Exhibit 99.2

Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases Blade Analyst Day February 22, 2022 Welcome! The event will start shortly.

Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases Blade Analyst Day February 22, 2022

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Today’s Agenda 6 Topic Speaker Welcome & Introductions Krishna Gorti, M.D., SVP – Investor Relations Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases Wendye Robbins, M.D., President & CEO Idiopathic Pulmonary Fibrosis Treatment Landscape and Needs Toby Maher, M.B., MSc, Ph.D., FRCP Professor of Medicine, USC Hastings Center for Pulmonary Research, Los Angeles Cudetaxestat Clinical Development Program Bassem Elmankabadi, M.D., SVP – Clinical Development Idiopathic Pulmonary Fibrosis Market Landscape and Opportunities Felix Karim, Ph.D., EVP – Business Development Neurodegeneration Market Landscape and Opportunities Felix Karim, Ph.D. Financial Overview Jean - Frédéric Viret, Ph.D., Chief Financial Officer Q&A Dr. Toby Maher & Blade Management Catalysts & Closing Wendye Robbins, M.D.MB0

7 Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases Wendye Robbins, M.D. President & CEO

Committed to Developing Cutting - Edge Treatments for Patients with Rare Progressive Diseases 8 5 - year survival rate of 50% 1 Median survival time of 3 - 5 years following diagnosis 2 Neurodegeneration Huntington’s Disease & SCA3 Fibrosis Idiopathic Pulmonary Fibrosis Autosomal dominant, inherited progressive loss of neuronal function Complications typically cause death 10 - 30 years after onset 3,4 1. American Thoracic Society, General Information About Pulmonary Fibrosis. 2. Lederer, 2018, NEJM. 3. Bates, 2015 Nat Rev Dis Primers . 4. Klockgether , 2019, Nat Dis Primers .

Blade Therapeutics Investment Thesis 9 4. Research and Markets. “Global Idiopathic Pulmonary Fibrosis (IPF) Market” summary. Posted December 2021. 5. iHealthcareAnalyst , Inc. (press releasee Nov. 5, 2021). Orphan Diseases Pursuing debilitating, progressive diseases in fibrosis and neurodegeneration Significant Market Strong projected growth in IPF market Large Unmet Need 40 - 75% of patients with IPF remain untreated with current therapies 1,2,3 ~$3.3B ~$8.8B (2027 estimate) 5 (2020) 4 Differentiated Pipeline Oral, small - molecule candidates with novel mechanisms of action and strong IP complemented by global commercial rights Phase 2 Ready Lead program targeting clinically - validated pathway for IPF as potential monotherapy or add - on to current therapies $280M Proposed Valuation compared to peer companies, prior M&A deals and external IPF market potential 1. Dempsey, 2021, Ann Am Thor Soc. 2. Lancaster, 2021, Respirol . 3. Maher, 2017, BMC Pulm Med.

Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases 10 1. Effects demonstrated in preclinical studies. 2. Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Experts in Biology of Cell and Tissue Damage Responses • Researching novel biological pathways foundational to cell - and tissue - damage responses • Developing potential disease - modifying therapeutics in fibrosis and neurodegeneration Differentiated Pipeline Led By Phase 2 - Ready Program in Fibrosis • Non - competitive autotaxin inhibitor with direct anti - fibrotic activity and differentiating characteristics 1 – planned phase 2 study in lung fibrosis in 2Q - 2022 • CNS - penetrant calpain inhibitor 1 for genetic orphan neurodegenerative conditions approaching planned phase 1 study in 2H - 2022 2 Deep Scientific & Industry Experience • Experienced management team and advisors with extensive expertise in fibrosis and neurodegeneration • Strong track record of development and approvals of innovative medicines at prior companies

Leadership with Deep Scientific and Industry Experience 11 Wendye Robbins, M.D. Chief Executive Officer Jean - Frédéric Viret, Ph.D. Chief Financial Officer Prabha Ibrahim, Ph.D. Chief Technical Officer Felix Karim, Ph.D. EVP, Business Development Bassem Elmankabadi, M.D. SVP, Clinical Development Daven Mody, PharmD SVP, Regulatory Affairs Michael Blash SVP, Communications

Developing Therapies to Target Key Pathways in Disease Progression 12 Target Pathway Potential Treatment Effects Diseases Autotaxin (ATX) Non - competitive, reversible inhibition supports potential for differentiated profile in fibrotic diseases and epithelial tumors Dimeric Calpains (CAPN) Inhibition shown to enhance autophagy and reduce protein aggregates in preclinical models Inhibition blocks myofibroblast activation / differentiation, thereby inhibiting extracellular matrix production, in preclinical models Huntington’s SCA3 IPF, SSc - ILD IPF, ILD NASH NASH Fibrotic diseases – idiopathic pulmonary fibrosis (IPF), systemic sclerosis – interstitial lung disease ( SSc - ILD), non - alcoholic steatohepatitis (NASH) Neurodegenerative diseases – Huntington’s disease (HD), spinocerebellar ataxia type 3 (SCA3, aka Machado - Joseph disease or MJD) Oncology

Differentiated Pipeline of Novel Product Candidates 13 * Orphan drug designations granted by FDA for IPF and for SSc . Compound & MoA Indication Est. Prevalence PC Ph1 Ph2 Ph3 Patent Expiry Fibrosis Cudetaxestat (BLD - 0409) Non - Competitive Autotaxin Inhibitor Idiopathic Pulmonary Fibrosis (IPF)* <200K (US) ~5M (WW) Orphan Disease 2034 – 2036 Systemic Sclerosis – Interstitial Lung Disease ( SSc - ILD)* ~47K (N. America) ~400 - 500K (WW) Orphan Disease Liver Fibrosis ~16M (US) up to 505M (WW) (NASH Prevalence) Neurodegeneration BLD - 2184 Calpain Inhibitor Poly - Q (HD, SCA3) Orphan Diseases 2037 – 2040

Multiple Milestones 14 * Pirfenidone and nintedanib. ** Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Indicates completed milestone. Completed and Potential Milestones Timing Cudetaxestat Phase 1 CYP - DDI study completed Nov - 2021 Cudetaxestat Phase 1 DDI study with approved IPF therapies completed* Jan - 2022 Cudetaxestat End - of - phase 1 meeting with FDA 1Q - 2022 Corporate Complete merger with Biotech Acquisition Company 1Q - 2022 Cudetaxestat American Thoracic Society presentations May - 2022 Cudetaxestat Initiate planned phase 2 study in IPF** 2Q - 2022 BLD - 2184 Initiate planned phase 1 study in healthy volunteers** 2H - 2022 Cudetaxestat Initiate planned phase 2 basket clinical study in SSc - ILD** 2H - 2022 Cudetaxestat First interim analysis for planned phase 2 study in IPF** 1H - 2023 BLD - 2184 Data read out for planned phase 1 study in healthy volunteers** 1H - 2023 Cudetaxestat Second interim analysis for planned phase 2 study in IPF** 2H - 2023

15 Fibrosis – Cudetaxestat Non - Competitive Autotaxin Inhibitor Targeting IPF

Autotaxin / Lysophosphatidic Acid (LPA) Drives Fibrosis 16 Innate Lymphoid Cells Macrophages LPA LPC LPA receptor Choline Autotaxin 1 Dysregulated Damage Response Fibrosis is triggered by dysregulated cell / tissue damage response following epithelial injury. 2 Release of Pro - fibrotic Mediators Pro - fibrotic mediators, cytokines and the enzyme autotaxin are released. Increased autotaxin levels produce excessive lysophosphatidic acid (LPA). 3 Autotaxin Production of LPA LPA binds to LPAR1 (receptor on myofibroblasts) and triggers signaling cascade resulting in migration, activation and release of additional mediators. 4 Myofibroblast Activation Excessive LPA activates myofibroblasts. 5 Secretion of ECM Proteins Activated myofibroblasts secrete ECM proteins (scarring) that disrupt normal organ architecture and function. 1 2 3 4 5 Damaged Epithelium Myofibroblasts Activated ECM Proteins Pro - fibrotic Mediators

Cudetaxestat – Phase 2 Ready, Targeting IPF 17 * Pending FDA review and feedback. Direct Anti - Fibrotic Activity Robust in vivo anti - fibrotic activity in preclinical models of lung and liver fibrosis Non - Competitive Autotaxin Inhibition Differentiating characteristics support potential treatment profile in fibrosis Extensive Phase 1 Clinical Program Phase 1 data demonstrated PK/PD correlation and biomarker activity; well tolerated with no drug - related SAEs in 200+ healthy volunteers Progressing Toward Planned Phase 2 IPF Study E nd - of - phase 1 package submitted to FDA 1Q - 2022 to further inform next phase of clinical development*

Non - Competitive Inhibitor Does not compete with LPC for binding Competitive Inhibitor Competes with LPC for binding Potent inhibitor results in no loss in potency Inhibition plateaus and results in reduced potency Non - Competitive Inhibition Supports Differentiated Profile in Fibrosis 18 * Plasma concentrations of LPC in an animal model of liver fibrosis are between 200 - 250 µM. Head - to - head clinical studies comparing cudetaxestat with currently approved or investigational therapies have not been conducte d. Above data from preclinical biochemical study. ATX Tripartite Active Site Substrate (LPC) in enzyme pocket Enzyme Products: LPA + Choline • Non - competitive inhibitor cudetaxestat shown to maintain potency in preclinical biochemical assay – Cudetaxestat expected to maintain potency in disease state – Potentially advantageous for efficacy and safety profile • 50% inhibition at 250 m M concentration of LPC* – Cudetaxestat: 8 nM – GLPG - 1690: ~400 nM (competitive inhibitor loses potency) High substrate (LPC) levels seen in diseased tissues and organs Adapted from Salgado - Polo, 2019, Cancers.

Cudetaxestat Displays Robust Activity ( in vivo ) on Lung Fibrosis Biomarkers and Pro - Fibrotic Genes 19 SMA (smooth muscle actin), collagen 1A1 and assembled collagen data from preclinical study conducted in mouse bleomycin lung fib rosis model dosed once daily. PAI - 1, IL - 6 and CTGF (connective tissue growth factor) data from preclinical study conducted in mouse bleomycin lung fibrosis mo del dosed twice daily. SMA gene expression Marker of myofibroblast activation PAI - 1 gene expression Contributes to excessive ECM accumulation Assembled collagen Represents advanced fibrosis IL - 6 gene expression Pro - fibrotic cytokine Collagen 1A1 gene expression Primary component of fibrosis, produced by myofibroblasts CTGF gene expression Pro - fibrotic growth factor ANOVA One - Way *p<0.05 **p<0.01 ***p<0.001 ****p<0.0001 Saline Vehicle Cude 3mg/kg Cude 10mg/kg Cude 30mg/kg

Supporting Peer Clinical Evidence on Lung Function (FVC) 20 BMS - 986020 (LPA1 antagonist) Ph2 1 Significant FVC benefit at wk 26 in BID group in IPF Tocilizumab (IL - 6R antagonist) Ph3 2 Significant FVC benefit at wk 48 in SSc - ILD Pamrevlumab (anti - CTGF mAb ) Ph2 3 Significant FVC benefit at wk 48 in IPF Cudetaxestat - Ph1 MAD in Healthy Volunteers LPA Reduction (P eak - to - trough variation) 100 mg QD 300 mg QD 2a-d1 2a-d72a-d142b-d1 2b-d72b-d142c-d1 2c-d72c-d142d-d1 2d-d72d-d14 0 20 40 60 80 100 M e a n % L P A R e d u c t i o n f r o m B a s e l i n e E m a x o r E t r o u g h Emax Etrough 5 00 mg QD 750 mg QD Cudetaxestat - Mouse Bleo Lung model IL - 6 gene expression Cudetaxestat - Mouse Bleo Lung model CTGF gene expression 1. Palmer, 2018, Chest. 2. Khanna, 2020, Lancet. 3. Richeldi , 2020, Lancet.

Completed Preclinical Studies Support Safety Profile of Cudetaxestat 21 * 13 - week dosing tolerated up to 300 mpk . Completed Studies Findings Toxicology Rat 4 - week GLP tox NOAEL 100 mpk Dog 4 - week GLP tox NOAEL 300 mpk Rat 26 - week GLP tox NOAEL 30 mpk (male) / 75 mpk (female) Dog 39 - week GLP tox* In - life completed Safety Pharmacology Dog cardiovascular No adverse findings; NOAEL 1000 mpk Rat respiratory No adverse findings; NOAEL 750 mpk Rat Irwin No adverse findings; NOAEL 750 mpk hERG in vitro IC 50 = 49.4 µM (corrected for plasma protein binding) Gene Tox Ames Negative In vitro micronucleus Negative Drug - Drug Interactions In vitro and in vivo profiling vs. approved IPF therapies (pirfenidone, nintedanib) Unlikely DDI potential with approved IPF therapies

Decisive Actions by Blade to Set Clear Path to Planned Phase 2 Studies of Cudetaxestat 22 Completed Phase 1 4Q - 2021 – Jan - 2022 1Q - 2021 Assessed GLPG - 1690 Study Implications Successfully completed Ph1 DDI studies on CYPs and DDI with approved IPF therapies ‒ Cudetaxestat well tolerated with no reports of drug - related SAEs End - of - phase 1 data package submitted to FDA “Given the known safety/tolerability issues with SoC (pirfenidone/nintedanib)…” 3 ‒ Evaluate potential DDI effect on various transporters (e.g., P - gp ) and CYPs ‒ Conduct dedicated DDI study to evaluate PK between cudetaxestat and approved IPF therapies 4 prior to dose ranging studies Pursued Stepwise Approach Mid - 2021 S tatements from Gilead and Galapagos ‒ IDMC recommendation: “… ziritaxestat’s benefit - risk profile no longer supported continuing these studies.” 1 ‒ “… it's nothing that popped up that has linked to a mechanism of action that we could explain as of today” 2 Blade proactively sought pre - IND FDA feedback 1. Gilead news release, 10 - Feb - 2021. 2. Galapagos earnings call transcript, 19 - Feb - 2021. 3. FDA pre - IND correspondence with Blade Therapeutics. 4. Approved IPF therapies = nintedanib and pirfenidone.

P - gp in vitro assay using nintedanib as substrate P - gp transporter in vitro assay using quinidine as substrate DDI Profiles of Cudetaxestat (BLD - 0409) and GLPG - 1690 23 1. Wind, 2019, Clin. Pharm. 2. Esbriet® (pirfenidone) USPI. Compound P - gp Inhibition (IC 50 µM) P - gp Substrate (Efflux Ratio @ 10µM) Cudetaxestat Very Weak (64.6 µM) Not a substrate (1.7) GLPG - 1690 Moderate (7.8 µM) Yes (60) Nintedanib Weak (>30 µM) 1 Yes (16) Pirfenidone Weak (>100 µM) 2 Not a substrate Compound P - gp Inhibition (IC 50 µM) Cudetaxestat 39.8 µM GLPG - 1690 3.84 µM • Nintedanib known to be a substrate for P - glycoprotein (P - gp ) 1 ‒ P - gp transporter functions as a biological barrier by excreting certain compounds out of cells (e.g., in gastrointestinal tract, liver, and kidney) • Cudetaxestat is neither a substrate nor an inhibitor of P - gp at physiological concentrations • GLPG - 1690 is both a substrate and an inhibitor of P - gp

Nintedanib Exposure Comparison ± Cudetaxestat or GLPG - 1690 (preclinical model) 24 Preclinical study conducted in rat model. Nintedanib Plasma Conc. vs Time Nintedanib alone (30 mg/kg) Nintedanib + BLD - 0409 (75 mg/kg) Nintedanib + GLPG - 1690 (60 mg/kg) Nint+BLD-0409 Nint Alone Nint+GLPG-1690 0 100 200 300 400 500 N i n t e d a n i b P l a s m a C o n c . ( n g / m L ) Nint+BLD-0409 Nint Alone Nint+GLPG-1690 0 1000 2000 3000 4000 5000 N i n t e d a n i b A U C . ( h * n g / m L ) • Nintedanib C max and AUC − Increased when co - administered with GLPG - 1690 by 2.5X and 4X respectively (p<0.0001) − No statistically significant change when co - administered with BLD - 0409 ns ns **** **** Nintedanib Cmax ± BLD / GLPG Nintedanib AUC ± BLD / GLPG

Cudetaxestat – Well - Defined Development Pathway in Lung Fibrosis 25 * Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Completed and Potential Milestones Timing Phase 1 CYP - DDI study completed Nov - 2021 Phase 1 DDI study with approved IPF therapies (pirfenidone, nintedanib) completed Jan - 2022 End - of - phase 1 meeting with FDA 1Q - 2022 Initiate planned phase 2 clinical study in IPF* 2Q - 2022 • 52 - week study (N=160) to provide efficacy and safety data o Blinded interim 12 - week analysis (from LPI) o Blinded interim 26 - week analysis (from LPI) o Study completion 1H - 2023 2H - 2023 1H - 2024 Initiate planned phase 2 basket clinical study in SSc - ILD* 2H - 2022

26 Neurodegeneration – BLD - 2184 CNS - Penetrant Calpain Inhibitor for Poly - Q Neurodegenerative Conditions

Calpains Implicated in Progression and Autophagy of Neurodegenerative Diseases 27 Weber, 2018, Neuropharmacol . Gafni, 2002, J Neurosci . Calpain inhibition shown in preclinical models to r educe cleavage of mutant proteins, aggregation and enhances clearance via autophagy Mutant gene w/ expanded CAG repeats Mutant protein w/ expanded poly - Q repeats CALPAIN (cleaves mutant protein and generates toxic fragments) BLD inhibitor (reduces cleavage & aggregates) Protein a ggregates (neurotoxicity) M isfolded (toxic) fragments CALPAIN (cleaves machinery and inhibit s autophagy) Lysosomal clearance ATG5 beclin - 1 LAMP A utophagy BLD inhibitor (increases autophagy) Huntington’s Disease (HD) HTT G ene and Spinocerebellar Ataxia Type 3 (SCA3) Weber, 2019, BioMed Res Int.

Calpain Inhibitors Demonstrate Preclinical Evidence of Neuroprotective Effects 28 1. Weber, 2018, Neuropharmacol . Gafni, 2002, J Neurosci . Weber, 2019, BioMed Res Int. 2. Robinson, 2021, Cells. Novel Target for Disease Progression 1 Calpains shown in preclinical studies to regulate formation of toxic proteins and autophagy (intracellular clearance), key components in incurable neurodegenerative Poly - Q diseases (HD, SCA3) Preclinical Evidence of Neuroprotection 2 Improvements in biomarkers, motor function and enhanced autophagy in SCA3 preclinical models (mouse, zebrafish models) Development Candidate Selection Ongoing preclinical and nonclinical activities in preparation for initiating planned phase 1 study (2H - 2022)

Planned Clinical Development in Fibrosis and Neurodegeneration 29 Note: clinical studies listed above are contingent upon regulatory review and feedback (e.g., FDA and ex - US regulatory authoriti es). * Study currently tentative and in early planning. Ph1 (Healthy Volunteers) Ph2 BLD - 2184 Poly - Q ND (HD, SCA3) 1H - 20 22 2H - 20 22 1H - 2023 2 H - 2023 1 H - 2024 Ph2 IPF IA#1 (12W) IA#2 (26W) Cudetaxestat IPF & SSc - ILD (Ph2 IPF OLE*) (Ph2 SSc - ILD basket study*)

Blade Therapeutics Investment Thesis 30 4. Research and Markets. “Global Idiopathic Pulmonary Fibrosis (IPF) Market” summary. Posted December 2021. 5. iHealthcareAnalyst , Inc. (press release Nov. 5, 2021). Orphan Diseases Pursuing debilitating, progressive diseases in fibrosis and neurodegeneration Significant Market Strong projected growth in IPF market Large Unmet Need 40 - 75% of patients with IPF remain untreated with current therapies 1,2,3 ~$3.3B ~$8.8B (2027 estimate) 5 (2020) 4 Differentiated Pipeline Oral, small - molecule candidates with novel mechanisms of action and strong IP complemented by global commercial rights Phase 2 Ready Lead program targeting clinically - validated pathway for IPF as potential monotherapy or add - on to current therapies $280M Proposed Valuation compared to peer companies, prior M&A deals and external IPF market potential 1. Dempsey, 2021, Ann Am Thor Soc. 2. Lancaster, 2021, Respirol . 3. Maher, 2017, BMC Pulm Med.

31 IPF Treatment Landscape and Needs Toby Maher, M.B., MSc, Ph.D., FRCP USC Hastings Center for Pulmonary Research, Los Angeles Dr. Maher is not an employee or an affiliate of Blade, and the slides he presented did not address Blade or its operations. His slides have been intentionally omitted.

32 Cudetaxestat Clinical Development Program Bassem Elmankabadi, M.D. Senior Vice President, Clinical Development

Extensive Phase 1 Clinical Study Program 33 All Phase 1 studies outlined above were conducted in healthy volunteers. Study 1 SAD/MAD (N=80) Study 2 Relative Bioavailability (N=34) Study 3 CYP - DDI (N=16) Study 4 DDI with Approved IPF Therapies (N=83) Evaluated safety, tolerability, PK and PD of single and multiple ascending doses of cudetaxestat to facilitate dose/dosing regimen selection for future studies Investigated relative bioavailability of new tablet formulation of cudetaxestat to oral solution formulation Evaluated effect of cudetaxestat on PK of a combination of probe substrates for CYP450 enzymes Assessed effect of cudetaxestat on PK of two approved drugs for IPF (pirfenidone and nintedanib) Objective

Consistent Tolerability in Phase 1 Clinical Studies 34 Study 1 SAD/MAD (N=80) Study 2 Relative Bioavailability (N=34) Study 3 CYP - DDI (N=16) Study 4 DDI with Approved IPF Therapies (N=83) • PK/PD correlation with sustained target engagement (LPA) • Data support clinical once - daily dose up to 750 mg or 500 mg BID (fed) • Comparable PK and PD profile between the two formulations • No alteration of plasma levels of substrates for CYP3A4, 2B6, 1A2, and 2C9; weak inhibition of CYP2D6 and induction of CYP2C19 • Co - administration w/ pirfenidone or nintedanib was well tolerated, with no reports of drug - related serious adverse events Summary Findings Cudetaxestat well tolerated with no reports of drug - related serious adverse events across all Phase 1 studies in healthy volunteers

Cudetaxestat Phase 1 Study Demonstrated Tolerability, PK and Biomarker Activity 35 6 single ascending dose (SAD) cohorts completed; 100, 300, 500, 750, 1000 mg 4 multiple ascending dose (MAD) cohorts completed; 100, 300, 500, 750 mg (fed) Demonstrated PK/PD correlation in healthy volunteer MAD Data support clinical once - daily dose up to 750 mg or 500 mg BID (fed) Well - tolerated at target doses with no treatment - emergent serious adverse events (SAEs) 100 - Fasted 300 - Fasted 500 - Fasted 750 - Fed (Normal diet) Daily Dose (mg) Peak - to - trough variation in LPA reduction (Emax and Etrough ) 2a-d1 2a-d72a-d142b-d1 2b-d72b-d142c-d1 2c-d72c-d142d-d1 2d-d72d-d14 0 20 40 60 80 100 M e a n % L P A R e d u c t i o n f r o m B a s e l i n e E m a x o r E t r o u g h Emax Etrough

Cudetaxestat Phase 2 Study Summary Design in IPF* 36 * Pending FDA review and feedback. Study Title: A phase 2, randomized, double - blinded, placebo - controlled, efficacy and safety of cudetaxestat (BLD - 0409) assessed across three dose ranges with or without a standard of care (nintedanib or pirfenidone) in patients with idiopathic pulmonary fibrosis (IPF) Screening / Enrollment Patient Population IPF patients (ATS, ERS, JRS, ALAT criteria) treated with or without approved IPF therapy (nintedanib or pirfenidone) Follow - Up Safety Assessments (4W +/ - 3 days) End of Treatment Primary Endpoints Change in Forced Vital Capacity (FVC) (L) from baseline at week 52 Time to disease progression Treatment (N=160) 52 - week duration IA#1 (12W) IA#2 (26W) Cudetaxestat High - Dose (n=40) Matching placebo (n=40) Cudetaxestat Mid - Dose (n=40) Cudetaxestat Low - Dose (n=40) 2Q - 2022 1H - 2024

Cudetaxestat Phase 2 Study Summary Design in IPF* 37 * Pending FDA review and feedback. ** Select adjudicated endpoints and assessments noted. Primary Endpoints • Change in Forced Vital Capacity (FVC) (L) from baseline at Week 52, assessed by clinic spirometry • Time to disease progression, defined as absolute percent predicted FVC ( FVCpp ) decline of ≥10% or death, whichever occurs first Secondary Endpoints** • Time to first acute IPF exacerbation during study • Time to all - cause mortality during study • Time to first respiratory hospitalization during study Exploratory Endpoints** • Percent change from baseline in LPA • Biomarkers of collagen and extracellular matrix biosynthesis, fibrosis, epithelial damage, and inflammation Interim Analyses (Blinded) • Conduct at 12 and 26 weeks to assess biomarkers (LPA target engagement, PRO - C3, PRO - C6) Safety** • Treatment - emergent adverse events • Assessment of vital signs, clinical laboratory parameters, and electrocardiograms

Cudetaxestat Phase 2 Basket Study in SSc - ILD Preliminary Design* 38 * Pending FDA review and feedback. ** Select adjudicated endpoints and assessments noted. Design • Multicenter, double - blind, randomized, placebo - controlled clinical study • Patients with interstitial lung disease secondary to systemic sclerosis (ACR/EULAR criteria) • 48 - week treatment duration Primary Endpoint • Change from baseline in FVC (L) Secondary Endpoints** • Composite endpoints • Composite Response Index in Systemic Sclerosis (CRISS) score • Health Assessment Questionnaire Disability Index (HAQ - DI) • Absolute FVCpp • Change in Modified Rodnan Skin Score ( mRSS )* • All cause mortality Safety** • Treatment - emergent adverse events • Assessment of vital signs, clinical laboratory parameters, and electrocardiograms

Cudetaxestat Planned Development Milestones 39 Note: clinical studies listed above are contingent upon regulatory review and feedback (e.g., FDA and ex - US regulatory authoriti es). * Study currently tentative and in early planning. Ph2 IPF IA#1 (12W) IA#2 (26W) Cudetaxestat IPF & SSc - ILD (Ph2 IPF OLE*) 1H - 20 22 2H - 20 22 1H - 2023 2 H - 2023 1 H - 2024 (Ph2 SSc - ILD basket study*)

40 Idiopathic Pulmonary Fibrosis Market Landscape and Opportunities Felix Karim, Ph.D. Executive Vice President, Business Development

IPF Epidemiology and Prevalence Estimates 41 1. Nalysynk , 2012, Eur Resp Rev. 2. Raghu, 2006, AJRCCM. 3. Natsuizaka , 2014, AJRCCM. * Prevalence varies by stringency of diagnosis, as defined in Nalysynk , 2012, Eur Resp Rev. Majority of patients with IPF are over 55 years old IPF Prevalence Estimates Prevalence Rate Prevalence US 1,2 Narrow Case Definitions* 14 - 28 / 100K ~45 - 90K Broad Case Definitions* 43 - 63 / 100K ~140 - 208K EU 1 1.3 - 23 / 100K ~6 - 120K Japan 3 10 / 100K ~13K

Lung Function Decline is the Hallmark of IPF 42 Kim, 2015, Respir Med. Lederer, 2018, NEJM. • IPF patients have a very poor prognosis − 5 - year survival rate of 50% 1 − Median survival time of 3 - 5 years following diagnosis 2 • Disease progression is highly variable • Acute exacerbations (~5 - 10% of patients annually) are the leading cause of hospitalization and death Adapted from Kim, 2015, Respir Med. 1. American Thoracic Society, General Information About Pulmonary Fibrosis. 2. Lederer, 2018, NEJM.

Current Approved Anti - Fibrotic Therapies for IPF 43 1. Noble, 2016, Eur Resp J. 2. Richeldi , 2014, NEJM. 3. Guler , 2021, AJRCCM. 4. Esbriet® (pirfenidone) USPI and Ofev ® (nintedanib) USPI. Esbriet ® (pirfenidone) and Ofev ® (nintedanib) • Only approved (standard of care) anti - fibrotic therapies • Approved based on slowing the decline of FVC from baseline − Reduced FVC decline from baseline by 40 – 55% vs. pbo 1,2 • Neither is curative nor showed a mortality benefit Guler , 2021, AJRCCM FVC (Force Vital Capacity) Product Safety / Tolerability 4 TEAE treated placebo Pirfenidone – Nausea 36% 16% – Rash 30% 10% – Dyspepsia 19% 7% – Liver enzyme elevation 4% 1% Nintedanib – Diarrhea 76% 32% – Nausea 32% 14% – Vomiting 25% 10% – Liver enzyme elevation 13% 3% Both treatments have significant safety/tolerability issues 4

Current IPF Treatment Paradigm Results in Significant Undertreatment 44 1. Dempsey, 2021, Ann Am Thor Soc. 2. Lancaster, 2021, Respirol . 3. Maher, 2017, BMC Pulm Med. 4. Wright, 2021, BMJ Open Respir Res. Real - world studies indicate 40 - 75% of patients remain untreated with SoC (pirfenidone or nintedanib ) 1,2,3 Note: Figure adapted from real - world data – see references cited below *No official standard exists for classifying disease severity in IPF. Physician - based judgments are highly subjective but do fal l into frequently noted characteristics (e.g., Mild = ppFVC > 80%; Moderate = ppFVC 55 - 80%; Severe = ppFVC <55%) IPF ~140K US & ~120K EU (estimated prevalence) ~30 - 40% discontinue anti - fibrotic treatment within one year 1,4 Safety/tolerability issues w/ SoC limit patient compliance 1,4 “Watch - and - wait” often used for mild / non - progressing patients Comorbidities, tolerability and access issues limit use for severe patients 2 Mild * 20 – 30% Moderate * ~50% Severe * 20 – 30% Treated ~30% Untreated SoC Treated ~60% Untreated SoC Treated ~40% Untreated

Significant Addressable Market Opportunity in IPF 45 1. Dempsey, 2021, Ann Am Thor Soc. 2. Lancaster, 2021, Respirol . 3. Maher, 2017, BMC Pulm Med. 4. Wright, 2021, BMJ Open Respir Res. 5. Research and Markets. “Global Idiopathic Pulmonary Fibrosis (IPF) Market” summary. Posted December 2021. 6. iHealthcareAnalyst , Inc. (press release Nov. 5, 2021). 7. Drugs.com. ~48% Untreated ~52% SoC Treated ~30 - 40% annual discontinuation 1,4 Current IPF Market 1,2,3,4 ~$3.3B ~$8.8B 2027 estimate 6 2020 5 Global IPF Market Market CAGR 7.3% driven by increased prevalence and incidence, premium - priced drugs, and approval of new treatments Annual list pricing for SoC anti - fibrotic therapies (2021) ‒ P irfenidone (patent expiry 2026): ~$130K/yr 7 ‒ N intedanib (patent expiry 2029): ~$145K/yr 7

IPF – Key Competitors in Clinical Development Includes all phase 3 programs and key phase 2 programs. PAH = pulmonary arterial hypertension. SoC = pirfenidone or nintedanib. 46 Company Stage Product MOA ROA, Dosing, Molecule Differentiators LOE Ph 3 Pamrevlumab Anti - CTGF mAb IV, Q3W mAb ± IV monotherapy only 2035 Ph 3 PRM - 151 Pentraxin - 2 protein IV, Q4W recomb protein ± IV add - on only, no monotherapy activity 2036 Ph 3 Treprostinil Prostacyclin analog Inhaled, QID small mol ± Inhaled add - on, reduces PAH 2028 Ph 2 GB - 0139 Galectin - 3 inhibitor Inhaled, QD small mol ± Inhaled monotherapy only - DDI w/ SoC 2033 Ph 2 BMS - 986278 LPA1 antagonist PO, BID small mol + Oral mono - or add - on therapy to SoC 2034 Ph 2 HZN - 825 LPA1 antagonist PO, QD or BID small mol ± Oral monotherapy only 2034 Ph 2 PLN - 74809 Integrin α v β 1 / α v β 6 antagonist PO, QD small mol + Oral mono - or add - on therapy to SoC 2037 Ph 2 Ready Cudetaxestat (BLD - 0409) ATX inhibitor (non - competitive/allosteric) PO, QD or BID small mol + Oral mono - or add - on therapy to SoC 2034 - 2036

Systemic Sclerosis ( SSc ) Pathophysiology / Progression / Demographics 47 1. National Scleroderma Foundation. 2. Denton, 2017, Lancet. 3. Bergamasco, 2019, Clin Epi. 4. Chifflot , 2008, Semin Arthritis Rheum. 5. Olson, 2018, Eur Resp Rev. 6. Goh, 2017, Arthritis Rheumatol . SSc is heterogeneous autoimmune disease often leading to chronic organ/tissue fibrosis • Majority of SSc patients exhibit some lung fibrosis – interstitial lung disease ( SSc - ILD) 2 • Progression of SSc - ILD is highly variable – typically slower than IPF 6 • North America SSc - ILD prevalence ~47K 3 • Global SSc - ILD prevalence ~400 – 500K 3,5 • Two primary disease segments: limited cutaneous ( lcSSc ) and diffuse cutaneous ( dcSSc ) • Organ fibrosis leads to morbidity / mortality - dcSSc entails greater risk for organ involvement • Onset is most frequently 25 – 55 years 1 • 3 - 4x more common in women than men 1 US prevalence rate of ~27.6 / 100K (~91K SSc patients in US 4 )

SSc - ILD Approved Treatments 48 1. Coherent Market Insights (press release Nov. 30, 2021). 2. Drugs.com No consensus approach to disease management 3 • Immunosuppressive therapies are longstanding SoC 2 approved therapies • Ofev ® (nintedanib) and Actemra ® (tocilizumab) approved based on slowing the decline in FVC • KOL recommendations for use/adoption are emerging 4 2028 Global SSc - ILD Market Opportunity $2.5B Nintedanib (oral dose, BID) Pricing ~$145 K/yr 2 Tocilizumab (IL - 6R antagonist mAb – SC/Q1W) Pricing ~$59 K/yr 2 1 3. Denton, 2017, Lancet. 4. Khanna, 2022, Arthritis Rheumatol .

SSc - ILD – Key Competitors in Clinical Development 49 Includes all phase 3 programs and key phase 2 programs. SoC = Mycophenolate mofetil. Company Stage Product MOA ROA, Dosing, Molecule Differentiators LOE Ph 2 HZN - 825 LPA1 antagonist PO, QD or BID small mol + Oral mono - or add - on therapy to SoC ± Excludes use of nintedanib or tocilizumab 2034 Ph1b/2 ACE - 1334 TGF - beta 1, 3 ligand trap SC, Q2W or Q4W recombinant protein + Oral mono - or add - on therapy to SoC + Add - on w/ nintedanib or tocilizumab Not disclosed Ph 2 Ready Cudetaxestat (BLD - 0409) ATX inhibitor (non - competitive/ allosteric) PO, QD or BID small mol + Oral mono - or add - on therapy to SoC + Add - on w/ nintedanib or tocilizumab 2034 - 2036

Supporting Peer Clinical Evidence on Lung Function (FVC) 50 BMS - 986020 (LPA1 antagonist) Ph2 1 Significant FVC benefit at wk 26 in BID group in IPF Tocilizumab (IL - 6R antagonist) Ph3 2 Significant FVC benefit at wk 48 in SSc - ILD Pamrevlumab (anti - CTGF mAb ) Ph2 3 Significant FVC benefit at wk 48 in IPF Cudetaxestat - Ph1 MAD in Healthy Volunteers LPA Reduction (P eak - to - trough variation) 100 mg QD 300 mg QD 2a-d1 2a-d72a-d142b-d1 2b-d72b-d142c-d1 2c-d72c-d142d-d1 2d-d72d-d14 0 20 40 60 80 100 M e a n % L P A R e d u c t i o n f r o m B a s e l i n e E m a x o r E t r o u g h Emax Etrough 5 00 mg QD 750 mg QD Cudetaxestat - Mouse Bleo Lung model IL - 6 gene expression Cudetaxestat - Mouse Bleo Lung model CTGF gene expression 1. Palmer, 2018, Chest. 2. Khanna, 2020, Lancet. 3. Richeldi , 2020, Lancet.

51 Neurodegeneration Market Landscape and Opportunities Felix Karim, Ph.D. Executive Vice President, Business Development

Significant Needs in Orphan Neurodegenerative (Poly - Q) Diseases 52 Physio - pedia.com – Huntington Disease. Huntington Study Group. Physio - pedia.com. Machado - Joseph Disease (Spinocerebellar Ataxia Type 3). Ruano , 2014, Neuroepidemiol . Nobrega , 2018, Adv Exp Med Biol. NIH - NINDS. Huntington’s Disease (HD) Spinocerebellar Ataxia 3 (SCA3) (aka, Machado - Joseph Disease or MJD) Prevalence ~5.7 per 100K (US, CA, EU, Australia) ~20 – 50K (US) ~2.7 per 100K (global) ~2K (US), ~5K (EU), ~1.7K (JP), ~5K (BR), ~20 – 100K (PRC) Disease Autosomal dominant (poly - Q) progressive neurodegeneration Autosomal dominant (poly - Q) progressive neurodegeneration Diagnosis Movement disorder (rapid, jerky), psychiatric and dementia Cerebellar ataxia, muscle weakness and loss of muscle mass Significant unmet need for disease - modifying therapies that are safe and well - tolerated

HD – Misfolded Proteins Trigger Progressive Neurodegenerative Diseases 53 1. Drugs.com. 2. Austedo ® ( deutetrabenazine ) USPI. 3. Podvin , 2019, J Neurol. 4. Singh, 2021, Curr Gene Ther . • Current SoC is symptomatic treatment and supportive care − Chorea treated with antipsychotics and dopamine - depleting agents − List price of deutetrabenazine $55 – $155K/ yr ($4.6K - $14K depending on dose) 1,2 • HD complications typically cause death 10 - 30 years after onset Number of CAG repeats in HTT gene 3,4 Juvenile - onset HD Adult - onset HD Normal 48 - 121 36 - 75 6 - 35

SCA3 (aka Machado - Joseph Disease or MJD) 54 1. Nobrega , 2018, Adv Exp Med Biol. 2. NIH - NCBI (https://www.ncbi.nlm.nih.gov/books/NBK1196/). SCA3 Subtype 1 Time of Onset Rate of Progression Type 1 Early onset 5 - 30 (mean 24 yrs ) Fast Type 2 Average onset (mean ~36 yrs ) Intermediate Type 3 Late onset (mean ~50 yrs ) Slow • Clinically heterogeneous ‒ Subtypes classified based on phenotype and progressive disease • Mean age of onset: ~40 years 1 ‒ Most patients require a wheelchair 10 - 15 years after disease onset 2 • No approved therapy to treat underlying disease ‒ Current SoC is symptomatic treatment and supportive care

HD – Key Competitors in Clinical Development Includes all phase 3 programs and key phase 2 programs. 55 Company Stage Product MOA ROA, Dosing, Molecule Differentiators LOE Prilenia Ph 3 Pridopidine Sigma type 1 receptor agonist PO, BID small mol • mRNA splicing modulator 2020 Annexon Ph 2 ANX - 005 Complement C1q mAb antagonist IV, Q2W mAb • Targets aberrant complement - mediated (C1q) 2037 AOP Orphan Pharma Ph 2 Selisistat SIRT1 Inhibitor PO, QD small mol • To enhance clearance of mutant Htt protein Unclear Novartis Ph 2 Branaplam SMN2 modulator PO, QW small mol • Stabilizes SMN2 mRNA splicing modulator 2035 Roche Ph 2 Tominersen Antisense targeting HTT gene Intrathecally Q8W or Q16W antisense • No clinical benefit for most HD patients • May also impact normal HTT gene product 2032 UniQure Ph 2 AMT - 130 HTT gene silencing (miRNA) 3 intra - brain injections one - time gene therapy AAV - miRNA • Adeno - assoc. virus (AAV) delivery of miRNA 2037 - 2038 Ph 2 pepinemab (VX15/2503) SEMA4D antagonist IV, Q4W mAb • Didn’t meet pre - specified co - primary endpoints • >beneficial changes in more advanced disease 2030 - 2038 Ph 1 - ready BLD - 2184 Calpain inhibitor PO, QD or BID small mol • Reduce mutant protein fragments • Enhance autophagy - clearance • Reduce mutant protein aggregates 2037 – 2040

Limited Competitive Pipelines in SCA3 Includes global phase 3 programs and key phase 2 programs. 56 Company Stage Product MOA ROA, Dosing, Molecule Differentiators LOE Ph 3 Troriluzole Tripeptide prodrug conjugate of riluzole PO, QD small mol • Increase glutamate uptake from the synapse • Reduce ataxia in all SCA diseases 2036 Ph 2 Trehalose Low mol weight disaccharide IV, Q24W small mol • Reduce mutant protein aggregates • Enhance autophagy 2033 Novartis Ph 2 Rimtuzalcap SK channel activator (calcium - activated K+ channels) PO, BID small mol • Reduce tremors and ataxia in all SCA diseases Not Disclosed Ph 1 - ready BLD - 2184 Calpain inhibitor PO, QD or BID small mol • Reduce mutant protein fragments • Enhance autophagy - clearance • Reduce mutant protein aggregates 2037 – 2040

57 Financial Overview Jean - Frédéric Viret, Ph.D. Chief Financial Officer

Biotech Acquisition Company Overview 58 • Nasdaq - listed SPAC (Nasdaq: BIOT) completed $230 million IPO on January 28, 2021 • SPAC affiliated with SPRIM, a global healthcare consulting firm and clinical research organization • SPRIM Global Investments is a leading life sciences venture capital firm with in - depth understanding of clinical - stage biotech companies Competitive Differentiation Decades of diverse experience operating businesses and driving value creation across 17 countries Management team has worked together for more than 20 years and has strong record of working with clinical - stage biotech companies Deep industry and life science experience

Uses ($mm) Equity Issued to Blade Shareholders $280.0 Cash to Balance Sheet $229.3 Estimated Transaction Expenses $25.0 Total Uses $534.3 Transaction Overview 59 Post - Money Valuation Transaction Sources and Uses Pro Forma Ownership (1) Assumes 28.0 million shares issued to Blade’s existing shareholders (with no portion of the merger consideration rolled into assumed in - the - money options), approximately 2.4 million PIPE shares, 23.0 million BAC public shares, and 4.6 million founder shares. Assumes no redemptions by BAC’s existing shareholders. Excludes the impact of 6.0 million BAC private placement warrants and 11.5 million BAC public warrants. (2) Excludes 3.5 million Blade earn - out shares not yet issued (to be issued to Blade if the VWAP of BAC is greater or equal to $15.00 over 20 trading days within any 30 trading days within 5 years after close) and any awards to be issued under an expected new equity incentive plan. Founder shares exclude 1.15 million previously issued shares that will be placed in escrow (to be released to the sponsor if the VWAP of BAC is greater or equal to $15.00 over 20 trading days within any 30 trading days within 5 years after close). Assumes PIPE shares are issued at a price of $10.00. (3) Blade estimated closing cash balance of $1mm and estimated closing debt balance of $2.8mm (4) Assumes no redemptions by BAC’s existing shareholders. (5) Consists of existing Blade investors. (1) (3) (3) (4) (4) (2) (4) 48.3% 4.2% 39.6% 7.9% Existing Blade Shareholders PIPE Investors BAC Public Shareholders BAC Sponsor Shares Sources ($mm) Blade Shareholder Equity Rollover $280.0 BAC Cash in Trust 230.0 PIPE 24.3 Total Sources $534.3 (5) PF Transaction ($mm or mm, except share price) Combined Company Share Price $10.00 PF Shares Outstanding 58.0 Total Equity Value $580.3 Less: Pro Forma Cash (230.3) Plus: Debt 2.8 Total Enterprise Value $352.8

Strategic and Smart Capital to Advance Novel Therapies in Unmet Needs in Orphan Diseases 60 * Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Backed by experienced life - science and strategic investors with deep experience investing in fibrosis therapeutic area • Expected differentiated competitive support post de - SPAC Minimum cash condition of $75 million • Allows sufficient runway through at least 1Q - 2024 Multiple anticipated near - and long - term clinical milestones* • Phase 2 trial in IPF for cudetaxestat with anticipated interim analyses in 1H - 2023 and 2H - 2023 • Phase 1 trial for BLD - 2184 in healthy volunteers with anticipated data readout in 1H - 2023

Q&A 61

62 Catalysts & Closing Wendye Robbins, M.D. President & CEO

Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases 63 1. Effects demonstrated in preclinical studies. 2. Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Experts in Biology of Cell and Tissue Damage Responses • Researching novel biological pathways foundational to cell - and tissue - damage responses • Developing potential disease - modifying therapeutics in fibrosis and neurodegeneration Differentiated Pipeline Led By Phase 2 - Ready Program in Fibrosis • Non - competitive autotaxin inhibitor with direct anti - fibrotic activity and differentiating characteristics 1 – planned phase 2 study in lung fibrosis in 2Q - 2022 • CNS - penetrant calpain inhibitor 1 for genetic orphan neurodegenerative conditions approaching planned phase 1 study in 2H - 2022 2 Deep Scientific & Industry Experience • Experienced management team and advisors with extensive expertise in fibrosis and neurodegeneration • Strong track record of development and approvals of innovative medicines at prior companies

Multiple Milestones 64 * Pirfenidone and nintedanib. ** Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Indicates completed/achieved milestone. Completed and Potential Milestones Timing Cudetaxestat Phase 1 CYP - DDI study completed Nov - 2021 Cudetaxestat Phase 1 DDI study with approved IPF therapies completed* Jan - 2022 Cudetaxestat End - of - phase 1 meeting with FDA 1Q - 2022 Corporate Complete merger with Biotech Acquisition Company 1Q - 2022 Cudetaxestat American Thoracic Society presentations May - 2022 Cudetaxestat Initiate planned phase 2 study in IPF** 2Q - 2022 BLD - 2184 Initiate planned phase 1 study in healthy volunteers** 2H - 2022 Cudetaxestat Initiate planned phase 2 basket clinical study in SSc - ILD** 2H - 2022 Cudetaxestat First interim analysis for planned phase 2 study in IPF** 1H - 2023 BLD - 2184 Data read out for planned phase 1 study in healthy volunteers** 1H - 2023 Cudetaxestat Second interim analysis for planned phase 2 study in IPF** 2H - 2023

Blade Therapeutics Investment Thesis 65 4. Research and Markets. “Global Idiopathic Pulmonary Fibrosis (IPF) Market” summary. Posted December 2021. 5. iHealthcareAnalyst , Inc. (press releasee Nov. 5, 2021). Orphan Diseases Pursuing debilitating, progressive diseases in fibrosis and neurodegeneration Significant Market Strong projected growth in IPF market Large Unmet Need 40 - 75% of patients with IPF remain untreated with current therapies 1,2,3 ~$3.3B ~$8.8B (2027 estimate) 5 (2020) 4 Differentiated Pipeline Oral, small - molecule candidates with novel mechanisms of action and strong IP complemented by global commercial rights Phase 2 Ready Lead program targeting clinically - validated pathway for IPF as potential monotherapy or add - on to current therapies $280M Proposed Valuation compared to peer companies, prior M&A deals and external IPF market potential 1. Dempsey, 2021, Ann Am Thor Soc. 2. Lancaster, 2021, Respirol . 3. Maher, 2017, BMC Pulm Med.

Developing Cutting - Edge Treatments for Debilitating Fibrotic and Neurodegenerative Diseases Blade Analyst Day February 22, 2022

Role of ATX / LPA Signaling Pathway in Pulmonary Fibrosis 67 Adapted from Suryadevarant , 2020, J. Mol. Sci. A ) Lung e pithelial cells - LPA activates the LPA receptor (LPA 2 ) to generate reactive oxygen species to promote cell death pathway, and directs the fibrogenic signaling via α v β 6 and TGF - β B ) Lung vascular endothelial cells - LPA/LPA 1 signaling activates cytoskeletal changes and VE - cadherin - mediated junctional disruption resulting in vascular leaking. C ) Fibroblast cells - LPA signaling results in enhanced TGF - β production and secretion, and in turn myofibroblast activation/differentiation leading to fibrotic gene expression, including CTGF, Col1A1 and TGF - β

Cudetaxestat Displays Robust Activity ( in vivo ) on Lung Fibrosis 68 SMA (smooth muscle actin), collagen 1A1 and assembled collagen data from preclinical study conducted in mouse bleomycin lung fib rosis model dosed once daily. PAI - 1, IL - 6 and CTGF (connective tissue growth factor) data from preclinical study conducted in mouse bleomycin lung fibrosis mo del dosed twice daily. SMA gene expression Marker of myofibroblast activation Collagen 1A1 gene expression Primary component of fibrosis, produced by myofibroblasts Assembled collagen Represents advanced fibrosis ANOVA One - Way *p<0.05 | **p<0.01 ***p<0.001 | ****p<0.0001 Saline Vehicle Cude 3mg/kg Cude 10mg/kg Cude 30mg/kg Bleomycin + Vehicle Bleomycin + cudetaxestat 30 mg/kg

Cudetaxestat Displays Robust Activity ( in vivo ) on Key Fibrotic Genes 69 TGF β = Transforming Growth Factor beta. α V Integrin gene expression Pro - fibrotic signaling TGF β 2 gene expression Pro - fibrotic growth factor β 6 Integrin gene expression Pro - fibrotic signaling ANOVA One - Way *p<0.05 | **p<0.01 ***p<0.001 | ****p<0.0001 SalineVehicle 409 0 20 40 60 80 100 TGFB2 Gene Counts T G F B 2 C P M ✱✱✱✱ ✱✱ SalineVehicle 409 0 20 40 60 80 100 TGFB3 Gene Counts T G F B 3 C P M ✱✱✱✱ ✱✱✱✱ SalineVehicle 409 0 50 100 150 200 250 TGFBR3 Gene Counts T G F B R 3 C P M ✱✱✱ ✱✱✱ α X Integrin gene expression Pro - fibrotic signaling TGF β 3 gene expression Pro - fibrotic growth factor TGF β R3 gene expression Anti - fibrotic growth factor receptor

SSc - ILD Treatment Paradigm – KOL Opinion on Management of SSc - ILD 70 Adapted from Khanna, 2022, Arthritis Rheumatol . ILD on HRCT Subclinical Clinical HRCT fibrosis <5 - 10% Asymptomatic Normal PFTs HRCT fibrosis >10% Symptomatic Risk of Progression Low High TCZ MMF CYC Close Monitoring Quiescent disease Active disease w/ skin, musculoskeletal manifestations Extrapulmonary Manifestations MMF CYC NINT MMF TCZ CYC RTX TCZ: Tocilizumab MMF: Mycophenolate Mofetil CYC: Cyclophosphamide NINT: Nintedanib RTX: Rituximab

BLD - 2184 – Development Candidate for Neurodegenerative Diseases 71 Neuroprotective Effects in SCA3 Model Fewer Ataxin - 3 inclusions and decreased loss of dopaminergic neurons (mutant hATXN3 lentiviral mouse model) Potent and active against cysteine proteases in preclinical models Good oral bioavailability and CNS penetration with long half - life Preclinical evidence in mouse models Attenuation of disease effects in SCA3 model IND - enabling studies completed Phase 1 planned to initiate 2H - 2022

BLD - 2184 Planned Phase 1 Study Design* 72 ** Pending regulatory review and feedback (e.g., FDA or ex - US regulatory authorities). Study Title: Phase 1A, Randomized, Double - Blind, Placebo - Controlled, Single & Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, and Pharmacokinetics of BLD - 2184 in Healthy Volunteers Eligibility confirmation Healthy volunteers (HVs) Part 2 – MAD (N=32) Multiple Ascending Doses Part 1 – SAD (N=40) Single Ascending Dose • 5 cohorts • Assess PK parameters • 4 cohorts • Assess maximal tolerable dose 2H - 2022 1H - 2023 Screening / Enrollment End of Study Drug Administration (N=72)

Glossary of Terms ALAT – La Asociación Latinoamericana de Tórax ATS – American Thoracic Society ATX – Autotaxin CAG – Cytosine, Adenine, Guanine CAPN – Dimeric Calpains CRISS – Composite Response Index in Systemic Sclerosis CTGF – Connective Tissue Growth Factor CYC – Cyclophosphamide dcSSc – Diffuse Cutaneous Systemic Sclerosis DDI – Drug - Drug Interaction ECM – Extracellular Matrix ERS – European Respiratory Society FVC L – Forced Vital Capacity, Liters FVCpp – Forced Vital Capacity Percent Predicted HAQ - DI – Health Assessment Questionnaire Disability Index HD – Huntington’s Disease HV – Healthy Volunteers lcSSc – Limited Cutaneous Systemic Sclerosis IL - 6 – Interleukin 6 IPF – Idiopathic Pulmonary Fibrosis JRS – Japanese Respiratory Society 73 LPA – Lysophosphatidic Acid LPC – Lysophosphatidylcholines LPI – Last Patient In MJD – Machado - Joseph Disease MMF – Mycophenolate Mofetil mRSS – Modified Rodnan Skin Score NINT – Nintedanib NOAEL – No Observed Adverse Effect Level PAI - 1 – Plasminogen Activator Inhibitor 1 PD – Pharmacodynamic P - gp – P - glycoprotein PK – Pharmacokinetic PRO - C3 – N - terminal Pro - peptide of Collagen Type III PRO - C6 – C - terminal Pro - peptide of Collagen Type VI RTX – Rituximab SAE – Serious Adverse Event SCA3 – Spinocerebellar Ataxia 3 SSc - ILD – Systemic Sclerosis - Interstitial Lung Disease SMA – Spinal Muscular Atrophy TCZ – Tocilizumab

Toby Maher, M.B., MSc, Ph.D., FRCP Professor of Medicine, USC Hastings Center for Pulmonary Research, Los Angeles 74 Dr. Maher runs an active clinical and translational research program. His research interests include biomarker discovery, the lung microbiome and host immune response in the pathogenesis of idiopathic pulmonary fibrosis (IPF). He is also actively involved in designing and running clinical trials in fibrotic lung disease. He has been involved in >50 trials, from phase 1b through phase 4, and is currently running studies assessing IPF, scleroderma, rheumatoid arthritis and inflammatory myositis. Dr. Maher and his team have recruited over 1,000 subjects to more than 35 clinical studies in the last 8 years. Dr. Maher received his medical degree from University of Southampton Faculty of Medicine and has been in practice for more than 20 years. He trained in Respiratory Medicine at the Royal Brompton Hospital. During his training, he gained an MSc in Respiratory Medicine from Imperial College London. In 2005, Dr. Maher was awarded a Wellcome Trust Clinical Research Fellowship undertaken at the Centre for Respiratory Research, University College London and culminated in the award of a Ph.D. As well as publishing original research, expert reviews and book chapters, Dr. Maher acts as an expert reviewer for a number of international medical and respiratory journals. He is an Associate Editor for American Journal of Respiratory and Critical Care Medicine and is a past Senior Editor of Respirology and past Associate Editor of PLOSOne . He is on the Editorial Board of the European Respiratory Journal, the European Respiratory Review and F1000 Journal and on the Advisory Board of Lancet Respiratory Medicine.