R&D Day for Investors and Analysts

R&D Day for Investors and Analysts November 16, 2020 Seagen 2020 R&D Day

Clay Siegall, Ph.D. Roger Dansey, M.D. Nancy Whiting, Pharm.D Megan O’Meara, M.D. Shyra Gardai, Ph.D.

President & Chief Chief Medical Officer EVP, Corporate Strategy VP, Early Stage Executive Director, Executive Officer Alliances and Development Immunology Communications

2 Forward-Looking Statements

Certain of the statements made in this presentation are forward looking, such as those, among others, relating to the Company’s potential to achieve the noted development and regulatory milestones in 2021 and in future periods; anticipated activities related to the Company’s planned and ongoing clinical trials; the potential for the Company’s clinical trials to support further development, regulatory submissions and potential marketing approvals in the U.S. and other countries; the opportunities for, and the therapeutic and commercial potential of ADCETRIS, PADCEV, TUKYSA, tisotumab vedotin and ladiratuzumab vedotin and the Company’s other product candidates and those of its licensees and collaborators; the potential to submit a BLA for accelerated approval of tisotumab vedotin; the potential for data from the EV-301 and EV-201 cohort 2 clinical trials to support additional regulatory approvals of PADCEV; the potential for the approval of TUKYSA by the EMA; the therapeutic potential of the Company’s SEA technology and of the Company’s early stage pipeline agents including SGN-B6A, SGN-STNV, SGN-CD228A, SEA-CD40, SEA-TGT, SEA-BCMA and SEA-CD70; as well as other statements that are not historical fact. Actual results or developments may differ materially from those projected or implied in these forward-looking statements. Factors that may cause such a difference include without limitation: the risk that the Company or its collaborators may be delayed or unsuccessful in planned clinical trial initiations, enrollment in and conduct of clinical trials, obtaining data from clinical trials, planned regulatory submissions, and regulatory approvals in the U.S. and in other countries in each case for a variety of reasons including the difficulty and uncertainty of pharmaceutical product development, negative or disappointing clinical trial results, unexpected adverse events or regulatory actions and the inherent uncertainty associated with the regulatory approval process; risks relating to the Company’s collaboration agreements and its ability to achieve development and commercialization progress thereunder; and risks related to the duration and severity of the COVID-19 pandemic and resulting global economic, financial and healthcare system disruptions. More information about the risks and uncertainties faced by Seagen is contained under the caption “Risk Factors” included in the Company’s Quarterly Report on Form 10-Q for the quarter ended September 30, 2020 filed with the Securities and Exchange Commission. Seagen disclaims any intention or obligation to update or revise any forward-looking statements, whether as a result of new information, future events or otherwise, except as required by law.

3 CEO Strategic Overview

Clay Siegall, Ph.D. President & Chief Executive Officer A Global Oncology Company

Innovative research and Three approved therapies Our Mission the leader in ADCs fueling with multi-indication opportunities robust pipeline of targeted in blood cancers and solid tumors Discovering, developing, medicines for cancer and commercializing transformative cancer Expanding U.S. and ex-U.S. medicines to make a Proven, world-class drug footprint complements strategic development driving patient- partnerships to reach patients globally meaningful difference focused clinical programs in people’s lives

5 The Pace of Our Progress is Accelerating

TUKYSA approved in 5 countries

Positive topline results from two PADCEV trials

Positive data from pivotal trial of tisotumab vedotin***

ADCETRIS global sales >$1B Global collaborations with Merck on ladiratuzumab vedotin and TUKYSA PADCEV approved by FDA** Robust pipeline of programs with first- and/or Initiated Positive results from operations best-in-class potential ADCETRIS FDA-approved TUKYSA® HER2CLIMB trial and expanded to 6 Expanding global footprint indications; global POLIVY® approved by FDA 1998 approvals in >70 countries* and EMA (Roche) BLENREP® approved by FDA and EMA (GSK)

6 *in collaboration with Takeda **in collaboration with Astellas ***in collaboration with Genmab Our Strategic Priorities Support Long-term Growth

1 2 3 4

Execute commercially Maximize the potential Advance our late-stage Conduct innovative R&D to of our three approved programs toward securing maintain a robust early-stage products approvals for new products pipeline of novel targeted therapies

• ADCETRIS is the foundation of care • Broad clinical development of • Tisotumab vedotin could be our • Seven phase 1 programs, including for CD30+ lymphomas ADCETRIS, PADCEV and TUKYSA 4th approved drug ADCs and I-O agents to address important unmet needs • Strong PADCEV and TUKYSA U.S. • Collaborating with Merck accelerates • Goal to submit 3-4 INDs per year launches and expands ladiratuzumab vedotin • Trials designed to inform early development • Preparing to launch TUKYSA ex-U.S. go/no-go decisions

7 Seagen is Advancing Multiple Targeted Therapies for Cancer

ADCs harness the specificity of Targeting the Antibody-Drug monoclonal antibodies and the outside of the cell: Conjugates (ADCs) potency of cytotoxic agents Potential to improve • Sugar-engineered patient outcomes with antibodies (SEA) targeted therapies

Targeting signaling Activating pathways inside immune cells: the cell: CANCER CELL • Sugar-engineered IMMUNE CELL antibodies (SEA) • Small molecule TKIs Various combinations of these novel modalities are likely to be the future of treatment in oncology Hematologic Malignancies Solid Tumors Investigating Broadly is Pipeline Clinical Our and Late Stage Approved Early Stage Early Study planned / underway / planned Study Approved indication *IND submitted November 2020 November submitted *IND SGN SEA SGN SEA SEA SGN SEA LV TV TUKYSA PADCEV ADCETRIS ------CD70 TGT CD40 BCMA STNV* B6A CD228A • Bladder • Breast

Lung

Head and Neck

CRC

Melanoma

Pancreatic

Cervical

Ovarian

Uterine 9 GEC

Prostate

Mesothelioma

cSCC

Endometrial

Biliary Tract • HL • ALCL • CTCL • PTCL

DLBCL

AML/MDS Small Molecule TKI Molecule Small 8 Technology Sugar - antibody (SEA) load load Vedotin - MMAE ADC MMAE engineered engineered ADC Sandy ® Treated for urothelial cancer PADCEV (enfortumab vedotin) with PADCEV. Antibody-Drug Conjugate (ADC) Targeting Nectin-4

Roger Dansey, M.D. Chief Medical Officer

In collaboration with Nectin-4 is Expressed Across the Spectrum of Urothelial Cancer

Locally Advanced / Non-muscle Invasive Bladder Cancer Muscle Invasive Bladder Cancer Metastatic UC (NMIBC) (MIBC) (la/mUC)

Typically treated with TURBT and BCG* Typically treated with cystectomy +/- platinum Limited treatment options Bladder lumen

Lamina propria

Inner muscle

Outer muscle

Tis Ta T1 T2a T2b T3 T4 Carcinoma Non-invasive Tumor invades Tumor invades Tumor invades Tumor invades Tumor invades In situ papillary connective tissue Superficial muscle deep muscle perivesical tissue adjacent tissue carcinoma and organs

*TURBT: Transurethral Resection of Bladder Tumor Adapted from Springer Nature: Knowles MA and Hurst CD. Nature Rev Cancer. 2015;15(1):25-41 BCG: Bacillus of Calmette and Guerin vaccine 11 Broad PADCEV Development Program in Urothelial Cancer

MONOTHERAPY COMBINATION w/ KEYTRUDA® (PEMBROLIZUMAB) MONOTHERAPY

FDA-approved Expand FDA Expand into mUC Pursue first-line mUC Advance into Explore indication indication globally muscle-invasive non-muscle bladder cancer invasive disease Accelerated Global trial ✓ approval pathway

EV-201 Cohort 1 EV-201 Cohort 2 EV-301: randomized EV-103 Cohort K: EV:302: randomized KEYNOTE 905/ Non- muscle-invasive trial randomized to to PADCEV plus EV-303 and another bladder cancer mUC following mUC post-PD1 PADCEV +/- KEYTRUDA vs planned trial platinum and PD(L)-1 mUC post-platinum Clinical trial plans in KEYTRUDA chemotherapy and PD(L)-1 Two randomized trials development for Cis-ineligible patients in cis-ineligible and BCG-unresponsive Cis-eligible and cis-eligible patients ineligible patients PADCEV administration into the bladder feasible based on preclinical data

mUC: metastatic urothelial cancer

12 PADCEV Induces High Response Rates and Prolongs PFS and OS in Previously Treated mUC

EV-201 cohort 2 and EV-301 supplemental BLA planned in 1Q21

EV-201 COHORT 2 (N~91) EV-301 (N~600)

Hazard ratio 0.70 ORR 52% [95% CI: 40.8, 62.4] OS [95% CI: 0.56, 0.89] P=0.001 Hazard ratio 0.61 DOR 10.9 mos PFS [95% CI: 0.50, 0.75] P<0.00001 Tolerable with a manageable safety profile* PADCEV arm adverse events consistent with USPI*

• Full data to be presented at an upcoming medical meeting • At a planned interim analysis, the IDMC recommended the study be stopped for efficacy

EV-201 COHORT 1 (N=125) • Full data to be presented at an upcoming medical meeting

ORR 44% [95% CI: 35.1, 53.2]

DOR 7.6 mos

Tolerable with a manageable safety profile*

13 *See important safety information on PADCEV.com Promising Data with PADCEV plus KEYTRUDA Support Registration Trials in First-line mUC

Maximal Target Lesion Reduction by PD-L1 status Progression-Free and Objective Response Rate per Investigator Survival

Median PFS: 12.3 months (95% CI: 7.98, -) Best Response

73% ORR  • Confirmed CR/PR 12-month PFS rate: 50.1% 93% had tumor reduction (95% CI: 33.0, 65.0)

N=45; 20 Events

Overall Survival Median OS: not reached 12-month OS rate: 81.6% *Combined positive score high ≥10 (95% CI: 62.0, 91.8) N=45; 7 Events Safety profile appears consistent with individual components of the combination, including rash, hyperglycemia, peripheral neuropathy and immune-mediated events

Data presented at ASCO GU 2020 14 Rosenburg et.al.; Abstract #441 PADCEV Plus KEYTRUDA Vedotin ADCs and PD(L)-1 Inhibitors

Shyra Gardai, Ph.D. Executive Director, Immunology Scientific Rationale for Combining Vedotin (MMAE)-Based ADCs with PD(L)-1 Inhibitors

ADCs linked to MMAE induce cell death in a manner consistent with immunogenic cell death (ICD), and may enhance antitumor immunity

MMAE disrupts microtubules ICD causes release of DAMPs activate innate cells T cell responses can be causing ER stress and an immune-activating molecules that can initiate antitumor further augmented by PD-1/L1

immunogenic cell death (ICD) (DAMPs1; ATP, HMGB1, CRT) T cell responses inhibitors

DAMP=Damage-associated molecular patterns 1. Cao et al. AACR 2016. 2. Cao et al. Cancer Res 2017;77(13 suppl): Abstract 5588. 3. Cao et al. Cancer 16 Res 2018;78(13 Suppl): Abstract 2742. 4. Alley et al. Cancer Res 2019;79(13 Suppl): Abstract 221. MMAE Disrupts Microtubules Causing ER Stress, the First Step of ICD

In vitro, ladiratuzumab vedotin (LV) induces ER stress responses that increase over time Microtubule stabilizing agents do no induce an ER stress response which is required for ICD

Untreated LV Paclitaxel Docetaxel hours 48 96 120 48 96 120 48 96 120 48 96 120

pJNK

Microtubule disruption Microtubule stabilization

17 Cao et al., AACR, 2018 #2742. Preclinical data set. Vedotin ADCs Cause Tumor Cells to Release Immune Activating Molecules (DAMPs)

In vitro, PADCEV selectively induces release of immune activating molecules (DAMPs) from tumor cells MMAE free drug payload drives similar responses

18 Liu et al. AACR, 2019 #, 5581. Preclinical data set. PADCEV Induces Immune Cell Activation and TME Changes Required for Antigen Recognition by T cells in Preclinical Models

PADCEV recruits activated macrophages to tumors and modifies the TME (MHC-I) to support T cells responses that are important for PD1 agent activity

Antigen Recognition Receptors Macrophage Activation Macrophage Infiltration (MHC Class I)

Untreated PADCEV

19 Liu et al. AACR, 2019 #, 5581. Preclinical data set. Vedotin ADCs are Preferred Partners for PD-1 Agents

TV induced tumor cell death drives T cell responses (IFNγ) which is amplified by PD1 blockade with pembrolizumab

20 Gray et al., SITC, 2020 #618. Preclinical data set. Vedotin ADCs Induce ICD More Robustly Than an ADC Bearing a Topoisomerase-Ι Inhibitor

ER Stress Induction DAMP Release (ATP) Innate Immune Cell Activation

Microtubule Disruption- Vedotin (vc-MMAE ADC) 21 Topoisomerase-Ι Inhibition- Camptothecin (Exatecan ADC) Klussman et al., SITC 2020 #618 Preclinical data set. Clinical Development of PADCEV in Combination with KEYTRUDA

Roger Dansey, M.D. Chief Medical Officer Two Potential Opportunities for Approval in First-line mUC

Potential U.S. accelerated Randomized, Phase 3 trial approval pathway EV-302 EV-103 Cohort K

Cohort K added in January 2020 to PADCEV + KEYTRUDA vs ongoing EV-103 trial Platinum + Gemcitabine

Randomizing 150 cisplatin-ineligible Enrolling patients regardless of platinum patients to PADCEV +/- KEYTRUDA eligibility or PD(L)-1 expression

Primary endpoint ORR, supported by Seagen, Astellas and Merck jointly funding duration of response First patient treated in April 2020

23 Advancing PADCEV + KEYTRUDA Data to Evaluate PADCEV in Muscle Invasive Bladder Cancer (MIBC)

An estimated 28,000 people in the U.S. present annually with MIBC Approximately 50% will progress to metastatic urothelial cancer Additional phase 3 trial Treatment goal to prevent metastases and maximize survival in cisplatin-eligible patients to open shortly

KEYNOTE-905 (EV-303) KEYTRUDA KEYTRUDA • Enrolling cisplatin-ineligible patients CYSTECTOMY • N=836 PADCEV + PADCEV + Dual primary endpoints KEYTRUDA KEYTRUDA • Pathologic complete response • Event-free survival Direct to Observation cystectomy

Both phase 3 studies operationalized by Merck 24 PADCEV is Rapidly and Specifically Internalized into Urothelial Cells that Express Nectin-4

Tumor regression is observed following two doses of PADCEV in a Nectin-4 protein is highly expressed in NMIBC preclinical orthotopic bladder tumor model PADCEV detected by immunohistochemistry following a Systemic ADC exposure is 200-1000X lower than IV administration single dose into the bladder (intravesical) of a healthy rat Consistent with lack of exposure, no systemic toxicity was observed NMIBC phase 1 intravesical dose finding study under development

6 hrs post-dose PADCEV Exposure in Serum Following IV or Intravesical Administration

IV Dose Administration

15X IV Dose by Intravesical Administration

25 Seagen data on file PADCEV Being Evaluated in Other Nectin-4 Expressing Solid Tumors

Nectin-4 is expressed in multiple Ongoing EV-202 Trial in Locally Advanced or solid tumors Metastatic Malignant Solid Tumors

Breast Breast Primary Endpoint • Confirmed objective response rate

Secondary Lung Lung Endpoints • Duration of response • Disease control rate • Progression-free survival Pancreas Head and Neck • Overall survival • Safety and tolerability

Ovarian Gastric /Esophageal

26 Broad PADCEV Development Program in Urothelial Cancer

MONOTHERAPY COMBINATION w/ KEYTRUDA® (PEMBROLIZUMAB) MONOTHERAPY

mUC: metastatic urothelial cancer

27 TUKYSA® (tucatinib) HER2 Tyrosine Kinase Inhibitor

Julie Treated for metastatic breast cancer on a tucatinib clinical trial

In collaboration with Broad TUKYSA Development Program Encompasses HER2+ Breast and GI Cancers

BREAST CANCER GI CANCERS OTHER TUMORS

Approved Move into earlier Advance into early- Expand into Pursue gastric Explore other solid indication lines of breast stage breast cancer colorectal carcinoma cancer tumors cancer (CRC) ✓

Metastatic breast Metastatic breast Adjuvant, high risk of Metastatic CRC Metastatic gastric HER2+ and HER2 cancer; 1 or more prior cancer; prior taxane relapse mutant HER2-regimen in and trastuzumab MOUNTAINEER MOUNTAINEER-02 metastatic setting COMPASS HER2 RD HER2CLIMB-02 Phase 2 pivotal Phase 2/3 Phase 2 basket trial Randomized phase 3 HER2CLIMB Randomized phase 3 Phase 1b trial evaluating Phase 1b trial evaluating 1L combination 1L combination

mUC: metastatic urothelial cancer

29 Successful HER2CLIMB Trial Supported FDA and Four Ex-US Approvals; MAA Under Review in EU

HER2+ metastatic breast cancer patients previously treated with trastuzumab, pertuzumab and T-DM1

Randomized to TUKYSA + trastuzumab + capecitabine or placebo + trastuzumab + capecitabine (n=612)

PFS by BICR in patients PFS by BICR Overall Survival with brain metastases N=480* N=612 N=291

Risk of progression or Risk of death was Risk of progression or death was reduced by reduced by death was reduced by 46% 34% 52% 95% CI: 0.42 to 0.71, P<0.001 95% CI, 0.50 to 0.88, P=0.005 95% CI, 0.34 to 0.69, P<0.001

PFS: progression-free survival; BICR: blinded independent central review *The primary endpoint of PFS was assessed in the first 480 patients enrolled. Murthy RK, et al. N Engl J Med 2020;382:597-609. 30 Intracranial Response Rate (ORR-IC) in Patients with Active Brain Metastases and Measurable Intracranial Lesions at Baseline

Confirmed Objective Response Rate (RECIST 1.1)

P=0.03* IC, % (95% CI) (95% % IC, ORR -

Screening Post-cycle 6 N=55 N=20

*Stratified Cochran-Mantel-Haenszel P value Images Seagen data on file: ONT-380-005 31 Data presented by N. Lin, ASCO 2020 TUKYSA Improves CNS-PFS and OS in Patients with Brain Mets

CNS-PFS Benefit in Patients with Brain Metastases OS Benefit in Patients with Brain Metastases

HR (95% CI) P Value Median OS (95% CI): HR (95% CI) P Value

TUC+Tras+Cape 9.9 months (8.0, 13.9) TUC+Tras+Cape 18.1 months (15.5, NE) 0.58 (0.40, 0.85) 0.005 0.32 (0.22, 0.48) <0.00001 Pbo+Tras+Cape 4.2 months (3.6, 5.7) Pbo+Tras+Cape 12.0 months (11.2, 15.2)

70.1%

Median Median 40.2% 46.7%

CNS-PFS: time from randomization to disease progression in the brain or death by investigator assessment. HR: hazard ratio computed from Cox proportional hazards model using stratification factors (ECOG performance status: 0/1, and Region of world: North America/Rest of World) at randomization. All P values are nominal. Data presented by N. Lin, ASCO 2020 Evaluating TUKYSA Combined with KADCYLA (T-DM1) in Two Registrational Trials in Earlier Stages of HER2+ Breast Cancer

HER2CLIMB-02 COMPASS HER2 RD 1st and 2nd-line metastatic setting Adjuvant HER2+ breast cancer trial in high-risk non-pathologic complete response (pCR) patients Goal to establish TUKYSA + KADCYLA as a new standard of care Despite improving outcomes, KADCYLA had no impact on the development of brain metastases with ~half of all disease recurrences occurring in the brain1

Unresectable locally advanced or metastatic HER2+ BC HER2+ BC with residual invasive disease after neoadjuvant N=460 therapy of taxane & trastuzumab followed by surgery N=801

TUKYSA + Placebo + TUKYSA + KADCYLA Placebo + KADCYLA KADCYLA KADCYLA

Primary Endpoint Key Secondary Objectives Primary endpoint Progression-free survival Overall survival Invasive disease-free survival Objective response rate

1. N Engl J Med 2019; 380:617-628 33 MOUNTAINEER Trial: Encouraging Interim Data Suggest Additional Opportunity for TUKYSA in HER2+ Colorectal Cancer

Best RECIST Phase 2 trial evaluating TUKYSA plus Response trastuzumab in HER2+ metastatic CRC Compared to Baseline • Trial enrolling total of ~110 patients to enable potential accelerated approval • Primary endpoint confirmed ORR

Randomize TUKYSA + Trastuzumab Excludes 1 subject with PD on day 1 due to brain metastasis Patient Population 3L+, HER2+ mCRC Time on Treatment TUKYSA* *If non-response or progression, crossover to TUKYSA + trastuzumab

• Additional phase 1b signal finding safety study combining oxaliplatin-based chemotherapy to enable 1L CRC trial Interim data as presented at ESMO 2019 Strickler, et.al.; abstract 527PD

34 Evaluating TUKYSA in Gastric Cancer

Approximately 20-30% of gastric cancers are HER2+1

Once a patient progresses on first line therapy, there are no approved Additional phase 1b signal HER2-target agents finding safety study combining MOUNTAINEER-02 is a global trial including Asia to support approval oxaliplatin-based chemotherapy to enable 1L gastric cancer trial

MOUNTAINEER-02 Phase 2/3 blinded, randomized trial in HER2+ gastroesophageal cancers TUKYSA+ trastuzumab + paclitaxel + ramucirumab Co-primary Patient Population (N=235) • 2L HER2+ GEC Cancer endpoints Go/No-Go Randomized • Progression-free survival to Phase 3 Safety Lead-in: • Overall survival • TUKYSA + trastuzumab + paclitaxel + paclitaxel + ramucirumab ramucirumab • (N=30-48) (N=235)

Additional 30 patients randomized to TUKYSA + ramucirumab and paclitaxel to assess contribution of components 1. Van Cutsem, E. et al. Gastric Cancer 18, 476–484 (2015). 35 Broad TUKYSA Development Program Encompasses HER2+ Breast and GI Cancers

BREAST CANCER GI CANCERS OTHER TUMORS

Approved Move into earlier Advance into early- Expand into Pursue gastric Explore other solid indication lines of breast stage breast cancer colorectal carcinoma cancer tumors cancer (CRC) ✓

mUC: metastatic urothelial cancer

36 ADCETRIS® (brentuximab vedotin) ADC Targeting CD30

Nancy Whiting, Pharm.D. Mike EVP, Corporate Strategy, Alliances and Communications Treated with ADCETRIS for classical Hodgkin Lymphoma

In collaboration with ADCETRIS Use Across Hodgkin and Non-Hodgkin Lymphoma

Six Indications in the U.S.

Frontline HL Stage 3/4: ADCETRIS + AVD (ECHELON-1)

Frontline PTCL CD30-expressing: ADCETRIS + CHP (ECHELON-2)

Post-Transplant HL High-risk (AETHERA trial) Hodgkin lymphoma

Relapsed/Refractory Systemic ALCL CD30-expressing CTCL (ALCANZA trial)

Several Additional NCCN Guidelines Listings*

Frontline HL Age 60+: ADCETRIS + dacarbazine, ADCETRIS + AVD (sequential) HL: ADCETRIS, ADCETRIS + bendamustine, ADCETRIS + OPDIVO® (nivolumab)

HL age 60+: ADCETRIS Relapsed/Refractory Diffuse large B-cell lymphoma (DLBCL): ADCETRIS

Primary mediastinal B-cell lymphoma (PMBCL): ADCETRIS + OPDIVO

*Not approved uses 38 ECHELON-1: 5 Years is a Critical Clinical Milestone and Data Continue to Demonstrate Durability of Benefit

• A+AVD continues to demonstrate a robust and durable treatment benefit across, independent of stage, risk factor or PET2 status • The sustained PFS benefit with A+AVD is coupled with a manageable safety profile with symptoms of peripheral neuropathy improving or resolving over time and similar pregnancy rates in both treatment arms.

PFS AT 4 YEARS OF FOLLOW UP (ITT) DISEASE STAGE IPS RISK FACTOR PET2 STATUS

Stage 3 IPS 0-1 PET2-positive HR=0.593 HR=0.666 HR=0.676 (0.384-0.914) (0.385-1.149) (0.393-1.256)

N=1,334 Stage 4 IPS 2-3 PET2-negative HR=0.747 HR=0.771 HR=0.703 (0.557-0.904) (0.541-1.099) (0.512-0.892)

IPS 4-7 HR=0.595 Bartlett, et.al.; ASH 2019 Abstract #4026 (0.392-0.904)

Straus, et.al.; ASH 2020 Abstract #2973

39 ADCETRIS Potential Development Opportunities in Non-Hodgkin Lymphoma, Solid Tumors and HIV

Phase 3 trial

Relapsed/refractory DLBCL ADCETRIS + RITUXAN® (rituximab) + REVLIMID® (lenalidomide)

Exploratory trials

Relapsed/refractory solid tumors ADCETRIS + KEYTRUDA

HIV immunologic non-responders ADCETRIS

40 Expanding into CD30+ and CD30- R/R DLBCL

Objectives R/R DLBCL remains a high unmet medical need • Phase 3 registrational trial ADCETRIS + Revlimid demonstrated encouraging activity in R/R DLBCL • Establish ADCETRIS + Revlimid + Rituxan as a investigator-sponsored study1 new standard of care • Total population ORR=57% • CD30+ ORR 73% • CD30- ORR 46%

Patient Population ADCETRIS + Primary Endpoint • R/R DLBCL Revlimid + Rituxan • Progression-free survival • CD30+ or CD30- • Prior ASCT and / or CAR-T R or ineligible 1:1 Secondary Endpoint • N=~400 • ORR, OS, CR, DoR and Revlimid + Rituxan Safety

41 1. Professor N. Bartlett, Personal Communication CD30+ T regulatory Cells are Clearly Enriched Within Solid Tumors Unlike Other T regulatory Targets Such as CD25

CD30+ T cells in NSCLC (Single Cell RNAseq) CD30+ Tregs in Solid Tumors

CD25+ T cells in NSCLC (Single Cell RNAseq) CD30 (+) FoxP3 (+) CD30(+)/FoxP3(+)

Example of dual IHC staining of a heavily infiltrated pancreatic tumor showing co-localization of CD30 with a subset of FOXP3+ cells.

42 Guo, X. et al, Nat Med 24, 978–985 Grogan et al., SITC 2020 #696. Preclinical data set. Preclinical Data Demonstrate Significant Direct Treg Depletion in Solid Tumors

In vitro, ADCETRIS shows selective depletion of activated Tregs and restores cytotoxic CD8+ T cells Murine CD30-ADC depletes Tregs more robustly than unarmed antibodies in a syngeneic solid tumor mouse model

In vitro ADCETRIS Depletion of CD30+ Tregs In vivo Depletion of Tumor CD30+ Tregs by CD30 ADC

43 Grogan et al., SITC 2020 #696 & data on file. Preclinical data set. Phase 2 Exploratory Trial to Evaluate CD30+ Treg Depletion in Solid Tumors

Patient Population NSCLC with primary resistance to previous CPI Primary Endpoint • Metastatic disease • Confirmed ORR • CPI-containing regimen is the immediate prior NSCLC with acquired resistance to previous CPI therapy Secondary • N~60 Endpoints Cutaneous melanoma with primary resistance to • Safety previous CPI Study Treatment • Duration of response • Progression-free survival • ADCETRIS + KEYTRUDA Cutaneous melanoma with acquired resistance to previous CPI

44 Exploring ADCETRIS in HIV

• While there have been significant improvements in HIV prevention and treatment, there are >1.2 million people living with HIV and ~16,000 patients die from HIV annually in the US • Despite adequate antiretroviral therapy, ~10% of patients do not achieve a CD4+ T cell count greater than 200 cells/µl and are considered immunological non-responders (INRs)1 • INRs are at high risk for opportunistic infections, AIDS-related malignancies, and increased mortality • There are currently no approved therapies for INR patients with HIV, representing a high unmet need

45 J Leukoc Biol. 2020 Apr; 107(4): 597–612. Sustained Improvement in CD4+ and CD8+ T-Cell Counts with ADCETRIS+AVD Treatment

Tregs have been implicated as a cause of INR; preclinical data demonstrated ADCETRIS is capable of selective depletion of Tregs With A+AVD, CD4+ and CD8+ T cells increased in majority of INR patients after 1st cycle T cell counts are maintained up to 12 months after the last dose of ADCETRIS

ADCETRIS Depletes Activated Distribution of CD4 Count (Overall) T cell Subsets

Grogran et al., SITC 2020 #696. Preclinical data set. Median CD4+ T-cell Count at diagnosis: 289 cells/ul Rubenstein et.al, ASH 2019 46 Median CD4+ T-cell Count after Cycle 1: 545 cells/ul Phase 2 Exploratory Study of ADCETRIS in HIV to Confirm Immune Reconstitution in Patients Without Malignancy

Primary Endpoint • Increase the CD4+ count

Target Population Key Secondary Endpoints • age ≥ 18, HIV-1+ without malignancy • Safety and tolerability ADCETRIS x 2-4 doses + • cART ≥ 2 years • Duration of response • CD4 between 51 & 200 antiretroviral therapy • Kinetics of CD4 and CD8 T cell counts • No detectable viral load • Rate of opportunistic infections

47 Advancing Our Late-Stage Pipeline

Nancy Whiting, Pharm.D. EVP, Corporate Strategy, Alliances and Communications Tisotumab Vedotin (TV) Could Become Seagen’s 4th Commercial Asset

Ongoing TV Clinical Trials • ADC targeting Tissue Factor Trial Name Therapeutic Area • Initial focus in recurrent/metastatic cervical cancer innovaTV 204 Recurrent/metastatic cervical cancer • Current therapies generally result in limited Cervical cancer (1L or recurrent); monotherapy and objective response rates of <15% with median innovaTV 205 overall survival ranging from 6.0 to 9.4 months combinations with KEYTRUDA or chemotherapy • Positive results from pivotal innovaTV 204 innovaTV 207 Solid tumor basket trial trial support planned Biologics License Application in Q1 2021 innovaTV 208 Platinum resistant ovarian cancer • Trial in cervical cancer evaluating TV in combination with KEYTRUDA or with Advanced solid malignancies (Japanese patients) and standard of care chemotherapy innovaTV 206 expansion cohort in recurrent/metastatic cervical cancer for potential approval in Japan • Additional trials in other solid tumors In collaboration with:

49 Tisotumab Vedotin Phase 2 Pivotal Trial: innovaTV 204

Key Eligibility Primary Endpoint Criteria • Confirmed ORR per • Recurrent or metastatic independent imaging cervical cancer review committee (IRC) • Progressed during or after doublet chemotherapy Tisotumab vedotin with bevacizumab Until PD or Secondary (if eligible) 2.0 mg/kg IV Q3W unacceptable toxicity Endpoints • Received ≤2 prior • ORR per investigator systemic regimens • DOR, TTR, and PFS by IRC and investigator N=101 • OS • Safety

50 InnovaTV 204 Demonstrated Clinically Meaningful and Durable Responses

N=101 DURATION OF RESPONSE

Confirmed ORR (95% CI),a % 24 (15.9−33.3) 1.00 CR, n (%) 7 (7) 0.80

PR, n (%) 17 (17) 0.60 Median DOR (95% CI) 0.40 SD, n (%) 49 (49) 8.3 months 0.20 (4.2−NR) PD, n (%) 24 (24)

Remaining in Response in Remaining 0 0 2 4 6 8 10 12 Not evaluable, n (%) 4 (4) Time (months) No. at risk24 22 16 11 8 3 0

Data cutoff: February 06, 2020. Median duration of follow-up: 10.0 months. aBased on the Clopper-Pearson method. CI, confidence interval; CR, complete response; DOR, duration of response; IRC, independent review committee; NR, not reached; ORR, objective response rate; PD, disease progression; PR, partial response; SD, stable disease.

51 Target Lesions Reduced in 79% of Patients with ≥1 Post-baseline Scan

100 Positive innovaTV 204 results support 75 planned BLA 50 submission in Q1 2021 25 Initiating a phase 3 0 trial in 2+L mCC to -25 serve as confirmatory

From Baseline (%) trial and to support -50 potential global approvals -75 Confirmed Best Overall Response CR PR SD PD Maximum Change in Target Lesion Size Lesion Target in Maximum Change -100

Data cutoff: February 06, 2020. Median duration of follow-up: 10.0 months. + indicates a change greater than 100%. Horizontal dashed lines indicate 20% increase and 30% decrease in target lesion diameters from baseline for RECIST v1.1 assessment. Colored bars represent the best overall confirmed response. CR, PR, SD, and PD were based on RECIST v1.1 as evaluated by IRC. CR, complete response; IRC, independent review committee; PD, disease progression; PR, partial response; RECIST v1.1, Response Evaluation Criteria In Solid Tumors version 1.1; SD, stable disease.

52 Tissue Factor is Highly Expressed and TV is Active in Multiple Other Solid Tumors

NSCLC • Tissue factor (TF) is widely expressed in multiple solid tumors • Cervical • Ovarian • NSCLC • Head and neck • Phase 1 study of TV in multiple solid tumors demonstrated objective responses in all tumor Ovarian Cancer types tested, except prostate • Two ongoing trials evaluating TV in solid tumors, including every three weeks and weekly dosing • Basket trial in colorectal, NSCLC, pancreatic and head & neck cancers • Trial in platinum-resistant ovarian cancer

53 Ladiratuzumab Vedotin Ladiratuzumab Vedotin (LV) is an Emerging Late-Stage Program

• ADC targeting LIV-1, which is broadly expressed Ongoing LV Clinical Trials in breast cancer and other solid tumors Trial Name Therapeutic Area • Encouraging single-agent and KEYTRUDA combination data reported in TNBC SGNLVA-001 Metastatic breast cancer (TNBC and HER+) Phase 1 • Clinical development focused on optimizing dose and schedule SGNLVA-002 1L metastatic TNBC in combination with Phase 1/2 KEYTRUDA • Development program with Merck in triple- SGNLVA-005 negative breast cancer, HR+ breast cancer and Solid tumor basket trial other LIV-1-expressing solid tumors Phase 2

In collaboration with:

55 LV is Active as Monotherapy and Activates Innate Immune Cells in the Tumor Microenvironment (TME)

• LV monotherapy results in immune activation in the TME in patients with metastatic TNBC with a significant induction of macrophage infiltration, induces MHC, co-stimulatory molecules, and PD-L1 expression

• LV-induced TME changes in cancer patients are consistent with preclinical evidence that LV induces ICD

Baseline C1D5

CD68 CD68

Data presented at SABCS, December 2017 PD-L1 PD-L1

Presented at SITC 2020 56 LV + KEYTRUDA is Active in TNBC with Evidence of Potent Immune Activation and Adaptive Immune Response

CD3 CD8 CD68 PD-L1

>90% of subjects achieved tumor reduction Baseline

CD3 CD8 CD68 PD-L1 C1D5

Similar response rate in both PD-L1 positive and PD-L1 negative patients Figure 4. Representative IHC pictures showing the increased infiltration of CD3+ and CD8+ T cells, CD68+ macrophages, and increased PD-L1 staining in C1D5 biopsy as compared to baseline biopsy collected from an LVA- Data presented at SABCS December 2019 002 patient. Brown color indicates cells stained positive for each marker.

Data presented at SITC 2020

57 Weekly Dosing Reduces Peak-to-Trough Fluctuations and Increases Exposure to High Drug Concentrations

• Concentrations for high drug-to-antibody ratio (DAR) species drop to zero for Q3W due to faster clearance

• Higher Ctrough maintained for all species with weekly dosing • Increased exposure to high DAR species with weekly dosing

ADC with DAR ≥ 4 ADC with DAR 2-3 Weekly Dosing Ongoing

Dose Level – 3 1.75 mg/kg

Dose Level – 2 1.50 mg/kg

Dose Level – 1 1.25 mg/kg

Dose Level – 0 3 mg/kg Q3WK 1.00 mg/kg 1 mg/kg Q1WK Dose Level – 1 0.75 mg/kg

58 Based on preclinical data Clinical Vignette: LV Monotherapy Weekly Dosing in TNBC

Baseline Post-Baseline Scan 1 49-year-old female with metastatic triple negative breast cancer (TNBC) Locally advanced TNBC diagnosed in May 2018 • No response to neoadjuvant 4-drug regimen • Disease progression on adjuvant 3-drug regimen LV treatment 1.25 mg/kg every week started in April 2020 • Achieved a confirmed partial response • Remained on treatment for 6 cycles • Adverse events included Grade 2 fatigue, peripheral sensory neuropathy, anorexia and pain

59 Clinical Vignette: LV Weekly Dosing in HR+ Breast Cancer

Baseline Post-Baseline Scan 1 Post-Baseline Scan 2 59-year-old female with endocrine-refractory, hormone receptor positive metastatic breast cancer Stage IIA breast cancer diagnosed in 2017 • Recurrence identified in Aug 2019 • Prior therapy includes 2 hormonal therapies, chemotherapy and PD-L1 inhibitor LV treatment 1.25mg/kg every week started in March 2020 • Achieve confirmed partial response • Remained on treatment for 7 cycles • Related adverse events encountered: • Grade 2 sensory peripheral neuropathy, alopecia

60 LV Basket Study Currently Enrolling Patients with Advanced Solid Tumors

1+ 2+ 3+

LIV1 is broadly expressed across multiple solid tumors, including lung, head and neck, gastroesophageal, melanoma and prostate cancers Trial evaluating weekly dosing with primary endpoint of ORR

Squamous NSCLC Carcinoma

61 Advancing our Late-stage Programs

TISOTUMAB VEDOTIN LADIRATUZUMAB VEDOTIN

• TV BLA will be submitted to FDA in 1Q21 • LV has demonstrated encouraging and if approved, is poised to become our activity as monotherapy and in 4th commercial product combination with KEYTRUDA, with biopsy-demonstrated potent immune • Multiple additional trials of TV, as activation in the tumor microenvironment monotherapy or in combination with KEYTRUDA or chemotherapy, in cervical • Clinical development focused on cancer and in other solid tumors ongoing optimizing dose and schedule in breast cancer • Solid tumor basket trial ongoing • Collaboration with Merck will accelerate development

62 Early-Stage ADC Pipeline

Megan O’Meara, M.D. Vice President, Early-Stage Development Early-Stage Pipeline Employs Novel ADCs and Empowered Antibodies

SGN-B6A ADC Technology • Clinically validated auristatin payloads SGN-STNV • Novel drug linkers • Unique targets with first-in-class antibodies SGN-CD228A

SEA-CD40 SEA Technology • Enhanced engagement of activating SEA-TGT Fc gamma receptor • Amplified immune agonism SEA-BCMA • Direct tumor cell killing

SEA-CD70

Early pipeline as of November 2020

64 Integrin Beta-6: ADC Target with High Expression in NSCLC and Head and Neck Cancer

Integrin Beta-6 target Purposeful antibody design • High expression in tumors including NSCLC and head & neck • Unique specificity to beta-6; avoids other integrins • Key biological role in activation of TGF-beta • Greater tumor selectivity • Poor prognostic indicator in multiple cancer types • Reduced normal tissue binding

Integrin Beta-6 IHC

Non-Small Cell Lung Head & Neck

Adapted from Desgrosellier et al, Nat Rev Cancer 2010 Lyon et al AACR 2020 65 SGN-B6A Vedotin ADC with Rapid Internalization and Strong Preclinical Activity

ADC rapidly internalizes and traffics to lysosomes Activity in head & neck xenograft model

Beta-6 staining on membranes Colocalization in lysosomes

0 hr 4 hr

Phase 1 trial ongoing in tumors including NSCLC, head & neck, gastric, esophageal

66 Lyon et al AACR 2020. Preclinical data set. Clinicaltrials.gov: NCT04389632 Sialyl Thomsen-nouveau (STn) is a First-in-Class Carbohydrate Target for Vedotin ADC

Sialyl Thomsen-nouveau (STn) Features SGN-STNV • STn is a tumor-associated carbohydrate antigen • Present on multiple tumor associated glycoproteins (e.g. CA-125, MUC1) • Almost-ubiquitous expression across multiple tumors including NSCLC, ovarian, gastric • Expression of STn is rare in normal tissues compared to cancer tissue • Correlated with poor prognosis & chemo resistance

Schultz et al, Cancer and Metastasis Rev 2012 Pinho et al, Nat Rev Cancer 2015 Eavarone et al, PLOS One 2018

67 SGN-STNV: STn Vedotin ADC with Target Expression and Preclinical Activity Across Multiple Solid Tumors

IHC Examples Across Tumor Types Preclinical Activity Across PDX Models

NSCLC

Ovarian cancer

Gastric cancer

IND submitted Nov 2020; Phase 1 trial targeting early 1Q21

68 Seagen data on file CD228: Biologically Relevant Cancer Target with Low Normal Tissue Expression

CD228 (melanotransferrin; p97) is an oncofetal protein first identified on melanoma cells • Low normal tissue expression • High expression in multiple tumor types including melanoma, colorectal, breast, lung

Possible role in tumor migration and proliferation • Tumors exploit remodeling function to promote invasiveness and metastasis • High expression a poor prognostic indicator

Rolland et al, Pigment Cell and Mel Res 2009 Sandall et al, AACR 2019 Sandall et al, AACR 2020 69 SGN-CD228A Pairs CD228 Antibody with Novel Linker Technology

Anti-CD228A monoclonal antibody CD228 antibody PEGylated glucuronide linker • Superior drug delivery ability compared to other CD228 antibodies tested despite similar binding affinity Monomethyl auristatin E (MMAE)

MMAE with novel PEGylated glucuronide linker 8-load MMAE • Increased drug loading (8-load) compared to 4-load 4-load vedotin vedotin • Improved linker stability 3-4 FOLD MORE MMAE DELIVERED INSIDE CELLS

• Enhanced intracellular drug release and retention Intracellular MMAE Retention of MMAE in Cells

) 400 60 • Maintains immunogenic cell death MOA nM 300 40

200

20 100

Intracellular MMAE IntracellularMMAE ( 0 0 % % Cellular Retention Burke et al, Mol Cancer Ther, 2017 SK-MEL-5 A2058 SK-MEL-5 A2058 Sandall et al, AACR 2019 70 8 6 8 6 SGN-CD228A Is Highly Active in Preclinical Melanoma Models

A2058 MELANOMA XENOGRAFT MODEL MELANOMA PDX MODELS

Untreated 1400 CD228-vedotin, 3 mg/kg

)

3 CD228-vedotin, 1 mg/kg 1200 SGN-CD228A, 3 mg/kg SGN-CD228A, 1 mg/kg 1000

800

600 Single Dose 400 3/5 transient CRs

Mean TumorVolume (mm 200 Percent Tumor Volume Change (%) Change Volume Tumor Percent 5/5 CRs 0 0 10 20 30 40

Days post tumor implant

Phase 1 trial ongoing in solid tumors including melanoma, NSCLC, breast, mesothelioma

Sandall et al, AACR 2019 Sandall et al, AACR 2020 71 Clinicaltrials.gov: NCT04042480 Sugar-Engineered Antibody (SEA) Technology

Shyra Gardai, Ph.D. Executive Director, Immunology Seagen Proprietary SEA-Technology Creates Empowered Antibodies

Sugar-Engineered Antibody (SEA) technology is an elegant platform that uses a small molecule inhibitor added to existing mAb-producing cells to generate nonfucosylated antibodies

Stable Antibody =H Producing Cells + H= =H

Nonfucosylated antibodies enhance engagement with the activating FcγRIIIa receptor and have minimal binding to inhibitory FcγRIIb receptor • Increased affinity for activating FcγRIIIa receptor results in amplified killing of antigen positive cells • Preferential enhancement of activating FcγRIIIa binding amplifies immune cell activation

73 Four SEA Empowered Antibody Programs are in Ongoing Phase 1 Trials

ADCC Killing of Antigen (+) Cells Receptor Clustering & Agonism Receptor Agonism/Synapse Formation

Myeloid Cells Myeloid Cells

T Cells

FcyRIIIa SEA-BCMA FcyRIIIa SEA-CD40 FcyRIIIa SEA-TGT (CD16) (CD16) (CD16) SEA-CD70 NK Cells T Cells NK Cells SEA-TGT Monocytes

Program Disease Area SEA MOA

SEA-CD40 Pancreatic cancer Enhanced Immune Agonism/ADCC

SEA-TGT Solid tumors and lymphomas Enhanced Immune Agonism/ADCC

SEA-BCMA Multiple myeloma Enhanced ADCC

SEA-CD70 AML and MDS Enhanced ADCC

1.Okeley NM, et al. Proc Natl Acad Sci USA 2013;110(14):5404–9; 2. Field JJ, et al. Cancer Res 2016;76(14 suppl):Abstract 4005; 3. Gardai SJ, et al. Cancer Res 2016;76 (14 suppl):Abstract 499; 4. Gardai SJ, et al. J Clin Oncol 2015;33(suppl 15):3074. 74 SEA-CD40 Activates CD40+ Innate Cells to Initiate a T cell Response in Preclinical Models

SEA-CD40 MOA requires receptor clustering and agonism enabled by SEA technology

APC (Myeloid Cells)

Increased binding of nonfucosylated backbone to FcγRIII results in increased: • Crosslinking and agonism of CD40 on Antigen Presenting Cell CD40 (APC; myeloid cells) • CD40 signaling resulting in elevated chemokines, cytokines, FcyRIIIa SEA-CD40 and up-regulated co-stimulatory receptors (CD16) • Kick-starts antigen specific CD8 T cell responses

NK Cells Monocytes

75 SEA-CD40 Nonfucosylated Differentiated Backbone

SEA-CD40 uniquely binds to activating FcγR with limited binding to the inhibitory FcγR

SEA-CD40* APX005 S267E 21.4.1 G12 Antibody Class Humanized IgG1 Humanized IgG1 Fully human IgG2 Fully human IgG1 Fc backbone modification ↑FcRγIIIa ↓FcγRIIb ↓FcγRIIIa binding ↑FcγRIIa&b Native Native

*parent antibody is dacetuzumab; 1Based on sequence in US patent US9676861B2; 2Based on sequence in South Korea patent SK20170041790A, 3Based on clone described in Cancer Immunology Research March 2015 3; 236.

76 Zeng et al, SITC, 2020 #438. Preclinical data set. SEA-CD40 Distinctly Amplifies an Immune Response to Chemotherapy

Immune Activating Cytokine (IFNγ)

Abraxane Treated Pancreatic Tumor Cells

Activating FcγRIIIa Binding

77 Zeng et al, SITC, 2020 #438. Preclinical data set. SEA-CD40 Amplifies Chemotherapy and PD-1 Antitumor Activity in Preclinical Models

SEA-CD40 + Abraxane combo SEA-CD40 + PD1 combo SEA-CD40 + Abraxane+ PD1 combo

78 Zeng et al, SITC, 2020 #438. Preclinical data set. SEA-TGT Optimized for Fc Effector Function and has Differentiated Antitumor Activity in Preclinical Models

Binding Activating Fc Receptors

IgG4 IgG1-effector null IgG1 IgG1-Fc Optimized

SEA-TGT

Disrupts TIGIT ligand interactions and relieves Disrupts TIGIT ligand interactions and relieves suppressive checkpoint signaling suppressive checkpoint signaling Engages and activates myeloid cells resulting in generation of antigen (+) CD8 T cells Depletes TIGIT+ T regulatory T cells

SEA-TGT binds with nM affinity to human, mouse and SEA-TGT nonfucosylated antibody backbone is cyno TIGIT and blocks inhibitory signals optimized for FcγR binding

79 SEA-TGT Has Differentiated Binding to Activating and Inhibitory Fc Receptors

FcγRIIIa (Activating) FcγRIIb (Inhibitory)

80 Smith et al., SITC 2020 # 250. Preclinical data set. SEA-TGT Distinctly Engages Antigen Presenting Cells to Drive T cell Responses

In Vitro Myeloid Cytokines Peptide-Stimulated T Cells

81 Smith et al., SITC 2020 # 250. Preclinical data set. Nonfucosylated SEA-TGT Drives Robust Depletion of T regulatory Cells with Minimal Impact of CD8 Effector T cells

In Vitro Human Treg Depletion In Vitro Human CD8+ T Cell Depletion

82 Smith et al., SITC 2020 # 250. Preclinical data set. SEA-TGT Induces Robust and Curative Antitumor Responses in Preclinical Models

Syngeneic Model Syngeneic Model

83 Smith et al., SITC 2020 # 250. Preclinical data set. SEA-TGT Increases Several MOAs Through Distinct FcγR Binding

ADCC Killing of Antigen (+) Cells Receptor Agonism/Synapse Formation

Myeloid Cells T Cells

FcyRIIIa SEA-TGT (CD16) FcyRIIIa SEA-TGT (CD16)

NK Cells T Cells

MOA examination and backbone comparison in preclinical models

T reg CD8 CD8 naïve Myeloid depletion memory recall antigen response cell activation Anti-TIGIT Null (No effector function) - ++ -/+ -

Anti-TIGIT IgG1 (Standard effector function) ++ ++ ++ -/+

SEA-TGT (Enhanced effector function) ++++ +++ ++++ +++

(++++) maximal activity relative to other, (-) molecule inactive 84 Early-Stage SEA Pipeline

Megan O’Meara, M.D. Vice President, Early-Stage Development SEA-CD40 Monotherapy with Evidence of Clinical and Biological Activity

Dose Responsive Innate Cytokine Induction SEA-CD40 monotherapy evaluated in Phase 1 with recommended dose of 30 mcg/kg every 3 weeks

Predominant toxicity was infusion related reactions; mitigated by slow infusion

Evidence of clinical activity observed in solid tumors and lymphomas Log2 Fold Change fromBaseline • Prolonged stable disease in heavily pre-treated tumors • 1 PR in basal cell carcinoma; 1 PR and 1 CR in follicular lymphoma Activated CD8+ T cells (CD69+)

Pharmacodynamic biomarker changes observed in patients support proposed MOA Log2 Fold Change fromBaseline 4H 24H 72H EOI1 168H

Grilley-Olson et al, ASCO 2018 PRE1 Neff La Ford et al AACR 2020 86 SEA-CD40 Phase 1 Trial in Frontline Metastatic Pancreatic Cancer

Enrollment ongoing with SEA-CD40 + pembrolizumab + gemcitabine + nab-paclitaxel

Phase 1 Study Design Adults with Key Endpoints: advanced Safety & Tolerability Advanced malignancies malignancies Objective Response SEA-CD40 by IV infusion or SC injection Rate

Frontline metastatic pancreatic cancer SEA-CD40 + pembrolizumab + gemcitabine + nab- paclitaxel Actively enrolling

Coveler et al ASCO 2020 87 Clinicaltrials.gov: NCT02376699 Clinical Vignette: Pancreatic Cancer Patient Treated with SEA-CD40 + PD-1 + Chemo with Deep and Durable Response

80 yr-old woman with pancreatic cancer Months on Treatment • Surgical resection  gemcitabine + cisplatin  capecitabine + radiation 0 2 4 6 8 10 12 • Pancreatic tumor recurred with abdominal metastases 0% -10% Treated with SEA-CD40 + pembro + gemcitabine + nab-paclitaxel • Adequately tolerated without dose-limiting toxicities -20% • Stopped chemo after cycle 11 due to fatigue; continued SEA-CD40 + pembro -30% -40% Partial response at cycle 4, deepening over time -50% Remains on-treatment ~ 1 year without progression Change Sizein Tumor Change -60%

Tumor Reduction on CT Scan (all 4 target lesions decreased in size) Monocyte activation CD8+ T cell activation C1D1 C2D1 C4D1 C5D1 C9D1 C1D1 C2D1 C4D1 C5D1 C9D1

Baseline Month 10 88 SEA-TGT Phase 1 Trial Ongoing in US and Europe

Dose escalation Dose expansion

Malignant melanoma Advanced solid Primary Objectives: tumors and Non-small cell lung cancer • Safety lymphomas • Tolerability Gastric cancer • Identify MTD

Head and neck cancer Key Secondary Breast cancer Objectives: • Antitumor activity Ovarian cancer • PK

DLBCL

SEA-TGT + PD-1 Combo Cohorts

Clinicaltrials.gov: NCT04042480 89 SEA-TGT Pharmacodynamic Changes Observed at 1st Dose Level

Phase 1 monotherapy dose escalation cohorts enrolling solid tumors and lymphomas

Pharmacodynamic changes consistent with MOA observed early in dose escalation

STRONG TIGIT ENGAGEMENT AND REDUCTION IN TREGS SEEN IN BOTH PATIENTS ENROLLED IN COHORT 1 Evidence of SEA-TGT biological activity at lowest dose

TIGIT Expression on Tregs Decrease in Tregs

SEA-TGT SEA-TGT SEA-TGT SEA-TGT

001 001 002 002 - treatment) Free TIGIT (% Tregs) (% TIGIT Free Tregs (% of Pre

90 SEA-BCMA Blocks Proliferative Signaling and Displays Enhanced ADCC

B-cell Maturation Antigen (BCMA): • Validated target expressed on myeloma • Minimal normal tissue expression • Mediates cell proliferation and survival • Ligands APRIL and BAFF bind to BCMA and mediate pro-survival cellular signals

Proposed MOA based on preclinical data 91 SEA-BCMA Phase 1 Study Ongoing in R/R Multiple Myeloma

Monotherapy expansion cohorts “A” vs “B” ongoing to determine optimal dosing schedule

SEA-BCMA + dexamethasone cohort “C” ongoing to evaluate safety and activity in combination

Dose escalation A Additional Expansion Dose Level 5 Monotherapy Expansion B Dose Level 4 Intensified Dosing Monotherapy Cohort Dose Level 3 C Dose Level 2 SEA-BCMA + Dexamethasone Dose Level 1 Combo Cohort

92 Clinicaltrials.gov: NCT03582033 Clinical Vignette: VGPR Achieved in Late-Line Myeloma with SEA-BCMA Monotherapy

83 year-old man with IgG lambda light chain myeloma relapsed/refractory after 6 prior lines of therapy • Enrolled on 1600mg every 2 weeks escalation cohort • Achieved very good partial response (VGPR) at Cycle 1 with >90% reduction in serum free light chains (sFLC) • Remained on treatment until progression after 8 months • Study drug was well-tolerated with only 1 related AE (worsening of baseline Grade 1 hypertension to Grade 2)

BCMA+ myeloma cells in bone RAPID DECREASE OF SFLC AFTER 1ST DOSE COMPLETE BCMA SATURATION AT C2D22 marrow at baseline

Free membrane BCMA Baseline 30000 C2D22 (mg/L) 20000 sFLC 10000 Not detectable

Free membraneFree BCMA MFI 0 Baseline 10003-0015 C2D22

Months from C1D1

93 SEA-CD70 May Impart Anti-tumor Activity Through Multiple MOAs

CD70 is Expressed in Myeloid Malignancies (IHC)

AML with antecedent MDS AML AML

Global Phase 1 study ongoing in MDS and AML • Initial monotherapy trial • Potential for addition of combination cohorts

Regional collaboration with 94 Seagen data on file Four SEA Empowered Antibody Programs are in Ongoing Phase 1 Trials

ADCC Killing of Antigen (+) Cells Receptor Clustering & Agonism Receptor Agonism/Synapse Formation

Myeloid Cells Myeloid Cells

T Cells

FcyRIIIa SEA-BCMA FcyRIIIa SEA-CD40 FcyRIIIa SEA-TGT (CD16) (CD16) (CD16) SEA-CD70 NK Cells T Cells NK Cells SEA-TGT Monocytes

Program Disease Area SEA MOA

SEA-CD40 Pancreatic cancer Enhanced Immune Agonism/ADCC

SEA-TGT Solid tumors and lymphomas Enhanced Immune Agonism/ADCC

SEA-BCMA Multiple myeloma Enhanced ADCC

SEA-CD70 AML and MDS Enhanced ADCC

Clay Siegall, Ph.D. President and CEO Seagen is Well-Positioned to Deliver on our Strategy for Growth and Achieve our Mission of Addressing Unmet Needs of Cancer Patients

Maximize Advance Innovate Pursue the potential of our our late-stage programs in R&D to maintain strategic corporate three approved toward securing a robust early-stage development products approvals pipeline opportunities that meet for new products of novel targeted our criteria therapies Question and Answer Period