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Platform with Potential to Impact Millions of Patients February 16, 2021Exhibit 99.1 Targeting the Chromatin Regulatory System A Product Platform with Potential to Impact Millions of Patients February 16, 2021
Precision Oncology: Novel Biology with Breadth and Depth Large Market
Potential / Precision Approach Experienced Leadership Team Expertise across drug discovery, clinical development Biology implicated in up to 50% of cancer potentially and commercialization impacting ~2.5 million patients Over
220 drug candidates into the clinic and over 30 drugs approved Novel Biology and Targets Multiple Drugging Approaches Targeting the chromatin regulatory system Synthetic lethality Integrated and scalable platform
Protein degradation Chromatin remodeling complexes, transcription factors, Transcription factor disruptors and other components Potential applications beyond oncology in diseases including virology, autoimmune disease and neurology
2Precision Oncology: Novel Biology with Breadth and Depth Large Market Potential / Precision Approach Experienced Leadership Team Expertise across drug discovery, clinical development Biology implicated in up to 50% of cancer
potentially and commercialization impacting ~2.5 million patients Over 220 drug candidates into the clinic and over 30 drugs approved Novel Biology and Targets Multiple Drugging Approaches Targeting the chromatin regulatory system
Synthetic lethality Integrated and scalable platform Protein degradation Chromatin remodeling complexes, transcription factors, Transcription factor disruptors and other components Potential applications
beyond oncology in diseases including virology, autoimmune disease and neurology 2
On Track for Entry Into the Clinic with First Two Programs Precision
Oncology / Breadth and Depth Global Program / Target Modality Discovery IND-enabling Phase 1 Phase 2 Phase 3 Rights AML FHD-286 Enzyme inhibitor (BRG1 / BRM) Uveal melanoma FHD-609 Protein degrader Synovial sarcoma (BRD9) Enzyme inhibitor BRG1
mutated Selective BRM & protein degrader cancers ARID1A mutated Selective ARID1B Protein degrader cancers Partnered program Transcription factor disruptor (undisclosed) Gene Traffic Control Platform Using our proprietary Gene Traffic
Control platform, we have identified additional genetically determined dependencies to drug using enzymatic inhibitors, protein degraders and transcription factor disruptors 3On Track for Entry Into the Clinic with First Two Programs Precision
Oncology / Breadth and Depth Global Program / Target Modality Discovery IND-enabling Phase 1 Phase 2 Phase 3 Rights AML FHD-286 Enzyme inhibitor (BRG1 / BRM) Uveal melanoma FHD-609 Protein degrader Synovial sarcoma (BRD9) Enzyme inhibitor BRG1
mutated Selective BRM & protein degrader cancers ARID1A mutated Selective ARID1B Protein degrader cancers Partnered program Transcription factor disruptor (undisclosed) Gene Traffic Control Platform Using our proprietary Gene Traffic
Control platform, we have identified additional genetically determined dependencies to drug using enzymatic inhibitors, protein degraders and transcription factor disruptors 3
Our Gene Traffic Control Platform Makes It Possible to Understand and
Drug Genetic Dependencies within the Chromatin Regulatory System Integrated, Scalable, Efficient - Repeatable Paradigm Production of Discovery and Translation to Clinic Chromatin Regulatory Target Identification Targeted Protein Optimization
of and Identification of System Components And Validation Degradation Chemical Matter Biomarkers at Scale & Proprietary Assays 4Our Gene Traffic Control Platform Makes It Possible to Understand and Drug Genetic Dependencies within the Chromatin
Regulatory System Integrated, Scalable, Efficient - Repeatable Paradigm Production of Discovery and Translation to Clinic Chromatin Regulatory Target Identification Targeted Protein Optimization of and Identification of System Components And
Validation Degradation Chemical Matter Biomarkers at Scale & Proprietary Assays 4
Experienced Leadership Team with Industry Leading Advisors and Investors
SENIOR LEADERSHIP TEAM Adrian Gottschalk, President & CEO Carl Decicco, Ph.D., CSO Sam Agresta, M.D., M.P.H., CMO Michael LaCascia, CLO Development through commercialization in >200 drugs transitioned to the clinic, Global drug approval
experience, Former GC, Vertex Pharmaceuticals, global law multiple therapeutic areas across >25 20 approvals 3 drug approvals and compliance experience, 2 drug approvals drug programs Steve Bellon, Ph.D., SVP, Drug Discovery Allan Reine,
M.D., CFO Carlos Costa, SVP, HR Fanny Cavalie, SVP, Business & Operations 20+ years in industry drugging novel targets, 15 years biotech investor and public 20+ years worldwide experience across Global development through launch for >20
drugs, incl. bromo platform at Constellation multiple countries and regions portfolio and BD strategy experience company CFO BOARD OF DIRECTORS SCIENTIFIC AND OTHER ADVISORS Doug Cole, M.D. Adrian Gottschalk Charles Sawyers, M.D. David Schenkein,
M.D. Flagship Pioneering - Foghorn President & CEO MSKCC, HHMI - SAB Chair General Partner, GV Board Chair; Founder Jose Baselga, M.D., Ph.D. Cigall Kadoch, Ph.D. Gerald Crabtree, M.D. Tony Kouzarides, Ph.D. Gurdon Institute -
University of Cambridge AstraZeneca R&D Oncology Dana-Farber, Broad, HMS; Founder Stanford, HHMI; Founder Scott Biller, Ph.D. Adam Koppel, M.D., Ph.D. Faheem Hasnain Ian Smith Bain Capital Life Sciences Gossamer Bio, Chair of Mirati Former COO
Vertex Pharmaceuticas, Former CSO and Strategic Advisor, Agios Chair of Solid Bio., Chair of ViaCyte Simba Gill, Ph.D. Michael Mendelsohn, M.D. Craig Peterson, Ph.D. Cardurion Pharmaceuticals Professor UMass Medical School Evelo Biosciences, Partner
at Flagship Pioneering 5Experienced Leadership Team with Industry Leading Advisors and Investors SENIOR LEADERSHIP TEAM Adrian Gottschalk, President & CEO Carl Decicco, Ph.D., CSO Sam Agresta, M.D., M.P.H., CMO Michael LaCascia, CLO Development
through commercialization in >200 drugs transitioned to the clinic, Global drug approval experience, Former GC, Vertex Pharmaceuticals, global law multiple therapeutic areas across >25 20 approvals 3 drug approvals and compliance experience, 2
drug approvals drug programs Steve Bellon, Ph.D., SVP, Drug Discovery Allan Reine, M.D., CFO Carlos Costa, SVP, HR Fanny Cavalie, SVP, Business & Operations 20+ years in industry drugging novel targets, 15 years biotech investor and
public 20+ years worldwide experience across Global development through launch for >20 drugs, incl. bromo platform at Constellation multiple countries and regions portfolio and BD strategy experience company CFO BOARD OF DIRECTORS SCIENTIFIC AND
OTHER ADVISORS Doug Cole, M.D. Adrian Gottschalk Charles Sawyers, M.D. David Schenkein, M.D. Flagship Pioneering - Foghorn President & CEO MSKCC, HHMI - SAB Chair General Partner, GV Board Chair; Founder Jose Baselga, M.D., Ph.D.
Cigall Kadoch, Ph.D. Gerald Crabtree, M.D. Tony Kouzarides, Ph.D. Gurdon Institute - University of Cambridge AstraZeneca R&D Oncology Dana-Farber, Broad, HMS; Founder Stanford, HHMI; Founder Scott Biller, Ph.D. Adam Koppel, M.D., Ph.D.
Faheem Hasnain Ian Smith Bain Capital Life Sciences Gossamer Bio, Chair of Mirati Former COO Vertex Pharmaceuticas, Former CSO and Strategic Advisor, Agios Chair of Solid Bio., Chair of ViaCyte Simba Gill, Ph.D. Michael Mendelsohn, M.D. Craig
Peterson, Ph.D. Cardurion Pharmaceuticals Professor UMass Medical School Evelo Biosciences, Partner at Flagship Pioneering 5
The Chromatin Regulatory System Orchestrates Gene ExpressionThe
Chromatin Regulatory System Orchestrates Gene Expression
The Chromatin Regulatory System Orchestrates Gene Expression Two Major
Components Work in Concert - Chromatin Remodeling Complexes and Transcription Factors 1 3 Work together to orchestrate Once chromatin unpacked, gene expression gene expression can occur Chromatin Chromatin remodeling Transcription Factor complex
Normal gene expression Right genes Chromatin - compacted 2 form of DNA inside the TF's guide chromatin remodeling nucleus of the cell complexes to the right locations 7The Chromatin Regulatory System Orchestrates Gene Expression Two
Major Components Work in Concert - Chromatin Remodeling Complexes and Transcription Factors 1 3 Work together to orchestrate Once chromatin unpacked, gene expression gene expression can occur Chromatin Chromatin remodeling Transcription Factor
complex Normal gene expression Right genes Chromatin - compacted 2 form of DNA inside the TF's guide chromatin remodeling nucleus of the cell complexes to the right locations 7
Breakdowns in the Chromatin Regulatory System Lead to Disease Mutations
in Chromatin Remodeling Complex Result in Abnormal Gene Expression Mutated or Overexpressed TF Hijacks Chromatin Remodeling Complex to Wrong Location DISEASE DISEASE 8Breakdowns in the Chromatin Regulatory System Lead to Disease Mutations in
Chromatin Remodeling Complex Result in Abnormal Gene Expression Mutated or Overexpressed TF Hijacks Chromatin Remodeling Complex to Wrong Location DISEASE DISEASE 8
Chromatin Regulatory System Implicated in Over 50% of Cancers
Potentially Impacting Over 2.5M Patients 28 Chromatin Remodeling BAF Complex and Associated Transcription Factors Complexes and >1,000 TFs + BAF Complex Subunits Estimate >100 Transcription Mutated and Dysregulated Factors Associated with just
in Cancer the BAF Complex 9Chromatin Regulatory System Implicated in Over 50% of Cancers Potentially Impacting Over 2.5M Patients 28 Chromatin Remodeling BAF Complex and Associated Transcription Factors Complexes and >1,000 TFs + BAF Complex
Subunits Estimate >100 Transcription Mutated and Dysregulated Factors Associated with just in Cancer the BAF Complex 9
Mutations Lead to Disease Specific Genetic Dependencies on the
Chromatin Regulatory System Novel Targets Tailored Drugging Approaches Enzymatic Inhibitors: Highly selective and allosteric Mutations in Chromatin small molecule inhibitors Remodeling Complexes ATP ADP Targeted Protein Degradation: Transcription
Factor Bi-functional protein degraders for Mutations / Overexpression targets with no enzymatic activity Potential Mutations that Impinge on Transcription Factor druggable the Chromatin Regulatory Disruptors: sites Disrupt interactions between
System chromatin remodeling complexes and transcription factors 10Mutations Lead to Disease Specific Genetic Dependencies on the Chromatin Regulatory System Novel Targets Tailored Drugging Approaches Enzymatic Inhibitors: Highly selective and
allosteric Mutations in Chromatin small molecule inhibitors Remodeling Complexes ATP ADP Targeted Protein Degradation: Transcription Factor Bi-functional protein degraders for Mutations / Overexpression targets with no enzymatic activity Potential
Mutations that Impinge on Transcription Factor druggable the Chromatin Regulatory Disruptors: sites Disrupt interactions between System chromatin remodeling complexes and transcription factors 10
Pursuing a Precision Oncology Approach Each Program is Based on a
Genetically Defined Dependency Mutation / Target Patient Program Genetic Dependency Drug Approach Abberation Population* AML Elevated BRG1 expression BRG1 (20,000) Enzymatic Inhibitor FHD-286 SOX10 / MITF / BAF Uveal Melanoma GNAQ/GNA11 complex
(5,000) Synovial Sarcoma Protein Degrader FHD-609 SS18-SSX1, SSX2, SSX4 BRD9 (>1,800) BRG1 mutated cancers Enzymatic Inhibitor / Protein Selective BRM BRG1 BRM Degrader (>100K) ARID1A mutated cancers Protein Degrader Selective ARID1B ARID1A
ARID1B (>175K) Specific TF - Chromatin Transcription Factor Disruptor Transcription Factors Various Various Remodeling Complex *U.S., EU5, Japan 11Pursuing a Precision Oncology Approach Each Program is Based on a Genetically Defined
Dependency Mutation / Target Patient Program Genetic Dependency Drug Approach Abberation Population* AML Elevated BRG1 expression BRG1 (20,000) Enzymatic Inhibitor FHD-286 SOX10 / MITF / BAF Uveal Melanoma GNAQ/GNA11 complex (5,000) Synovial Sarcoma
Protein Degrader FHD-609 SS18-SSX1, SSX2, SSX4 BRD9 (>1,800) BRG1 mutated cancers Enzymatic Inhibitor / Protein Selective BRM BRG1 BRM Degrader (>100K) ARID1A mutated cancers Protein Degrader Selective ARID1B ARID1A ARID1B (>175K) Specific
TF - Chromatin Transcription Factor Disruptor Transcription Factors Various Various Remodeling Complex *U.S., EU5, Japan 11
FHD-286: Clinical Entry Point - AML and Uveal Melanoma FHD-286 is a
Potent, Selective, Allosteric, Small Molecule Inhibitor of the BRG1 and BRM subunits of the BAF complexFHD-286: Clinical Entry Point - AML and Uveal Melanoma FHD-286 is a Potent, Selective, Allosteric, Small Molecule Inhibitor of the BRG1 and BRM
subunits of the BAF complex
FHD-286 Targets Abnormal Dependencies on BAF in Cancer BAF Chromatin
Remodeling Complex BRG1/BRM ATPase Target / Approach Small molecule, allosteric, oral enzymatic inhibitor Acute myelogenous leukemia (AML) Uveal melanoma Indications Indication expansion work ongoing in
multiple solid tumors AML: BRG1 elevated in blast cells Mutation / Aberration Uveal Melanoma: GNAQ/GNA11 mutated UM is driven by an abnormal dependency on BAF BRG1 BRM Program Status On track for clinical data as early as
Q4'21 BRG and BRM Subunits AML: Over 20,000 relapsed and/or New Patients refractory patients Impacted BRM/BRG1 is the engine (ATPase) of the BAF chromatin / year* Uveal melanoma: Over 5,000 patients remodeling complex
BRG1 & BRM are highly similar proteins * US, EU5, Japan 13FHD-286 Targets Abnormal Dependencies on BAF in Cancer BAF Chromatin Remodeling Complex BRG1/BRM ATPase Target / Approach Small molecule, allosteric, oral
enzymatic inhibitor Acute myelogenous leukemia (AML) Uveal melanoma Indications Indication expansion work ongoing in multiple solid tumors AML: BRG1 elevated in blast cells Mutation / Aberration Uveal
Melanoma: GNAQ/GNA11 mutated UM is driven by an abnormal dependency on BAF BRG1 BRM Program Status On track for clinical data as early as Q4'21 BRG and BRM Subunits AML: Over 20,000 relapsed and/or New Patients refractory
patients Impacted BRM/BRG1 is the engine (ATPase) of the BAF chromatin / year* Uveal melanoma: Over 5,000 patients remodeling complex BRG1 & BRM are highly similar proteins * US, EU5, Japan 13
Therapeutic Rationale for AML: Blast Cells Dependent on BRG1-BAF
Cancerous blast Intervention cells rely on elevated decreases BRG1- BRG1-BAF BAF activity expression BRG1 BRG1 expression expression level level Disease State Treatment with FHD-286 Differentiation HSC Loss of blast phenotype / AML blasts stuck in
BAF-dependent proliferative phase Apoptosis 14Therapeutic Rationale for AML: Blast Cells Dependent on BRG1-BAF Cancerous blast Intervention cells rely on elevated decreases BRG1- BRG1-BAF BAF activity expression BRG1 BRG1 expression expression level
level Disease State Treatment with FHD-286 Differentiation HSC Loss of blast phenotype / AML blasts stuck in BAF-dependent proliferative phase Apoptosis 14
Treatment with FHD-286 of Patient-Derived AML Tumor Samples was
Associated with both Differentiation and Cytoreduction Patient #1 Sample BM-de novo AML Patient #2 Sample BM-secondary AML Patient #3 Sample BM-secondary AML Exposure-dependent differentiation effect and cytoreduction (Cytoreduction is equivalent to
standard of care) Total Blasts Differentiation-like Blasts Immature Blasts Patient #1 Sample: Example of exposure-dependent differentiation effect 15Treatment with FHD-286 of Patient-Derived AML Tumor Samples was Associated with both Differentiation
and Cytoreduction Patient #1 Sample BM-de novo AML Patient #2 Sample BM-secondary AML Patient #3 Sample BM-secondary AML Exposure-dependent differentiation effect and cytoreduction (Cytoreduction is equivalent to standard of care) Total Blasts
Differentiation-like Blasts Immature Blasts Patient #1 Sample: Example of exposure-dependent differentiation effect 15
Dose-Dependent Tumor Growth Inhibition Observed with FHD-286 Treatment
in AML CDX Models Tumor Volume Body Weight 120 1250 1000 110 750 100 MV4-11 500 CDX Model 90 (FLT3 ITD, MLL-AF4) 250 0 80 0 7 14 21 0 7 14 21 Days Post Treatment Days Post Treatment Tumor Volume Body Weight 3200 120 2400 110 OCI-AML2 1600 100 CDX
Model (MII-AF6, DNMT3a mut.) 800 90 0 80 0 7 14 21 0 7 14 21 Days Post Treatment Days Post Treatment 16 3 3 Tumor Volume (mm ) Tumor Volume (mm ) Body Weight Change (%) Body Weight Change (%)Dose-Dependent Tumor Growth Inhibition Observed with
FHD-286 Treatment in AML CDX Models Tumor Volume Body Weight 120 1250 1000 110 750 100 MV4-11 500 CDX Model 90 (FLT3 ITD, MLL-AF4) 250 0 80 0 7 14 21 0 7 14 21 Days Post Treatment Days Post Treatment Tumor Volume Body Weight 3200 120 2400 110
OCI-AML2 1600 100 CDX Model (MII-AF6, DNMT3a mut.) 800 90 0 80 0 7 14 21 0 7 14 21 Days Post Treatment Days Post Treatment 16 3 3 Tumor Volume (mm ) Tumor Volume (mm ) Body Weight Change (%) Body Weight Change (%)
Therapeutic Rationale for Uveal Melanoma: Dependency on Overexpression
of the MITF / SOX10 Transcription Factors and the BAF Complex Inhibiting BRG1/BRM to shut down the abnormal TF interaction with the BAF complex Biology Validation of Dependency and Approach MITF ChIPseq Over 85% of uveal melanoma cancers have GNAQ
or GNA11 mutations MITF SOX10 ChIPseq SOX10 17Therapeutic Rationale for Uveal Melanoma: Dependency on Overexpression of the MITF / SOX10 Transcription Factors and the BAF Complex Inhibiting BRG1/BRM to shut down the abnormal TF interaction with the
BAF complex Biology Validation of Dependency and Approach MITF ChIPseq Over 85% of uveal melanoma cancers have GNAQ or GNA11 mutations MITF SOX10 ChIPseq SOX10 17
FHD-286 was Associated with Dose-Dependent Tumor Regression in Uveal
Melanoma CDX Models at Tolerated Doses Tumor Volume Body Weight MP-46 uveal melanoma 1200 120 CDX model 900 110 Dose-dependent tumor growth 600 100 inhibition 300 90 Well tolerated 0 80 0 7 14 21 28 0 7 14 21 28 Days Post Treatment
Days Post Treatment Tumor Volume Body Weight 900 120 92-1 uveal melanoma 750 CDX model 110 600 Dose-dependent tumor growth 450 100 inhibition 300 90 Tumor regression at 1.5 mg/kg, 150 PO, QD 0 80 0 5 10 15 20 0 5 10 15 20
Well tolerated Days Post Treatment Days Post Treatment 18 3 3 Tumor Volume (mm ) Tumor Volume (mm ) Body Weight Change (%) Body Weight Change (%)FHD-286 was Associated with Dose-Dependent Tumor Regression in Uveal Melanoma CDX Models at Tolerated
Doses Tumor Volume Body Weight MP-46 uveal melanoma 1200 120 CDX model 900 110 Dose-dependent tumor growth 600 100 inhibition 300 90 Well tolerated 0 80 0 7 14 21 28 0 7 14 21 28 Days Post Treatment Days Post Treatment Tumor Volume
Body Weight 900 120 92-1 uveal melanoma 750 CDX model 110 600 Dose-dependent tumor growth 450 100 inhibition 300 90 Tumor regression at 1.5 mg/kg, 150 PO, QD 0 80 0 5 10 15 20 0 5 10 15 20 Well tolerated Days Post Treatment
Days Post Treatment 18 3 3 Tumor Volume (mm ) Tumor Volume (mm ) Body Weight Change (%) Body Weight Change (%)