Slide 1: Unique biology, Precision therapeutics, Broad impact
Unique biology Precision therapeutics Broad impact FHTX August 2026 NASDAQ LISTED
Slide 2: Forward Looking Statements
Forward Looking Statements 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- looking s
Slide 3: Foghorn is a Leader in Chromatin Biology, Successfully Drugging Challenging Targets
Foghorn is a Leader in Chromatin Biology, Successfully Drugging Challenging Targets Multi-billion $ First-and-Best-in-Class Selective Target Strategic Partnership: Opportunities Approaches Engagement Multiple Programs Targeting chromatin Unlocking Innovating selective Leveraging a proven regulation
Slide 4: Chromatin Regulatory System Orchestrates Gene Expression
Chromatin Regulatory System Orchestrates Gene Expression: Multiple Opportunities for Targets and Therapeutics Chromatin Regulatory System genes are implicated across a wide range of cancers Chromatin Remodeling Complexes – specialized multiprotein machines that Chromatin – compacted Transcription Fa
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 2. Chemistry, Biochemistry & Formulations Track record Track record with previously of delivering undruggable targets precision therapeutics 1. Chromatin Biology Deep mechanistic understanding
Slide 6: Precision Therapies with Potential for Multi-billion Dollar Opportunities
Precision Therapies with Potential for Multi-billion Dollar Opportunities Therapeutic Area Program Disease Area Preclinical Phase 1 Next Clinical Milestone Phase 1a Monotherapy Data; Selective SMARCA2 SMARCA4-mutant cancers (e.g., NSCLC) Dose Expansion Decision Inhibitor FHD-909* Selective EP300 Deg
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 Strong Momentum and Ongoing Discovery Economics Shared Vision Programs • $300 million cash • Lilly is a leading oncology company • Three additional programs as part of with a tr
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 Leader in Unique Area Large Market Well- Value Major Strategic of Cancer Biology Potential Funded Drivers Collaboration Chromatin biology is $167.6 million in cash Strategic collaboration with Foghorn is a leader in
Slide 9: Selective SMARCA2 Program
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 Selective SMARCA2 Selective SMARCA2 Inhibitor FHD-909* Degrader Exploit the synthetic lethal relationship between SMARCA2 and Biology mutated SMARCA4 Phase 1 monotherapy dose escalation Advancing t
Slide 11: Selective SMARCA2 Inhibition: Exploiting Synthetic Lethal Relationship
Selective SMARCA2 Inhibition: Promising Strategy to Exploit Synthetic Lethal Relationship Between SMARCA2 and Mutant SMARCA4 Healthy Cells Cancer Cells BAF BAF BAF Complex Complex Complex SMARCA2i Mutant SMARCA4 SMARCA2 SMARCA4 SMARCA2 SMARCA4 No SMARCA4 Mutations SMARCA4 Mutation SMARCA4 Mutation a
Slide 12: SMARCA4 is Mutated in Up to 10% of NSCLC
SMARCA4 is Mutated in Up to 10% of NSCLC; Up to 5% of Solid Tumors SMARCA4 mutated across a broad range of tumors Accounts for ~5% of solid tumors 12 | AACR GENIE via cBioPortal
Slide 13: FHD-909: Goal 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 Relevant treatment regimens in each line of therapy for metastatic NSCLC* 1st Line NSCLC Pembrolizumab-based regimens Other immune checkpoint inhibitor-based regimens 2nd Line NSCLC Chemotherapy-based Chemotherapy-b
Slide 14: Significant Unmet Medical Need in NSCLC Metastatic Setting for SMARCA4 Patients
Significant Unmet Medical Need in NSCLC Metastatic Setting for SMARCA4 Patients Frontline NSCLC Metastatic – PD1 + Chemo1 Significant Unmet Need in SMARCA4-mutated NSCLC Response Rate (%) PFS (months) OS (months) • Poor response to 1L chemo-immunotherapy for patients with SMARCA4 mutations1 39.1% Si
Slide 15: SMARCA4 Mutations are Consequential in NSCLC
SMARCA4 Mutations are Consequential – in NSCLC, Patients with Mutated SMARCA4 Have Significantly Worse Clinical Outcomes Overall Survival for SMARCA4 wt vs SMARCA4 mut1; SMARCA4 Mutated in Up to 10% of NSCLC Tumors, Frontline Metastatic NSCLC w/ Chemoimmunotherapy Minimal Overlap w/ Other Mutations2
Slide 16: SMARCA4 and KRAS Co-Occurring Mutations Have Worse Outcomes
When SMARCA4 and KRAS Mutations Co-Occur, Patients Have Even Worse Outcomes to Standard of Care Treatment Overall Response Rate (ORR) Progression-Free Survival (PFS) Overall Survival (OS) Median PFS, months (95% CI) Median OS, months (95% CI) P = 0.03 KRAS mut + SMARCA4 wt (n:159): 4.1 (2.8–6.0) KRA
Slide 17: A First-in-Human Phase 1 Trial of FHD-909
A First-in-Human Phase 1 Trial of FHD-909 in Advanced Solid Tumor Patients with SMARCA4 Mutations Phase 1b Dose Expansionb Phase 1a Dose Escalation Presence of a Known or Likely Loss of Function of SMARCA4 Advanced solid tumors with any Cohort A1 SMARCA4 alteration Randomized (mTPI-2 method with bac
Slide 18: FHD-909 with Anti-PD1 Demonstrates Complete and Durable Regression
FHD-909 in Combination with Anti-PD1 Demonstrates Complete and Durable Regression Double Combo Efficacy (LY4050784, anti-PD1, chemo) MB49 SMARCA4 KO Syngeneic Model % body weight change Body weight percentage change (%) • FHD-909 monotherapy demonstrates better efficacy (tumor regression) than chemo
Slide 19: Lack of Tumor Formation in CR Mice Suggests Immune Memory
Lack of Tumor Formation in CR Mice After Re-inoculation Suggests Immune Memory Formation Re-challenge of Mice After CR with FHD-909 + Anti-PD1 Combos Tumor volume (mm3) (~70 days after dosing stopped) • Complete response (CR) mice were re-challenged with MB49 SMARCA4-KO cells alongside age-matched n
Slide 20: Degrader Programs
Degrader Programs • Selective EP300 Degrader • Selective CBP Degrader • Selective ARID1B Degrader 20
Slide 21: Developing a Portfolio of Novel and Selective Degraders
Developing a Portfolio of Novel and Selective Degraders with Blockbuster Potential Selective EP300 Selective CBP Selective ARID1B Degrader Degrader Degrader • Heme malignancies (including MM and • ER+ breast cancer • Mutated in up to 5% of all DLBCL) and prostate solid tumors • Highly selective and
Slide 22: CBP and EP300 Proteins – A Decades-long Challenge in Selectivity
CBP and EP300 Proteins – A Decades-long Challenge in Selectivity Ac CoA CBP and EP300 Biology CBP/ EP300 • CBP and EP300 are highly homologous, paralog histone CoA acetyltransferases regulating enhancer-mediated transcription and protein stability • Dysregulation of CBP and EP300 has been implicated
Slide 23: Selective EP300 Degrader
Selective EP300 Degrader For CBP-mutant and EP300-dependent Cancers 23
Slide 24: Summary: Selective EP300 Degrader for Heme Malignancies and Prostate Cancer
Summary: Selective EP300 Degrader for Heme Malignancies and Prostate Cancer Asset Description Initial Opportunity (U.S.) EP300-dependent Target / • E1A binding protein p300 (EP300) Hematological Incidence* Approach Malignancies • Targeted protein degrader MM 31K • Broad range of heme malignancies In
Slide 25: EP300 Degradation Shows Anti-Proliferative Activity in Hematological Malignancies
EP300 Degradation Shows Anti-Proliferative Activity in Broad Range of Hematological Malignancies Anti-Tumor Activity Across Full Range of Heme Sub-Lineages (~ 70% of All Tested Cell Lines are Sensitive) MM: Multiple Myeloma; DLBCL: Diffuse Large B-Cell Lymphoma; AML: Acute Myeloid Leukemia; BL: Burk
Slide 26: EP300 Degradation Results in Tumor Growth Inhibition in MM, DLBCL and Prostate Models
EP300 Degradation Results in Significant Tumor Growth Inhibition in MM, DLBCL and Prostate Models Multiple Myeloma (MM1S) CDX DLBCL (KARPAS422) CDX AR+ Prostate (VCaP) CDX 3,000 2,000 Vehicle Vehicle FHT-EP300d - 53, SC, 10mg/kg (QD) FHT-EP300d - 32, SC, 10mg/kg (BID) 2,500 FHT-EP300d - 53, SC, 30mg
Slide 27: FHT-273 Shows Superior Efficacy and Tolerability Compared to Inobrodib
Selective EP300 Degrader FHT-273 Shows Superior Efficacy and Tolerability Compared to Clinical Benchmark Inobrodib FHT-101273 Demonstrates Dose-responsive Efficacy, Including Selective Degrader Spares Platelets Complete Responses, in MM1S CDX Model Vehicle Vehicle CCS1477(Inobrodib), 20mpk, QD, p.o
Slide 28: VHL-based EP300 Degrader Maintains Activity in IMiD Resistant Cell Lines
VHL-based Selective EP300 Degrader Maintains Activity in IMiD Resistant Cell Lines dEP300-9 pomalidomide lenalidomide dEP300-9 mezigdomide iberdomide Resistant MM1S cell lines were developed through 5–6 months of in vitro exposure to gradually increasing concentrations of lenalidomide, pomalidomide,
Slide 29: EP300 Degrader Superior in IMiD Resistant Multiple Myeloma Model
Selective EP300 Degrader Shows Superior Efficacy Compared to Pomalidomide and Inobrodib in an IMiD Resistant Multiple Myeloma Model Pomalidomide-resistant Multiple Myeloma CDX (MM1S-PomR) Treated with EP300d-007 4000 3000 2000 Vehicle 1000 Pomalidomide, 10mpk, QD, p.o. CCS1477 (Inobrodib), 20mpk, QD
Slide 30: FHT-273: Potent and Selective EP300 Degrader
FHT-273: Potent and Selective EP300 Degrader FHT-273 Rapidly and Potently Degrades EP300, but Not Its Global Proteomics Confirms that FHT-273 Paralog CBP is Selective FHT-273 EP300 Kinetics FHT-273 DC50 0.3nM Dmax 96% Rate 1.8 hr-1 FHT-273 CBP Kinetics 333nM FHT-273/DMSO 8hr Log2FC 30 |
Slide 31: Development Vision: EP300 in Hematological Malignancies
Development Vision: EP300 in Hematological Malignancies Dose Expansion/ Phase 1a Dose Escalation Registration Explore Combinations Patients with r/r hematological Register in specific hematological malignancies malignancies single agent or MM DLBCL as part of combination regimen e Dose Level n EP300
Slide 32: Selective CBP Degrader, FHT-171
Selective CBP Degrader, FHT-171 For EP300-mutant and CBP-dependent Cancers 32
Slide 33: Summary: Selective CBP Degrader for CBP-dependent & EP300-mutant Cancers
Summary: Selective CBP Degrader for CBP-dependent & EP300-mutant Cancers Asset Description Initial Opportunity (U.S.) CBP-dependent Incidence* • CREB binding protein (CBP) Cancers** Target / Approach • Targeted protein degrader ER+ breast 210K NA NA cancer EP300 mut. EP300 mut. EP300 mut. Incidence*
Slide 34: FHT-171 Disrupts Estrogen Receptor Signaling in Breast Cancer
FHT-171 Disrupts Estrogen Receptor (ER) Signaling in Breast Cancer FHT-171 Reduces ER Levels in Wildtype ESR1 FHT-171 Suppresses ER Target Genes, Breast Cancer Cell Lines T47D and CAMA1 Comparable to Fulvestrant 1.5 T47D Set of Estrogen Controlled Genes ER levels normalized to DMSO control 1.0 HALLM
Slide 35: FHT-171 Demonstrates Anti-tumor Efficacy in Resistant ER+ Breast Cancer Models
FHT-171 Demonstrates Anti-tumor Efficacy as a Monotherapy in Standard-of-care Resistant ER+ Breast Cancer Models ER+ Metastatic Breast Cancer CDX ER+ Metastatic Breast Cancer PDX ER+ Metastatic Breast Cancer PDX (ST941C; ESR1m) (ST4887B, ESR1 wt) (ST4680D, ESR1m) 1000 1000 Tumor Volume (mm3) +/- SEM
Slide 36: FHT-171 Shows No Impact on Platelet Counts and Spared Megakaryocytes
CBP FHT-171 Shows No Impact on Platelet Counts and Spared Megakaryocytes • Platelet Counts Post Two Weeks of Dosing Human Megakaryocyte Cell Viability Assay (In Vivo – Control Mice) (In Vitro**) Vehicle 2,500 FHT-171, 10mg/kg, SC, QD Dual BD inhibitor, (GNE-781), 30mg/kg, PO, BID Dual BD inhibitor (
Slide 37: FHT-171: Potent and Selective CBP Degrader
CBP FHT-171: Potent and Selective CBP Degrader • FHT-171 Rapidly and Potently Degrades CBP, Global Proteomics Confirms that but not its Paralog EP300 FHT-171 is Selective FHT-171 CBP Kinetics Dmax: 97% Max Rate: 3.2 hr-1 DC50: 30pM FHT-171 EP300 Kinetics Dmax: 5% Max Rate: N/A 100nM CBPd-171/DMSO 3h
Slide 38: Selective CBP Degradation Results in 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) 1,500 Vehicle Tumor Volume (mm³ + SEM) FHT-CBPd-59, 10mg/kg (QD) Tumor Volume (mm3 ± SEM
Slide 39: Long-Acting Injectable Formulation Enables Weekly Sub-cutaneous Delivery
Long-Acting Injectable Formulation of CBPd-171 Enables Weekly Sub-cutaneous (SC) Delivery Tumor Growth Inhibition Observed in EP300mut (AGS) Gastric Model (Daily Injections and SC weekly LAI Injection) • Weekly LAI injection of CBDd-171 results in Tumor Volume (mm³ + SEM) efficacy comparable to dail
Slide 40: Development Vision: CBP Degrader as Combination Partner in ER+ Breast Cancer
Development Vision: CBP Degrader has the Potential to be an Attractive Combination Partner in ER+ Breast Cancer and Beyond Phase 1b Dose Expansion / Phase 1a Dose Escalation Registration Combination ER+ BC patients who failed Expansion cohorts Advance selected combinations at least 2L in advanced /
Slide 41: Selective ARID1B Degrader
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 Asset Description Initial Opportunity (U.S.) ARID1A mut. ARID1A mut. Incidence* Frequency Incidence Target / • ARID1B Approach • Targeted protein degrader Endometrial cancers 66K 38% 25K Gastric 37K 20% 7K Stage
Slide 43: ARID1B: Drugging A Previously Undruggable Target
ARID1B: Drugging A Previously Undruggable Target ARID1A/B Drug Targeting Considerations BAF Nucleosome • Large and highly unstructured protein ~ 240 kDa • No known enzymatic function • Member of large, multi-subunit complex • High sequence homology (~60%) to ARID1A Approach • Discover binders to ARI
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 FHT-654: DC50: 0.35 uM CEREBLON DC50: 3.7 uM VHL 44 | ARID1B-HiBiT HCT116 Colorectal Cell Line
Slide 45: Selective ARID1B Degradation Demonstrated by Global Proteomics
Selective ARID1B Degradation Demonstrated by Global Proteomics FHT-654 Cereblon-based Degrader ARID1A Log2FC ARID1B degrader 2.5uM/DMSO 24 hr 45 | 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 ARID1B 48h Downregulated Upregulated Protein expression Gene 48h Gene 48h Relative expression Relative expression Relative expression 63 M 25 n M 50 n M 63 M 63 O nM 12 nM 10 n M 25 n M 50 n M 10 n M 12 nM 25 nM 50
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 Leader in Unique Area Large Market Well- Value Major Strategic of Cancer Biology Potential Funded Drivers Collaboration Chromatin biology is $167.6 million in cash Strategic collaboration with Foghorn is a leader in
Slide 48: Unique biology, Precision therapeutics, Broad impact
Unique biology Precision therapeutics Broad impact August 2026 48
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 NCI-H2126 Reduction in Tumor Volume NCI-H2126 Body Weight TumorVolume Tumor (mm33)) volume (mm Genetic Background: SMARCA4 W764R, TP53 E62*, STK11-/-, CDKN2A-/-, KEAP1 R272C 51 | Note: All
Slide 52: FHD-909 Monotherapy Activity Across SMARCA4-mutant NSCLC Models
FHD-909 Monotherapy Demonstrated Strong In Vivo Activity Across SMARCA4-mutant NSCLC Models at Tolerated Doses A549 Model RERF-LC-AI Model NCI-H1793 Model 500 Vehicle Control FHD-909, 20mg/kg, BID, PO FHD-909, 40mg/kg, BID, PO 400 FHD-909, 60mg/kg, BID, PO 300 200 100 0 7 14 21 28 Days of Dosing (Do
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 FHD-909 + cisplatin + pemetrexed A549 (SMARCA4mt, KRAS G12S) 1200 In vivo, combining FHD-909 with cisplatin and pemetrexed increased antitumor 1000 effect, r
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 FHD-909 + cisplatin + paclitaxel RERF-LC-AI (SMARCA4mt) 1400 In vivo, combining FHD-909 with cisplatin 1200 and paclitaxel increased antitumor effect, Tumor Volum
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 NCI-H2030, Lung, NSCLC PATU-8988T, Pancreas, PDAC A549, Lung, NSCLC SMARCA4-/- KRAS(G12C) SMARCA4 - / fusion, KRAS(G12D)* SMARCA4 Q729fs/H736Y, KRAS(G12S) 120 [LY4066434](nM) 100 900 Inhibition (%) Inhibition (%)
Slide 56: FHD-909 with KRAS Inhibitors Synergistic In Vivo (olomorasib)
Combination of FHD-909 with KRAS Inhibitors Demonstrates Synergistic Activity in SMARCA4, KRAS Co-mutated Human NSCLC Xenograft Models In Vivo 3000 FHD-909 + olomorasib (KRAS G12C inh) NCI-H2030 (SMARCA4mt, KRAS G12C) ## synergistic (p<0.05) 2500 Tumor Volume (mm3) 2000 Combination of FHD-909 with o
Slide 57: FHD-909 with KRAS Inhibitors Synergistic In Vivo (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) Combination of FHD-909 with pan-KRAS inhibitor resulted in synergistic antitumor activity and sustained tu
Slide 58: FHD-909 with Pembrolizumab Enhanced 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 FHD-909 (20 mg/kg) + pembrolizumab FHD-909 (40 mg/kg) + pembrolizumab A549 (SMARCA4mt, KRAS G12S) A549 (SMARCA4mt, KRAS G12S) FHD-909 sensitized the tumor cell
Slide 59: Selective SMARCA2 Degrader Achieved Complete Degradation In Vitro
Selective SMARCA2 Degrader Achieved Complete SMARCA2 Degradation and Cell Growth Inhibition In Vitro SMARCA2 / SMARCA4 HIBIT Data A549 Ten-Day Proliferation Assay 100 SMARCA2 75 % Degradation 50 25 0 SMARCA4 1E-3 0.01 0.1 1 10 Concentration (uM) Degraders Caused Time- and Dose-dependent SMARCA2 Degr
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 Theoretical Experimental Experimental Kinetic Profile Kinetic Profile Rate vs. Dmax Native Deg Rate Target Level Fractional Loss Dmax10 Dmax25 Dmax50 Dmax80 Dmax95 Time • Slower rates lead to partial degradation, faster rates to complete loss • Rate i
Slide 62: Degradation Rate Dictates Dmax – Program Independent
Degradation Rate Dictates Dmax – Program Independent Foghorn BRD9 Program Foghorn CBP Program Foghorn EP300 Program Large scale experimental kinetic analysis for a program reveals the relationship between rate and Dmax 62 |
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 Prelude SMARCA2 (VHL) Degrader Prelude SMARCA2 (CRBN) Degrader Concentration Concentration Rate max (ƛ) hr-1: 1.5 Rate max (ƛ) hr-1: 0.4 Fractional Luminescence Fractional Luminescence Hook Effect Loss Loss Hook Effect (
Slide 64: Foghorn Analysis and Dmax Results Match Published Prelude Data
Foghorn Analysis and Dmax Results Match Published Prelude Data Prelude Published Data Foghorn Replicated Data from Prelude Patents Prelude PRT3789 (VHL) 1 Prelude (VHL) Degrader % Degradation Prelude PRT7732 (CRBN) 2 % Degradation Prelude (CRBN) Degrader % Protein 1. AACR-NCI-EORTC 2023 Poster B113