Forma Therapeutics Holdings Inc
Forma Therapeutics — Investor Day (May 2022)
85 slides from Forma Therapeutics's investor day presentation, May 26, 2022
Slide 1: Research and Development Day May 26, 2022
Research and Development Day May 26, 2022 8:00–10:00 a.m. EDT Exhibit 99.2
Slide 2: Legal Disclaimer
Legal Disclaimer This Presentation contains forward-looking statements and information of Forma Therapeutics Holdings, Inc. (“we,” “us,” “our,” “Forma” or the “Company”) within the meaning of the Private Securities Litigation Reform Act of 1995 relating to our current and future prospects and our op
Slide 3: Today's Agenda
Today’s Agenda Opening Remarks Frank Lee, President and Chief Executive Officer Expanding Etavopivat Development Patient perspective Development program overview Phase 1 trial in SCD Unmet need in bone marrow failure syndromes Ify Osunkwo, M.D., Chief Patient Officer Patrick Kelly, M.D., Chief Medic
Slide 4: Opening Remarks
Frank Lee President, Chief Executive Officer, Director Opening Remarks
Slide 5: The Science of Giving a Damn
The Science of Giving a Damn
Slide 6: Our 2024 Vision
Expanding Pipeline delivering one IND every other year Our 2024 Vision Trusted Partner to the communities we serve Recognized Leader in rare hematologic diseases and cancers Fully Integrated capabilities and commercial engine
Slide 7: Robust Research and Development Pipeline
Robust Research and Development Pipeline BRCA, breast cancer gene; HRD, homologous recombination deficiencies; IDH1m, isocitrate dehydrogenase 1 mutations; mCRPC, metastatic castration-resistant prostate cancer; MDS, myelodysplastic syndrome, NTD, non-transfusion dependent; PKR, pyruvate kinase-R; R
Slide 8: Today's Highlights
Etavopivat: Exploring impact on transfusion burden in SCD, Thalassemia and Lower-risk MDS Additional analysis of pain events from Phase 1 study provides further support for potential to demonstrate VOC benefit First look at research pipeline with FT-3171 (USP1) and focus on Red Blood Cell health FT-
Slide 9: What's It Like To Be A Patient With...
Ifeyinwa (Ify) Osunkwo, M.D., M.P.H. Senior Vice President, Chief Patient Officer What's It Like To Be A Patient With...
Slide 10: THERAPEUTICS.
THERAPEUTICS. forma
Slide 11: STROKE
STROKE rs) forma THERAPEUTICS.
Slide 12: THERAPEUTICS.
THERAPEUTICS.
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Slide 14: The Challenges of Transfusion Dependency
The Challenges of Transfusion Dependency Iron overload Liver cirrhosis Heart failure Endocrinopathies Infertility Alloimmunization Infection Limited providers / medical centers with expertise Blood supply Out of pocket costs Transportation Covid 19 ORGAN COMPLICATIONS ACCESS QUALITY OF LIFE Time awa
Slide 15: Key Unmet Needs of Patients with SCD, Thalassemia and MDS
Key Unmet Needs of Patients with SCD, Thalassemia and MDS SICKLE CELL DISEASE THALASSEMIA MDS Pain – VOC (managed at home or acute care) Chronic pain - daily Pain (chronic) Short of breath Bruising/bleeding Fatigue Fatigue Fatigue Infections Infections Infections Joint damage Bone deformities Bone p
Slide 16: Slide 16
Slide 17: Etavopivat
Joyce and daughter Aaron, 26, living with SCD Etavopivat
Slide 18: Etavopivat Development
Patrick Kelly, M.D. Senior Vice President, Chief Medical Officer Etavopivat Development
Slide 19: Etavopivat Development Highlights
Etavopivat Development Highlights Successfully creating a global development program during a global pandemic Phase 1 Study in SCD complete: focus on the dataset supporting etavopivat's potential for VOC reduction Phase 2/3 Hibiscus Study on track for interim analysis 1 (IA1) in late 2022 Phase 2 tr
Slide 20: Unmatched in Expertise and Broad Geographical Presence
Unmatched in Expertise and Broad Geographical Presence We are where the patients are 18 countries >120 Global study sites 9 Forma Physicians 7 Adult or Pediatric hematologists Medical leads in the EU and Africa Ghana Nigeria Kenya Egypt Saudi Arabia Oman Turkey Greece Germany France Spain Italy UK L
Slide 21: Etavopivat Compound Profile
Novel small molecule designed to improve RBC health Selective activator of PKR enzyme in RBCs Multi-modal effects (↓2,3-DPG and ↑ATP) Once-daily dosing with low DDI potential Safety profile suitable for pediatric development Phase 1 trial completed Etavopivat Compound Profile
Slide 22: Etavopivat Phase 1 Trial in Sickle Cell Disease
Cameron Trenor, M.D. Executive Director, Clinical Development Etavopivat Phase 1 Trial in Sickle Cell Disease
Slide 23: Etavopivat SCD Phase 1 Trial Design and Results Summary
Etavopivat SCD Phase 1 Trial Design and Results Summary BID=twice daily; QD=every day; wk=week 1. Kalfa TA, et al. Blood. 2019;134(suppl 1):616. 2. Estepp JH, et al. Hemasphere. 2020;4:709-10. Study Design: Arms/dosing Objectives Inclusion criteria PHASE 1 RESULTS HIGHLIGHTS: 400 mg once daily for u
Slide 24: Etavopivat Improves Multiple Risk Factors Associated with VOC Pathophysiology
Increased inflammation, thrombophilia and adhesion: Decreasing inflammation, thrombotic and adhesion markers associated with an increased risk for VOC Poor RBC flexibility: Decreasing HbS polymerization, improving RBC hydration, AND reduces dense cells improves RBC flexibility Increased intravascula
Slide 25: Fewer VOCs Than Expected During Etavopivat Treatment
Fewer VOCs Than Expected During Etavopivat Treatment Cohort N Prior History Once-Daily Etavopivat On-Treatment N Annualized VOCa Rate (no. events) Annualized VOCb Rate (no. events) Exposure Duration (Patient Years) Etavopivat 2-wk cohorts 16 0.88 (13) 0.00 (0) 0.61 Etavopivat 12-wk cohort 15 0.93 (1
Slide 26: Daily Pain in Sickle Cell Disease is Common
Daily Pain in Sickle Cell Disease is Common Most sickle cell pain crises are managed at home Adapted from Smith, WR, et al. Ann Intern Med 2008; 148:94 -101 39% Days “Mild Pain” SCD PATIENT PAIN DIARIES ~3/4 of sickle pain managed at home “SCD-related pain” reported as adverse events in clinical tri
Slide 27: Sickle Cell Pain Improves Over Time on Etavopivat
*1 VOC requiring hospitalization Covid-associated: uncomplicated outcome > 3 VOCs expected based on prior history and treatment duration (>3.3 yrs cumulative daily dosing) Sickle Cell Pain Improves Over Time on Etavopivat 80% reduction in pain events over 12 weeks of treatment Number of Pain Events
Slide 28: Etavopivat Development
Patrick Kelly, M.D. Senior Vice President, Chief Medical Officer Etavopivat Development
Slide 29: Phase 2/3 Hibiscus Study of Etavopivat in SCD
Open-label Extension etavopivat Selected Dose 52 WEEK Phase 2/3 Hibiscus Study of Etavopivat in SCD Enrolling and remains on track for IA1 (dose selection) late 2022, IA2 (Hb response) late 2023 and final analysis (VOC & Hb response) late 2024 Dose Determination 60-90 patients, randomized 1:1:1 PLAC
Slide 30: Near-Term Etavopivat Development Program in Sickle Cell Disease
2021 2022 2022 2023 Near-Term Etavopivat Development Program in Sickle Cell Disease: Data supporting the Hibiscus Accelerated Approval Submission HVS-101 Ph 1 OLE HEM-301 Hibiscus – Phase 3 HEM-301 Hibiscus – Phase 2 SCD Dose Selection Exercise tolerance study HEM-201: TDT / NTDT & SCD Chronic Trans
Slide 31: Data Package Planned to Support Accelerated Approval Submission
Data Package Planned to Support Accelerated Approval Submission Additional studies planned to further support approval pathways and differentiate etavopivat Stroke Risk Reduction Functional Exercise Capacity Other End Organ Measures Data from current clinical program anticipated to support submissio
Slide 32: Ischemic Stroke is a Devastating Consequence of SCD
Ischemic Stroke is a Devastating Consequence of SCD DeBaun, MR and Kirkham, FJ. Blood 2016; 127:829-38 Early intervention (TCD) has reduced the risk of overt stroke from 10% to 1% by 18 years of age Risk of a silent cerebral infarct (SCI) by age 35 is >50% Chronic transfusion therapy remains the sta
Slide 33: Mechanism of Action
Mechanism of Action Etavopivat is an investigational, once daily, selective erythrocyte pyruvate kinase (PKR) activator PKR activation results in decreased 2,3-DPG and increased ATP in RBCs PKR Activation May Reduce Transfusion Burden in Patients with Hemolytic Anemias and Bone Marrow Failure Syndro
Slide 34: Etavopivat in TD SCD and Thalassemia: The Gladiolus Study Design
Etavopivat in TD SCD and Thalassemia: The Gladiolus Study Design This is a global, Phase 2, open-label study (NCT04987489) with initial results expected late 2022 PRIMARY OBJECTIVE: SCD on chronic transfusions and Transfusion-Dependent Thalassemia (TDT): Reduction in transfusions over a 12-week trea
Slide 35: Etavopivat in MDS: Study Design
Etavopivat in MDS: Study Design This is a global, Phase 2, open-label study with FPI expected in second half 2022 with initial results expected mid-2023 PRIMARY OBJECTIVE: Hematologic Response after 16 weeks of daily etavopivat treatment PATIENT POPULATION: Adults (≥18 years) with Very Low to Interm
Slide 36: Unmet Need in Bone Marrow Failure Syndromes
Michael Savona, M.D. Chair, MDS/MPN International Working Group; Head, Hematology, Cellular Therapy and Stem Cell Transplantation, Beverly and George Rawlings Directorship in Hematology Research; Professor of Medicine and Cancer Biology, Department of Internal Medicine, Vanderbilt University School
Slide 37: Disclosures
Disclosures I have the following financial relationships to disclose: Advisory and consulting: Abbvie, Celgene, CTI, Forma Therapeutics, Geron, Karyopharm, Novartis, Ryvu, Taiho, Takeda, TG Therapeutics; Research Support: ALX Oncology, Astex, Incyte, Takeda, TG Therapeutics; Equity: Karyopharm, Ryvu
Slide 38: "Lower Risk" Disease Related Mortality in MDS
“Lower Risk” Disease Related Mortality in MDS Neukirchen et al. Leukemia Research 2014. < 60 yo > 60 yo
Slide 39: "Lower Risk" Disease Related Mortality in MDS
“Lower Risk” Disease Related Mortality in MDS Neukirchen et al. Leukemia Research 2014. > 60 yo Median Age of Diagnosis of MDS is between 70-73 years
Slide 40: Transfusions are the Mainstay of Treatment; Can Result in Iron Overload
Transfusions are the Mainstay of Treatment for Patients with Hemolytic Anemias and Bone Marrow Failure, and Can Result in Iron Overload Most complications of iron overload are partially or completely irreversible Normal total body iron: 4,000-5,000 mg No natural way of excreting excess iron Preventi
Slide 41: Transfusion Burden has Profound Effect on Outcome in MDS
Transfusion Burden has Profound Effect on Outcome in MDS Lemos et al. European J of Haematology. 2021 107(1): 3-23. Transfusion Independence predicts strongly for improved survival is MDS – regardless of HSCT
Slide 42: Early Erythropoiesis Stimulation in Low Risk MDS Remains Standard of Care
Recombinant erythropoietin can lead to long term responses in LR-MDS with MDS with isolated anemia epo levels < 500, usually <200 considerable variation in dose and schedule Low thromboembolic risk if given with lower Hgb* Sequencing of ESAs with other therapy for LR-MDS - Unclear Early Erythropoies
Slide 43: ECOG 2905 – ESA+Len is Superior to ESA Alone
ECOG 2905 – ESA+Len is Superior in ESA Alone in ESA-Refractory LR-MDS
Slide 44: Luspatercept in MDS
Luspatercept in MDS Suragani R, et al. Nature Med 2014 Zhou L, et al. Blood 2008 Erythropoiesis TGF-β Superfamily Ligands: GDF11, etc. Smad2/3 Luspatercept Fusion protein containing modified activin receptor type IIB (ActRIIB) Activin Receptor Domain Human IgG Fc Domain Mechanism is distinct from er
Slide 45: Medalist Phase 3 Study in Low Risk MDS-RS
Medalist Phase 3 Study in Low Risk MDS-RS Fenaux et al, NEJM, 2020. 382:140-151
Slide 46: Functional PK-R Deficiency Associated with Anemia of MDS
Functional PK-R Deficiency Associated with Anemia of MDS
Slide 47: Functional PK-R Deficiency Leads to Ineffective RBC Production
Reduced PK-R activity in erythroid progenitors reduces ATP by glycolysis, increasing dependence on oxidative pathway (mitochondrial) for ATP = increased oxidative stress Myeloid Neoplasms Evolve in Inflammatory Niche that Leads to Functional PK-R Deficiency = Ineffective RBC Production/Survival Hb=h
Slide 48: Functional PK-R Deficiency Leads to Ineffective RBC Production
Myeloid Neoplasms Evolve in Inflammatory Niche that Leads to Functional PK-R Deficiency = Ineffective RBC Production/Survival Hb=hemoglobin ↓ RBC lifespan ↑ Ineffective erythropoiesis 2,3-DPG PEP Lactate ATP ATP PKR Oxy -Hb Deoxy-Hb Glucose Pyruvate ↓ Hb-O2 binding ↑ Oxidative stress ↑ Membrane dama
Slide 49: Functional PK-R Deficiency Leads to Ineffective RBC Production
Myeloid Neoplasms Evolve in Inflammatory Niche that Leads to Functional PK-R Deficiency = Ineffective RBC Production/Survival Hb=hemoglobin ↓ RBC lifespan ↑ Ineffective erythropoiesis ↑ Anemia ↑ Transfusions 2,3-DPG PEP Lactate ATP ATP PKR Oxy -Hb Deoxy-Hb Glucose Pyruvate ↓ Hb-O2 binding ↑ Oxidativ
Slide 50: PKR Activation May Reduce Transfusion Burden in Bone Marrow Failure Syndromes
PKR Activation May Reduce Transfusion Burden in Patients with Bone Marrow Failure Syndromes Hb=hemoglobin; MoA=mechanism of action ↑ Hb-O2 binding ↓ Oxidative stress ↓ Membrane damage ↑ RBC lifespan ↓ Ineffective erythropoiesis ↓ Anemia ↓ Transfusions 2,3-DPG PEP Lactate ATP ATP PKR Oxy -Hb Deoxy-Hb
Slide 51: Clonal Hematopoiesis is a Normal Process of Aging
Clonal Hematopoiesis is a Normal Process of Aging Hematopoietic stem cells (HSCs) are rare and quiescent blood cells (1:10,000 blood cells) yet there are billions of HSC cell divisions in a human lifetime Replication errors are largely repaired, but errors which are not repaired are propagated Propa
Slide 52: Clonal Hematopoiesis is Age-Associated Phenomenon
Clonal Hematopoiesis is Age-Associated Phenomenon Which Becomes Pathologic Over Time in the Minority of Patients CH occurs in 1% of 60yo, 10% of 70yo, 30% of 90yo While CH in small variant allele fractions are ubiquitous (0.2% VAF in 95% of population), the term of CH refers to clones present in a s
Slide 53: CH+ Cytopenias = CCUS
CH+ Cytopenias = CCUS Clonal Cytopenias of Unknown significance = CCUS CHIP CCUS MDS AML CCUS implies: Absence of other cause of cytopenias (e.g. hemolysis, bleeding, nutritional, infectious or metabolic disorder) and lack of dyplasia on BMBx
Slide 54: CCUS is a Newly Recognized Clonal Disorder Needing Intervention
Ineffective hematopoiesis and marrow inflammation is NOT limited to low risk MDS alone, it is a problem with patients with all chronic hematologic malignancies. CCUS, even in the absence of progression to MDS leads to Hb < 10g/dL and diminished quality of life CCUS Observation alone Therapy needed A
Slide 55: Summary
Lower risk MDS is not low risk and is associated with serious morbidity and higher mortality than realized Iron overload from chronic transfusions is a significant risk factor Current therapy for lower risk MDS is variably effective and is NOT benign Luspatercept provides a new approach specifically
Slide 56: Acknowledgments
The patients The MDS and Clonal Hematopoiesis Community Acknowledgments The Biff Ruttenberg Foundation Serodino Family Compact Lovell Family Fellowship Beverly and George Rawlings Directorship in Hematology Research
Slide 57: Research Pipeline and Red Blood Cell Health
David N. Cook, Ph.D. Senior Vice President, Chief Scientific Officer Research Pipeline and Red Blood Cell Health
Slide 58: Research Pipeline and RBC Health Highlights
Research Pipeline and RBC Health Highlights Our strategy is to select programs based on scientific promise, patient need and strategic fit with our focus on rare hematology and oncology Our pipeline reflects a rich heritage – with FT-3171, a USP1 inhibitor, now in IND-enabling studies New programs i
Slide 59: Building a Deep Preclinical Pipeline
Building a Deep Preclinical Pipeline INDICATION RBC Metabolism Rare Hematology COMPOUND/FOCUS AREA HIT-TO-LEAD LATE EARLY Rare Hematology HbF Inducer Rare Hematology Membrane Stabilizer Type 1 IFN-Driven Cancers Oncology Oncology Synthetic Lethality Oncology FT-3171 (USP1)
Slide 60: Role of RBCs in Human Biology
Regulate vasodilation via export of nitric oxide (NO) Regulate vasodilation via export of ATP Cholesterol trafficking Activation of systemic innate immune responses via TLR9 signaling Carry O2 to tissues Carry CO2 to lungs Role of RBCs in Human Biology RBCs comprise more than 80% of cells in the bod
Slide 61: RBC Health Opportunity
We believe there are chronic diseases where improving RBC health will make a substantial improvement in quality of life. Relevant mechanisms include increasing ATP using etavopivat and other intracellular RBC targets that improve function. RBC Health Opportunity
Slide 62: An Illustrative Example: RBC Dysfunction in Type 2 Diabetes
An Illustrative Example: RBC Dysfunction in Type 2 Diabetes (T2D) T2D patients have poor oxygen delivery to skeletal muscle tissue Altered RBCs in T2D: Less deformable Increased blood viscosity Less NO Excessive ROS (reactive oxygen species) RBCs induce endothelial damage and prolong ischemia-reperf
Slide 63: FT-7051
FT-7051
Slide 64: FT-7051 Program in Metastatic Castration-Resistant Prostate Cancer
FT-7051 Program in Metastatic Castration-Resistant Prostate Cancer (mCRPC) Sylvie Guichard, Ph.D. Program Lead FT-7051 Executive Director, Translational Science
Slide 65: FT-7051 Program Highlights
FT-7051 Program Highlights 25 patients enrolled as of May 12, 2022 Heavily pre-treated population (lines of therapy, genetics and disease burden) Drug exposures in the predicted efficacious exposure range supported by target engagement biomarkers Alternative schedule of administration based on PK/PD
Slide 66: Prostate Cancer
Prostate Cancer Nearly all patients who respond to current mCRPC therapies acquire resistance AR-v7 splice variant confers treatment resistance to anti-androgens and reduces median overall survival Anti-androgens now used in mCSPC increases future patient need in mCRPC 2nd leading cause of cancer de
Slide 67: FT-7051 is an Inhibitor of CBP/p300, an Essential Co-Activator for AR
FT-7051 is an Inhibitor of CBP/p300, an Essential Co-Activator for AR Inhibition of CBP/p300 is expected to reduce AR-dependent gene expression and result in clinical benefit in mCRPC & other AR+ cancers <1 nM potency with > 200-fold selectivity against target family Mechanism-based antitumor activi
Slide 68: FT-7051 Antitumor Effect Compared to Enzalutamide in PDX Model
FT-7051 Demonstrated Similar Antitumor Effect Compared to Enzalutamide in an Enzalutamide-Sensitive Prostate PDX Model Pharmacodynamic modulation with FT-7051 differentiated from enzalutamide FT-7051 has significant antitumor activity in enzalutamide-sensitive PDX model Source: Forma internal data
Slide 69: The Courage Study: First-In-Human Phase 1 Study
The Courage Study is a First-In-Human, Multi-Center, Open-Label Phase 1 Study to Evaluate Safety and Tolerability and Determine Phase 2 Dose Twenty-five patients enrolled as of May 12, 2022 Advanced patient population: Median of 3 lines of therapy for mCRPC, of which ~60% had prior taxane therapy
Slide 70: Current Dose Levels of FT-7051 are at Predicted Efficacious Exposures
FT-7051 is absorbed following oral administration with a time to maximum concentration (Tmax) of 1- 4 hr and an estimated elimination half-life (t1/2) of ~ 2-4 hr Predicted efficacious exposure target achieved at dose levels > 150 mg Steady state levels are similar to single dose exposures with mini
Slide 71: Target Engagement Biomarkers Show Rapid and Sustained Modulation
Target Engagement Biomarkers Show Rapid and Sustained Modulation Rapid downregulation of CBP target gene in blood Pathway modulation maintained 24 hr post-dose Pre-dose 24 hr post-dose Recovery to baseline before next daily dose Supporting strategy for monitoring on/off dosing schedule H3K27Ac Sourc
Slide 72: Safety Data Update
On-target toxicity of hyperglycemia observed in patients with glucose intolerance or diabetes Manageable and monitorable with standard treatment Additional AEs such as fatigue and GI events appear cumulative with 3-week on/1-week off schedule Evaluating an alternative dose schedule at the predicted
Slide 73: FT-3171 Program
Maria D. Ribadeneira, Ph.D. Program Lead FT-3171 Executive Director DMPK and Toxicology FT-3171 Program USP1 inhibitor for the treatment of advanced solid tumors
Slide 74: USP1 Program Highlights
Untapped DNA damage repair pathway A differentiated USP1 inhibitor with high potency, exquisite selectivity, and favorable tolerability Once-daily dosing as monotherapy or in combinations including PARPi Evidence of antitumor activity across multiple tumor types First half 2023 IND filing anticipate
Slide 75: USP1 Modulates a DNA Damage Repair Pathway Distinct from PARP1/2
USP1 Modulates a DNA Damage Repair (DDR) Pathway Distinct from PARP1/2 and Other DDR Targets Bulky Adducts and Replication Fork Stalling Translesion Synthesis (TLS) Therapeutic Target: USP1 Single-Stranded Breaks Base Excision Repair (BER) Therapeutic Targets: PARP1/2 APE1 Double-Strand Breaks Non-H
Slide 76: Therapeutic Hypothesis
Therapeutic Hypothesis USP1 inhibition drives accumulation of ubPCNA (ubiquitinated proliferating cell nuclear antigen), leading to replication fork destabilization, DNA damage, and tumor cell death USP1 Inhibition Induces Synthetic Lethality in BRCAmt Tumors Source: 1. Lim et al., 2018, Molecular C
Slide 77: FT-3171 Demonstrates High Selectivity, Target Engagement and Potency
Potent, dose dependent induction of Ub-PCNA and inhibition of proliferation by FT-3171 Exquisite selectivity of FT-3171 for USP1/UAF1 * w/ WDR20 Greater than 1000-fold selectivity across a panel of 44 DUBs USP1 Inhibitor (FT-3171) Demonstrates High Selectivity, with Robust Target Engagement and Pote
Slide 78: FT-3171 Upregulates Ub-PCNA, Inducing DNA Damage
Cell cycle arrest Cell death ↑Ub-PCNA USP1 PCNA FT-3171 Increased UbPCNA DNA damage Antitumor activity FT-3171 Upregulates Ub-PCNA, Thus Inducing DNA Damage that Drives Antitumor Activity in BRCA1mt Tumors Source: Forma internal data from mouse Xenograft model -MDA-MB-436 cells Vehicle ↑ -H2AX
Slide 79: USP1 Inhibition Demonstrates Monotherapy Antitumor Activity in PDX Models
USP1 Inhibition Demonstrates Monotherapy Antitumor Activity in Diverse Patient Derived Xenograft (PDX) Tumor Models Source: Forma internal data Subcutaneous patient derived xenograft (PDX) efficacy screen in N=1, 2-arm study for each model. PDX fragments were implanted into NOD SCID or Balb/c nude m
Slide 80: Homologous Recombination Deficiencies: Opportunity Beyond BRCAmt Tumors
Homologous Recombination Deficiencies (HRD): Potential Broad Opportunity for FT-3171 Beyond BRCAmt Tumors Source: Heeke et al. (2018). Prevalence of Homologous Recombination-Related Gene Mutations Across Multiple Cancer Types. JCO precision oncology, 2018, PO.17.00286. https://doi.org/10.1200/PO.17.
Slide 81: In Closing…
Frank Lee Chief Executive Officer In Closing…
Slide 82: Today's Highlights
Etavopivat: Exploring impact on transfusion burden in SCD, Thalassemia and Lower-risk MDS Additional analysis of pain events from Phase 1 study provides further support for potential to demonstrate VOC benefit First look at research pipeline with FT-3171 (USP1) and focus on Red Blood Cell health FT-
Slide 83: Anticipated Near-term Events
Anticipated Near-term Events Clinical Data Milestones Etavopivat – Phase 2/3 in SCD (IA1) Etavopivat – Phase 2 in Thalassemia and TD-SCD (initial results) FT-7051 – Phase 1 in mCRPC (data update) Clinical Study Initiations Etavopivat – Phase 2 in Lower-Risk MDS Etavopivat – Phase 2 in Pediatric SCD
Slide 84: Q&A
Rick, living with prostate cancer Q&A
Slide 85: The Science of Giving a Damn
The Science of Giving a Damn
Forma Therapeutics Holdings — Investor Day (May 2022) on 6ix