Syndax Pharmaceuticals, Inc. · NASDAQ:SNDX
Syndax Pharmaceuticals — Investor Day (July 2026)
81 slides from Syndax Pharmaceuticals's investor day presentation, Jul 14, 2026
Slide 1: Syndax 2026 R&D Event
Syndax 2026 R&D Event July 14, 2026 Exhibit 99.2
Slide 2: Forward-looking statements disclosure
Forward-looking statements disclosure This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Words such as "may," "will," "expect," "plan," "anticipate" and similar expressions (as well as other words or expressions referenci
Slide 3: Syndax is delivering for patients and driving substantial long-term value
Syndax is delivering for patients and driving substantial long-term value Proven ability to translate scientific discoveries into novel therapies, with 3 FDA approvals between 2 drugs and thousands of patients treated Fully integrated biotech with deep expertise and strong partnerships with leading
Slide 4: Advancing the standard of care with two first- and best-in-class medicines
Advancing the standard of care for R/R NPM1m AML and KMT2Ar acute leukemia and chronic GVHD with two first- and best-in-class medicines Revuforj® (revumenib) and Niktimvo™ (axatilimab-csfr) were both annualizing at ~$200M as of 1Q26, advancing the company towards profitability First and only menin i
Slide 5: Syndax is driving innovation for patients
Syndax is driving innovation for patients
Slide 6: Expanding our pipeline to fuel the next phase of innovation and growth
Expanding our pipeline to fuel the next phase of innovation and growth R/R, relapsed or refractory; NSCLC, non-small cell lung cancer + Ongoing trials across the acute leukemia treatment continuum Positioned to be the 1st menin inhibitor approved in frontline AML Ongoing trials in frontline cGVHD an
Slide 7: Today's speakers
Today’s speakers Syndax speakers Nick Botwood, MBBS Head of R&D and Chief Medical Officer Peter Ordentlich, PhD Chief Scientific Officer and Founder Toby M. Maher, MD, PhD Professor of Clinical Medicine and Director of Interstitial Lung Disease, Keck Medical School of University of Southern Californ
Slide 8: Today's agenda
Today’s agenda Introduction Driving long-term growth through innovation Michael A. Metzger, Syndax Pharmaceuticals An R&D engine built to deliver breakthroughs Nick Botwood, MBBS, Syndax Pharmaceuticals Revuforj (revumenib) & Next-Gen Menin Inhibitors Advancing our leadership in menin inhibition Nic
Slide 9: An R&D engine built to deliver breakthroughs
An R&D engine built to deliver breakthroughs Nick Botwood, MBBS Head of Research & Development and Chief Medical Officer
Slide 10: World-class R&D organization and partnerships
WORLD-CLASS R&D ORGANIZATION PARTNERSHIPS WITH LEADING RESEARCHERS DEEP MECHANISTIC UNDERSTANDINGS FULLY INTEGRATED CAPABILITIES Talented team with extensive experience developing novel medicines and building leading franchises Trailblazers in menin, CSF-1R, and EGFR inhibition In-house expertise sp
Slide 11: Proven track record of delivering breakthroughs
Proven track record of delivering breakthroughs 1L, frontline; R/R, relapsed or refractory; MF, myelofibrosis; FIH, first-in-human First to clinically validate menin inhibition in acute leukemia 2020 First and only FDA-approved menin inhibitor for R/R KMT2A translocated acute leukemia patients ≥ 1 y
Slide 12: Multiple opportunities for expansion with revumenib and axatilimab
R/R, relapsed or refractory; 1L, frontline; AML, acute myeloid leukemia; SOC, standard of care; HSCT, hematopoietic; MRD, measurable residual disease; cGVHD, chronic graft-versus-host disease; rux, ruxolitinib; IPF, idiopathic pulmonary fibrosis; *Trials led by Incyte. Asset Setting Pre-clinical Ph
Slide 13: A growing pipeline of differentiated assets
R/R, relapsed or refractory; 1L, frontline; AML, acute myeloid leukemia; SOC, standard of care; HSCT, hematopoietic; MRD, measurable residual disease; cGVHD, chronic graft-versus-host disease; rux, ruxolitinib; IPF, idiopathic pulmonary fibrosis; NSCLC, non-small cell lung cancer. *Trials led by Inc
Slide 14: Advancing our leadership in menin inhibition
Advancing our leadership in menin inhibition Nick Botwood, MBBS Head of Research & Development and Chief Medical Officer
Slide 15: Positioned to continue leading menin inhibition in acute leukemia and beyond
Positioned to continue leading menin inhibition in acute leukemia and beyond Only menin inhibitor approved for R/R NPM1m AML + KMT2A translocated acute leukemia in adults and children Only menin inhibitor with presented data showing clinical activity in NUP98r BROADEST INDICATION & CLINICAL ACTIVITY
Slide 16: Pioneering menin inhibition across multiple acute leukemia settings
Break Through Cancer Rev + ven for MRD clearance INTERCEPT Rev for MRD relapse Dose optimization + MenTain Rev as post-HSCT maintenance Global pivotal 1L trials underway with dual primary endpoints to support potential for accelerated and full approval RELAPSED / REFRACTORY MAINTENANCE & MRD RELAPSE
Slide 17: Pioneering menin inhibition across multiple acute leukemia settings
Break Through Cancer Rev + ven for MRD clearance INTERCEPT Rev for MRD relapse Dose optimization + MenTain Rev as post-HSCT maintenance Global pivotal 1L trials underway with dual primary endpoints to support potential for accelerated and full approval RELAPSED / REFRACTORY MAINTENANCE & MRD RELAPSE
Slide 18: Following the science to unlock the full potential of menin inhibition
Following the science to unlock the full potential of menin inhibition Emerging data highlights the potential for revumenib in multiple diseases Myelofibrosis (MF) selected as the next area for expansion based on: High unmet need Compelling preclinical data Strategic fit Potential for early clinical
Slide 19: Library of next-gen menin inhibitors
Leading menin inhibition into the future with a library of next-gen molecules plus the ability to leverage revumenib to de-risk development in new areas Revumenib will be leveraged in preclinical and proof-of-principle clinical studies to generate data that informs development of next-gen molecules
Slide 20: Menin inhibition in myelofibrosis
Menin inhibition in myelofibrosis John D. Crispino, PhD, MBA Director, Division of Experimental Hematology, St. Jude Children's Research Hospital
Slide 21: New therapeutic strategies are needed in myelofibrosis
New therapeutic strategies are needed in myelofibrosis (MF) MF, a type of myeloproliferative neoplasm (MPN), affects ~20,000 people in the U.S. MF is associated with: Extramedullary hematopoiesis contributing to hepatosplenomegaly Increased levels of inflammatory cytokines mediating debilitating sym
Slide 22: Menin inhibition is a promising new target in MF
Menin inhibition is a promising new target in MF Wen et al. Cancer Cell 2026. MF is characterized by an accumulation of atypical megakaryocytes (MKs), which contribute to fibrosis by secreting factors that increase collagen deposition Emerging data reveal that menin is a novel dependency in prolifer
Slide 23: Revumenib selectively inhibits megakaryopoiesis
Our recently published preclinical data show revumenib selectively inhibits megakaryopoiesis Wen et al. Cancer Cell 2026. CFU, colony-forming units; BFU, burst forming units CFU-Granulocytes/macrophages BFU-Erythroid Revumenib reduced megakaryocyte progenitors (MKPs) and the formation of immature an
Slide 24: Loss of menin phenocopies revumenib
Loss of menin (MEN1) phenocopies revumenib, confirming on-target effect of the drug Control MEN1 g1 MEN1 g13 Revumenib MEN1 knockouts Both revumenib and MEN1 loss substantially decreased MKPs and immature MKs Wen et al. Cancer Cell 2026.
Slide 25: Revumenib improves peripheral blood counts in MPN animal models
Revumenib alone and in combo with ruxolitinib improves peripheral blood counts in MPN animal models Days of treatment Days of treatment Days of treatment Control Revumenib Ruxolitinib Revumenib + ruxolitinib Wen et al. Cancer Cell 2026.
Slide 26: Revumenib increases survival and normalizes spleen weight
Revumenib increases survival and normalizes spleen weight in combination with ruxolitinib in MPN animal models Control Revumenib Ruxolitinib Revumenib + ruxolitinib Rev + rux combo notably reduced spleen weight Both single agent arms and the rev + rux combo showed extended survival compared to the c
Slide 27: Revumenib suppressed TGF-β, megakaryocyte accumulation, and fibrosis
Revumenib alone and in combo with ruxolitinib suppressed levels of TGF-β, megakaryocyte accumulation, and fibrosis more than ruxolitinib alone Control Revumenib Ruxolitinib Revumenib + ruxolitinib Both rev arms decreased TGF-β, an inflammatory & profibrotic cytokine Both rev arms decreased MK number
Slide 28: Revumenib normalizes bone marrow cellularity and abrogates fibrosis
Revumenib as a single agent and in combo with ruxolitinib normalizes bone marrow cellularity and abrogates fibrosis in MPN animal models Control Revumenib Ruxolitinib Revumenib + ruxolitinib Wen et al. Cancer Cell 2026.
Slide 29: Revumenib targets malignant MKPs in MF patient samples
Revumenib targets malignant megakaryocyte progenitors (MKPs) in MF patient samples Wen et al. Cancer Cell 2026. Samples include CALR and JAK2 mutant cases. HSPCs, hematopoietic stem and progenitor cells; DMSO = vehicle In vitro, revumenib reduced MKs and MKPs derived from human MF samples In vivo, r
Slide 30: Unique and complementary mechanism of action in myelofibrosis
Revumenib could provide a unique and complementary mechanism of action in myelofibrosis Revumenib’s effects are mediated by downregulation of key MKP genes, such MEF2C and MEIS1 Control Revumenib Revumenib reduced expression of key menin-KMT2A target genes in MKPs and MKs MK MKP Wen et al. Cancer Ce
Slide 31: Summary
Summary Menin inhibition suppresses megakaryopoiesis in times of stress or disease when progenitors are highly proliferative; on-target effect in MF is driven in part by downregulation of MEF2C and MEIS1 Revumenib has anti-tumor effects in multiple MPN mouse models as a single agent and in combinati
Slide 32: Menin inhibition in MF - Next steps
Menin inhibition in MF - Next steps Nick Botwood, MBBS Head of Research & Development and Chief Medical Officer
Slide 33: Leveraging revumenib to de-risk development of SNDX-62122 in MF
Leveraging revumenib to inform and de-risk development of SNDX-62122 in MF Publish preclinical MF data Initiate revumenib proof-of-principle MF trial in 4Q26 IND, investigational new drug Anticipated path forward Submit IND for SNDX-62122 (next-gen menin inhibitor) in 2027 Initiate Ph 1 of SNDX-6212
Slide 34: Phase 1/2 proof-of-principle trial in MF expected to initiate in 4Q26
Phase 1/2 proof-of-principle trial of menin inhibition in MF expected to initiate in 4Q26 in partnership with the MPN-RC consortium Key inclusion criteria: Myelofibrosis (MF) diagnosis Post-ET MF Post-PV MF DIPSS Int-1 or higher Platelet count ≥ 75 x 109/L (N ≈ 30) R/R MF with prior treatment with J
Slide 35: Q&A – Revumenib and Next-Gen Menin Inhibitors
Q&A – Revumenib and Next-Gen Menin Inhibitors Nick Botwood, MBBS Head of R&D and Chief Medical Officer Michael A. Metzger Chief Executive Officer and Director Peter Ordentlich, PhD Chief Scientific Officer and Founder John D. Crispino, PhD, MBA Director, Division of Experimental Hematology, St. Jude
Slide 36: Unlocking the potential of CSF-1R inhibition
Unlocking the potential of CSF-1R inhibition Peter Ordentlich, PhD Chief Scientific Officer and Founder
Slide 37: Axatilimab development driven by understanding of the CSF-1R pathway
Axatilimab development driven by deep mechanistic understandings of the CSF-1R pathway Colony stimulating factor 1 receptor (CSF-1R) signaling is essential for the activation, proliferation, and differentiation of monocytes and monocyte-derived macrophages Axatilimab is a monoclonal antibody that bl
Slide 38: Following the science to unlock the full potential of CSF-1R inhibition
Following the science to unlock the full potential of CSF-1R inhibition BEYOND IPF R/R cGVHD 1L cGVHD Pivotal trial showed robust responses across all organs studied, including in the lung and skin FDA approved in 2024 for cGVHD patients with ≥2 prior lines of therapy Ongoing trials could advance ax
Slide 39: Clinical perspective on IPF and CSF-1R inhibition
Toby M. Maher, MD, PhD Professor of Clinical Medicine and Director of Interstitial Lung Disease, Keck Medical School of University of Southern California Clinical perspective on IPF and CSF-1R inhibition
Slide 40: Syndax 3*
Syndax 3* TRACHEA BRONCHIAL BRONCHIOLAR REGION bronchus OROPHARYNGEAL REGION (mouth and nose) bronchiole _%ae—Alveoli & lveo eo) 2 2 ALVEOLAR REGION ~~ “Sebronchiole ; 40
Slide 41: IPF – Histology
IPF – Histology
Slide 42: Idiopathic pulmonary fibrosis
Idiopathic pulmonary fibrosis Maher TM JAMA 2024
Slide 43: IPF is one of several interstitial lung diseases
IPF is one of several interstitial lung diseases with shared pathophysiology
Slide 44: IPF is a complex, multi-factorial disease
IPF is a complex, multi-factorial disease GENETIC SUSCEPTIBILITY
Slide 45: Evolving treatment landscape in IPF
Evolving Tx landscape and multiple emerging modalities could advance patient outcomes in IPF Combination approaches targeting multiple pathways will likely be needed to meaningfully impact survival in IPF FDA approved drugs Notable emerging candidates with distinct mechanisms Pirfenidone (Esbriet) N
Slide 46: Real-world outcomes with first generation antifibrotics
Real-world outcomes with first generation antifibrotics underscore need for new therapeutic approaches in IPF General population Pirfenidone Best supportive care Guenther et al. Respir Res. 2018; Fisher et al. J Manag Care Spec Pharm 2017. Antifibrotic Tx No antifibrotic Tx
Slide 47: Pirfenidone and nintedanib use and persistence in the US
Pirfenidone and nintedanib use and persistence in the US Anti-fibrotic use in US Anti-fibrotic persistence in US Dempsey T et al Annals ATS 2021 Ortiz et al BMJ Respir Open 2024
Slide 48: Monocyte-derived alveolar macrophages are a promising target in IPF
The monocyte-derived alveolar macrophages is a promising target in IPF Byrne et al. J Exp Med 2020 Oldham et al ERJOR 2022
Slide 49: Higher monocyte levels associated with shorter survival in IPF
Scott et al. Lancet Respir Med 2019. Higher monocyte levels are associated with shorter survival in IPF and other fibrotic diseases
Slide 50: Axatilimab targets a novel pathway in IPF
Axatilimab targets a novel and potentially complementary pathway in IPF Axatilimab is a CSF1R-blocking antibody targeting monocyte-derived alveolar macrophages
Slide 51: Axatilimab has shown strong activity across multiple organs in cGVHD
Axatilimab has shown strong activity across multiple organs in cGVHD Wolff et al. NEJM 2024.
Slide 52: Safety profile observed in cGVHD
Safety profile observed in cGVHD highlights axatilimab’s combination potential Wolff et al. NEJM 2024.
Slide 53: Data in cGVHD-related BOS shows antifibrotic activity in the lung
Data in cGVHD-related bronchiolitis obliterans syndrome (BOS) shows axatilimab has antifibrotic activity in the lung Salhotra et al. Axatilimab in Patients With Lung Chronic Graft-Versus-Host Disease and Related Bronchiolitis Obliterans Syndrome: Results From the AGAVE-201 Study. Oral presentation a
Slide 54: MAXPIRe Phase 2 trial of axatilimab in IPF
MAXPIRe is a robust Phase 2 trial of axatilimab in IPF Randomized, double-blind, placebo-controlled, multi-center international trial Key eligibility criteria: ≥40 yrs of age HRCT confirming IPF diagnosis FVC ≥45% of predicted normal (PN) FEV1/FVC ≥0.7 DLCO ≥30% and ≤90% PN Stable background use of
Slide 55: Summary
Summary IPF is a deadly and progressive disease Current therapies slow but do not prevent progression of fibrosis There is an increasing drive to combine therapies in IPF CSF-1R positive macrophages play an important role in fibrogenesis Axatilimab has been shown to be effective in GVHD – a disease
Slide 56: Q&A - Axatilimab
Q&A - Axatilimab Nick Botwood, MBBS Head of R&D and Chief Medical Officer Michael A. Metzger Chief Executive Officer and Director Peter Ordentlich, PhD Chief Scientific Officer and Founder Toby M. Maher, MD, PhD Professor of Clinical Medicine and Director of Interstitial Lung Disease, Keck Medical S
Slide 57: Expanding our pipeline into EGFRm NSCLC with SNDX-4321
Expanding our pipeline into EGFRm NSCLC with SNDX-4321 Nick Botwood, MBBS Head of Research & Development and Chief Medical Officer
Slide 58: Allosteric inhibitors reshaping the standard of care
Allosteric inhibitors are increasingly reshaping the standard of care for difficult-to-treat cancers Future Allosteric inhibitors bind to non-active sites rather than the ATP-binding site on tyrosine kinases; their binding induces a conformational change that ‘locks’ the kinase in an inactive state
Slide 59: Addressing unmet needs in EGFRm NSCLC with a novel approach
Syndax aims to address significant unmet needs in EGFRm NSCLC with a novel approach Note: This is an illustrative figure that does not depict every approved or investigational therapy targeting EGFRm NSCLC. EGFRi, EGFR inhibitor BI-8128 TAS3351 SNDX-4321 ATP Binding Site SNDX-4321 Binding Site 3rd g
Slide 60: SNDX-4321, a mutant-selective, allosteric EGFR inhibitor for NSCLC
Michael J. Eck, MD, PhD Professor, Department of Cancer Biology, Dana-Farber Cancer Institute Professor, Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School SNDX-4321, a mutant-selective, allosteric EGFR inhibitor for non-small cell lung cancer (NSCLC) Disclosure st
Slide 61: SNDX-4321 builds on Dana-Farber's work on allosteric EGFR inhibitors
SNDX-4321 builds on Dana-Farber Cancer Institute’s pioneering work on allosteric EGFR inhibitors SNDX-4321 allosteric binding site ATP site (binding site for osimertinib + other EGFR inhibitors) SNDX-4321: Binds at a pocket adjacent to the active (ATP) site that is only accessible with L858R and cer
Slide 62: SNDX-4321 potential to advance the treatment paradigm for EGFRm NSCLC
SNDX-4321 has the potential to advance the Tx paradigm for EGFRm NSCLC SNDX-4321 allosteric binding site ATP site (binding site for osimertinib + other EGFR inhibitors) Excellent selectivity, oral bioavailability, and brain penetration Efficacy in multiple tumor models as a single-agent or in combin
Slide 63: Significant unmet needs remain in EGFRm NSCLC
Significant unmet needs remain in EGFRm NSCLC despite recent advances ~200,000 people are diagnosed with NSCLC annually in the U.S. alone1 Worldwide ~1/3 of NSCLC patients have EGFR mutations2 The most common EGFR mutations are exon 19 deletions and L858R point mutations Osimertinib +/- chemotherapy
Slide 64: SNDX-4321 could address areas of high unmet need
SNDX-4321 has the potential to address several areas of high unmet need in EGFRm NSCLC Patients with L858R have poorer outcomes than those with ex19 deletions Patients with atypical mutations have poorer outcomes than those with classical mutations Preclinical data show activity against certain atyp
Slide 65: Patients with L858R NSCLC have poorer outcomes
Jänne et al. NEJM 2026. Patients with L858R NSCLC have poorer outcomes than those with ex19del 1 48-month OS in 1L EGFRm advanced NSCLC L858R ex19del FLAURA2 showed that even with the addition of chemotherapy, L858R patients continue to have shorter OS than ex19del patients
Slide 66: EGFRm NSCLC patients with CNS metastases fare worse
EGFRm NSCLC patients with CNS metastases fair worse than those without 48-month OS in 1L EGFRm advanced NSCLC (Includes both L858R and ex19del patients) With CNS metastases Without CNS metastases 2 Jänne et al. NEJM 2026. FLAURA2 showed that even with the addition of chemotherapy, patients with CNS
Slide 67: Atypical activating EGFR mutations have shorter time to treatment failure
Patients with atypical activating EGFR mutations have shorter time to treatment failure as compared with classical mutations 3 Atypical variants account for up to ~20% of EGFRm NSCLC (excluding exon20 insertions); most common atypical mutations are G719X, S768I, and L861Q Frequency of atypical EGFR
Slide 68: On-target EGFR mutations confer resistance to osimertinib
On-target mutations in EGFR confer resistance to osimertinib Passaro et al. Nat Cancer 2021. C797S (most common), L718X, L792F, G796S and others Up to ~20% after 2nd line Tx Up to ~12% after 1st line Tx 4
Slide 69: SNDX-4321 is a mutant-selective and potent allosteric EGFR inhibitor
Preclinical studies show: Negligible activity against wild-type EGFR Activity against L858R, with or without common resistance mutations to osimertinib (e.g., C797S) Activity against certain atypical mutations including L861Q, one of the most common atypical variants No activity against exon 19 dele
Slide 70: SNDX-4321 is effective in the CNS in intracranial xenograft model
SNDX-4321 is effective in the CNS in intracranial xenograft model Subcutaneous tumor implant Intracranial tumor implants H1975 (L858R/T790M) dual subcutaneous/intracranial model, 21 days dosing, QD SNDX-4321, 25 mg/kg Osimertinib, 25 mg/kg Vehicle control SNDX-4321, 5 mg/kg
Slide 71: SNDX-4321 is highly active as a single agent in L858R PDX models
SNDX-4321 is highly active as a single agent in L858R NSCLC PDX models Vehicle SNDX-4321, 5 mg/kg QD SNDX-4321, 15 mg/kg QD SNDX-4321, 50 mg/kg QD PDX LUN439 (L858R) NSCLC model PDX, patient-derived xenograft SNDX-4321 inhibits growth of L858R containing tumors in a dose-dependent fashion
Slide 72: Combination therapy is the more significant opportunity
While SNDX-4321 is highly active as a single agent, the more significant opportunity is for combination therapy Advantages of allosteric approach, especially for combination therapy: Bind outside ATP site, yielding excellent kinome-wide selectivity Better/different tox profile as compared with ATP-s
Slide 73: In vivo studies show benefit of combining SNDX-4321 with osimertinib
In vivo efficacy studies show benefit of combining SNDX-4321 with osimertinib Combination of SNDX-4321 and osimertinib was well-tolerated Clear combination benefit in terms of delayed regrowth and survival Vehicle control Osimertinib, 20 mg/kg SNDX-4321, 25 mg/kg Osimertinib, 20 mg/kg + SNDX-4321, 2
Slide 74: Summary – SNDX-4321
Summary – SNDX-4321 Novel, mutant-selective allosteric EGFR inhibitor that could address EGFRm NSCLC populations with significant unmet needs, such as those with L858R mutations, CNS metastases, atypical mutations, or resistance to osimertinib Highly active as a single agent and in combination with
Slide 75: SNDX-4321 - Next steps
SNDX-4321 - Next steps Nick Botwood, MBBS Head of Research & Development and Chief Medical Officer
Slide 76: SNDX-4321 clinical development plan
SNDX-4321 clinical development plan designed to efficiently generate safety and efficacy data that support allosteric approach in EGFRm NSCLC Complete IND-enabling studies IND submission by YE 2026 Evaluate with osimertinib in 1L NSCLC patients with susceptible EGFR mutations Initiate Ph 1 trial in
Slide 77: Q&A - SNDX-4321
Q&A - SNDX-4321 Nick Botwood, MBBS Head of R&D and Chief Medical Officer Michael A. Metzger Chief Executive Officer and Director Michael J. Eck, MD, PhD Professor, Department of Cancer Biology, Dana-Farber Cancer Institute; Professor, Department of Biological Chemistry and Molecular Pharmacology, Ha
Slide 78: Closing remarks
Michael A. Metzger Chief Executive Officer and Director Closing remarks
Slide 79: Syndax is delivering for patients and driving substantial long-term value
Syndax is delivering for patients and driving substantial long-term value Proven ability to translate scientific discoveries into novel therapies, with 3 FDA approvals between 2 drugs and thousands of patients treated Fully integrated biotech with deep expertise and strong partnerships with leading
Slide 80: Continued focus on revenue growth and pipeline progress with near-term catalysts
Continued focus on driving revenue growth and pipeline progress, with multiple near-term catalysts and blockbuster opportunities Acute Leukemia Advance global enrollment in pivotal 1L trials of revumenib New 1L, maintenance, real-world, and R/R revumenib data in 2H26 + beyond Publish R/R NUP98r AML
Slide 81: Slide 81