Foghorn Therapeutics Inc. · NASDAQ:FHTX
Foghorn Therapeutics — Investor Presentation (May 2026)
64 slides from Foghorn Therapeutics's investor presentation, May 7, 2026
Slide 1: Unique biology, Precision therapeutics, Broad impact
Unique biology Precision therapeutics Broad impact NASDAQ LISTED FHTX May 2026 Exhibit 99.2
Slide 2: Forward Looking Statements
| Forward Looking Statements 2 This presentation contains forward-looking statements that are based on management's beliefs and assumptions and on information currently available to management. All statements other than statements of historical facts contained in this presentation are forward- looki
Slide 3: Foghorn is a Leader in Chromatin Biology, Successfully Drugging Challenging Targets
| Foghorn is a Leader in Chromatin Biology, Successfully Drugging Challenging Targets 3 Targeting chromatin regulation Implicated in up to 50% of all tumors Multi-billion $ Opportunities Unlocking selectivity of previously undruggable targets First-and-Best-in-Class Approaches Innovating selective p
Slide 4: Chromatin Regulatory System Orchestrates Gene Expression
| Chromatin Regulatory System Orchestrates Gene Expression: Multiple Opportunities for Targets and Therapeutics 4 Chromatin – compacted form of DNA inside the nucleus of the cell Chromatin Remodeling Complexes – specialized multiprotein machines that allow access to DNA Targets: SMARCA2, ARID1B Tran
Slide 5: Foghorn's Platform Has Delivered Precision First-in-Class Therapeutics
| Foghorn’s Platform Has Delivered Precision First-in-Class Therapeutics, and is Poised to Unlock New Biology 5 1. Chromatin Biology 2. Chemistry, Biochemistry & Formulations 3. Degraders / Selective Targeting Deep mechanistic understanding of chromatin regulatory system Expertise in rules of degrad
Slide 6: Foghorn: Precision Therapies with Potential for Multi-Billion Dollar Opportunities Across Oncology
| Foghorn: Precision Therapies with Potential for Multi-Billion Dollar Opportunities Across Oncology 6 Modality Program and Partner Phase 1 Enzyme Inhibitors Protein Degraders FHD-909* (Selective SMARCA2) 3 Discovery Programs Undisclosed Partnered** Undisclosed Disease SMARCA4-mutant cancers (e.g.,
Slide 7: FHD-909 is Being Developed in Collaboration with Lilly
| FHD-909 is Being Developed in Collaboration with Lilly; Landmark Agreement Signed in December 2021 Significant Upfront and Economics Strong Momentum and Shared Vision Ongoing Discovery Programs • $300 million cash • $80 million in Foghorn common stock at a price of $20 per share • 50/50 U.S. econo
Slide 8: Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer
| Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer 8 Large Market Potential Chromatin biology is implicated in up to 50% of tumors, potentially impacting ~2.5 million patients Foghorn’s current pipeline potentially addresses more than 500,000 of these patients Broa
Slide 9: Selective SMARCA2 Program For SMARCA4-mutant Cancers
Selective SMARCA2 Program For SMARCA4-mutant Cancers • FHD-909 (LY4050784) – Selective SMARCA2 Inhibitor 9
Slide 10: SMARCA2: Clinical-stage FHD-909 Inhibitor and Preclinical Degrader
| SMARCA2: Clinical-stage FHD-909 Selective SMARCA2 Inhibitor and Preclinical Selective SMARCA2 Degrader 10 Selective SMARCA2 Inhibitor FHD-909* Selective SMARCA2 Degrader Biology Exploit the synthetic lethal relationship between SMARCA2 and mutated SMARCA4 Status Phase 1 monotherapy dose escalation
Slide 11: Selective SMARCA2 Inhibition Exploits Synthetic Lethal Relationship
| Selective SMARCA2 Inhibition: Promising Strategy to Exploit Synthetic Lethal Relationship Between SMARCA2 and Mutant SMARCA4 11 No SMARCA4 Mutations SMARCA4 Mutation SMARCA4 Mutation and SMARCA2i Cell Survival Cell Death Healthy Cells Cancer Cells SMARCA4 SMARCA2 BAF Complex BAF Complex Mutant SMA
Slide 12: SMARCA4 is Mutated in Up to 10% of NSCLC; Up to 5% of Solid Tumors
| SMARCA4 is Mutated in Up to 10% of NSCLC; Up to 5% of Solid Tumors 12 SMARCA4 mutated across a broad range of tumors Accounts for ~5% of solid tumors AACR GENIE via cBioPortal
Slide 13: FHD-909: Overall Goal is to Become a First-Line Treatment for SMARCA4-mutated NSCLC
| FHD-909: Overall Goal is to Become a First-Line Treatment for SMARCA4- mutated NSCLC 13 1st Line NSCLC Pembrolizumab-based regimens Other immune checkpoint inhibitor-based regimens Chemotherapy-based regimens 2nd Line NSCLC Chemotherapy-based regimens Ramucirumab (anti-VEGF) + chemotherapy Checkpo
Slide 14: Significant Unmet Medical Need in NSCLC Metastatic Setting for SMARCA4 Patients
| 14 Significant Unmet Medical Need in NSCLC Metastatic Setting for SMARCA4 Patients ~15 months ~8 months 1L (SMARCA4 WT) 1L (SMARCA4 Mut) 39.1% 21.9% 2.7 months Response Rate (%) PFS (months) OS (months) Significant Unmet Need Frontline NSCLC Metastatic – PD1 + Chemo1 Source: 1. Alessi, J Thorac On
Slide 15: SMARCA4 Mutations are Consequential in NSCLC
| NSCLC patients with SMARCA4 mutations: ─ Poor prognosis ─ Shorter overall survival ─ Less responsive to immune checkpoint inhibitors ─ Clinically definable, high unmet need population SMARCA4 Mutated in Up to 10% of NSCLC Tumors, Minimal Overlap w/ Other Mutations2 Overall Survival for SMARCA4 wt
Slide 16: SMARCA4 and KRAS Co-Mutations Have Even Worse Outcomes
| When SMARCA4 and KRAS Mutations Co-Occur, Patients Have Even Worse Outcomes to Standard of Care Treatment In response to PD(L)-1 therapy, patients with co-occurring SMARCA4 and KRAS mutations have a shorter ORR, PFS, and OS than patients with only KRASmut 16 Overall Response Rate (ORR) Source: Ale
Slide 17: First-in-Human Phase Trial of FHD-909 in SMARCA4-Mutated Solid Tumors
| A First-in-Human Phase 1 Trial of FHD-909 in Advanced Solid Tumor Patients with SMARCA4 Mutations Phase 1a Dose Escalation Advanced solid tumors with any SMARCA4 alteration (mTPI-2 method with backfillinga) Dose Level 1 Dose Level 2 Dose Level 3 Dose Level n Phase 1b Dose Expansionb Presence of a
Slide 18: FHD-909 with Anti-PD1 Demonstrates Complete and Durable Regression
| FHD-909 in Combination with Anti-PD1 Demonstrates Complete and Durable Regression 18 Double Combo Efficacy (LY4050784, anti-PD1, chemo) B o d y w e ig h t p e rc en ta g e c h a n g e (% ) • FHD-909 monotherapy demonstrates better efficacy (tumor regression) than chemo or anti-PD1 (progressive dis
Slide 19: Lack of Tumor Formation in CR Mice After Re-inoculation
| Lack of Tumor Formation in CR Mice After Re-inoculation Suggests Immune Memory Formation 19 Re-challenge of Mice After CR with FHD-909 + Anti-PD1 Combos • Complete response (CR) mice were re-challenged with MB49 SMARCA4-KO cells alongside age-matched naïve controls • 0% tumor take in CR mice vs. 1
Slide 20: Degrader Programs
Degrader Programs • Selective CBP Degrader • Selective EP300 Degrader • Selective ARID1B Degrader 20
Slide 21: Multi-billion Dollar Opportunities for Each Program
| Multi-billion Dollar Opportunities for Each Program Developing a Portfolio of Novel and Selective Degraders with Blockbuster Potential 21 Selective ARID1B Degrader Selective CBP Degrader • Mutated in up to 5% of all solid tumors • First to demonstrate robust and selective degradation of the protei
Slide 22: CBP and EP300 Proteins: A Decades-long Challenge in Selectivity
| CBP and EP300 Proteins – A Decades-long Challenge in Selectivity 22 CBP and EP300 Biology • CBP and EP300 are highly homologous, paralog histone acetyltransferases regulating enhancer-mediated transcription and protein stability • Dysregulation of CBP and EP300 has been implicated in multiple canc
Slide 23: Selective CBP Degrader, FHT-171
Selective CBP Degrader, FHT-171 For EP300-mutant and CBP-dependent Cancers 23
Slide 24: Summary: Selective CBP Degrader
| Summary: Selective CBP Degrader for CBP-dependent & EP300-mutant Cancers 24 • CREB binding protein (CBP) • Targeted protein degrader Gynecological cancers1 Other cancers2 Bladder cancer ER+ breast cancer Target / Approach • Preclinical • IND-enabling studies in 2026 Stage / Next Milestone • Highly
Slide 25: FHT-171 Disrupts Estrogen Receptor Signaling in Breast Cancer
| FHT-171 Reduces ER Levels in Wildtype ESR1 Breast Cancer Cell Lines T47D and CAMA1 FHT-171 degradation of CBP disrupts and suppresses ER signaling in a potentially ESR1 mutation agnostic manner FHT-171 Disrupts Estrogen Receptor (ER) Signaling in Breast Cancer 25 0.0 0.5 1.0 1.5 Day 7 Day 14 Day 2
Slide 26: FHT-171 Demonstrates Anti-tumor Efficacy as Monotherapy in ER+ Breast Cancer
| FHT-171 Demonstrates Anti-tumor Efficacy as a Monotherapy in Standard-of-care Resistant ER+ Breast Cancer Models ER+ Metastatic Breast Cancer CDX (ST941C; ESR1m) ER+ Metastatic Breast Cancer PDX (ST4887B, ESR1 wt) ER+ Metastatic Breast Cancer PDX (ST4680D, ESR1m) 26 T u m o r V o lu m e ( m m 3 )
Slide 27: FHT-171 Shows No Impact on Platelet Counts
| FHT-171 Shows No Impact on Platelet Counts and Spared Megakaryocytes • C B P Platelet Counts Post Two Weeks of Dosing (In Vivo – Control Mice) Human Megakaryocyte Cell Viability Assay (In Vitro**) *CCS1477 (Inobrodib) inhibition study used 3 weeks of dosing Platelet counts are unaffected by select
Slide 28: FHT-171: Potent and Selective CBP Degrader
| FHT-171: Potent and Selective CBP Degrader • C B P Global Proteomics Confirms that FHT-171 is Selective 28 FHT-171 Rapidly and Potently Degrades CBP, but not its Paralog EP300 Dmax: 97% Max Rate: 3.2 hr-1 DC50: 30pM Dmax: 5% Max Rate: N/A 100nM CBPd-171/DMSO 3hr Log2FC FHT-171 CBP Kinetics FHT-171
Slide 29: Selective CBP Degradation Shows Anti-Tumor Activity in EP300-mutant Models
| Selective CBP Degradation Results in Significant Anti-Tumor Activity in EP300-mutant Solid Tumor Models EP300mut Bladder Cancer CDX (639V) EP300mut Gastric Cancer CDX (AGS) EP300mut Gastric Cancer PDX (ST020326) T u m o r V o lu m e (m m ³ + S E M ) B o d y W ei g h t C h an g e (% ) 20 30 40 50 6
Slide 30: Long-Acting Injectable Formulation of CBPd-171 Enables Weekly Delivery
| Long-Acting Injectable Formulation of CBPd-171 Enables Weekly Sub-cutaneous (SC) Delivery 30 Tumor Growth Inhibition Observed in EP300mut (AGS) Gastric Model (Daily Injections and SC weekly LAI Injection) • Weekly LAI injection of CBDd-171 results in efficacy comparable to daily SC injections in A
Slide 31: Development Vision: CBP Degrader as Combination Partner
| 31 Development Vision: CBP Degrader has the Potential to be an Attractive Combination Partner in ER+ Breast Cancer and Beyond Phase 1b Dose Expansion / Combination ER+ BC patients who failed at least 2L in advanced / metastatic setting In parallel, explore combos Dose Level 1 Dose Level 2 Dose Lev
Slide 32: Selective EP300 Degrader
Selective EP300 Degrader For CBP-mutant and EP300-dependent Cancers 32
Slide 33: Summary: Selective EP300 Degrader for Heme Malignancies and Prostate Cancer
| Summary: Selective EP300 Degrader for Heme Malignancies and Prostate Cancer 33 • E1A binding protein p300 (EP300) • Targeted protein degrader MM AML + MDS DLBCL Target / Approach • Preclinical • IND-enabling studies in 2026 Stage / Next Milestone • Deeper efficacy response vs non- selective molecu
Slide 34: EP300 Degradation Shows Anti-Proliferative Activity in Hematological Malignancies
| EP300 Degradation Shows Anti-Proliferative Activity in Broad Range of Hematological Malignancies 34MM: Multiple Myeloma; DLBCL: Diffuse Large B-Cell Lymphoma; AML: Acute Myeloid Leukemia; BL: Burkitt’s Lymphoma; PTCL: Peripheral T-cell Lymphomas; T-ALL: T-cell Acute Lymphoblastic Leukemia; B-ALL:
Slide 35: EP300 Degradation Results in Tumor Growth Inhibition in MM, DLBCL and Prostate Models
| Multiple Myeloma (MM1S) CDX DLBCL (KARPAS422) CDX AR+ Prostate (VCaP) CDX EP300 Degradation Results in Significant Tumor Growth Inhibition in MM, DLBCL and Prostate Models 35 B o d y W ei g h t C h an g e ( % ) 5 10 15 20 25 30 35 40 45 0 500 1,000 1,500 2,000 Vehicle FHT-EP300d - 32, SC, 50mg/kg
Slide 36: FHT-273 Shows Superior Efficacy and Tolerability Compared to Inobrodib
| • The max efficacious dose for inobrodib results in stasis with daily dosing. However, inobrodib use in the clinic is limited by thrombocytopenia, which requires dosing holidays • Selective EP300 degraders can achieve deeper responses at tolerated doses with no thrombocytopenia Selective EP300 Deg
Slide 37: VHL-based EP300 Degrader Maintains Activity in IMiD Resistant Cell Lines
| VHL-based Selective EP300 Degrader Maintains Activity in IMiD Resistant Cell Lines 37 Resistant MM1S cell lines were developed through 5–6 months of in vitro exposure to gradually increasing concentrations of lenalidomide, pomalidomide, iberdomide, or mezigdomide dEP300-9 dEP300-9 pomalidomide len
Slide 38: EP300 Degrader Superior in IMiD Resistant Multiple Myeloma Model
| 20 25 30 35 40 0 100 200 300 400 1000 2000 3000 4000 Days After Tumor Inoculation Vehicle FHT-EP300d-007, 30mpk, BID, s.c. CCS1477 (Inobrodib), 10mpk, BID (4d on / 3d off), p.o CCS1477 (Inobrodib), 20mpk, QD, p.o. Pomalidomide, 10mpk, QD, p.o. Selective EP300 Degrader Shows Superior Efficacy Compa
Slide 39: FHT-273: Potent and Selective EP300 Degrader
| FHT-273: Potent and Selective EP300 Degrader FHT-273 Rapidly and Potently Degrades EP300, but Not Its Paralog CBP Global Proteomics Confirms that FHT-273 is Selective 39 333nM FHT-273/DMSO 8hr Log2FC FHT-273 0.3nMDC50 96%Dmax 1.8 hr-1Rate FHT-273 EP300 Kinetics FHT-273 CBP Kinetics
Slide 40: Development Vision: EP300 in Hematological Malignancies
| 40 Development Vision: EP300 in Hematological Malignancies e patients with r/r hematological malignancies Dose Level 1 Dose Level 2 Dose Level 3 Dose Level n Register in specific hematological malignancies single agent or as part of combination regimen AML/MDS T-Cell Malignancies Expand into earli
Slide 41: Selective ARID1B Degrader For ARID1A-mutant Cancers
Selective ARID1B Degrader For ARID1A-mutant Cancers 41
Slide 42: ARID1B is a Major Synthetic Lethal Target
| ARID1B is a Major Synthetic Lethal Target with Potential in Up To 5% of All Solid Tumors 42 • ARID1B • Targeted protein degrader Endometrial cancers Gastric cancers Bladder cancer Non-small cell lung cancer • Preclinical • In vivo proof-of-concept in 2026 • Multiple ARID1B binders with nM affinity
Slide 43: ARID1B: Drugging A Previously Undruggable Target
| ARID1B: Drugging A Previously Undruggable Target • Large and highly unstructured protein ~ 240 kDa • No known enzymatic function • Member of large, multi-subunit complex • High sequence homology (~60%) to ARID1A 43 ARID1A/B BAF Nucleosome PDB ID: 6LTJ • Discover binders to ARID1B • Use binders to
Slide 44: Progression of Both Cereblon and VHL-based Degraders in Parallel
| Maximum Optionality Achieved Through Progression of Both Cereblon and VHL-based Degraders in Parallel 44 C E R E B L O N V H L FHT-654: DC50: 0.35 uM DC50: 3.7 uM ARID1B-HiBiT HCT116 Colorectal Cell Line
Slide 45: Selective ARID1B Degradation Demonstrated by Global Proteomics
| Selective ARID1B Degradation Demonstrated by Global Proteomics 45 FHT-654 Cereblon-Based Degrader ARID1A Log2FC ARID1B degrader 2.5uM/DMSO 24 hr ARID1B-HiBiT HCT116
Slide 46: FHT-654 Modulates ARID1B Target Gene Expression
| FHT-654 Modulates ARID1B Target Gene Expression in HCT-116 Colorectal ARID1A-/- Cells DM SO 63 n M 12 5 nM 25 0 nM 50 0 nM 10 00 n M 63 n M 12 5 nM 25 0 nM 50 0 nM 10 00 n M R el at iv e ex p re ss io n DM SO 63 n M 12 5 nM 25 0 nM 50 0 nM 10 00 n M 63 n M 12 5 nM 25 0 nM 50 0 nM 10 00 n M R el at
Slide 47: Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer
| Developing First-in-Class Precision Medicines Targeting Major Unmet Needs in Cancer 47 Large Market Potential Chromatin biology is implicated in up to 50% of tumors, potentially impacting ~2.5 million patients Foghorn’s current pipeline potentially addresses more than 500,000 of these patients Bro
Slide 48: Unique biology, Precision therapeutics, Broad impact
Unique biology Precision therapeutics Broad impact 48 May 2026
Slide 49: Appendix
Appendix 49
Slide 50: SMARCA2 Program
SMARCA2 Program 50
Slide 51: FHD-909 Monotherapy Demonstrated Regression in NCI-H2126 Model
| FHD-909 Monotherapy Demonstrated Regression In Vivo in NCI-H2126 SMARCA4-mutant NSCLC Model at Tolerated Doses 51 NCI-H2126 Reduction in Tumor Volume NCI-H2126 Body Weight Genetic Background: SMARCA4 W764R, TP53 E62*, STK11-/-, CDKN2A-/-, KEAP1 R272C Note: All doses were well tolerated. Dosing hol
Slide 52: FHD-909 Monotherapy Strong In Vivo Activity Across SMARCA4-mutant NSCLC Models
| FHD-909 Monotherapy Demonstrated Strong In Vivo Activity Across SMARCA4-mutant NSCLC Models at Tolerated Doses 52 0 7 14 21 28 100 200 300 400 500 Days of Dosing (Dose Start Day1) Vehicle Control FHD-909, 20mg/kg, BID, PO FHD-909, 40mg/kg, BID, PO FHD-909, 60mg/kg, BID, PO A549 Model RERF-LC-AI Mo
Slide 53: FHD-909 with Standard Therapies in A549 Xenograft Model
| FHD-909 in Combination with Standard Therapies Demonstrates Significant Activity in the A549 (SMARCA4-mutant, KRAS G12S) Xenograft NSCLC Model 53 0 7 14 21 28 200 400 600 800 1000 1200 Days of Dosing (Dose Start Day 1) T u m o r vo lu m e (m m 3 ) * * * * ** ## Note: *p≤0.05 for pairwise compariso
Slide 54: FHD-909 with Standard Therapies in RERF-LC-AI Xenograft Model
| FHD-909 in Combination with Standard Therapies Demonstrates Significant Activity in the RERF-LC-AI (SMARCA4-mutant) Xenograft NSCLC Model 54 0 7 14 21 28 200 400 600 800 1000 1200 1400 Days of Dosing (Dose Start Day 1) T u m o r V o lu m e (m m 3 ) * * * * **# # Note: *p≤0.05 for pairwise comparis
Slide 55: Synergistic Activity of FHD-909 with KRAS Inhibitors In Vitro
| Synergistic Activity Observed for FHD-909 in Combination with KRAS Inhibitors In Vitro 55 In h ib it io n ( % ) In h ib it io n ( % ) FHD-909 + olomorasib (KRAS G12C inhibitor) FHD-909 + pan-KRAS inhibitor In h ib it io n ( % ) In h ib it io n ( % ) 1 10 100 1000 10000 -20 0 20 40 60 80 100 120 FH
Slide 56: FHD-909 with KRAS Inhibitors in Co-mutated NSCLC Xenograft Models (Olomorasib)
| Combination of FHD-909 with KRAS Inhibitors Demonstrates Synergistic Activity in SMARCA4, KRAS Co-mutated Human NSCLC Xenograft Models In Vivo FHD-909 + olomorasib (KRAS G12C inh) NCI-H2030 (SMARCA4mt, KRAS G12C) 56 0 7 14 21 28 0 500 1000 1500 2000 2500 3000 Days of Dosing (Dose Start Day1) T u m
Slide 57: FHD-909 with KRAS Inhibitors in Co-mutated NSCLC Xenograft Models (Pan-KRAS)
| Combination of FHD-909 with KRAS Inhibitors Demonstrates Synergistic Activity in SMARCA4, KRAS Co-mutated Human NSCLC Xenograft Models In Vivo FHD-909 + pan-KRAS inh A549 (SMARCA4mt, KRAS G12S) 57 Combination of FHD-909 with pan-KRAS inhibitor resulted in synergistic antitumor activity and sustain
Slide 58: FHD-909 with Pembrolizumab Enhances Anti-Tumor Activity in Humanized Model
| FHD-909 in Combination with Pembrolizumab Shows Significantly Enhanced Anti-Tumor Activity in A549 CD34+ HSC Humanized Xenograft NSCLC Model 58 FHD-909 sensitized the tumor cells to pembrolizumab treatment resulting in enhanced combination activity Pembrolizumab alone had no effect on tumor growth
Slide 59: Selective SMARCA2 Degrader Achieved Complete Degradation In Vitro
| Selective SMARCA2 Degrader Achieved Complete SMARCA2 Degradation and Cell Growth Inhibition In Vitro 59 Degraders Caused Time- and Dose-dependent SMARCA2 Degradation Antiproliferative Effects in A549-mutant NSCLC Model A549 Ten-Day Proliferation AssaySMARCA2 / SMARCA4 HIBIT Data SMARCA2 SMARCA4 %
Slide 60: Protein Degradation Importance of Rate Analysis
Protein Degradation Importance of Rate Analysis FHD-609 is a Selective, Potent, Protein Degrader of the BRD9 component of the BAF complex 60
Slide 61: Degradation Rates and Their Relationship to Dmax
| Degradation Rates and Their Relationship to Dmax 61 • Slower rates lead to partial degradation, faster rates to complete loss • Rate is an indicator of degrader efficiency. If rate is slow, the process is inefficient and reflective of a degrader which does not have a high turnover rate of target N
Slide 62: Degradation Rate Dictates Dmax – Program Independent
| Degradation Rate Dictates Dmax – Program Independent 62 Foghorn CBP ProgramFoghorn BRD9 Program Foghorn EP300 Program Large scale experimental kinetic analysis for a program reveals the relationship between rate and Dmax
Slide 63: Prelude VHL and CRBN Compounds Have Incomplete Dmax and Hook Effect
| Prelude VHL and CRBN Compounds Have Incomplete Dmax and also Have a Hook Effect 63 • Prelude’s SMARCA2 (VHL) degrader was faster and achieved improved Dmax across concentrations as compared to SMARCA2 (CRBN) • The SMARCA2 (CRBN) degrader is considerably slower and therefore even at high concentrat
Slide 64: Foghorn Analysis and Dmax Results Match Published Prelude Data
| Foghorn Analysis and Dmax Results Match Published Prelude Data 64 Prelude Published Data Prelude PRT3789 (VHL) 1 Prelude PRT7732 (CRBN) 2 % P ro te in Prelude (CRBN) Degrader Prelude (VHL) Degrader Foghorn Replicated Data from Prelude Patents 1. AACR-NCI-EORTC 2023 Poster B113 – Ito et al. 2. AACR
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