQVIA Biotech • Adora People & Medical • Bluprint Oncology We Thank the Patients, Their Families, and Caregivers for Their Contribution to This Ongoing Study

Presented at the 2026 ASCO Annual Meeting; May 29-June 2, 2026; Chicago, IL, USA

Expanding the reach of CAR-T cells with in vivo gene delivery

KLN-1010: A modified LVV generating anti-BCMA CAR-T cells in vivo3

In vivo CAR T with lentiviral particles1,2

VSV-G mutation Detargeted fusogen,

Reduced cost of goods and manufacturing Simplified logistics to expand access Elimi nates precondition ing chemothera py

T cell retargeting with CD3 tropism molecule

CAR molecule

In vivo CART generation

Proprietary, fully-human BCMA scFv Direct infusion

4-1BB CD3ζ

No ex vivo culture may increase T-cell fitness BCMA, B-cell maturation antigen; CAR, chimeric antigen receptor; CD3, cluster of differentiation 3; CD3ζ, cluster of differentiation 3 zeta chain; LVV, lentiviral vector; scFv, single-chain variable fragment; VSV-G, vesicular stomatitis virus glycoprotein. 1. Bot A et al. Nat Rev Drug Discov. 2025 Sep 30. doi: 10.1038/s41573-025-01291-5; 2. Najibi AJ. T cell-specific in vivo transduction with preclinical candidate KLN-1010 generates BCMA-directed CAR-T cells with potent anti-multiple myeloma activity (abstract #48). Poster presented at: AACR Annual Meeting; April 5-10, 2024. 3. Wood JT et al. Toward treatment with gene-modified B cells engineered in vivo using iGPS particles (abstract #1281). Poster presented at: ASGCT 28th Annual Meeting; May 1317, 2025.

Deep, ongoing BM MRD-negative responses ORR (N=18) observed

Dose (IU/kg)

100 80

% of all patients

60 40

6 × 106

100%

100

(n=6)

22%

67%

22%

60 40

50%

PR VGPR

Median duration of follow-up: 2.8 months

4 × 10

VGPR

MRD-negative 10-6

sCR

MRD pending

MRD-negative 10-5

MRD-negative 10-5 (indeterminate 10-6) Progression

Best change from baseline (%)

SD 6

MRD positive

sBCMA (n=9)

1 11

Months post treatment

sCR

50 25

MRD-negative 10-5 or deeper

sFLC (n=16)

-50

-50 -75

-25

Response ongoing

Patients with ≥4 mo33% follow-up

Best change from baseline (%)

All patients

100%

20 0

% of MRD-evaluable patients

2× 107

MRD-negative BM responses (n=14)

-75

-100

Patients

BM, bone marrow; CR, complete response; D, study day; infectious unit; M,marrow study month; minimal NGS, -6 includes MRD indeterminate at 10 NGS result pending or IU, indeterminate. Bone biopsy MRD, performed M1,residual M3, M6,disease; M12, M18, andnext generation sequencing; ORR, overall response rate; PR, partial response; sCR, stringent complete response; sBCMA, soluble B-cell maturation antigen; SD, stable disease; sFLC, serum free light chain; VGPR, very good partial response. MRD-negative BM responses reported in n=13 patients with at least one evaluable post-treatment bone marrow assessment. M24. sBCMA data available in n=9 patients; sFLC data available in n=16 patients.

Conclusions  Lymphodepletion not required for in vivo CAR-T cell generation, expansion and persistence  Favorable safety and tolerability profiles using off-the-shelf product suggest outpatient dosing is feasible  All CRS events were Grade 1-2 with one Grade 3 ICANS event limited to 3 days; no delayed neurotoxicity was observed  Cytopenias and Grade 3-4 infections were notably limited  No IRRs observed following dexamethasone premedication implementation; SRC has approved outpatient dosing

 100% MRD-negative responses showed deepening of IMWG response  MRD-negative BM responses were sustained through 6 months  Earliest patients treated now in ongoing response at and beyond 9 months post-dosing  Similar persistent responses have been associated with durable remissions using ex vivo CAR-T cells in RRMM BM, bone marrow; CAR, chimeric antigen receptor; CRS, cytokine release syndrome; ICANS, immune effector cell-associated neurotoxicity syndrome; IMWG, International Myeloma Working Group; IRR, infusion-related reaction; MRD, minimal residual disease; RRMM, relapsed and refractory multiple myeloma; SRC, safety review committee.

CB-011, an allogeneic anti-BCMA CAR-T cell therapy with immune cloaking, in patients with relapsed/refractory multiple myeloma Long-term follow-up results from the CaMMouflage phase 1 trial

Binod Dhakal, Adriana Rossi, William Clark, Daniel Sherbenou, David Siegel, Manisha Bhutani, Faiz Anwer, Sham Mailankody, James Essell, Jay Spiegel, Douglas Sborov, Donna Marcy, Ine-Mari Bornman, Chris Holland, Jeffrey Hellman, Elizabeth Garner, Pingping Mao, Eric Stawiski, Enrique Zudaire, Tonia Nesheiwat, Socorro Portella, Wellington Sundar Jagannath, Luciano J. Costa EHAMendes, Oral Abstract #: S201

CB-011: a differentiated allogeneic CAR-T cell therapy for r/r MM B2M–HLA-E protein fusion insertion

CB-011 Manufactured from healthy donor T cells with 4-1BB Vispa-cel costimulatory domain Manufactured from

healthy donor T cells

Anti-BCMA CAR insertion

TCR knockout

B2M knockout

Rossi A et al. TANDEM 2026 presentation RDE: recommended dose for expansion r/r MM: relapsed/refractory multiple myeloma 1

CB-011 immune cloaking strategy enhances functional persistence and antitumor activity

450M cell dose selected as RDE following deep, durable responses and manageable safety profile1

CB-011 demonstrates potential to address unmet need in both BCMAnaïve and BCMA-exposed patients

CB-011 induces deep, durable responses at 450M in BCMAnaïve patients

83% ≥CR rate

92% ORR (11/12)

Patient ID

EMD (Y/N)

MRD neg1 (Y/N)

050-0003

008-0002

009-0003

030-0002

050-0006

009-1004

039-0001

Y N

Y Y

N Y N Y

039-0002 039-0003 016-0002 050-0004 008-0003

Y N

Day 28

(10/12)

3 mo

6 mo

9 mo

12 mo

91% MRD neg

(10/11 evaluable patients) 15 mo

18 mo

sCR: stringent CR CR: complete response VGPR: very good PR PR: partial response PD: progressive disease Withdrawal from trial Death

One patient who had previously withdrawn from the trial died on day 90 of treatment-related ICAHT; one patient died of pneumonia on day 50 (not treatmentrelated); one patient developed respiratory acidosis on Day 466 (not treatment-related) Data shown are from BCMA-naïve patients dosed at 450M cell dose with LD regimen of 500 mg/m2 cy and 30 mg/m2 flu daily x 3 days CONFIDENTIAL | EHA Presentation | June 2026 1 MRD negative at ≤10-5 ©2026 Caribou Biosciences, Inc. ICAHT: immune effector cell-associated hematotoxicity; M: million; mo: month; MRD: minimal residual disease; ORR: overall response rate; PFS: progression-free survival

Part 4 – Future Approaches to Myeloma Discussion

What excited you about these future approaches?

Key Takeaways from Relapsed Therapy 1. Talquetamab + Daratumumab +/- Pomalidomide is a highly effective regimen 2. Teclistamab monotherapy is more effective than triplets and feasible in early relapse 3. Cytogenetic risk status subgroup analysis of TEC-3 suggests teclistamabdaratumumab can overcome much of high risk disease 4. Etentamig is a novel bispecific with little/no step-up dosing, outpatient monthly dosing with potential of no CRS with prophylactic tocilizumab 5. CelMods are being developed that are more potent than IMiDs in combinations, include Mezigdomide-Carfilzomib 6. A GPRC5 targeted CAR T is being developed with promising efficacy 7. in vivo CAR T is feasible with less toxicity than ex vivo CAR T and promising efficacy © 2026, International All rightsmeans reserved. IMF Confidential 8. Allo CARMyeloma T isFoundation. novel of delivering CAR T

Part 5 – This JUST in! Updates since ASCO/EHA... a. Isatuximab On Body Injector (OBI) b. Iberdomide, Daratumumab, Dexamethasone c. ENDURANCE trial results – maintenance lenalidomide

Isatuximab SC OBI Preparation and Administration The on-body delivery system is an investigational device evaluated in phase 3 trials for hands-free delivery of the fluid bolus over a shorter duration than IV infusion

Step 1: Fill

Step 2: Place on patient

Step 3: Administer

OBI, on-body injector; SC, subcutaneous. Images courtesy of Sikander Ailawadhi, MD. Ailawadhi S, et al. J Clin Oncol. 2025;43:2527-2537. These materials are provided to you solely as an educational resource for your personal use. Any commercial use or distribution of these materials or any portion thereof is strictly prohibited.

Patient and HCP Preference for Isatuximab OBI Versus Manual Administration in the IZALCO Trial Patient preference

HCP preference

OBI

74.5%

OBI

Manual

17.0%

Manual

No preference

8.5%

No preference

From C7, after receiving SC or OBI, all patients could choose either method

78.9% 0% 21.1%

90% chose to

continue with the OBI

Iberdomide – the first CELMod is approved!

SUCCESSOR-2

CELMoD Mechanism of Action •

Mezi and iberdomide (Iber) are CELMoDs that bind cereblon uniquely and more effectively, delivering superior MM cell killing and immune stimulation, compared to IMiDs 1

IMiD

Faster and more complete target protein degradation

Ub Ub Ub Ub

Direct MM cell cytotoxicity and activity in IMiD resistance

Aiolos/ Ikaros

Cereblon (~20% in active state)

T/NK cell activation and mitigation of immune exhaustion

CELMoD Aiolos/ Ikaros

Cereblon (50%-100% in active state)

Single enantiomer/substrate preference potentially minimizing nonhematological effects

• Mezi is being investigated in combination with PIs in two phase 3 trials: SUCCESSOR-1 and SUCCESSOR-2 4 –

Richardson PG, et al. ASCO 2026, Presentation LBA7506

Overall Survival – Fixed duration vs Continuous Lenalidomide

Part 5 – This JUST in! Updates since ASCO/EHA... - Discussion What do you think of the On-Body Injector? How will Iberdomide be an attractive option in relapse? Will ENDURANCE mean less maintenance therapy? © 2026, International Myeloma Foundation. All rights reserved. IMF Confidential

AUDIENCE Q & A

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155+ Support Groups Across the US and beyond

We are happy to help connect you with an existing support group or help you form a new one! SGTeam@myeloma.org

SHARED EXPERIENCE GROUPS Shared experience groups are designed as a supplemental support for specific populations of patients, in addition to their local Support Groups MM Families For patients & care partners with young children Living Solo & Strong For patients without a care partner

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Living with High-Risk Multiple Myeloma For high-risk myeloma patients & care partners

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Beyond the Data: A Patient & Care Partner Conversation on Myeloma Research from ASCO