2Q25 (L)earnings August 2025
This presentation of Recursion Pharmaceuticals, Inc. (“Recursion,” “we,” “us,” or “our”) and any accompanying discussion contain statements that are not historical facts may be considered forward-looking statements under federal securities laws and may be identified by words such as “anticipates,” “believes,” “estimates,” “expects,” “intends,” “plans,” “potential,” “predicts,” “projects,” “seeks,” “should,” “will,” or words of similar meaning and include, but are not limited to, statements regarding Recursion’s ability to demonstrate the potential of technology-driven approaches to increase speed, quality and the scalability of drug discovery; Recursion's future as a leader in TechBio and ability to deliver better treatments to patients faster; Recursion’s OS industrializing first- and best- in-class drug discovery; our ability to industrialize clinical development and the effect of doing so on clinical trial outcomes; the occurrence or realization of potential milestones; current and future preclinical and clinical studies, including timelines for enrollment in studies, data readouts, and progression toward IND- enabling and other potential studies; advancements of our pipeline, partnerships, and data strategies; the potential size of the market opportunity for our drug candidates; outcomes and benefits from licenses, partnerships and collaborations, including option exercises by partners and the amount and timing of potential milestone payments; the initiation, timing, progress, results, and cost of our research and development programs; advancements of our Recursion OS; the potential for additional partnerships; our ability to identify viable new drug candidates for clinical development and the accelerating rate at which we expect to identify such candidates including our ability to leverage the datasets acquired through the license agreement into increased machine learning capabilities and accelerate clinical trial enrollment; Recursion’s cash position and cash runway; the completion of core integration plans and the results of the business combination with Exscientia; and many others. Other important factors and information are contained in Recursion’s most recent Annual Report on Form 10-K, Quarterly Report on Form 10-Q, and the Company’s other filings with the U.S. Securities and Exchange Commission (the “SEC”), which can be accessed at https://ir.recursion.com, or www.sec.gov. All forward-looking statements are qualified by these cautionary statements and apply only as of the date they are made. Recursion does not undertake any obligation to update any forward-looking statement, whether as a result of new information, future events or otherwise. Certain information contained in this presentation relates to or is based on studies, publications, surveys and other data obtained from third-party sources and the company’s own internal estimates and research. While the company believes these third-party sources to be reliable as of the date of this presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third- party sources. In addition, all of the market data included in this presentation involves a number of assumptions and limitations, and there can be no guarantee as to the accuracy or reliability of such assumptions. Finally, while the company believes its own internal research is reliable, such research has not been verified by any independent source. Information contained in, or that can be accessed through our website is not a part of and is not incorporated into this presentation. Cross-trial or cross-candidate comparisons against other clinical trials and other drug candidates are not based on head-to-head studies and are presented for informational purposes; comparisons are based on publicly available information for other clinical trials and other drug candidates. Any non-Recursion logos or trademarks included herein are the property of the owners thereof and are used for reference purposes only. Important Information 2
Recursion OS 2.0
Recursion’s unbiased platform approach delivers a strong internal and partnered portfolio 4 • Powered by proprietary and fit- for-purpose scaled data • End-to-end capabilities spanning novel target discovery, precision chemistry and optimized clinical trials • Built upon iterative cycles of dry- lab predictions and wet-lab validation to accelerate learning Models Portfolio Compute Data Generation & Validation
Boltz-2: Open-source model with MIT commoditizing binding affinity prediction approaching FEP accuracy at 1000x speed 5 Over 171K downloads and 41.5K unique users in less than two months Designed for drug discovery and virtual screening Contact/pocket constraints — ensure output follows respects given conditions Allows users to specify an experimental modality to emulate Template steering — allows users to input reference templates that embed prior knowledge
ClinTech: Industrialize clinical development by building an end-to- end platform to increase probability of success 6 • Patient-platform connectivity • Enables target validation and patient stratification • Supports expansion into new indications • More robust trial planning via clinical trial simulations • Potential for up to 30% more patients receive optimal dose • Potential for 50% faster enrollment projections through high quality sites • 2+ months faster trial activation Powered by integrated tech stack, RWE, and agentic solutions Strategic Partnerships Causal AI applied to human genomics Intelligent clinical trial design AI-powered recruitment & execution
REC-4539 for Small-Cell Lung Cancer (target: LSD1) is on strategic pause. Delivering Pipeline Advancements and Partnership Value 7 Target Disease Indication Late Discovery Preclinical Phase 1/2 Pivotal/Phase 3 Oncology REC-617 CDK7 Advanced Solid Tumors REC-1245 RBM39 Biomarker-Enriched Solid Tumors & Lymphoma REC-3565 MALT1 B-Cell Malignancies REC-7735 PI3Kα H1047R Breast Cancer Rare Disease REC-4881 MEK1/2 Familial Adenomatous Polyposis REC-102 ENPP1 Hypophosphatasia Partnerships Therapeutic Area Highlights Roche and Genentech Neuroscience & Oncology First neuroscience phenomap in human cell context. One optioned Gi oncology program continues to advance. Potential for up to 40 compound programs Sanofi Oncology & Immunology Milestones achieved across four distinct BIC and FIC discovery programs in 18 months; potential for several program milestones upcoming Bayer Oncology Advancing multiple programs with previously “undruggable” targets to lead series milestones Merck KGaA, Darmstadt, Germany Oncology & Immunology Multi-year collaboration to identify and advance first-in-class and best-in-class programs
Recursion brings medicines to clinic faster and at lower cost 0 10 20 30 40 50 60 Industry Recursion T im e t o c a n d id a te I D ( m o n th s ) Go faster 0 5 10 15 20 25 30 Industry Recursion C o s t to I N D ( $ M ) Spend less 0 500 1,000 1,500 2,000 2,500 3,000 Industry Recursion Highly productive compound design # s y n th e s iz e d t o c a n d id a te 0 2 4 6 8 10 12 14 Industry Recursion T im e t o h it p a c k a g e ( m o n th s ) Quickly validate hypotheses (Far Left): Time from hypothesis screening to validated hit package for legacy Recursion programs. (Center Left): Legacy Exscientia compounds synthesized from hit to candidate ID. (Center Right): Total molecule-related spend from hypothesis screening to the completion of IND-enabling studies for legacy Recursion novel chemical entity (NCE) programs that advanced to clinical trials. The cost to IND has been inflation-adjusted using the US Consumer Price Index (CPI) (Far Right). Time to validated lead is the average of >280 legacy Recursion programs since late 2017 through 2024. Industry data adapted from Paul, et al., Nature Reviews Drug Discovery (2010) 9, 203–214 8
Building Momentum: Portfolio Advancement Fueled by Platform Insights
REC-4539 for Small-Cell Lung Cancer (target: LSD1) is on strategic pause. Delivering Pipeline Advancements and Partnership Value 10 Target Disease Indication Late Discovery Preclinical Phase 1/2 Pivotal/Phase 3 Oncology REC-617 CDK7 Advanced Solid Tumors REC-1245 RBM39 Biomarker-Enriched Solid Tumors & Lymphoma REC-3565 MALT1 B-Cell Malignancies REC-7735 PI3Kα H1047R Breast Cancer Rare Disease REC-4881 MEK1/2 Familial Adenomatous Polyposis REC-102 ENPP1 Hypophosphatasia Partnerships Therapeutic Area Highlights Roche and Genentech Neuroscience & Oncology First neuroscience phenomap in human cell context. One optioned Gi oncology program continues to advance. Potential for up to 40 compound programs Sanofi Oncology & Immunology Milestones achieved across four distinct BIC and FIC discovery programs in 18 months; potential for several program milestones upcoming Bayer Oncology Advancing multiple programs with previously “undruggable” targets to lead series milestones Merck KGaA, Darmstadt, Germany Oncology & Immunology Multi-year collaboration to identify and advance first-in-class and best-in-class programs
Advancing programs with strong therapeutic rationale, powered by Recursion OS Addressable patient populations estimate based on annual US+EU5 and currently identified indications 1. Includes ovarian cancer, breast cancer, non-small cell lung cancer (NSCLC), colorectal cancer, pancreatic cancer, head and neck cancer 2. Biomarker-enriched 3. Diagnosed patients Note: REC-4539 | LSD1: Precision designed for reversibility and CNS penetration. Strategic pause to ensure a competitive Target Product Profile 11 REC-617 | CDK7 Solid tumors1 Optimized PK/PD for wider therapeutic index ~185,000 addressable patients REC-1245 | RBM39 Solid tumors2, Lymphoma Phenotypic insight reveals novel MOA for synthetic-lethal targeting in genomically unstable cancers ~100,000+ addressable patients REC-4881 | MEK1/2 Familial adenomatous polyposis (FAP) Phenotypic insight on MEK1/2 inhibition for APC-mutant FAP ~50,000 addressable patients REC-3565 | MALT1 B cell malignancies Potential for lower UGT1A1 inhibition and off-target AEs ~41,000 addressable patients REC-7735 | PI3Kα H1047R Breast Cancer Selective and wider therapeutic index ~11,000 addressable patients REC-102 | ENPP1i Hypophosphatasia (HPP) Oral, highly selective & potent, suitable for lifetime dosing ~7,8003 addressable patients
Recursion OS 2.0: Efficiently delivering novel insights, precision design, and optimized clinical trials 12 Nomination Workflow Scientific Agents Transcriptomics Assay & Models ML-based Patient Connectivity (RWD) LLMs & Graphs MOA Deconvolution Scaled Binding Affinity Predictions Phenomics Assay & Models AI-powered Biological Insights Clinical Trial Design ClinTech Workflow AI-powered Recruitment Causal AI Patient stratification & indication selection AI-informed Clinical Development Design Workflow Automated ADMET Automated Chemistry Automated Biology 3D Protein & Atomistic Models Molecular Property Prediction & Design Scientific Agents AI-enabled Precision Design
REC-1245 (RBM39 degrader): Novel biological insight drives clinical program 13 Design Workflow Automated ADMET Automated Chemistry Automated Biology 3D Protein & Atomistic Models Molecular Property Prediction & Design Scientific Agents AI-enabled Precision Design Nomination Workflow Scientific Agents Transcriptomics Assay & Models ML-based Patient Connectivity (RWD) LLMs & Graphs MOA Deconvolution Scaled Binding Affinity Predictions Phenomics Assay & Models AI-powered Biological Insights Clinical Trial Design ClinTech Workflow AI-powered Recruitment Causal AI Patient stratification & indication selection AI-informed Clinical Development
Platform links RBM39 biology to CDK12, a key regulator of DNA damage response genes (DDR) and replication stress (RS) Genetic-Chemical ConvergenceCDK12 Axis RecapitulatedAI-guided Multimodal Mapping Deep genome coverage across major DDR pathways in HUVEC PhenoMap1 • Whole Genome CRISPR knockouts; close to 1 million compounds profiled • Vast DDR network resolution unattainable with single-readout screens 1. List of DDR genes and pathways obtained from Knijnenburg 2018 CDK12 and Cyclin K (CCNK) share a similar signature in phenomic readout • CDK12 kinase activity requires CCNK binding, a well-established dependency • Validates approach and potential for novel AI-driven mechanistic and patient insights 14 RBM39 loss mimics CDK12 inhibition, providing a druggable potential analog • Suppresses DDR networks and cell-cycle pathways • Potential for tumor-selective activity with a wider therapeutic index SimilarOpposite CCNK CDK12 CDK12 CCNK REC-1245 | RBM39 degrader
Multi-Omics insights link RBM39 dependency to transcription- replication stress and DNA repair vulnerabilities Epigenetic Regulation Cell Cycle Control Transcription DNA Damage Repair RBM39 & REC-1245 Clusters across various mechanisms of replication stress and DNA repair vulnerabilities REC-1245 | RBM39 degrader
Selective degradation of RBM39 impairs splicing, compromising DDR pathways and transcriptional regulation 2 3 1 1. RBM39 Degradation • REC-1245 recruits RBM39 & DCAF15 for rapid proteasomal degradation • Loss of this splice adaptor destabilizes the spliceosome 2. DDR Gene Silencing • Long repair transcripts (BRCA1/2, ATR, etc.) retain introns and degrade • Fork protection fails, marked by rising γH2AX and stalled replication 3. Mitotic Collapse • Compromised G2/M checkpoints push cells into mitosis without repair • Resulting chromosomal breakage drives tumor cell death 16 RBM39 degradation recapitulates CDK12 loss, potentially enabling a synthetic-lethal opportunity in genomically unstable cancers REC-1245 | RBM39 degrader
Target tumors characterized by drivers of genomic instability arising from replication stress potentially linked to RBM39 dependency 17 1. da Costa 2022, NRDD 2. Internal company estimates. Assumes US+EU5 addressable incidence with biomarker-enriched solid tumors and other select histologies. 3. Cell lines were assigned to broad pathway dysregulation contexts based on 1 or more documented alteration from CCLE/GSDC databases C T G I C 5 0 ( µ M ) In vitro: cell viability with REC-12453 Emerging preclinical data uncover replication stress as a potential signature for REC-1245 sensitivity • REC-1245 also demonstrates concentration-dependent increases in γH2AX in high replication stress driven human cancer cells in vitro (data not shown) Replication stress and DNA repair vulnerabilities span several solid tumors and blood cancers • Including colorectal, endometrial, lung, breast, sarcoma, bladder, ovarian, pancreatic, DLBCL and AML • Correlates with clinically actionable alterations • E.g., MYC/MYCN amplification, SWI/SNF loss, MSI-H, HRR defects • Potential to meaningfully expand beyond initial patient population Broad patient subsets with replication stress and DNA repair vulnerabilities1 Epigenetic Dysregulation Cell Cycle Alterations Oncogenic Drivers DDR Defects >100,000 patients in US & EU5 per year2 REC-1245 | RBM39 degrader
Emerging preclinical data suggests greater sensitivity with REC- 1245 in high replication stress and DDR vulnerable tumors 18 1. N=4 mice per group. REC-1245 demonstrates reduction in tumor volume across different tumors with high-RS signatures and DNA repair vulnerability1 Vehicle BID REC-1245 10 mg/kg BID A2780 (Ovarian) Epigenetic dysregulation Days post treatment T u m o r V o lu m e ( m m 3 ) HEC-251 (Endometrial) Cell cycle alterations Days post treatment T u m o r V o lu m e ( m m 3 ) LS513 (CRC) Oncogenic drivers Days post treatment T u m o r V o lu m e ( m m 3 ) TOV-21G (Ovarian) DDR Defects, MSI-H Days post treatment T u m o r V o lu m e ( m m 3 ) REC-1245 | RBM39 degrader
Mechanistic Validation RBM39 Degradation % R B M 3 9 D e g r a d a t io n (N o rm a li ze d -V e h ic le ) Concentration (nM) Recursion OS Insight Platform derived insight to unlocking comprehensive genomic instability vulnerabilities 19 Preclinical Data Days post treatment T u m o r V o lu m e ( m m 3 ) Ovarian CDX Model: OVK18 (MSI-H) REC-1245 induces significant tumor regressions in an ovarian CDX • Model driven by elevated replication stress REC-1245 translates phenotypic insights • Driving rapid and potent RBM39 degradation in human PBMCs within 24 hours RBM39 loss mimics CDK12 deficiency • 204 candidates synthesized to candidate ID (REC-1245) • Advanced program from target ID to IND-enabling studies in 18 months REC-1245 | RBM39 degrader CDK12 RBM39CDK13 RBM39 CDK12 CDK13
Phase 1/2 monotherapy dose escalation ongoing with early safety/PK data anticipated 1H26 20 Clinical Updates • First patient dosed in 4Q24 • Early safety and PK from monotherapy trial in 1H26 Monotherapy data update expected in 1H26 REC-1245 monotherapy dose escalation Minimum efficacious dose REC-1245 monotherapy dose confirmation RP2D REC-1245 monotherapy Tumor-specific expansion cohorts Dose Escalation & Confirmation Dose Expansion DAHLIA patient population: • Multi-omic guided insights for initial advanced solid tumor population • Cancers with high genomic instability (e.g., endometrial) • Biomarker enriched populations (e.g., 2L+ MSI-H/dMMR1) Cohort 1 TBD Cohort 2 TBD DAHLIA: A Study of REC-1245 in Participants With Unresectable, Locally Advanced, or Metastatic Cancer; NCT06678659 1. Progressed on, been ineligible for, or intolerant to at least on prior checkpoint inhibitor REC-1245 | RBM39 degrader
REC-617 (CDK7 inhibitor): Precision design for optimal therapeutic index and causal AI for indication validation 21 Design Workflow Automated ADMET Automated Chemistry Automated Biology 3D Protein & Atomistic Models Molecular Property Prediction & Design Scientific Agents Nomination Workflow Scientific Agents Transcriptomics Assay & Models ML-based Patient Connectivity (RWD) LLMs & Graphs MOA Deconvolution Scaled Binding Affinity Predictions Phenomics Assay & Models Clinical Trial Design Clintech Workflow AI-powered Recruitment Causal AI Patient stratification & indication selection AI-enabled Precision DesignAI-powered Biological Insights AI-informed Clinical Development
22 AI-guided precision design for optimized therapeutic index High permeability, rapid absorption, low efflux Target affinity and selectivity CDKC IC50 (nM) CDK family selectivity Cell potency HCC70 (breast cancer) IC50 (nM) OVCAR-3 (ovarian cancer) IC50 (nM) Safety and metabolism hERG IC50 (μM) Human microsome Clint μL/min/mg Human hep Clint μL/min/106 cells ADME Caco-2 A2B (efflux) 106 cm/s pH 7.4 μg/mL F % (p.o.) • Generative AI models used to design novel scaffolds • Active learning and experimental data leveraged rapidly to optimize ADME • 136 novel compounds to Candidate ID in <12 months Designed to optimize PK/PD and maximize potential therapeutic index REC-617 achieves peak exposures in the clinic exceeding CDK7 IC80 and well below CDK2 IC80 • AI-designed molecule achieves rapid, potent CDK7 inhibition 1. CDK7 IC80 reflects biochemical in vitro potencies on file REC-617 | CDK7 inhibitor As of the November 2024 data cut, REC-617 showed one confirmed partial response and multiple cases of stable disease, with a favorable safety profile and no maximum tolerated dose reached
AI-enabled causal inference strengthens preclinical data for indication selection of ovarian cancer for ELUCIDATE 23 1. Besnard et al, AACR (2022) 2. Causal inference framework based on a network-informed directed acyclic graph (DAG) to assess CDK7’s impact on clinical outcomes. Patients were indexed on their date of NGS sequencing and followed until death or censoring with 10 + years of patient follow available. The model adjusts for relevant clinical and genomic confounders, including BRCA status, treatment history, and tumor genomics. Ovarian cell line sensitive to CDK7 inhibition with REC-617 • Unbiased analysis of over 360 cell lines in glo titer assay Cell Panels Causal Inference using Omics and Clinical data CDK7 emerges as a likely driver of poor survival in ovarian cancer based on a causal inference framework leveraging multi-omic and clinical data • Over ~32K patient records using DNA, RNA and clinical outcomes Impact • Supports preclinical findings with causal inference using omics and patient data • 1st indication: 2L+ platinum- resistant ovarian cancer (PROC) Potent tumor regression with REC-617 treatment • <10 hours of exposure above IC80 to optimize benefit-risk In vivo Models CDX Model: OVCAR1 Patient Data: Ovarian Cancer2Cell Line: OVCAR3 S u rv iv a l p ro b a b ili ty Number of months post-sequencing REC-617 | CDK7 inhibitor
Phase 1/2 single-arm combination in ovarian cancer initiated 1H25 24 ELUCIDATE: Study to Assess GTAEXS617 in Patients With Advanced Solid Tumors; NCT05985655 1. SOC includes single-agent chemotherapy, bevacizumab ± chemotherapy, PARP inhibitors in select patients Clinical Updates • Early data indicates favorable safety profile • Maximum Tolerated Dose (MTD) not yet reached ✓ Combination escalation initiated 1H25 • 2L PROC selected as first cohort • Site selection & activation in process Monotherapy data update expected in 2H25 Single-Arm Tumor Expansion Cohorts Combination: REC-617 + SOC1 2L+ platinum-resistant ovarian cancer (PROC) Monotherapy Dose Escalation All-comers Patients with advanced solid tumors RP2D(s) Monotherapy: REC-617 Monotherapy: REC-617 R/R ovarian cancer Additional Combinations: REC-617 + SOC REC-617 | CDK7 inhibitor
Partnered Discovery Delivering on differentiated programs
Advancing partnership discovery by leveraging Recursion 2.0 26 4 Program milestone payments achieved in last 18 months Several programs advancing towards development candidate over next 12-15 months Continued program advancement in a GI oncology indication and multiple neuroscience programs into target validation advanced by leveraging the RecursionOS and Genentech's biology expertise Phenomaps in Neuroscience, GI Oncology • 1 trillion iPSC-derived cells • 100 billion GI Oncology relevant cells • 5,000 transcriptomes5 Potential for over $100 million in partnership milestones by end of 2026 Recursion & Bayer have nominated multiple early discovery precision oncology programs against previously “undruggable” targets Multiple-year collaboration to identify first-in-class and best-in-class targets
Financial Update
Well positioned to deliver on upcoming milestones 1. Cash, cash equivalents and restricted cash 2. YE2024 reported OpEx for Recursion and Exscientia combined, excluding non-cash GAAP items (e.g. share-based compensation). 2026 estimate of <$390 million cash burn 3. Risk-adjusted cash inflows from partnerships included in estimated cash runway 4. Cash burn, defined as operating cash flow less capital expenditures, excluding partnership and financing inflows, transaction expenses and severance 28 • $533.8 million in cash1 as of June 30, 2025 Cash, cash equivalents and restricted cash Operational cash inflows • $7 million Sanofi milestone payment • $28.6 million R&D tax credit • Potential for over $100 million in partnership inflows by end of 20263 • Expected 2025 cash burn4 of <$450 million • Expected 2026 cash burn4 of <$390 million Expected cash runway into the fourth quarter of 2027 Guidance 2Q25 Highlights 2025 & 2026 Streamlining of operations and infrastructure • Expected to reduce pro forma operating expenses by ~35% from 2024 to 20262
Looking ahead
Continuing our evolution to deliver differentiated, high-confidence programs 30 Differentiated, high quality programs with novel pathway biology, chemistry design, and competitive positioning emerging from evolving Recursion 2.0 platform Unique biologic insights identified from maps with different cell types MoA and Target deconvolution using Boltz-2, QM/MD, & CRISPR screens Patient strategy supported by translational models & RWE Illustrative
Internal and external pipeline momentum FY 2025 and 2026 upcoming pipeline catalysts Partnership Catalysts Potential for additional phenomap options Potential for multiple new project initiations Potential for multiple programs optioned by partners 2025 2026 H1 REC-617 (CDK7i) in advanced solid tumors Initiation of combination studies H2 REC-4881 (MEK1/2i) in FAP Additional safety and efficacy data from TUPELO REC-617 (CDK7i) in advanced solid tumors Additional Phase 1 data from ELUCIDATE REC-7735 (PI3Kα H1047Ri) DC nomination H1 REC-1245 (RBM39) Early safety and PK from monotherapy trial H2 REC-3565 (MALT1) Early safety and PK from monotherapy trial REC-102 (ENPP1i) Ph1 initiation – 2H26 31
