BeiGene Corporate Presentation

August 7, 20241

Disclosures
Certain statements contained in this presentation and in any accompanying oral presentation, other than statements of fact that are independently verifiable at thedate hereof, may constitute forward-looking statements. Examples of such forward-looking statements include statements regarding the projected size of certain
oncology market sectors; BeiGene's future income generation; BeiGene’s research, discovery, and pre-clinical and early-stage clinical programs and plans; recent
clinical data for BeiGene’s product candidates and approvals of its medicines; the conduct of late-stage clinical trials and expected data readouts; additional plannedcommercial product launches; the advancement of and anticipated clinical development, regulatory milestones and commercialization of BeiGene’s medicines anddrug candidates; and BeiGene’s path towards profitability and future strategic advantages. Actual results may differ materially from those indicated in the forwardlooking statements as a result of various important factors, including BeiGene's ability to demonstrate the efficacy and safety of its drug candidates; the clinical resultsfor its drug candidates, which may not support further development or marketing approval; actions of regulatory agencies, which may affect the initiation, timing andprogress of clinical trials and marketing approval; BeiGene's ability to achieve commercial success for its marketed medicines and drug candidates, if approved;
BeiGene's ability to obtain and maintain protection of intellectual property for its technology and medicines; BeiGene's reliance on third parties to conduct drug
development, manufacturing, commercialization, and other services; BeiGene’s limited experience in obtaining regulatory approvals and commercializing
pharmaceutical products; BeiGene's ability to obtain additional funding for operations and to complete the development of its drug candidates and achieve andmaintain profitability; and those risks more fully discussed in the section entitled “Risk Factors” in BeiGene’s most recent periodic report filed with the SEC, as well as
discussions of potential risks, uncertainties, and other important factors in BeiGene's subsequent filings with the SEC. All information in this presentation is as of thedate of this presentation, and BeiGene undertakes no duty to update such information unless required by law.
Some of the clinical data in this presentation relating to BeiGene’s investigational drug candidates is from pre-clinical studies or early phase, single-arm clinical trials.
When such data or data from later stage trials are presented in relation to other investigational or marketed drug products, the presentation and discussion are notbased on head-to-head trials between BeiGene’s investigational drug candidates and other products unless specified in the trial protocol. BeiGene is still conducting
pre-clinical studies and clinical trials and, as additional patients are enrolled and evaluated, data on BeiGene’s investigational drug candidates may change.
This presentation and any accompanying oral presentation contain data and information obtained from third-party studies and internal company analysis of such dataand information. BeiGene has not independently verified the data and information obtained from these sources. Forward-looking information obtained from thesesources is subject to the same qualifications noted above.
All trademarks, logos and brand names are the property of their respective owners.

2

Delivering On Our Key Priorities
A global oncology company discovering and developing innovative treatments thatare more accessible and affordable to cancer patients worldwide

Achieved

Diversified
global revenue

OpenedGlobal speed
and cost
advantaged$2.6B

Q2 2024

60%+

$800M

3,000+

24,000+*Q2 24
ending cash
balancereduction
in GAAP
operating loss;
Non-GAAP
income fromoperations (1)from theU.S. and Europe

flagship U.S.
Biologics
manufacturing
and clinicalR&D facility

ClinicalDevelopmentTeampatients in
140+ trials in
45+** countries
and regions

Strong revenue
growthStrong cash
position$929M / 56%
Q2 24 total
revenue / %growth overprior year

(1) Non-GAAP income from operations is a non-GAAP financial measure that excludes from the corresponding GAAP measurecosts related to share-based compensation, depreciation and amortization expense. A reconciliation of this non-GAAP measure to
the comparable GAAP measure is included in the Appendix to this presentation.
*Includes investigator initiated trials (IITs)**Includes countries and regions in which trials are planned to enroll

Enrolled3

Our Unique Model Has Enabled Fast Rise to Global
Oncology Leadership
GlobalOncology
Leadership

Top

15
Top

5
Top

5

Global oncology company by revenue – and rising – forinnovative therapies*

Company for completing phase 3 oncology trials in theindustry between 2017 and 2023

Company with number of oncology molecules advanced
into the clinic in the industry in the last four years

One of the largest oncology-focused R&D teams in the industry

More than 1.3M patients treated worldwide

Source: Evaluate Pharma Competitor Analyzer accessed 12/18/23 for cancer, blood & blood forming malignancies, excluding generics andbiosimilars; and IND data; Company filings, IQVIA, analyst reports. Citeline through competitor trial. Data analysis is as of January 2024.
*Based on Evaluate Pharma data assessed 08/05/24.

4

Global Clinical Development Pipeline
Phase 1
Sonrotoclax
 101/102 B-cell malignancies
 103 AML/MDS 105 MM t(11;14)
BGB-16673
 102 B-cell malignancies

BCL2i

BTK CDAC

BGB-21447
next gen BCL2i
 101 B-cell malignancies
Tislelizumab 103 SubQ formulation

Anti PD1

Phase 2

BGB-A3055
 101 Solid tumors

Anti CCR8

BGB-24714
 101 Solid tumors

SMAC mimetic

BGB-43395
 101/102 BC & Solid tumors

CDK4i

BG-685011
 101 BC & Solid tumors

CDK2i

BG-C90742
 101 BC & Solid tumors

B7H4 ADC

Ociperlimab
Anti TIGIT 900-105 NSCLC dose confirmation
 101 R/R DLBCL

BGB-45035
IRAK4 CDAC
 101 Immunology & Inflammation

BGB-15025
 101 Solid tumors

BGB-C354
 101 Solid tumors

B7H3 ADC

BGB-R046
 101 Solid tumors

IL-15 prodrug

Xaluritamig4
 20180146 mCRPC

Anti STEAP1xCD3

BGB-26808
 101 Solid tumors
BGB-30813
 101 Solid tumors

HPK1i
HPK1i
DGKζi

Phase 3

Zanubrutinib
 215 B-cell lymphoma 218 CD79B R/R DLBCL 217 Lupus nephritis

BTKi

BGB-16673
 101 R/R MCL, R/R CLL
Sonrotoclax
 201 R/R MCL
 202 R/R CLL
 203 R/R WM

Registration

Zanubrutinib
 306 TN MCL
 308 R/R MZL, R/R FL
 309 pMN

BTKi

Zanubrutinib
 304 TN CLL/SLL (JP) 305 R/R CLL/SLL (JP) 302 TN WM (JP)BTK CDAC

Sonrotoclax
 301 TN CLL

BCL2i

BCL2i

Tislelizumab 310 1L UBC
 311 LA ESCC
 314 R/R cHL

Anti PD1

TislelizumabAnti PD1
 315 Neo/adj NSCLC (CN) 305 1L GC/GEJC ITT (US, EU) 306 1L ESCC (US, EU, JP) 302 2L ESCC (JP)Blinatumomab4
Anti CD3xCD19
 20190359 Ped. R/R BP-ALL (initiation act.)

Pamiparib
 302 2L MTx gBRCAm PSOC

LBL-0075
 201 MSS-CRC
 202 1L ESCC

Anti LAG3

Ociperlimab
 302 1L NSCLC PDL1-high

BGB-A445
 201 Melanoma, UC

Anti OX40

Umbrella Studies
 LC-201 1L NSCLC LC-203 2L+ NSCLC LC-202 Neoadj NSCLC HNSCC-201 1L HNSCCIO Combos

Zanidatamab3
Anti HER2 BsAb
 203 HER2+ 2L BTC (CN)

PARPi
Anti TIGIT

Zanidatamab3
 301 1L HER2+ GEA

Anti HER2 BsAb

Tarlatamab4 20210004 2L SCLC
 20200041 1L ES-SCLC
 20230016 LS-SCLC

Anti DLL3xCD3Tarlatamab4
Anti DLL3xCD3
 20230273 3L SCLC (initiation activities)

Heme

Lung

Pan-Tumor/Other
Registration includes select accepted submissions
1) Ensem collaboration2) DualityBio collaboration
3) Zymeworks/Jazz collaboration4) Amgen collaboration
5) Leads Biolabs collaboration
Please refer to our most recent 10-K filing for a full list of our commercial products, including in-licensed products, as well as commercial rights and collaboration details.

BTKi

GI

Breast/Gyn
Non-Oncology

Please see clinical trials details in a “BeiGene Q2 Clinical
Trials Portfolio” presentation found on
https://ir.beigene.com

5Financial
Highlights

6Strong Growth in Product Revenue and Diversified
Mix in Geographies and Products
Revenue Growth

Q2 2024 Total Revenue by Region

1000

900
800

Global Revenue Mix

Global Product Revenue(US $M)

9%
1%

700
600
500
400
300

Significant global productrevenue growth

52%

38%

• 1-year CAGR of 66%• 3-year CAGR of 88%

200
100
0

U.S.

Europe

ROW

China

7

Significant Progress Toward Income Generation
Gross Margin (%)
Now among the highest across global
oncology companies1 with sales mix shift toward
internally developed products

85
83

Reduced loss from operations
and achieved adjusted income
from operations 2 (US $M)

Loss fromoperations (GAAP)

Adjusted income(loss) from operations(Non-GAAP)

Q2 2023

Q2 2023

Q2 2024

Q2 2024

48
77
(107)
(193)
(319)

+$241 a 125%
improvement+$212M a 66%
improvement

Q2 2022

Q2 2023

Q2 2024(1) Defined as companies deriving 40% or more of sales from oncology and 15% or more of sales outside of the U.S.
(2) Adjusted Income (Loss) from Operations is a non-GAAP financial measure that excludes from the corresponding GAAP measure costs related to share-based compensation,
depreciation and amortization expense. A reconciliation of this non-GAAP measure to the comparable GAAP measure is included in the Appendix to this presentation.

8

Leader in
Hematology

9Compelling and Leading Hematology Portfolio
BTK

BCL2

inhibitor

inhibitor

BTK
CDAC

BRUKINSA

Sonrotoclax

BGB-16673

Best-in-class BTKi

Differentiated efficacy
and safety

Clinically meaningful efficacy
and favorable safety data

Only BTKi demonstrating
H2H superiority

1000+ patients enrolled

Broadest label

Already inpivotal stage
Best-in-class potential
and broader usability by
all physicians$15B BTKi class$4B BCL2i classprojected in 2028*

projected in 2028**Source: Evaluate Pharma
CDAC – Chimeric Degradation Activation Compound300+ patients enrolled
Distinct MOA, agnosticof mutations
Most advanced BTK
degrader addressing BTKi
resistant patients10

Establishing BTKi Leadership
BRUKINSA is emerging as the BTKi class leader in the U.S. in new patient starts across all
approved indications• BTKi is the cornerstone therapy and the standardof care for non-Hodgkin’s lymphoma

BRUKINSA
Global Revenues ($M)

$700

637

• Global BTKi market was $8.8B in 2023

$600

• CLL is the largest indication for BTKi, accounting
for 80% of the market

489

$500
413
$400

358

• CLL market is expected to reach $12B in 2030*

308
$300
211
$200
$100
7

16

18

22

Q2
'20

Q3
'20

Q4
'20

Q1
'21

42

66

88

104

129

155

• BRUKINSA Q2 global revenue increased 107%from the prior-year period

176

$0

*Source: Evaluate Pharma July 2024

Q2
'21

Q3
'21

Q4
'21

Q1
'22

Q2
'22

Q3
'22

Q4
'22

Q1
'23

Q2
'23

Q3
'23

Q4
'23

Q1
'24

Q2
'24

• Given its best-in-class profile, as demonstrated inhead-to-head clinical trials for CLL, BRUKINSA iswell positioned to become the leading BTKi
11

BRUKINSAFoundational asset in hematology portfolio, only BTKi to demonstrate superiority
in safety and efficacy

BTK
inhibitor

Best-in-Class
BTKi• Engineered to havesustained/complete
target coverage;
substantially longer
exposure thanacalabrutinib andibrutinib• Sustained superiority of
PFS in H2H R/R CLL
vs ibrutinib1 while
acalabrutinib showed
non-inferiority• Strong efficacy acrossindications among
BTKis• Deep and durable
responses acrossindications

Favorable Safety• Superior safetyincluding cardiac
profile in two H2H
studies vs. ibrutinib• Well-tolerated inacalabrutinib intolerant
patients2 and improved
safety in those who
switched fromibrutinib3

Combination of
ChoiceBroadest Label• 5 approved
indications in the USA• Only BTKi approved inFL

Combination partner withsonrotoclax, TEVIMBRA,
and external assets tomaximize lifecycle value• Only BTKi with flexible
dosing schedule (QD or
BID)• Low treatment-related
infections, A-fib, GI
symptoms, headache,cough and fatigue
compared withacalabrutinib4

1 Brown et al. Extended Follow-up of ALPINE Randomized Phase 3 Study Confirms Sustained Superior Progression-Free Survival of Zanubrutinib Vs. Ibrutinib for Treatment of R/R CLL/SLL. ASH 2023
2 Shadman et al. Zanubrutinib in Acalabrutinib-Intolerant Patients with B-Cell Malignancies. ASH 2023
3 Garcia – Sanz et al. Clinical Outcomes in Patients with Waldenström Macroglobulinemia Receiving Ibrutinib on the Phase 3 ASPEN Study ≥1 Year After Transitioning to Zanubrutinib. ASH 2023
4 Hwang el al. Comparison of Treatment-Emergent Adverse Events of Acalabrutinib and Zanubrutinib: Meta-Analysis by Mayo Clinic. EHA 2023

12

BRUKINSA December 2023 U.S. Label Update
ALPINE PFS superiority in R/R CLL (HR 0.65, p=0.0024)1; sustained with extended follow-up2

PFS superiority sustained
at 39 months

PFS superiority in patientswith del(17p)/TP53

PFS events, n (%)

Separation of PFS curves continues BRUKINSA
130 (39.8)
at median 39 months follow-up
159 (48.9)
Ibrutinib
where acalabrutinib curves
HR (95% CI) 0.68 (0.53-0.86)
crossed in ELEVATE-RR and
P=0.0011
showed non-inferiority (HR=1)

PFS events, n (%)

PFS superior benefit over ibrutinib
31 (41.3)
BRUKINSA
demonstrated in patients with46 (61.3)
Ibrutinibdel(17p)/TP53mut; in this subset
acalabrutinib was only non-inferior HR (95% CI) 0.52 (0.33-0.83)
P=0.0047
to ibrutinib also with HR =1

1 USPI label for superiority based on median follow-up of 29.6 months ASH 2022
2 Brown et al. Extended Follow-up of ALPINE Randomized Phase 3 Study Confirms Sustained Superior Progression-Free Survival of Zanubrutinib Vs. Ibrutinib for Treatment of R/R CLL/SLL ASH 2023

13

Sonrotoclax
Potential best-in-class BCL2 inhibitor with differentiated profile

BCL2
inhibitor

More potent
andspecific BCL2i

Enablesbroader clinicaluse• Greater potencyvs. venetoclax inpreclinical models• Shorter half-life vs.
venetoclax and no
drug accumulation
leading to a better
safety profile• Active against
mutated G101V
BCL2 (known
resistancemechanism tovenetoclax)*• Higher selectivity
towards BCL2
believed to translate
to improved
tolerability• Easier ramp-up
and eliminating
monitoring unlocks
use by all
physicians*Liu et al.; Sonrotoclax overcomes BCL2 G101V mutation–induced venetoclax resistance inpreclinical models of hematologic malignancy. Blood 2024; 143 (18): 1825–1836.

Improvedclinical profile

Broaddevelopment
plan

Extends ourfootprint in otherheme malignancies• With 1000+
patients treated,clinical experience
reinforces preclinical data andsupports thepotential to be bestin-class• Initiated Phase 3
registrational
study in TN CLL
with potential to be
best in disease
fixed duration
combination and
SOC globally• Compelling efficacy
and safety data in
AML/MDS in
combination withazacytidine• Safe and tolerable
in combination with
BRUKINSA; deep
and durable
responses in TN
CLL are better
than reported
venetoclax
combos at same
timepoints• Monotherapy
potential in postBTKi setting withearly registration
options in CLL,
WM and MCL in key
countries• Encouraging datawith potential to be
first BCL2i
approved in
MM with t(11,14)

14

BTK Degrader (BGB-16673)
CDAC platform developed by BeiGene is the most advanced BTK degrader in the clinic

BTK
CDAC

Clinically Meaningful
Efficacy Data

Favorable
Safety Profile

RobustRegistration Plan

Growing Our
Hematology Leadership• BTK degradation
observed at lowest dosein patients with BTK
mutations1• Lack of IMiD activity vs.
competitors allows
improved safety. Low
grade 3/4 neutropenia inheavily pre-treatedpatients• Expansion cohorts in
R/R CLL and R/R MCL
are currently enrolling• Become SOC therapy
for patients progressing
after BTKi

• Expect to initiate Phase
3 clinical trial in R/R CLL
in 4Q24/1Q25• Potential to move toearlier lines of therapy• Clinical responses
observed acrossseveral B-cell
histologies and inpatients who received
prior cBTKi and
ncBTKi1• Shorter time toresponse than BTKis• Can penetrate the blood
brain barrier*• Safe and tolerable in
300+ patients treated• Degradation may
expand into additional
disease areas (LBCL,
Richter's, Follicular)• Potential to be
combined with othernovel agents andbecome a backbone

1 Seymour et al. First Results from a Phase 1, First-in-Human Study of the Bruton’s

Tyrosine Kinase (BTK) Degrader BGB-16673 in Patients (Pts) with Relapsed or Refractory(R/R) B-Cell Malignancies. ASH 2023
*based on internal preclinical data

15

Diverse Solid
Tumor Portfolio

16

TEVIMBRA-Centered Pan Tumor Pipeline
Poised for Global Patient Impact
TEVIMBRA
accomplishments

TEVIMBRA is an optimal
combination partner• 13 indications approved in China including recent
1L ES-SCLC approval• Global approvals including 1L/2L NSCLC in EU, AUS and
2L ESCC in US, AUS have been achieved. Multiple global
approvals expected in 2024.
• 1L ESCC and 1L GC BLAs under review in the US and
EU. BLA reviews ongoing in AUS, Japan and Brazil.
• More than 1.2 million patients treated worldwide, including
the first European patient treated with TEVIMBRA following
launch in Austria• Strong data in broad set of indications• Preparing to launch in multiple indications on 5 continents• Diverse pipeline combinations enable multiple immunemodulating approaches• $158 million in Q2 2024 revenue• >40 internal and external combination studies ongoing17

Solid Tumor Portfolio: Clinical Stage Assets
Next wave of immuno-oncology programs in combination with TEVIMBRA
Phase 3Phase 2Phase 1

• Ph3 NSCLC PD-L1+ completed enrollment in Q1• Upcoming POC readouts in NSCLC, CRC, ESCC, and HNSCC• Upcoming POC readout in 1L HNSCC• Upcoming POC readouts in 1L NSCLC and UBC• Ongoing Ph2 in 1L NSCLC (1G)
• Ph2 dose established; ongoing expansion in 1L GC

TIGIT
LAG3
TIM3
OX40
HPK1
CCR8

Next Wave of
IO Assets• FSE achieved August 2023
• Ongoing Ph1 dose escalation in monotherapy and Tisle combo

CRC= colorectal cancer
ESCC = esophageal squamous cell carcinoma
HNSCC = head and neck squamous cell carcinomaL= line of therapy
LAG3 = Lymphocyte-activation gene 3
NSCLC = non-small cell lung cancer
UBC= urinary bladder cancer

PD-L1
POC
RCC
TIGIT
TIM3
FSE

= programmed death-ligand 1= proof of concept= renal cell carcinoma= T-cell immunoglobulin and ITIM domain= T-cell membrane protein 3= first subject enrolled

18Innovative Solid Tumor NME Early Pipeline
Differentiated molecules with multiple modalities in priority tumor types
Lung

Breast/Gynecologic

GI

Pan-Tumor

PanKRASi

CDK4i*PanKRASi

SMAC Mimetics*

MTA Cooperative
PRMT5i

CDK2i*

FGFR2b ADC

DGKζi*EGFR CDAC

Next-genBCL2i*

CEA ADCHPK1i*

CEA ADC

B7H4 ADC*

GPC3 x 4-1BB

CCR8*

B7H3 ADC*

Claudin6 x CD3

IL-15 prodrug*

MUC1 x CD16A

EGFR x MET Tsp

BeiGene has global rights for CDK2 (Ensem partnership) andB7H4 ADC (DualityBio partnership)* In the clinic

Small molecule

Protein degrader

Bi/Tri-specific

mAb

ADC

Cytokine therapy

19

Exciting Early Solid Tumor Programs to Deliver FIC/BIC Molecules
Targeted TX

DegraderADC• High potency and CDK4 selectivity with brain penetrability• Best in class preclinical characteristics

CDK4i
PanKRASi
Differentiated
New Molecules• Broad activity against KRAS mutations in multiple tumor types​• Limits toxicity by sparing other RAS proteins• 15% of all tumor types including NSCLC are MTAP deleted• High potency and selectivity with brain penetrability

PRMT5i

EGFR CDAC
FGFR2b ADC
B7H3 ADC
B7H4 ADC• Differentiated MoA (degrader) to abolish EGFR activity• Broad mutation coverage which may prevent resistance• Potential first-in-class ADC for upper GI and breast cancers• Pre-clinical corneal toxicity less than with competitor molecule• Consistent expression in thoracic and squamous histology cancers• High drug antibody ratio (DAR8) enhances toxin delivery• High expression in breast and gynecologic cancers• Good efficacy in heterogeneous pre-clinical models

Slide to follow
Detailed descriptions included in appendix slides

20

CDK4 Inhibitor
Next-generation CDK4 inhibitor aiming for better efficacy and less toxicity

BGB-43395 is a potential best-in-class
CDK4 inhibitor spares CDK-6 mediated andoff-target toxicities•

Highly potent and selective compared with all approved
and investigational CDK4/(6)i agents•

Well tolerated in GLP TOX study w/o concerningneutropenia or GI toxicity issues

Strongest CDK4i Potency
CDK4 potency in MCF-7 proliferation assay
Proliferation IC50 nM

Despite CDK4/6 inhibitor success (estimated peaksales over $18B), unmet medical need still exists
as all have been associated with dose-limiting
toxicities and development of resistance mutations

356

Dose escalation in monotherapy (dose level 5) and incombination with fulvestrant and letrozole (dose level 2)
is ongoing towards the predicted efficacious dose range
with PK as expected•

No dose limiting toxicities observed•First clinical data abstract submitted to SABCS 2024

Atirmociclib (PF-07220060) is CDK4 inhibitor from Pfizer
CDK4 cellular IC50 measured through pRB in Jeko-1
CDK6 cellular IC50 measured through pRB in Pfeiffer with CDK4 KO

326
126

Palbociclib

Ribociclib

Abemaciclib

Atirmociclib

BG CDK4i

Greatest CDK4i to CDK6i selectivity*38
CDK6/CDK4 IC50 Fold

•

544
4.3x

Potential first-in-class in other tumor types
including ovarian, endometrial cancer, lung,and prostate
Currently in phase 1 development

BG CDK4i

639

16

21

BG CDK4i

7.7
1.3
Palbociclib

Ribociclib

Abemaciclib

Atirmociclib

BG CDK4i

21

Amgen Development Collaboration Progress
Two priority programs in Amgen’s oncology pipeline

Tiered mid-single digit royalties on net sales of potential blockbuster products globally;
developing these assets with commercial rights in China
IMDELLTRA (tarlatamab-dlle) first-in-class (DLL3 x
CD3) First T-cell engager to demonstrate activity in small
cell lung cancer. U.S. drug-treated population of ~35K
across all lines of disease• FDA approved1 in May 2024 for the treatmentof adult patients with extensive-stage small
cell lung cancer (ES-SCLC)• Durable ORR of 40% at 10mg dose and est. OS
at 9 mos. was 68%2 in SCLC
• Global phase 3 trial in 1L ES-SCLC was
initiated; enrollment of global phase 3 trials
in 2L SCLC and limited-stage SCLC is ongoing

1 Accelerated approval. Continued approval may depend on confirmatory trials.
2 N Engl J Med 2023; 389:2063-2075, DOI: 10.1056/NEJMoa2307980
3 Cancer Discov. 2024 Jan 12;14(1):76-89. doi: 10.1158/2159-8290.CD-23-0964.
SCLC = small cell lung cancer, ES = extensive stage,
LS = limited stage, mCRPC = metastatic castration-resistant prostate cancer

Xaluritamig, first-in-class (STEAP1 x CD3)
Enrolling phase 1 dose expansion in prostate cancer.
STEAP1 is expressed in >80% of prostate cancer patients• January 2024 data3 provides compelling
proof-of-concept• Dose-exploration data from patients with
mCRPC with the majority of participants
having received 3 or more prior lines2• RECIST ORR of 41% at doses ≥0.75 mg3

22

Key Catalysts
Pipeline   Approved Products ✓BRUKINSA

Sonrotoclax• 2H24: WM and CLL/SLL JP approval• 2H24: Tablet formulation U.S./EU submission• 1H25: Tablet formulation U.S./EU approval

•
•
•
•

TEVIMBRABTK CDAC

•
•
•
•
•
•
•
•
•
•
•
•
•

• Initiate phase 3 in R/R CLL in 4Q24/1Q25• Ongoing expansion cohorts (potential registration intent) for R/R MCL and R/R CLL• Additional data read out in B-cell malignancies

1H24: 1L ES-SCLC CN approval ✓2H24: Q2W 2L ESCC U.S. submission ✓2H24: Neo/adj NSCLC CN approval
2H24: 1L NPC EU submission
2H24: 1L ES-SCLC EU submission
2H24: Neo/adj NSCLC EU submission
2H24: 1L ESCC U.S. approval*
2H24: 1L Gastric U.S. approval
1H25: 2L ESCC Q2W U.S. approval
1H25: 1L Gastric EU approval
1H25: 1L ESCC EU approval
1H25: 1L ESCC JP approval
1H25: 2L ESCC JP approval

Ongoing phase 3 in TN CLL
Initiate phase 3 in R/R CLL in 4Q24/1Q25
Initiate phase 3 in R/R MCL in 4Q24/1Q25
Additional data read outs in B-cell malignancies, MM, MDS and AML

Tislelizumab Combinations• Multiple lung cancer combination cohorts with BGB-A445 (anti-OX40), LBL-007 (anti-LAG3)and BGB-15025 (HPK1 inhibitor) expected to read out in 2024 and expected publication in 1H 2025
• Multiple GI combination cohorts with LBL-007 (anti-LAG3) expected to read out in 2024
Zanidatamab1• 2L HER2+ BTC CN submission in May 2024 ✓, CN approval projected in 2H 2025

Early Clinical Development• Phase 2 dose identification for SMAC mimetic, CCR8, DGKζ, CDK4i• Bring 10 NMEs2 into the clinic including EGFR CDAC, PRMT5, pan-KRAS, ADC programs,
and bispecific antibodies• Clinical validation of internal ADC platform – payload, linker and targets* Due to a delay in scheduling clinical inspections, the target PDUFA date of July 2024 was deferred
1 Jazz/Zymeworks collaboration; BeiGene has commercial rights in APAC (excluding Japan), Australia, New Zealand
2 5 NMEs brought into the clinic YTD 2024, including CDK2i, B7H4 ADC, IRAK4 CDAC, B7H3 ADC, IL-15 prodrug

23Completed Our Capital Investment in State-of-the-Art Manufacturing
Capabilities to Support Global Growth and Broad Portfolio
State-of-the-Art
Biologics
Manufacturing Facility
in Guangzhou

Multi-Functional
Manufacturing Facility
in Suzhou

U.S. Manufacturing Facility
at the Princeton West
Innovation Center, NJ

Experienced,
High-Quality
Manufacturing Partners• Current total capacityof 65,000L• Commercial-scale small• 42-acre of state-of-the-art
biologics manufacturing site

• Guangzhou South Campus
for ADC production opened
in April 2024

• Aligned with the design

Manufacturing
collaborations with leading
manufacturers in biologics
and small molecules

molecule drug products facility

criteria of U.S., EU, and China• Diamond Site opened in
November 2023 that
increased capacity by morethan 5 times• The site opened inJuly 2024• 1 million+ sq ft of spacefor future expansion

24Overview of State-of-the-Art Manufacturing Facility – Hopewell, NJ
First U.S Manufacturing Facility
Groundbreaking in April 2022

CUB

Warehouse

42-acre green-field site (1,800,000 ft2)
at Princeton Innovation Center

DS

DP

Lab

Phase I with 150,000 ft2 built

Expandable to Small Molecule and ADC

Grand Opening
July 2024

Platform standardization allowing efficient tech transfer and shared world-wide resources
DS | Drug SubstanceDP | Drug Product
CUB | Central Utility Building25

By 2025, We Expect to Have Transformed Into a Clear Leader
With a Path to Profitability and Strategic Advantages
Today 2025-2030 

Priority Solid Tumor Types and 2030 Market Size Estimate• Cost and speed
advantages• Well positioned withdiverse modalities• Clear path totransition to
cash producing
global enterprise• Diverse global
revenue mix for longterm growth

Lung

Breast/Gynecologic

GI

Pan-Tumor

$69B

$66B

$29B

--

Diversified Therapeutic Modalities
Small
Molecule

CDAC

mAb

ADC

BsAb/
TsAb

mRNA

Cell
Therapy

Future Cornerstone Programs
EGFR CDAC
2030 market size estimates from EvaluatePharma: Lung includes non small cell and small cell, Gynecologic
includes ovarian and cervical, GI includes colorectal, esophageal, gastric, liver, pancreatic, and stomach

CDK4

FGFR2b ADC

PanKRAS

PRMT526

Our Commitment to Responsible Business and Sustainability

Our ambition is to be a leading corporate
citizen, acting with courage, creativity, anddiscipline to provide equitable benefit to ourpatients, business, and society. Our strategy
for the coming years focuses on four areasaligned with BeiGene’s mission, vision andvalues. These focus areas are supported by
key strategic priorities.
Our 2023 Responsible Business andSustainability Report, published in April
2024, details our efforts in each of theseareas and describes recent progress.

27

28

Appendix

29

PanKRAS Inhibitor
Differentiated to address broad range of KRAS mutations in multiple tumor types
KRAS mutations found in ~19% of all tumor types*•

KRASmut shows the most robust cancer cell dependencies•

So far, no effective therapy for non-G12C KRASmut tumors

KRASmut prevalence in all cancers
New cancer patients with KRASmut /year in US

PanKRAS inhibitor is differentiated from mutation
selective KRAS inhibitor•

Address broader KRAS mutations•

Minimal impact on normal tissues due to
N/HRAS compensation

BGB-53038 demonstrates good potential inpreclinical studies•

Highly potent across different KRAS mutations•

High selectivity of KRAS sparing N/HRAS•

Robust efficacy in multiple KRAS-driven models

Indication

Non-G12C

G12C

PDAC

50,658659

CRC

70,486

4,065

LUAD

19,291

12,492Compensation Role of N/HRAS in Normal Tissue
Upstream signaling

KRas

NRas

HRas

On track to enter the clinic in 4Q, 2024
Normal cell proliferation, differentiation and survival
Pharmacol Res. 2019 Jan; 139:503-511
Zhu, C.et al. Mol Cancer 21, 159 (2022)
J Thorac Dis 2020;12(7):3776-3784

30

MTA-Cooperative PRMT5 Inhibitor
Next-generation PRMT5 inhibitor avoiding hematological toxicity
Stronger potency than leading competitors in MTAPDEL cells
MTA-cooperative
PRMT5iPRMT5i
Killing Selectivity
MTA-cooperative
killing selectivity

9
10

1

•

Brain penetrative and good intracranial efficacy•

On track to enter clinic in 4Q 2024

52
35

40

22

20

9

0

3

AM
G

-1
9

-9
0

8

2

-4
6

TN
G

19

TN
G

R
TX
-1
7

PR
M
T5
i

M

-1
9

3

8

AM
G

-4
6

-9
0

2

TN
G

19

TN
G

DEL

BG PRMT5i

18%

AMG-193

17.1%

TNG-908

6.8%

MRTX-1719 and TNG-462 are reported as
non-brain penetrative
PRMT5i, PRMT5 inhibitor; DEL, deletion
PRMT5: protein arginine methyltransferases 5
MTA:
methylthioadenosine
MTAP: methylthioadenosine phosphorylase*2020 Globocan; Konstantinos. M et al. Science. 2016, 351(6278): 1208-1213.

Mean EC50
fold change ofcell killing in 7
MTAPDEL and2 MTAPWT
cell lines

66

60

Higher brain penetration than most leading competitors
and good intracranial efficacy
Kpuu,brain (mouse)

Desirable half-life supports daily dosing

80

U87-luc2
OrthotopicMTAP
MTAP DELModel
U87-luc2
orthotopic
model
Vehicle, BID
BG PRMT5i, 35 mg/kg, BID

10 9

Bioluminescene(photon/second)

Highly potent and selective on MTAP-deletion cells

100

Higher brain penetration than most leading competitors
and good intracranial efficacy

Compelling pharmacological properties•

20

Mean EC50 Fold Change

27

100

RT
X17

10% in gastric adenocarcinoma and 28% in
esophageal adenocarcinoma

130

BG

•

8% in lung adenocarcinoma and 19% in lungsquamous cell carcinoma

321

1000

PR
M
T5
i

•

Different dotsin the “Tumor
Cells” panel
indicate
different tumor
cell lines. Del,
deletion.

M

MTAP-deletion is found in 15% of all tumor types*

Relative EC50 (nM)

PRMT5i
Killing Activity
MTA-cooperativeMTA-cooperative
PRMT5i killing
activity

BG

2nd generation, MTA-cooperative PRMT5 inhibitor
selectively kills MTAP-deletion tumor cells, yet spares
normal hematological cells

10 8

10 7

10 6
0

10

20

30

Days post treatment

31

EGFR CDAC
Truly differentiated MoA to completely abolish EGFR signaling
EGFR mutant NSCLC is a large oncogenedriven subgroup with estimated class peaksales of $12B

Broadest EGFRmut coverage while sparing WT EGFR

~50% lung adenocarcinoma in Asian and
15% in Caucasian*

WT

LR

D19

LT

DT

LC

DC

LTC

DTC

BG EGFR CDAC

BG-60366 is a novel, potentially best-in-class
EGFR degrader••

Broad coverage of EGFR mutations and destructionof EGFR scaffold function yields sustained
signaling inhibition
Non-redundant mechanisms may prevent the emergenceof resistance when used in early lines of therapy

Gefitinib (1G TKI)
Osimertinib (3G TKI)

IC50 >1000 nM

IC50 =100~1000 nM

IC50 =20~100 nM

IC50 <20 nM

Robust efficacy in both osimertinib-sensitive and resistant xenograft models
Promising preclinical candidate profile

On track to enter the clinic in 4Q, 2024

VehicleOsimertinib 25mpk QD
BG EGFR CDAC 3mpk QD
BG EGFR CDAC 10mpk QD

800

Osimertinibsensitive
HCC-827-D19
model

400

Vehicle QD
Osimertinib 25mpk QD
BG EGFR CDAC 3mpk QD
BG EGFR CDAC 10mpk QD

2400

Mean Tumor Volume(mm3 ± SEM)••

Highly potent across Osimertinib-sensitive and resistant
EGFR mutations
Spares WT EGFR and good proteome selectivity
Strong efficacy with oral, daily dosing

Mean Tumor Volume(mm3 ± SEM)

•

2000

Osimertinib
resistant
H1975L858R/C797S
model

1600
1200
800
400
0

0
0

4

8

12

16

Treatment Days

20

24

0

4

8

12

16

20

Treatment Days

WT: wild-type; LR: L858R; D19: exon 19 deletion; DT: exon 19 deletion/T790M; LT:
L858R/T790M; DC: exon 19 deletion/C797S; LC: L858R/C797S; DTC: exon 19
deletion/T790M/C797S; LTC: L858R /T790M/C797S* 2020 Globocan; Wang P, et al. J ThoracDis. 2017, 9(7): 1973-1979; Wen S, et al.
Oncologist. 2019, 24(11):e1070-e1081; J Clin Oncol . 2022 Feb 20;40(6):611-625.

32

BeiGene’s ADC Platform
Integrate innovations across essential ADC components to obtain BIC/FIC ADCs

Powerful discovery engine
generating fit-for-purpose Abs withhigh quality and efficiency

Homogenous and stableconjugation to create uniform
DAR/better stability
Antibody

Conjugation• Stable conjugator• Monoclonal Ab• Site specific conjugation• Multi-specific Ab• Flexibility on DAR optimization

Diverse payload MoA to unleash the fullpotential of ADC technology• Current portfolio focus: capitalize on near term
opportunities with proprietary and differentiatedTopo1i platform• Sustained investment on novel concepts covering
diverse MoAs and modalities (small molecule
inhibitors, degraders, immune modulators, etc)

Topo1i, Topoisomerase I inhibitor

Proprietary hydrophilic linker platform• Fine-tuned hydrophilicity to reduce
aggregation
PayloadLinker• High stability to minimize premature
warhead release in circulation

33

FGFR2b ADC
Differentiated modality to pursue best-in-class opportunity
Clinically validated target in upper GI cancers
with additional opportunity in breast cancer•

FGFR2bMedium GC PDX

DAR 8VehicleBG FGFR2b ADC, 3 mg/kg, once

1400

Bemarituzumab combo with chemo has shown
good efficacy
Opportunity to improve efficacy and reduce ocular toxicity*

PayloadTopoI inhibitor

Stableconjugator

1200
1000
800

****

•

FGFR2b positive (IHC 2+/3+) in ~ 24%
gastric cancer (GC)1

Tumor Volume (mm3 ± SEM)•

BG FGFR2b ADC Generates Strong Efficacy

600
400
200
0
1

Tumor-directed toxin delivery•

Bystander effect to address tumor heterogeneity•

Spares on-target corneal toxicity via weaker
ligand blockade

5

7

9

11 13 15 17 19 21 23

Treatment days

Potential first-in-class ADC with differentiatedantibody backbone to reduce toxicity•

3

TopoI - Topoisomerase I

BG FGFR2b ADC Spares Corneal Toxicity In Mouse✱✱✱✱

Antibody

FGF7-FGFR2b

FGF10-FGFR2b

BG FGFR2b ADC

Weaker blocker

Non blocker

Bemarituzumab

Strong blocker

Strong blocker

Cornea Thickness(um)On track to enter the clinic in 2H 2024

60

40

ns

VehicleBG FGFR2b ADC
Bemarituzumab

200
BG FGFR2b ADC, 10 mg/kg, Q2W x 2 / Bemarituzumab, 10 mg/kg, BIW x 8
1 Lancet Oncol 2022; 23: 1430–40* Bemarituzumab only benefits a subset of patients with relatively higher FGFR2b expression* Bemarituzumab led to 26% treatment discontinuation caused by on-target corneal toxicity

34

B7-H3 ADC
BIC potential with stable DAR8 and strong bystander effectHighly expressed in multiple tumor types,
including lung, GI, head and neck andgynecological cancers*

BG B7-H3 ADC
OC

25%

Proprietary drug-linker with strong bystander
effect to address tumor heterogeneity•

Stable conjugator to improve stability andtumor presence

FSD achieved July 24
Michiko Yamato et al., Mol Cancer Ther, 2022
LUSC: lung squamous cell carcinoma; LUAD: lung adenocarcinoma; ESCC:
Esophageal squamous cell carcinoma; CPRC: castration-resistant prostate cancer;
HNSCC, Head and neck squamous cell carcinoma; EC: endometrial cancer; OC:ovarian cancer
DS-7300 is B7-H3 ADC lead competitor from Daiichi Sankyo

BeiGeneadvantage

DAR

4

8

Higher DAR

TopoI inhibitorhydrophilic
linkerStronger
bystander
effectStableconjugator

Better stability

Traditional Cysteine
conjugation

TopoI, Topoisomerase I

Robust efficacy in DS-7300 resistant PDX models

Lead competitor
biosimilar used as
benchmarkMean Tumor Volume (mm3 ± SEM)•

BG B7H3 ADC

Conjugation

Differentiated drug design with BIC potential
High DAR (DAR8) to enhance payload delivery

DS-7300

Payload-Linker DXd-GGFG

Clinical validation by DS-7300 in small celllung cancer•

Attribute

VehicleDS-7300 10mpk
BG B7-H3 ADC 5mpk

2500
2000
1500
1000
500
0
0

7

14

21

Treatment Days

28

Mean Tumor Volume (mm3 ± SEM)

B7-H3
LUSC LUAD ESCC CPRC HNSCC EC
Expression
Medium/
High
84%
39%
80%
74%
74%
89%
(H-score101-300)

BG B7-H3 ADC: differentiated molecular design

VehicleDS-7300 10mpk
BG B7-H3 ADC 5mpk

2000
1500
1000
500
0
0

7

14

21

28

Treatment Days

35

B7-H4 ADC
Asset to potentially boost ADC pipeline in breast and gynecologic cancers
ADC target with broad expression in breast andgynecologic cancers•~45% in triple-negative breast cancer•~60% in endometrial carcinomas•~50% in ovarian cancer

BG B7-H4 ADC molecular design• Clinically validated drug linker design• Non-Pgp substrate payload• Strong bystander effect• DAR6 to balance efficacy and toxicity

BG-C9074 has enhanced probability of success
Early clinical proof of concept by HS-20089 and SGNB7H4V in breast cancer•

Robust ADC design leveraging technology from Duality
Bio, a clinically validated ADC platform•

Robust efficacy in PDX models

Robust efficacy in B7-H4 low/heterogeneous PDX model
2100

Tumor volume (mm3)•Currently enrolling monotherapy dose level 2
with PK as expected

HS-20089 and SGN-B7H4V are B7H4 ADC from GSK/Hansoh and Pfizer/Seagen, respectively
ADC = antibody-drug conjugate
DAR = drug-to-antibody ratio
IHC = immunohistochemistry
PDX = patient-derived xenograft
42nd Annual J.P. Morgan Healthcare Conference. 8Jan24.
Available at: https://ir.beigene.com/ Accessed 15Jan24

Endometrial cancer(IHC 2+)

1800
1500

VehicleB7H4 ADC, 3mg/kg, QW*4

1200

B7H4 ADC, 10mg/kg, QW*4

900
600
300
0
0

7

14

21

28

35

42

49

Treatment days

36

CEA ADC
Differentiated ADC design aiming for better efficacy in CEA+ lung and GI cancers
CEACAM5 (CEA) is a well-established TAA highly
expressed in lung and GI cancer*
Medium to low
CEA expression

Attribute

SAR701

BG CEA ADC

BeiGene advantage

Payload

DM4

Proprietary TopoI
inhibitor• Payload MoA is better fit for target
indications• Stronger bystander effect

DAR

4

8

• Higher DAR

LinkerSPDB
disulfide

Hydrophilic• Better ADC stability

Conjugation

LysineCysteine(w/ stableconjugator)• Better ADC homogeneity and stability

31%

Gastric

26%

22%

Colorectal

51%

36%

SAR701 demonstrated clinical activity in
CEAHigh lung cancer (20% ORR), yet withsignificant room to improve
Differentiated ADC design to enhance
efficacy benefit••

Different payload strategy: topoisomerase I inhibitor
High DAR (8), stable conjugator and hydrophilic
linker design

On track to enter clinic in 4Q, 2024

Superior ADC- bystander effect, stability and efficacy
Stronger bystander killing

100
80
60
40
20
0

SAR701
BG CEA ADC

45-fold

0.01

1
100
ADC(nM)

Better DAR stability
in mouse PK
SAR701
BG CEA ADC

150

Superior efficacy
CRC
PDX model
Mean Tumor Volume(mm3 ± SEM)

7%DAR (%, percent remaining)

Lung adenocarcinoma

CEA-negative Cell Killing (%)

Cancer typeHigh CEA
expression

BG CEA ADC with differentiated ADC design

100

50

0
0

100
200
Time(h)300

VehicleSAR701, 4 mpk
BG CEA ADC, 2 mpk

2000
1500
1000
500
0
0

10

20

30

40

Treatment Days

Topol, Topoisomerase I; SAR701 biosimilar used as benchmark; CRC: colorectal cancer* Stéphanie Decary et al., Clin Cancer Res, 2020 Dec 15;26(24): 6589-6599
SAR701 is in short for SAR408701, CEA ADC from Sanofi

37

Reconciliation and Calculation of Non-GAAP
Financial Measurements
Reconciliation to adjusted loss from operations($ in thousands)

Q2 2024

Q2 2023

GAAP loss from operations(107,161)(318,715)

Plus: Share based compensation

130,694

103,329

Plus: Depreciation

23,75421,307

Plus: Amortization of intangibles

1,177

1,028

Adjusted income (loss) from operations

48,464(193,051)

38