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DECODING BIOLOGY TO RADICALLY IMPROVE LIVES RECURSION JP Morgan Healthcare Conference January 10th, 2023
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initiation, timing, progress, results, and cost of our research and development programs and our current and future preclinical and clinical studies, the potential size of the market opportunity for our drug candidates, our ability to identify
viable new drug candidates for clinical development and the accelerating rate at which we expect to identify such candidates, our expectation that the assets that will drive the most value for us are those that we will identify in the future using
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reference purposes only. 2
RECURSION HAS AN OPPORTUNITY FOR ARBITRAGE IN THE DRUG DISCOVERY SPACE 50B 100M RECURSION 500K Eroom s Law: Drug discovery is
becoming slower and more expensive over time Moore s Law: Computing power becomes faster and less expensive over time 1962 1970 1980 1990 2000 2010 2020 10 1 0.1 NMEs per $B spent (inflation adjusted) Compute Power (Transistors per
Microprocessor) Adapted from Scannell et al and Our World in Data 3
Historical tools and the limits of human cognition have led to oversimplifying complex biological systems Traditional Approach to
Biology Recursion s Approach to Biology Well-known primary relationships between key members of five pathways: JAK/STAT | SWI/SNF | TGF ² | RAS | Proteasome All primary relationships found by the Recursion OS between key members of
five pathways: JAK/STAT | SWI/SNF | TGF ² | RAS | Proteasome 4 Recursion
Recursion recursion s map-based approach is designed to set the standard for drug discovery
in the 21st century Literature drives discovery. Informs target-based hypotheses Traditional drug discovery Recursion approach Data are an exhaust. Limited to testing hypotheses Linear process. Little cross-program learning or iteration Disparate
data generation. Siloed to individual programs and diseases Bespoke processes. Low-dimensional assays & biomarkers Vs Platforms drive discovery. Unbiased & target agnostic Data are our fuel.
Shape our hypotheses Virtuous cycles of atoms & bits. Iterative feedback accelerates learning Connected data across programs. Relatable high-dimensional data Industrialized to scale. Automation & standardization 5
Recursion Initiated 4 clinical trials in the first 3 quarters of 2022 (3 Ph2, 1 Ph1) Planning a 5th clinical trial to initiate (Ph2)
Novel oncology programs (Target Alpha, Target Gamma) nearing IND-enabling studies Advancing collaborations in Fibrosis (Bayer) and Neuroscience (Roche-Genentech) $13B in potential milestones across 50+ possible programs plus royalties We
believe that we have built one of the largest proprietary & relatable in-vitro biological and chemical datasets on Earth >21 petabytes of data and >3 trillion searchable relationships
maturing the techbio value proposition in 2022 6
Recursion our pipeline reflects the scale and breadth of our approach Phase 1 Phase 2 Phase 3 (APC; est. 50K) AXIN1/APC MUTANT CANCERS
(AXIN1/APC mutant cancers; est. 32K) KRAS/STK11-DRIVEN CHECKPOINT RESISTANCE (KRAS/STK11; est. 11K) MYC-DRIVEN ONCOLOGY (MYC; est. 54K1) CANCER IMMUNOTHERAPY TARGET ALPHA (Multiple; 72K2) CANCER IMMUNOTHERAPY
TARGET BETA (Multiple; 15K2) HRD-NEGATIVE OVARIAN CANCER TARGET GAMMA (HRD-negative ovarian cancer; 13K) Rare & Other CEREBRAL CAVERNOUS MALFORMATION (CCM; est.
360K3) NEUROFIBROMATOSIS TYPE 2 (NF2; est. 33K4) CLOSTRIDIUM DIFFICILE COLITIS (est. 730K) Partnership Programs MULTIPLE PROGRAMS ADVANCING SIMULTANEOUSLY More than a dozen early discovery and research programs in oncology, neuroscience,
inflammation & immunology, and rare disease All populations defined above are US and EU5 incidence unless otherwise noted. EU5 is defined as France, Germany, Italy, Spain and UK. (1) Our program has the potential to address a number of
indications driven by MYC alterations, totalling 54,000 patients in the US and EU5 annually. We have not finalized a target product profile for a specific indication. (2) Our program has the potential to address a number of indications in this
space. (3) Prevalence for hereditary and sporadic symptomatic population. (4) Annual US and EU5 incidence for all NF2-driven meningiomas. 7 7 Therapeutic Area Indication Late Discovery FAMILIAL
ADENOMATOUS POLYPOSIS Preclinical
Recursion mapping and navigating the complex systems of biology and chemistry has demonstrated leading indicators of efficiency Failing
faster and earlier to spend less Cost to IND ($M) 25 20 15 10 5 0 Industry 40 30 20 10 0 and go faster Screen Hit ID Validated Lead Advanced Candidate Development Candidate Stage Preliminary data shown is the average of
all our programs since late 2017. All industry data adapted from Paul, et al. Nature Reviews Drug Discovery. (2010) 9, 203 214 8 80% 75% 85% 64% 39% 50% 62% time to validated lead (mo)
How we build and navigate maps of biology and chemistry to turn drug discovery into a search problem recursion
We build biological and chemical datasets to map relationships across scales and understand the connectivity of the system recursion
Organism Level Invivomics Cell Level Phenotypes Phenomics Metabolates Level Metabolomics Protein Level Proteomics RNA Level Transcriptomics DNA Level (Population-Scale) Genomics Built and scaled Exploratory Aspirational Image adapted from
D Orazio, M., et al. Nature Scientific Reports 2022. 10
Recursion Robotic Automation at Scale Up to 2.2 Million wet-lab experiments per week profiling
genes and compounds, we believe we are one of the largest phenomics (human cellular image-based) data producers 2.2 Million Week Diverse Biological and Chemical Inputs 48 different human cell types >1.7 Million >500 Billion small molecule
library, we believe this scale is on par with some large pharma companies hiPSC-derived cells produced in 2022, we believe that we are one of the largest hiPSC- derived cell producers High-Dimensional Validation 150 Up to 100 15K near whole exomes
per week, we believe we are one of the largest transcriptomics data producers 50 log2(FC) Recursion OS Enables quality, relatability and scale of data >21 Petabytes Digitization of Biology and Chemistry >21 Petabytes of proprietary high-
dimensional data, we believe this is one of the largest relatable in vitro biological and chemical datasets Recursion Top 500 ML-Based Analysis Top 500 supercomputer across any industry (TOP500 List, Nov
2022), we leverage vast neural networks and multiomics approaches to extract features and drive insights >3 Trillion Novel Insights at Scale ML-Based Relationships relatable hypotheses across multiple
biological and chemical contexts 11
All Human Genes with Significant Effects in this Cellular Context Genome-scale mapping Recursion
This is a whole-genome arrayed CRISPR knock-out Map generated in primary human endothelial cells Every gene is represented in a pairwise way (each is present in columns and rows) Dark Red indicates phenotypic
similarity according to our neural networks while Dark Blue indicates phenotypic anti- similarity (which in our experience often suggests negative regulation) We can add the phenotypes of hundreds of thousands of small molecules at multiple doses
and query and interact with these maps using a web application Can show 100s of examples of known biology and chemistry 12
DOCK9 SLC39A1 ASB7 MEGF8 PRKCH SOCS3 PHF13 PPP1R9B TNKS1BP1 ZMYM3 FAM49B STK24 YWHAB IL6ST IL6R STAT3 IL6 JAK1 STAT3 ILGR ILGST WHAB
STK24 FAM49B One such example the JAK/STAT pathway clustered by strength of interaction, including both similar genes (red) and opposite genes (blue) Can wade into areas of novel biology and chemistry... 13
Enhancer module INTS13- Int-PP2A (phosphatase module) INTS8 -INTS14 INTSS INTS10 Endonuclease
module Central backbone INTS4 INTS11 INTS7- INTS9 SOSS complex -INTS1 INTS3 (N terminus) INIP INTS2 INTS6 Assembled complex -PP2A-C PPZA-A NABP1/2 INTS6 (C terminus)
INTS3 dimer (C terminus) Endonuclease module Int-PP2A (phosphatase module) Central backbone Phenomics TVN (below diagram) vs. Centerscale (above diagram) INTS9 INTS11 INTS4 INTS7 Similar INTS2 INTS8 INTS1
INTS6 Opposite C7orf26 INTS10 Maps reveal known and novel biology In 2022, new independent research identified a previously unknown gene, C7orf26, as part of the Integrator complex Maps jointly developed by Recursion and Genentech replicated this
same result Demonstrates accuracy and consistency across different map building approaches O Recursion. Genentech A Member of the Roche Group Recursion INTS13 INTS14 Trademarks are the property of their respective owners and used for informational
Value driven by partnerships, clinical and preclinical programs Recursion
How we create value using our maps of biology and chemistry Discovery Partnerships Partnership strategy Partner in complex therapeutic
areas requiring large financial commitment and competitive market dynamics Leverage partner knowledge and clinical development capabilities Fibrosis Neuroscience *and a single oncology indication Other large, intractable areas
of biology Recursion OS Internal Pipeline Pipeline strategy Build wholly-owned pipeline in indications with potential for accelerated path to approval Oncology Rare Disease 16
Our existing partnerships represent some of the most significant scientific collaborations in biopharma Recursion
BAYER BAYER (Announced Sep 2020; Expanded Dec 2021) Fibrosis $30M upfront and $50M equity investment Up to or exceeding $1.2B in milestones for up to or exceeding 12 programs Mid single-digit royalties on net sales Recursion owns all
algorithmic improvements I I Roche Genentech A Member of the Roche Group (Announced Dec 2021) Neuroscience *and a single oncology indication $150M upfront and up to or exceeding $500M in research milestones and data usage options Up to
or exceeding $300M in possible milestones per program for up to 40 programs Mid to high single-digit tiered royalties on net sales Recursion owns or co-owns all algorithmic improvements Trademarks are
the property of their respective owners and used for informational purposes only. 17
Our pipeline reflects the scale and breadth of our approach Therapeutic Area Indication Oncology FAMILIAL ADENOMATOUS POLYPOSIS (APC;
est. 50K) Rare & Other Partnership Programs MULTIPLE PROGRAMS ADVANCING SIMULTANEOUSLY AXIN1/APC MUTANT CANCERS (AXIN1/APC mutant cancers; est. 32K) KRAS/STK11-DRIVEN CHECKPOINT RESISTANCE (KRAS/STK11; est. 11K) MYC-DRIVEN ONCOLOGY (MYC; est. 54K1) CANCER IMMUNOTHERAPY TARGET ALPHA (Multiple; 72K2) CANCER IMMUNOTHERAPY TARGET BETA (Multiple; 15K2) HRD-NEGATIVE OVARIAN CANCER TARGET
GAMMA (HRD-negative ovarian cancer, 13K) CEREBRAL CAVERNOUS MALFORMATION (CCM; est. 360K³) NEUROFIBROMATOSIS TYPE 2 (NF2; est. 33K4) CLOSTRIDIUM DIFFICILE COLITIS (est. 730K) Late Discovery Preclinical
Phase 1 Phase 2 Phase 3 More than a dozen early discovery and research programs in oncology, neuroscience, inflammation & immunology, and rare disease Recursion All populations defined above are US and EU5 incidence
unless otherwise noted. EU5 is defined as France, Germany, Italy, Spain and UK. (1) Our program has the potential to address a number of indications driven by MYC alterations, totalling 54,000 patients in the US and EU5 annually. We have not
finalized a target product profile for a specific indication. (2) Our program has the potential to address a number of indications in this space. (3) Prevalence for hereditary and sporadic symptomatic population. (4) Annual US and EU5 incidence for
all NF2-driven meningiomas. 18
Phase 2 Trial Underway REC-994 for Cerebral Cavernous Malformation (CCM) PREVALENCE
~360,000 Symptomatic US + EU5, >1 million patients worldwide live with these lesions today CAUSE LOF mutations in genes CCM1, CCM2 & CCM3, key for maintaining the structural integrity of the vasculature due to unknown mechanisms
PATHOPHYSIOLOGY Vascular malformations of the CNS leading to focal neurological deficits, hemorrhage and other symptoms OUR REASON TO BELIEVE Efficacy in Recursion OS as well as functional validation via scavenging of massive superoxide accumulation
in cellular models; reduction in lesion number with chronic administration in mice KEY ELEMENTS Targeting sporadic and familial symptomatic CCM patients with CCM1, CCM2, and CCM3 mutations Phase 2 clinical trial initiated in Q1 2022 Phase 2a
Study Design: Once daily oral dosing US & EU Orphan Drug Designation Endpoints CCM Confirmed with MRI 1:1:1 High Dose Low Dose 52-Week Treatment 1 Safety and Tolerability Placebo
2 Imaging, neuro assessments and PROS Open Label Extension Julia living with CCM Recursion 19
Phase 2/3 Trial Underway REC-2282 for NF2-Mutated
Progressive Meningioma PREVALENCE ~33,000 US + EU5 CAUSE LOF mutations in NF2 tumor suppressor gene PATHOPHYSIOLOGY Inherited rare CNS tumor syndrome leading to loss of hearing and mobility, other focal neurologic deficits OUR REASON TO BELIEVE
Efficacy in Recursion OS, cellular, and animal models; suppression of aberrant ERK, AKT, and S6 pathway activation in a Phase 1 PD Study in NF2 patient tumors KEY ELEMENTS Targeting familial and sporadic NF2 meningioma patients Phase 2/3 clinical
trial initiated in Q2 2022 Oral bioavailability and CNS exposure together are unique among clinical-stage HDAC inhibitors Fast-Track and US Orphan Drug Designation Progressive NF2- mutated meningioma 1:1
REC-2282 40mg REC-2282 60mg Phase 2 6 x 1 Mo. Cycles Interim Analysis 20 x 1 Mo. Cycles Progressive NF2- mutated meningioma
REC-2282 Placebo 1 PFS 2 TTR, DOR & ORR 26 x 1 Mo. Cycles 20 Adaptive Phase 2/3 Study Design Phase 3 Ricki living with NF2
Phase 2 Trial Underway REC-4881 for Familial Adenomatous Polyposis (FAP) PREVALENCE ~50,000
PATHOPHYSIOLOGY US + EU5 Polyps throughout the GI tract with extremely high risk of malignant transformation CAUSE Inactivating mutations in the tumor suppressor gene APC OUR REASON TO BELIEVE Efficacy in the Recursion OS shows that specific MEK 1/2
inhibitors had an effect in context of APC LOF. Subsequent mouse model APCmin showed potent reduction in polyps and dysplastic adenomas Oral Dosing Fast-Track and US & EU Orphan Drug Designation Targeting Classical FAP
patients (w/ APC mutation) KEY ELEMENTS Phase 2 clinical trial initiated in Q3 2022 Phase 2 Study Design: Endpoints FAP with APC mutation 2:2:1 High Dose 1 A Polyp burden at 12M Open confirmed Low Dose Placebo 48 Week Treatment
2 PL, Safety, polyp # and Label histological grade Extension 21
Phase 1 Trial Underway REC-3964 for Clostridium difficile Colitis PREVALENCE ~730,000 US
+ EU5 CAUSE Release of C. difficile toxins by colonizing bacterium causes degradation of colon cell junction, toxin transit to bloodstream, and morbidity to host PATHOPHYSIOLOGY Highly recurrent infectious disease with severe diarrhea, colitis, and
risk of toxic megacolon, sepsis, and death OUR REASON TO BELIEVE Recursion OS identified a new chemical entity for recurrent C. difficile infection and potentially prophylaxis via glycosyl transferase inhibition with potential to be orally active
KEY ELEMENTS Orally active small molecule toxin effect inhibitor Non-antibiotic approach with potential for combination with SOC and other therapies for recurrent disease Designed for