Filed by Revolution Medicines, Inc.

Pursuant to Rule 425 under the Securities Act of 1933

and deemed filed pursuant to

14a-12

under the Securities Exchange Act of 1934

Subject Company: EQRx, Inc.

Commission File No.:

001-40312

Date: August 1, 2023

This filing relates to
the proposed transaction between Revolution Medicines, Inc. a Delaware corporation (“Revolution Medicines”), and EQRx, Inc., a Delaware corporation (“EQRx”), pursuant to the terms of that certain Agreement and Plan of Merger,
dated as of July 31, 2023 (the “Merger Agreement”), by and among Revolution Medicines, EQRx, Equinox Merger Sub I, Inc., a Delaware corporation and a wholly owned subsidiary of Revolution Medicines (“Merger Sub I”), and
Equinox Merger Sub II LLC, a Delaware limited liability company and a wholly owned subsidiary of Revolution Medicines (“Merger Sub II” and, together with Merger Sub I, the “Merger Subs” and each a “Merger Sub”).

On August 1, 2023, Revolution Medicines made available the following presentation:

Aug 1, 2023 On Target to Outsmart Cancer TM © 2023 Revolution Medicines

Legal Disclaimer This presentation contains forward-looking statements within the meaning of the Private
Securities Litigation Reform Act. All statements other than statements of historical facts contained in this presentation, including statements regarding the expected timing of closing of the proposed transaction with EQRx, Inc. (EQRx), the expected
benefits of the proposed transaction, our future results of operations and financial position, business strategy, prospective products, availability of funding, ability to manage existing collaborations and establish new strategic collaborations,
licensing or other arrangements, the scope, progress, results and costs of developing our product candidates or any other future product candidates, the potential market size and size of the potential patient populations for our product candidates,
the timing and likelihood of success of obtaining product approvals, plans and objectives of management for future operations, the scope of protection we are able to establish and maintain for intellectual property rights covering our product
candidates, future results of anticipated products, and the impact of the

COVID-19

pandemic on our business are forward-looking statements. These statements involve known and unknown risks, uncertainties and
other important factors that may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Because forward-looking
statements are inherently subject to risks and uncertainties, some of which cannot be predicted or quantified and some of which are beyond our control, you should not rely on these forward-looking statements as predictions of future events. The
events and circumstances reflected in our forward-looking statements may not be achieved or occur and actual results could differ materially from those projected in the forward-looking statements. The information included in these materials is
provided as of May 8, 2023, and is qualified as such. Except as required by applicable law, we undertake no obligation to update any forward-looking statements or other information contained herein, whether as a result of any new information,
future events, changed circumstances or otherwise. For a further description of the risks and uncertainties that could cause actual results to differ from those anticipated in these forward-looking statements, as well as risks relating to the
business of Revolution Medicines in general, see Revolution Medicines’ Quarterly Report on Form

10-Q

filed with the Securities and Exchange Commission on May 8, 2023, and its future periodic reports
to be filed with the Securities and Exchange Commission. This presentation concerns product candidates that are under clinical investigation and which have not yet been approved for marketing by the U.S. Food and Drug Administration (FDA). These
product candidates are currently limited by Federal law to investigational use, and no representation is made as to their safety or effectiveness for the purposes for which they are is being investigated. 2

Summary of Transaction and Business Updates Announced August 1, 2023 • RVMD to acquire EQRx in an

all-stock

transaction to gain more than $1B in additional capital • Strengthened balance sheet intended to support RVMD’s parallel, late-stage development for RAS(ON) Inhibitor pipeline, which includes

RMC-6236,


RMC-6291and


RMC-9805

•

RMC-6236

clinical activity data to be presented at ESMO
2023* on October 22 •

RMC-6236

supporting clinical data to be presented at 2023 Triple Meeting^ in October •

RMC-6291

initial clinical findings to be
presented at 2023 Triple Meeting in October • Deal expected to close in November 2023, subject to satisfaction of customary closing conditions • Stock exchange ratio to be determined using a blended average share price to account for
developments in our business and potential movement in RVMD share price • ~20% based on a determined RVMD share price at signing • ~80% based on RVMD share price as determined in close proximity to shareholder vote (subject to 6% discount)
• RVMD to continue focus on mission to discover, develop and deliver pioneering RAS(ON) Inhibitor drugs on behalf of patients with

RAS-addicted

cancers 3 * European Society for Medical Oncology Congress
(ESMO); Presentation No. 6520 ^


AACR-NCI-EORTC


International conference on Molecular Targets and Cancer Therapeutics (“Triple
Meeting”)

On Target to Outsmart Cancer HIGH UNMET NEED IN

RAS-ADDICTED

CANCERS
30% of human cancers(1), largely unserved by targeted therapeutics STRONG CLINICAL VALIDATION OF RASMUTANT AS CANCER DRIVER


Proof-of-principle


from

first-gen

KRASG12C inhibitors(2) DEEP, SCIENCE-DRIVEN CLINICAL AND PRECLINICAL PIPELINE RAS(ON) Inhibitors Groundbreaking class of drug candidates designed for robust cancer suppression RAS Companion Inhibitors
Class-leading drug candidates designed to counter treatment resistance (2) (1) Lumakras Prior et al. ,approved Cancer Research by the FDA 2020 in May 2021, Krazati approved by the FDA in December 2022

Excessive RAS(ON) Signaling Drives 30% of Human Cancers, Targeted by Our Pipeline Strategy

RAS-Addicted

Cancers = RAS(OFF) Normal RAS Cancer Mutations New patients per year (U.S.)(1) = RAS(ON) 230,000 All Cell Membrane 67,000 Lung cancer Tightly regulated Excessive control RAS(ON) cell proteins growth
RAS(ON) uncontrolled signaling cell growth drives 79,000 Colorectal cancer Exemplary G12C, G12D, G12V, G12R mutations in G13C, G13D 49,000 KRAS, HRAS Pancreatic cancer and/or NRAS Q61H, Q61K, Q61L 5 (1) Estimated using tumor mutation frequencies
from Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer =

non-small

cell lung cancer

Deep, Science-Driven Clinical and Preclinical Pipeline of Targeted Therapies for

RAS-Addicted

Cancers RAS(ON) Inhibitors RAS Companion Inhibitors 3 Clinical-stage 2 Drug Clinical-stage Candidates Drug Candidates RAS COOPERATING Development-stage TARGETS 2 Drug Candidates RAS(ON) 1

IND-ready

Drug Candidate Multiple pipeline CANCER + DRIVERS expansion programs 6

Groundbreaking RAS(ON) Inhibitors Bind Near RAS Cancer Mutation Hotspots and Suppress Cancer Signaling Bind
Suppress r Cyclophilin A

RAS-Q61


RAS-G12


RAS-G13

Inhibited RAS(ON) Oncogenic RAS(ON) Oncogenic RAS(ON) • Potent, selective,
oral and drug-like inhibitors • Deep and sustained suppression of RAS(ON) cancer signaling 7

Current Portfolio of RAS(ON) Inhibitors Targets Every RAS Cancer Mutation Hotspot(1) Relative Frequency in
Human RAS Cancers(2)

RMC-6236

MULTI/G12X Q61

RMC-0708

Q61H

RMC-6291

G12C G12

RMC-9805

G12D G13

RMC-8839

G13C (1) RAS cancer mutation hotspots defined as G12, G13 and Q61 8 (2) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated
patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail)

RMC-6236:



First-in-Class


RASMULTI(ON) Inhibitor with Broad Potential Against

RAS-Addicted

Cancers Preclinical Profile Colorectal Highly Potent and Selective RAS(ON) Inhibitor 32%
• Suppresses diverse mutant RAS cancer drivers Pancreatic and cooperating wild-type RAS proteins 32% 137,000 Robust Anti-tumor Activity in Cancer Models New KRASG12X patients • Deep and sustained inhibition drives durable
(1) anti-tumor activity in tumors with common per year (U.S.) RAS variants Lung Attractive PK/ADME Profile 30% • Favorable in vivo oral bioavailability, clearance and concentration in tumors for effective Other 6% target coverage in

RAS-addicted

cancer cells KRASG12X includes KRASG12D, KRASG12V, KRASG12R and KRASG12C 9 (1) Calculated using tumor mutation frequencies from Foundation Medicine Insights August 2020 and scaled to estimated patient
numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail); lung cancer =

non-small

cell lung cancer

RMC-6236:

Highly Active with Durable Benefit Across in Vivo Models of
Major Human Cancers with KRASG12X Drivers NSCLC PDAC CRC PFS 53% ORR (8/15) 61% ORR (11/18) 44% ORR (8/18)

RMC-6236

– Median not reached 100% DCR (15/15) 89% DCR (16/18) 56% DCR (10/18) Control –
Median 9 days 100 Free—75 mPD Tumors 50 0 mSD % 25 mPR Progression mCR 0 0 4 — 2 GP2D KP PAN022 PAN026 PAN1001 PAN038 PAN020 PAN003 PAN010 PAN014 PAN039 Capan PAN001 PAN045 PAN031 PAN028 HPAC PAN043 PAN009 CRC007 CRC043 CRC078 CRC022
CRC060 CRC1018 CRC050 CRC047 CRC044 CRC058 CRC051 CRC039 CRC012 SW620 CRC1009 SW403 CRC1005 0 20 40 60 80 100 Days on Treatment

RMC-6236

(n=191, 51 models) Control (n=215, 51 models) RVMD preclinical research
as of 06/01/22

RMC-6236

dosed at 25 mg/kg po qd;

n=1-10/group

Progression defined as tumor doubling from baseline NSCLC =

non-small

cell lung cancer; PDAC = pancreatic ductal adenocarcinoma; CRC = colorectal cancer 10 Responses assigned according to mRECIST (see appendix) ORR = objective response rate; DCR = disease control rate;
PFS = progression-free survival

RMC-6236

Phase 1/1b Trial: Clinical Translation of Preclinical Single
Agent Profile and Initial Platform Validation Preclinical Profile Aims of Phase 1/1b Clinical Trial(2) ü Oral dosing (daily and intermittent): drug and levels that drive sustained RAS pathway o Oral dosing: complete dose optimization and
suppression determine a dose for initiation of pivotal trials Safety ü Safety: well-tolerated in active range, dose- o Safety: characterize the safety and tolerability Dosing limiting toxicities “on target” and reversible profile of

RMC-6236

ü Long-term treatment(1) at active doses MUTANT ü Tumor selection: active in diverse RAS G12X o Patient selection: signal-seeking across NSCLC, pancreatic and CRC models; KRAS G12X Tumor diverse
KRAS tumors—most sensitive Activity: deep across G12X o Efficacy: characterize the ORR, and durability AntiActivity ü regressions KRAS of response and SD, of

RMC-6236

in patients tumors, especially
NSCLC and pancreatic G12X with KRAS tumors models (1) Long-term in mouse models defined as up to 90 days of treatment (2) Ongoing study,


RMC-6236-001—ClinicalTrials.gov


Identifier: NCT05379985

https://clinicaltrials.gov/ct2/show/NCT05379985?term=RMC-6236&draw=2&rank=1

11 KRASG12X includes KRASG12A, KRASG12D, KRASG12R, KRASG12S, KRASG12V ORR = overall response rate; SD = stable
disease

RMC-6236-001:


Treatment-Related
AEs Occurring in ≥ 10% of All Patients 10 mg QD 20 mg QD 40 mg QD 80 mg QD 120 mg QD Overall (N=3) (N=13) (N=9) (N=7) (N=4) (N=36) Preferred Any Grade Any Grade Any Grade Any Grade Any Grade Any Grade Term Grade ≥3 Grade ≥3 Grade
≥3 Grade ≥3 Grade ≥3 Grade ≥3 Rash (CMQ)* 0 0 2 0 4 0 6 0 4 0 16 0 (15.4%) (44.4%) (85.7%) (100%) (44.4%) Nausea 1 0 2 0 6 0 2 0 1 0 12 0 (33.3%) (15.4%) (66.7%) (28.6%) (25.0%) (33.3%) Diarrhoea 0 0 1 0 2 0 1 0 2 0 6 0
(7.7%) (22.2%) (14.3%) (50.0%) (16.7%) Fatigue 0 0 0 0 2 0 0 0 2 0 4 0 (22.2%) (50.0%) (11.1%) Vomiting 0 0 1 0 2 0 0 0 1 0 4 0 (7.7%) (22.2%) (25.0%) (11.1%) One related grade 4 adverse event of bowel perforation (also considered a serious adverse
event) was reported in a patient receiving 80 mg daily. The likely cause of the perforation was considered to be shrinkage of metastatic KRASG12V pancreatic cancer at the site of full-thickness bowel infiltration. EDC CMQ data = Customized as of
02/17/2023 MedDRA Query 12 *Consists of dermatitis acneiform, dermatitis psoriasiform, palmar-plantar erythrodysesthesia syndrome, rash maculo-papular, and rash pustular.

RMC-6236-001:


Change in Tumor
Burden from Patients with KRASG12X NSCLC or Pancreatic Cancer Treated at ≥ 40 mg Daily 120 mg QD 80 mg QD 40 mg QD = on treatment PDAC PDAC NSCLC PDAC PDAC PDAC NSCLC PDAC PDAC PDAC NSCLC PDAC G12V G12D G12A G12D G12D G12D G12D G12D G12V G12V
G12D G12D Most recent scan: C3D1 C3D1 C5D1 C3D1 C7D1 C3D1 C7D1 C3D1 C3D1 C3D1 C5D1 C5D1 EDC data as of 02/17/2023; efficacy evaluable patients defined as those in this data set with at least one post baseline response assessment or who have died or
have experienced clinical progression 13 *PR prior subsequently to the first post confirmed baseline as scan of 03/16/23. (n=12). Cycle time is 21 days. SD = stable disease, PR = partial response. NSCLC =

non-small

cell lung cancer; PDAC = pancreatic ductal adenocarcinoma.

RMC-6236-001


Case Report:
KRASG12D Pancreatic Cancer Patient • 76

year-old

male • KRASG12D pancreatic cancer diagnosed November 2017 • Treated with neoadjuvant chemotherapy, surgery, adjuvant chemotherapy 2018 •
Progressed with metastatic disease January 2022; treated with gemcitabine +

nab-paclitaxel

+ investigational therapy with SD as best response • November 2022 lung metastases • KRASG12D with

co-occurring

loss of P53, CDKN2A, CDKN2B and MTAP • Treated with

RMC-6236

80 mg daily 14

Updated


RMC-6236-001


Case
Report: Confirmed PR for KRASG12D Pancreatic Cancer Patient Target Lesion 1 (Lung RLL) Target Lesion 2 (Lung LLL)

Non-Target

Lesion (Lung LLL) SLD: Baseline 45.6 mm C7D1 6236, SLD: 8.0 mm Treatment

-On

RMC 15 RLL=right lower lobe; LLL=left lower lobe Images courtesy of


RMC-6236-001


study site with additional annotation by RVMD SLD
= sum of longest diameters per RECIST 1.1 (SLD values and red arrows highlighting detectable lesions)

Planning is Underway for Next Steps with

RMC-6236

Clinical Development
o Current


RMC-6236-001


trial: dose optimization for pivotal trials is Agent ongoing o One or more pivotal trials: late-stage evaluation of treatment with Single

RMC-6236

in patients with KRASG12X–bearing tumors potentially to begin in 2024 o Phase 1/2 clinical trial: evaluation of combination treatment with

RMC-6291

and

RMC-6236

in patients with KRASG12C–bearing tumors Combination potentially to begin in early 2024 16

RMC-6291:

Mutant-Selective RAS(ON) Inhibitor with


Best-in-Class


Potential for KRASG12C Cancers Preclinical Profile Highly Potent and Selective RAS(ON) Inhibitor Lung 76% • Highly active against KRASG12C • Covalent
for irreversible inhibition • Low

off-target

risk and acceptable safety profile 29,000 Robust Anti-tumor Activity in Cancer Models New KRASG12C patients • Rapid, deep and sustained inhibition drives
(1) durable anti-tumor effects across multiple per year (U.S.) G12C KRAS tumor types, with complete responses Colorectal in some models 18% Attractive PK/ADME Profile Pancreatic • Favorable in vivo oral bioavailability and 3% Other
clearance for effective target coverage in 3% KRASG12C-addicted cancer cells 17 (1) using Calculated cancer incidence using tumor from mutation ACS Cancer frequencies Facts and from Figures Foundation 2020 (see Medicine appendix Insights for
additional August detail); 2020 and lung scaled cancer to = estimated

non-small

patient cell lung numbers cancer

RMC-6291:

Superior Response Rates and Durability in Mouse Clinical
Trial with 25 KRASG12C NSCLC Models Responses PFS

RMC-6291

– Median not reached Adagrasib – Median not reached 72% (18/25) ORR 52% (13/25) ORR 100 Control – Median 9 days 92% (23/25) DCR 72%
(18/25) DCR mPD Free 75 -Tumors 50 mSD %    Progression 25 mPR mCR 0 0 20 40 60 80 100 Days on Treatment

RMC-6291

(n=108, 25 models) Adagrasib (n=118, 25 models) RVMD preclinical research
as of 11/20/22 Control (n=114, 25 models) Adagrasib dosed at 100 mg/kg po qd;

RMC-6291

dosed at 200 mg/kg po qd; n=3 to 10/group Progression defined as tumor doubling from baseline p<0.001 by

Log-rank

test

(RMC-6291

vs adagrasib treatment in the KM analysis ) 18 NSCLC =

Non-small

cell lung cancer Responses assigned according
to mRECIST (see appendix)

RMC-6291

Phase 1/1b Trial: Clinical Translation of Preclinical Single
Agent Profile and Initial Platform Validation Preclinical Profile Aims of Phase 1/1b Clinical Trial(2) ü Oral dosing (daily): drug levels that drive o Oral dosing: once daily or BID to reach active and maximal target crosslinking and sustained
exposures; surrogate markers of activity (ctDNA) RAS pathway suppression o Safety: short- and long-term safety and Safety ü Safety: well-tolerated in active range, highly tolerability at active exposures Dosing selective for KRASG12C o Dose:
complete dose optimization and ü Long-term treatment(1) at active doses determine a dose for initiation of pivotal studies G12C ü Tumor selection: active in KRASG12C NSCLC o Patient selection: KRAS solid tumors; and CRC tumor models,
including some KRASG12C(OFF) inhibitor-treated patients Tumor—resistant to KRASG12C(OFF) inhibitors included in dose escalation Activity ü Activity: deep and durable regressions across o Efficacy: initial clinical responses by RECIST; Anti
KRASG12C tumors, especially NSCLC formal


proof-of-concept


via expansion cohorts focused on NSCLC patients and potentially other tumor types, including CRC
(1) Long-term in mouse models defined as up to 90 days of treatment 19 (2) Ongoing study,


RMC-6291-001—ClinicalTrials.gov


Identifier: NCT05462717

https://www.clinicaltrials.gov/ct2/show/NCT05462717?term=RMC-6291&draw=2&rank=1

ctDNA = circulating tumor DNA

RMC-9805:



First-in-Class


Mutant-Selective RAS(ON) Inhibitor for KRASG12D Cancers Preclinical Profile Highly Potent and Selective RAS(ON) Inhibitor Pancreatic 38% 40% Colorectal    • Highly
active against KRASG12D • Covalent for irreversible inhibition • Low

off-target

risk and acceptable safety profile 55,000 Robust Anti-tumor Activity in Cancer Models New KRASG12D patients Rapid, deep
and sustained inhibition drives • per year (U.S.)(1) durable regressions in KRASG12D lung, pancreatic and colorectal cancers Attractive PK/ADME Profile Lung • Favorable in vivo oral bioavailability and Other 14% clearance for effective
target coverage in 8% KRASG12D-addicted cancer cells 20 (1) cancer Calculated incidence using from tumor ACS mutation Cancer Facts frequencies and Figures from 2020 Foundation (see appendix Medicine for additional Insights August detail); 2020 lung
cancer and scaled =

non-small

to estimated cell lung patient cancer numbers using

RMC-9805:

Selective, Covalent Binding and Inhibition of KRASG12D(ON)
with Apoptosis Induction in Vivo Selective Covalent Binding to KRASG12D(ON) RAS Signaling Inhibition and Apoptosis Induction(2) KRAS: WT G12D G13D G12C G13C

X-linked

KRAS KRAS Control

RMC-9805

H/NRAS Drug Exposure and Pathway RAS signaling Suppression after Oral Dosing(1) (pERK) Tumor PD Blood PK Tumor PK 150 10000 control 100 1000 Total expression    to 100 Conc Apoptosis
mRNA. 50 (nM) (cleaved caspase 3) %DUSP6 normalized 10 0 0.51 4 8 12 16 24 48 1 Time point(h) RVMD preclinical research

RMC-9805

dosed at 100 mg/kg po in HPAC subcutaneous xenograft model (PDAC, KRASG12D/WT)
21 (1) PK/PD data collected at indicated timepoints after a single dose (2) Histopathology data collected 24h after a single dose

RMC-9805:

Highly Active in Vivo Across Diverse KRASG12D Cancer Models
NSCLC PDAC CRC 67% ORR (6/9) 78% DCR (7/9) RVMD preclinical research as of 11/02/22

RMC-9805

dosed at 100 mg/kg po qd;

n=2-8/group

22 NSCLC Responses =

non-small

assigned cell according lung cancer; to mRECIST PDAC = (see pancreatic appendix) ductal adenocarcinoma; CRC = colorectal cancer ORR = objective response rate; DCR = disease control
rate

RMC-9805

Phase 1/1b Trial: Clinical Translation of Preclinical Single
Agent Profile Preclinical Profile Aims of Phase 1/1b Clinical Trial(2) ü Oral dosing (daily): drug levels that drive to reach active and maximal target crosslinking and sustained o Oral dosing: once daily or BID exposures; surrogate markers of
activity (ctDNA) RAS pathway suppression o Safety: short- and long-term safety and Safety ü Safety: well-tolerated in active range, highly tolerability at active exposures Dosing selective for KRASG12D (1) o RP2DS ü Long-term
treatment at active doses Patient selection: KRASG12D solid tumors ü Tumor selection: active in KRASG12D tumor o models across histotypes, including NSCLC, o Efficacy: initial clinical responses by RECIST; Tumor PDAC and CRC formal


proof-of-concept


via expansion cohorts—focused on distinct histotypes Activity ü Activity: deep and durable regressions across Anti KRASG12D tumors, especially NSCLC
and PDAC (1) Long-term in mouse models defined as up to 90 days of treatment (2) Site activation ongoing under an investigational new drug application 23 RP2DS = recommended Phase 2 dose and schedule; ctDNA = circulating tumor
DNA

RAS(ON) Inhibitors Drive Tumor Regressions in Models of Brain Metastasis LU99(1) LU99 HPAC high (NSCLC,
KRASG12C) (PDAC, KRASG12D) Control Brain Xenograft(1) Brain Xenograft(2) 1011 Adagrasib 1010 low 109 108

RMC-6236

(photons/sec) 107 Bioluminescence 106

RMC-6291

105 l b
6 1 l 5 (2) r o i 3 9 r o 0 HPAC t s 2 2 t 8 n r a 6 6 n 9 o — o

-g

C C C C a C Control d M M M A R R R

RMC-9805

Adagrasib RVMD preclinical dosed research at 100
mg/kg po bid,

RMC-6236

dosed at 25 mg/kg po qd,

RMC-6291

dosed at 100 mg/kg po bid,

RMC-9805

dosed at 100 mg/kg po qd 24 (1) LU99
intracranial xenograft model (NSCLC, KRASG12C/WT). Bioluminescence measured at end of study. (2) HPAC intracranial xenograft model (PDAC, KRASG12D/WT). Bioluminescence measured at end of study.

RAS(ON) Inhibitors Induce Anti-Tumor Immunity via Multiple Mechanisms in Immunocompetent Models Control Control
Control

Anti-PD1


Anti-PD1


Anti-PD1


RMC-6236


RMC-6291


RMC-9805

Combination Combination Combination G12C G12C G12D free 100 Mechanisms of Action—75 -Antigen presentation 50 ¯ Myeloid suppressive cells
progression 25

-T-cell

infiltration Tumors 0 % 0 25 50 75 100 0 25 50 75 100 0 25 50 75 100 Days post-tumor implant Additive Activity Supports Clinical Combination Strategies with Immune Therapies RVMD
preclinical research

RMC-9805

experiment conducted in CT26 syngeneic tumor model (KRASG12D);

RMC-6236

and

RMC-6291

experiments
conducted in CT26 model engineered to express KRASG12C 25

RMC-6236

Vertical dashed (25 mg/kg lines represent po qd) or

RMC-6291

treatment (200 stop; mg/kg Kaplan-Meier
po qd) dosed progression for 14 days; defined

RMC-9805

as tumor (100 doubling mg/kg from po qd) baseline dosed for 42 days;


anti-PD-1


(10 mg/kg ip biw, for 21 days)

RMC-0708:



First-in-Class


Mutant-Selective RAS(ON) Inhibitor for KRASQ61H Cancers Preclinical Profile Pancreatic Colorectal 23% Highly Potent and Selective RAS(ON) Inhibitor 22% • Highly active against KRASQ61H
•

Non-covalent,

highly selective over wild-type RAS • Low

off-target

risk and acceptable safety profile 10,000 Robust Anti-tumor Activity in Cancer Models New
KRASQ61H patients • Rapid, deep and sustained inhibition drives per year (U.S.)1) durable regressions in KRASQ61H lung, pancreatic and colorectal cancers Multiple Lung Myeloma Attractive PK/ADME Profile 26% 26% • Favorable in vivo oral
bioavailability and Other clearance for effective target coverage in 4% KRASQ61H-addicted cancer cells 26 using (1) Calculated cancer incidence using tumor from mutation ACS Cancer frequencies Facts and from Figures Foundation 2020 (see
Medicine appendix Insights for additional August detail); 2020 and lung scaled cancer to = estimated

non-small

patient cell lung numbers cancer

RMC-0708:

Sustained Pathway Inhibition in Vivo and Tumor Regressions in
KRASQ61H Cancer Models NSCLC(2) PDAC(3) Drug Exposure and Pathway 3 ) 2000 2000 Control Suppression after Oral Dosing(1,2) (mm e

RMC-0708

1500 1500 Tumor PD Blood PK Tumor PK Volum 100 1000 1000 10000 Dosing
Dosing Start Start mRNA Tumor 500 500 1000 Total control 0 0 50 Mean to 100 0 10 20 30 40 0 10 20 30 40 DUSP6 Conc . Days post-implant Days post-implant relative 10 (nM) %Tumor 200 200 0 1 0.5 1 2 4 8 24 48 72 Baseline Time (hours) post-dose Volume
100 100 From Tumor 5/5 CR 4/5 R 0 0 RVMD preclinical research Mean Change

RMC-0708

dosed at 30 mg/kg po qd (1) PK/PD data collected at indicated timepoints after a single dose %

-100


-100

(2) HCC2108 subcutaneous xenograft model (NSCLC, KRASQ61H/Q61H) (3)

T3M-4

subcutaneous xenograft model (PDAC,
KRASQ61H/WT) End of study 27 R = number of regressions >10% from initial; CR = number of regressions ≥80% from initial Each animal represented as a separate bar in waterfall plots

On Target to Outsmart Pancreatic Cancer: RAS(ON) Inhibitors Designed to Cover All KRASMUTANT Drivers(1)
Devastating disease >90% driven by KRAS mutations G12D

RMC-6236

&

RMC-9805

49,000 New KRASMUTANT pancreatic cancer G12V

RMC-6236

patients per year (U.S.)(1). No approved targeted therapies G12R

RMC-6236

Dismal survival rates Q61H G12C

RMC-6236

&

RMC-0708


RMC-6236

&

RMC-6291

Other(1)

RMC-6236

(1) Calculated using tumor mutation
frequencies from Foundation Medicine Insights August 2020 and scaled to estimated 28 patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020 (see appendix for additional detail);

RMC-6236

tested against all mutations occurring at >2% frequency in pancreatic cancer

RMC-6236

RAS Companion Inhibitors WT RAS

RMC-5552

Cooperating Designed to Suppress Targets and Pathways that mTORC1 Sustain

RAS-Addicted

RAS(ON) Cancers

RMC-4630

CANCER
DRIVERS SHP2

3 0 Evaluation of

RMC-4630

in Combination with Sotorasib in KRASG12C
Cancer Patients Phase 1/1b Clinical Trial(1) Aims of


RMC-4630-03


Phase 2 Trial(4) ü Selected single agent RP2DS: Oral dosing of o Dosing: Focused primarily on 200
mg D1D2 200 mg D1D2 weekly: well-tolerated, safety and weekly combined with sotorasib at 960 mg profile consistent with

on-pathway

inhibition daily ü Anti-tumor activity in certain KRASMUTANT and Safety o
Safety: short- and long-term safety and NF1LOF cancers evidenced by SD, PR and/or CR Dosing tolerability Amgen’s CodeBreaK 101c Clinical Trial(2) ü In KRASG12C patients, “the combination of o Patient Selection: NSCLC patients without
sotorasib with

RMC-4630

was safe and prior KRASG12C inhibitor treatment stratified tolerable”(3) with sotorasib at 960 mg po qd and Tumor into two cohorts: KRASG12C with or without


co-RMC-4630


at

140-200

mg po D1D2 weekly -Activity mutations such as KEAP1 or STK11 ü 75% ORR/100% DCR among KRASG12C Anti o
Efficacy: demonstrate clinical benefit additive

inhibitor-naïve

NSCLC patients treated at top to sotorasib two doses of

RMC-4630

(n=4) (1) Ongoing study,


RMC-4630-01—ClinicalTrials.gov


Identifier: NCT03634982

https://clinicaltrials.gov/ct2/show/NCT03634982?term=RMC-4630&draw=2&rank=1

(2) Ongoing study, CodeBreaK 101c—ClinicalTrials.gov Identifier: NCT04185883
https://clinicaltrials.gov/ct2/show/NCT04185883?term=codebreak+101&draw=2&rank=1 (3) Falchook et. al. Sotorasib in Combination with

RMC-4630,

a SHP2 Inhibitor, in KRAS p.G12C-Mutated NSCLC and Other
Solid Tumors. 2022 World Conference on Lung Cancer. August

6-9,

2022. Vienna, Austria. Abstract #OA03.03. (4) Ongoing study,


RMC-4630-03—ClinicalTrials.gov


Identifier: NCT05054725

https://clinicaltrials.gov/ct2/show/NCT05054725?term=RMC-4630&draw=2&rank=2

RMC-5552:



First-in-Class



Bi-steric

mTORC1-Selective Inhibitor for Cancers with Hyperactive mTOR Signaling Rapalogs mTOR Highly Potent and Selective mTORC1 Inhibitor active site

RMC-5552

inhibitors •

Bi-steric

mechanism enables selectivity for mTORC1 • Capable of reactivating the tumor suppressor 4EBP1 4EBP1 Anti-tumor mTORC1 substrates
Robust Anti-tumor Activity in Cancer Models S6K Anti-tumor • Selective inhibition of mTORC1 drives durable regressions in mTOR pathway-mutant models mTORC2 AKT substrate Toxicity and resistance Attractive PK/ADME Profile • Weekly dosing
provides favorable PK exposure and prolonged target modulation in vivo 31 Characterization above is based on RVMD preclinical research

RMC-5552:

Compelling Profile as a Potential Phase 1/1b Single Agent
Study RAS Companion Inhibitor Best Tumor Change in Efficacy Evaluable Patients Treated at 6 mg or 8 mg IV Weekly Preliminary radiologic and molecular 71% DCR(2) evidence of activity at tolerated doses: • Disease control across diverse tumors,
including durable stable disease • Objective response and regressions • Favorable changes in surrogate markers • 3 of 6 patients with stable disease and oncogenic mTOR pathway variants had molecular responses(1) (1) n = 6 molecular
response-evaluable patients with oncogenic mTOR pathway variants (2) n = 28 efficacy evaluable subjects. DCR = disease control rate. detected by ctDNA treated at 6 mg or higher majority dose. ”Oncogenic” defined as pathogenic *Patient
received one dose of 12 mg, followed by weekly doses of 6 mg, had complete loss of oncogenic PTEN variant by or likely pathogenic by blinded adjudication process using publicly available variant data. ctDNA, and has been on

RMC-5552

for >12 months. 32 Molecular response defined by 50% decrease or greater in mean VAF at C3D1 by #Patient received one dose of 10 mg, followed by weekly doses of 6 mg. Both patients were on

RMC-5552

for >24 weeks. Guardant360® Molecular Response algorithm. VAF = variant allele fraction Data as of 12/19/2022. PD = progressive disease, SD = stable disease, PR = partial response, mo =
months

RMC-5552

Phase 1/1b Trial: Clinical Optimization of Single Agent
Profile for Combination with RAS(ON) Inhibitor Portfolio Preclinical Profile Aims of Phase I/Ib Clinical Trial(1) and ü Dosing: Once weekly dosing achieves levels o Dosing: Establish optimal IV regimen based on that drive sustained inhibition
of mTORC1 safety, anti-tumor activity and surrogate markers Safety signaling and activation of 4EBP1 of activity (ctDNA) Dosing ü Safety: Well-tolerated, highly mTORC1 o Safety: Demonstrate short- and long-term selective safety and tolerability
at active exposures ü Single Agent: Strong activity in tumor models o Single Agent: Evidence of activity at tolerated Tumor with hyperactivated mTORC1 doses in tumors with hyperactive mTORC1 -Activity ü RAS Companion: Combinatorial
activity with signaling Anti RAS(ON) inhibitors o RAS Companion: Identify appropriate dose and schedule for initiation of combinations with RAS(ON) inhibitors (1) Ongoing study,


RMC-5552-001—ClinicalTrials.gov


Identifier: NCT04774952

https://clinicaltrials.gov/ct2/show/NCT04774952?term=rmc-5552&draw=2&rank=1

33 ctDNA = circulating tumor DNA

Overcoming Resistance:

RMC-6291

+

RMC-6236

Combination Induces Regressions in KRASG12C NSCLC Model 1000 Control ) 3 800

RMC-6291

(mm

RMC-6236

600 Combination
Volumestart Tumor 400 Dosing Mean 200 0 5 15 25 35 Days post-implant RASMULTI(ON) Inhibitor Deployed as a RAS Companion Inhibitor RVMD preclinical research

NCI-H2122

subcutaneous xenograft model (NSCLC,
KRASG12C/G12C)

RMC-6291

dosed at 100 mg/kg po qd;

RMC-6236

dosed at 10 mg/kg po qd 34

RMC-6291,


RMC-6236

and Combination—n = 15/group, Control – n=8 NSCLC =

non-small

cell lung cancer

Deep Pipeline of Targeted Therapies for Majority of

RAS-Addicted

Cancers PRECLINICAL

IND-ENABLING

CLINICAL PHASE 1 CLINICAL PHASE 2 CLINICAL PHASE 3 RAS(ON) INHIBITORS

RMC-6236

RASMULTI

RMC-6291

KRASG12C

RMC-9805

KRASG12D

RMC-0708

KRASQ61H

RMC-8839

KRASG13C Pipeline G12R, G12V, G13D, Expansion Q61X, other RAS COMPANION
INHIBITORS

RMC-4630(1)

SHP2

RMC-5552

mTORC1/4EBP1

RMC-5845(2)

SOS1 (1) (2)

IND-ready,

Sanofi collaboration active development on

RMC-4630/SAR442720

deferred terminated effective June 2023 35

Anticipated Milestones MILESTONE (EXPECTED TIMING) RAS(ON) INHIBITORS

RMC-6236

(RASMULTI) Report further evidence of


first-in-class


single agent activity (Oct 2023) Report preliminary evidence of
differentiation from KRASG12C(OFF) inhibitors

RMC-6291

(KRASG12C) (Oct 2023)

RMC-9805

(KRASG12D) Announce dosing of first patient (2H2023) RAS COMPANION INHIBITORS

RMC-4630

(SHP2) Provide topline data from


RMC-4630-03


(2H2023)

RMC-5552

(mTORC1/4EBP1) Report
additional evidence of single agent activity (4Q2023) 36

Financial Information Financial Position Cash, cash equivalents and marketable securities as of $909.8
million(1) March 31, 2023 2023 Financial Guidance 2023 GAAP net loss of $360 million to $400 million(2) (1) With current cash, cash equivalents and marketable securities, the company projects it can fund planned operations into 2025 (2)
Includes

non-cash

stock-based compensation expense of approximately $40 million to $50 million Financial guidance does not include impact of proposed EQRx acquisition 37

TM On Target to Outsmart Cancer Focused on serving high unmet needs across numerous cancers driven by diverse
RAS mutations First two targeted RAS(ON) Inhibitors have shown initial clinical activity and evaluation continues Targeted RAS Companion Inhibitors designed to counter drug resistance have shown initial clinical activity and evaluation continues
Development-stage portfolio covers RAS drivers of all major

RAS-addicted

cancers

Appendix • RAS cancer epidemiology statistics are estimated using tumor mutation frequencies from
Foundation Medicine Insights August 2020 and scaled to estimated patient numbers using cancer incidence from ACS Cancer Facts and Figures 2020: • RAS mutations include: KRAS G12(A,C,D,R,S,V), KRAS G13(C,D), KRAS Q61(H, K, L), KRAS A146T, KRAS
wild-type amplification, NRAS G12C, NRAS Q61(H,K,L,R,P), HRAS mutations of known/likely function (including HRAS Q61(H,L)), BRAF class 3 mutations, NF1 loss of function mutations, PTPN11 mutations of known/likely function. NF1 LOF mutations = 50% of
all NF1 mutations of known/likely function. BRAF class 3 mutations = D287H, D594(A,E,G,H,N,V,Y), F595L, G466(A,E,R,V,E,D,R), N581(I,S), S467L,T599I, V459L. • Includes 12 major types:

non-small

cell lung
cancer, colorectal, pancreatic adenocarcinoma, renal, gastroesophageal, head and neck squamous cell, ovarian and biliary cancers, acute myeloid leukemia, and advanced melanoma, bladder and uterine/endometrial cancers causing mortality. •
KRASQ61H epidemiology statistics include multiple myeloma in addition to 12 major types named above • Est. worldwide annual incidence of

RAS-mutated

cancers is 3.4 million per Prior et al., Cancer
Research 2020 • RAS mutations drive 30% of human cancers per Prior et al., Cancer Research 2020 • Mouse tumor responses on slides 9, 12 and 17 assigned according to mRECIST (modified from Gao et al. Nat Med. 2015): • mPD = progressive
disease; mSD = stable disease; mPR = partial response; mCR = complete response • PK = pharmacokinetic; ADME = absorption, distribution, metabolism, and excretion 39

Forward-Looking Statements

This presentation contains forward-looking statements within the meaning of federal securities laws, including the “safe harbor” provisions
of the Private Securities Litigation Reform Act of 1995. Such statements are based upon current plans, estimates and expectations of management of Revolution Medicines and EQRx in light of historical results and trends, current conditions and
potential future developments, and are subject to various risks and uncertainties that could cause actual results to differ materially from such statements. The inclusion of forward-looking statements should not be regarded as a representation that
such plans, estimates and expectations will be achieved. Words such as “anticipate,” “expect,” “project,” “intend,” “believe,” “may,” “will,” “should,” “plan,”
“could,” “continue,” “target,” “contemplate,” “estimate,” “forecast,” “guidance,” “predict,” “possible,” “potential,” “pursue,”
“likely,” and words and terms of similar substance used in connection with any discussion of future plans, actions or events identify forward-looking statements. All statements, other than historical facts, including express or implied
statements regarding the proposed transaction; the conversion of equity interests contemplated by the Merger Agreement; the issuance of common stock of Revolution Medicines contemplated by the Merger Agreement; the expected filing by Revolution
Medicines of a registration statement and Joint Proxy Statement/Prospectus to be included therein; the expected timing of the closing of the proposed transaction; the ability of the parties to complete the proposed transaction considering the
various closing conditions; the expected benefits of the proposed transaction; the competitive ability and position of the combined company; and any assumptions underlying any of the foregoing, are forward-looking statements. Important factors that
could cause actual results to differ materially from Revolution Medicines’ and EQRx’s plans, estimates or expectations described in such forward-looking statements could include, but are not limited to: (i) the risk that the proposed
transaction may not be completed in a timely manner or at all, which may adversely affect Revolution Medicines’ and EQRx’s businesses and the price of their respective securities; (ii) uncertainties as to the timing of the
consummation of the proposed transaction; (iii) the potential failure to receive, on a timely basis or otherwise, the required approvals of the proposed transaction, including stockholder approvals by both Revolution Medicines’
stockholders and EQRx’s stockholders, and the potential failure to satisfy the other conditions to the consummation of the transaction; (iv) that the proposed transaction may involve unexpected costs, liabilities or delays; (v) the
effect of the announcement, pendency or completion of the proposed transaction on each of Revolution Medicines’ or EQRx’s ability to attract, motivate, retain and hire key personnel and maintain relationships with customers, distributors,
suppliers and others with whom Revolution Medicines or EQRx does business, or on Revolution Medicines’ or EQRx’s operating results and business generally; (vi) that the proposed transaction may divert management’s attention from
each of Revolution Medicines’ and EQRx’s ongoing business operations; (vii) the risk of any legal proceedings related to the proposed transaction or otherwise, or the impact of the proposed transaction thereupon, including resulting
expense or delay; (viii) that Revolution Medicines or EQRx may be adversely affected by other economic, business and/or competitive factors; (ix) the occurrence of any event, change or other

circumstance that could give rise to the termination of the Merger Agreement relating to the proposed transaction, including in circumstances which would require Revolution Medicines or EQRx to
pay a termination fee; (x) the risk that restrictions during the pendency of the proposed transaction may impact Revolution Medicines’ or EQRx’s ability to pursue certain business opportunities or strategic transactions; (xi) the
risk that Revolution Medicines or EQRx may be unable to obtain governmental and regulatory approvals required for the proposed transaction, or that required governmental and regulatory approvals may delay the consummation of the proposed transaction
or result in the imposition of conditions that could reduce the anticipated benefits from the proposed transaction or cause the parties to abandon the proposed transaction; (xii) the risk that the anticipated benefits of the proposed
transaction may otherwise not be fully realized or may take longer to realize than expected; (xiii) the impact of legislative, regulatory, economic, competitive and technological changes; (xiv) risks relating to the value of Revolution
Medicines securities to be issued in the proposed transaction; (xv) the risk that integration of the proposed transaction post-closing may not occur as anticipated or the combined company may not be able to achieve the growth prospects expected
from the transaction; (xvi) the effect of the announcement, pendency or completion of the proposed transaction on the market price of the common stock of each of Revolution Medicines and the common stock and publicly traded warrants of EQRx;
(xvii) the implementation of each of Revolution Medicines’ and EQRx’s business model and strategic plans for product candidates and pipeline, and challenges inherent in developing, commercializing, manufacturing, launching, marketing
and selling potential existing and new products; (xviii) the scope, progress, results and costs of developing Revolution Medicines’ and EQRx’s product candidates and any future product candidates, including conducting preclinical
studies and clinical trials, and otherwise related to the research and development of Revolution Medicines’ and EQRx’s pipeline; (xix) the timing and costs involved in obtaining and maintaining regulatory approval for Revolution
Medicines’ and EQRx’s current or future product candidates, and any related restrictions, limitations and/or warnings in the label of an approved product; (xx) the market for, adoption (including rate and degree of market acceptance)
and pricing and reimbursement of Revolution Medicines’ and EQRx’s product candidates and their respective abilities to compete with therapies and procedures that are rapidly growing and evolving; (xxi) uncertainties in contractual
relationships, including collaborations, partnerships, licensing or other arrangements and the performance of third-party suppliers and manufacturers; (xxii) the ability of each of Revolution Medicines and EQRx to establish and maintain
intellectual property protection for products or avoid or defend claims of infringement; (xxiii) exposure to inflation, currency rate and interest rate fluctuations and risks associated with doing business locally and internationally, as well
as fluctuations in the market price of each of Revolution Medicines’ and EQRx’s traded securities; (xxiv) risks relating to competition within the industry in which each of Revolution Medicines and EQRx operate; (xxv) the
unpredictability and severity of catastrophic events, including, but not limited to, acts of terrorism or outbreak of war or hostilities; (xxvi) whether the termination of EQRx’s license agreements and/or discovery collaboration agreements
may impact its or Revolution Medicines’ ability to license in additional programs in the future and the risk of delays or unforeseen costs in terminating such arrangements; (xxvii) risks that restructuring costs and charges may be greater
than anticipated or incurred in different periods than anticipated; (xxviii) the risk that EQRx’s restructuring efforts may adversely affect its programs and its ability to recruit and retain skilled and motivated personnel, and may be
distracting to employees and management; and (xxix) the risk that EQRx’s restructuring or wind-down efforts may negatively impact its business operations and reputation with or ability to serve counterparties or may take longer to realize
than expected, as well as each of Revolution Medicines’ and EQRx’s response to any of the aforementioned factors. Additional factors that may affect the future results of Revolution Medicines and EQRx are set forth in their respective
filings with the U.S. Securities and Exchange Commission (the “SEC”), including each of Revolution Medicines’ and EQRx’s most recently filed Annual Reports on Form

10-K,

subsequent
Quarterly Reports on

Form 10-Q,

Current Reports on Form

8-K

and other filings with the SEC, which are available on the SEC’s website at www.sec.gov. See in
particular Item 1A of Revolution Medicines’ Quarterly Report on

Form 10-Q

for the quarterly period ended March 31, 2023 under the heading “Risk Factors,” and Item 1A of each of
EQRx’s Annual Report on Form

10-K

for the fiscal year ended December 31, 2022 and Quarterly Report on

Form 10-Q

for the quarterly period ended
March 31, 2023 under the headings “Risk Factors.” The risks and uncertainties described above and in the SEC filings cited above are not exclusive and further information concerning Revolution Medicines and EQRx and their respective
businesses, including factors that potentially could materially affect their respective businesses, financial conditions or operating results, may emerge from time to time. Readers are urged to consider these factors carefully in evaluating these
forward-looking statements, and not to place undue reliance on any forward-looking statements, which speak only as of the date hereof. Readers should also carefully review the risk factors described in other documents that Revolution Medicines and
EQRx file from time to time with the SEC. Except as required by law, each of Revolution Medicines and EQRx assume no obligation to update or revise these forward-looking statements for any reason, even if new information becomes available in the
future.

Additional Information and Where to Find It

In connection with the proposed transaction, Revolution Medicines and EQRx plan to file with the SEC and mail or otherwise provide to their respective security
holders a joint proxy statement/prospectus regarding the proposed transaction (as amended or supplemented from time to time, the “Joint Proxy Statement/Prospectus”). INVESTORS AND REVOLUTION MEDICINES’ AND EQRX’S RESPECTIVE
SECURITY HOLDERS ARE URGED TO CAREFULLY READ THE JOINT PROXY STATEMENT/PROSPECTUS IN ITS ENTIRETY WHEN IT BECOMES AVAILABLE AND ANY OTHER DOCUMENTS FILED BY EACH OF REVOLUTION MEDICINES AND EQRX WITH THE SEC IN CONNECTION WITH THE PROPOSED
TRANSACTION OR INCORPORATED BY REFERENCE THEREIN BECAUSE THEY WILL CONTAIN IMPORTANT INFORMATION ABOUT THE PROPOSED TRANSACTION AND THE PARTIES TO THE PROPOSED TRANSACTION.

Revolution Medicines’ investors and security holders may obtain a free copy of the Joint Proxy Statement/Prospectus and other documents that Revolution
Medicines files with the SEC (when available) from the SEC’s website at www.sec.gov and Revolution Medicines’ website at ir.revmed.com. In addition, the Joint Proxy Statement/Prospectus and other documents filed by Revolution Medicines
with the SEC (when available) may be obtained from Revolution Medicines free of charge by directing a request to Eric Bonach, H/Advisors Abernathy at

eric.bonach@h-advisors.global.

EQRx’s investors and security holders may obtain a free copy of the Joint Proxy Statement/Prospectus and other documents that EQRx files with the SEC
(when available) from the SEC’s website at www.sec.gov and EQRx’s website at investors.eqrx.com. In addition, the Joint Proxy Statement/Prospectus and other documents filed by EQRx with the SEC (when available) may be obtained from EQRx
free of charge by directing a request to EQRx’s Investor Relations at investors@eqrx.com.

No Offer or Solicitation

This communication is not intended to and shall not constitute an offer to buy or sell or the solicitation of an offer to buy or sell any securities, nor shall
there be any offer, solicitation or sale of securities in any jurisdiction in which such offer, solicitation or sale would be unlawful prior to registration or qualification under the securities laws of any such jurisdiction. No offering of
securities shall be made except by means of a prospectus meeting the requirements of Section 10 of the Securities Act of 1933, as amended.

Participants in the Solicitation

Revolution Medicines,
EQRx and their respective directors, executive officers, other members of management, certain employees and other persons may be deemed to be participants in the solicitation of proxies from the security holders of Revolution Medicines and EQRx in
connection with the proposed transaction. Security holders may obtain information regarding the names, affiliations and interests of Revolution Medicines’ directors and executive officers in Revolution Medicines’ Annual Report on Form

10-K

for the fiscal year ended December 31, 2022, which was filed with the SEC on February 27, 2023, and Revolution Medicines’ definitive proxy statement on Schedule 14A for its 2023 annual meeting of
stockholders, which was filed with the SEC on April 26, 2023. To the extent holdings of Revolution Medicines’ securities by Revolution Medicines’ directors and executive officers have changed since the amounts set forth in such proxy
statement, such changes have been or will be reflected on subsequent Statements of Changes in Beneficial Ownership on Form 4 filed with the SEC. Security holders may obtain information regarding the names, affiliations and interests of
EQRx’s directors and executive officers in EQRx’s Annual Report on

Form 10-K

for the fiscal year ended December 31, 2022, which was filed with the SEC on February 23, 2023, and in
certain of EQRx’s Current Reports on Form

8-K.

To the extent holdings of EQRx’s securities by EQRx’s directors and executive officers have changed since the amounts set forth in such Annual
Report on

Form 10-K,

such changes have been or will be reflected on subsequent Statements of Changes in Beneficial Ownership on Form 4 filed with the SEC. Additional information regarding the interests of
such individuals in the proposed transaction will be included in the Joint Proxy Statement/Prospectus relating to the proposed transaction when it is filed with the SEC. These documents (when available) may be obtained free of charge from the
SEC’s website at www.sec.gov, Revolution Medicines’ website at www.revmed.com and EQRx’s website at www.eqrx.com.