Investor Presentaiton
iber/mezi
Hematology
Reblozyl BET Inhibitor
Breyanzi golcadomide Abecma
alnuctamab
GPRC5D
BMS-986158: Potential-best in-class BET inhibitor with
broad applicability
BETi Mechanism of Action
Unmet need in MF remains for new treatments which
lead to strong & durable spleen volume reduction,
symptom improvement, and extended survival
BETI: Phase 1/2 study ongoing in MF2
Dose Escalation Phase
Dose Expansion Phase
Crosstalk
JAK21
BETi
1L MF (rux-naïve)
BMS-158 + ruxolitinib 15 mg BID
JAK-STAT signaling
BET (BRD2,BRD3, BRD4)
H3K6me1
H3K27ac
NF-kB
activation
Inflammatory
NF-KB1
genes
TGF-B
Proinflammatory
cytokines
GLI1
Bone marrow fibrosis
Inflammation signals
Extramedullary hematopoiesis
BET Inhibitors alone and in combination with JAK
inhibitors have shown clinical benefit in patients with MF1
Ill Bristol Myers Squibb™
1. Mascarenhas J, et al. Blood 2019; 134(suppl 1):670. 2. NCT04817007
1L MF (rux-naïve)
BMS-158 RP2D + ruxolitinib 10 mg BID
1L MF (add-on to rux)
BMS-158 RP2D + ruxolitinib previously
tolerated dose
2L MF (rux-exposed)
BMS-158+ fedratinib 400 mg QD
2L MF (rux-exposed)
BMS-158 RP2D + fedratinib 400 mg QD
•
•
2L MF (rux-exposed)
BMS-158 RP2D monotherapy
Primary Endpoint: Safety, tolerability, MTD and/or RP2D
Key Secondary Endpoint: Preliminary efficacy based on SVR
Proof-of-concept data anticipated in 2024
Not for Product Promotional Use
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