Proprietary Pipeline of Dual-Angiogenic & IO-Engaging (4-1BB) Bispecific Antibodies

TR009 (DLL4/VEGF BsAb) as a SINGLE AGENT Stabilized or Shrank 71% of tumors in 4th

Line+ Metastatic Gastric and Colorectal patientso Specific inhibitor of VEGF and DLL4/Notch1 pathways; MOA targets both tumor angiogenesis

and cancer stem cells (CSCs); overcomes multi-VEGF, EGFR, PD1/PDL1 resistance

o 38% gastric cancer patients had =>20% tumor shrinkage; 1 PR patient (tx ongoing)

o Unique DLL4 epitope binding vs. 2 other agents in class establishes differentiated safety profile

o Flagship Molecule with multiple solid tumor indications (next generation Avastin®)

2 Key TR009 Clinical Data Readouts Expected in 2020 (n=55), Fully Fundedo Phase 1B Monotherapy Expansion and Phase 1B Combination with Chemo/anti-PD1/PDL1

o Plan for FDA Phase 2 Master Protocol Filing (2021E); NMPA China/Japan Phase 2 IND(2021E)

o Plan for 4-1BB/BCMA first in class bispecific (multiple myeloma) to enter clinic H1’2021E

TRIGR Therapeutics was incorporated in April 2018 (Delaware)o $10M seed round financed the execution of 2 Global in-licensing agreements from ABL Bio

o Efficient corporate leadership and advisory structure

TRIGR Therapeutics Summary

Our Mission is to Develop Meaningful Treatments for Cancer Patients Worldwide

2

3 Bispecific Antibodies in the Pipeline(In-Licensed from TRIGR HOLDS GLOBAL DEVELOPMENT & COMMERCIAL RIGHTS*)

Proprietary Bispecific Antibody (BsAb) Platform Binds 2 Different Targets in One Molecule: o Conserves stability attributes of 1st generation mAb structure (IgG, Fc for PK/PD, symmetric tetravalent binding)

o Proprietary clones designed to enhance specificity / overcome toxicities known to other drugs in the class

Immune Cell Engaging BsAb (TRIA001 and TRIA002):

o Tumor Antigen Dependent 4-1BB crosslinking for tumor micro-environment localized immune cell activation

(reducing potential systemic toxicity, CRS – no liver tox seen in vivo with 41BB clone)

Pipeline Target Indication Phase 1A Phase 1B

TR009VEGF/DLL4

(Dual Angiogenic/DLL4

Notch1 Blocker)

Gastric, Colorectal, Ovarian, Pancreatic, NSCLC, GBM, TNBC, HCC

CompletedDose Expansion

&Combination

TRIA001*4-1BB/BCMA

(Immunotherapy)

Multiple MyelomaFirst in Class

INDQ1, 2021E

TRIA0024-1BB/+IO CheckPoint

(Immunotherapy)

Solid TumorsFirst in Class

INDQ4, 2021E

Off-the-shelf Alternative to CAR-T

ABL Bio retains S Korea rights to all compounds; TRIGR holds GLOBAL rights to all compounds, *Excluding Japan & certain Asia Pacific territories.

3

Leadership & Clinical Advisory Board

CORPORATE LEADERSHIP

George Uy (CEO, Founder), 35 yrs biopharma commercial leadership experience

Miranda Toledano (COO, CFO), 20 yrs biopharma / Wall St leadership experience

ACADEMIA

Professor Edward Chu MD, M.M.S. UPMC Hillman Cancer Center, University of Pittsburgh

Professor Yung-Jue Bang, MD, Seoul National University College of Medicine and Hospital

Professor Eric Van Cutsem, MD, PhD University of Leuven

Professor Howard Hochster, MD, Rutgers Robert Wood Johnson Medical School

Professor Jin Li, MD, Tongji University Shanghai East Hospital

Professor Patricia M. LoRusso, DO, Yale Cancer Center

PHARMA EXPERIENCE

Dr. Jean-Pierre Bizzari, MD former EVP and Global Head of Oncology at Celgene, Sanofi-

Aventis, Servier

Dr. Joanna Horobin M.B., Ch.B., former CEO Syndax, CMO (Verastem/ Idera), Sanofi

Dr. Ye Hua, MD, MPH, CEO Bionova, former Clinical Head at Hutchison MediPharm

4

5

TR009(Anti-VEGF/DLL4 BsAb)

Anti-Angiogenesis TherapyA Cornerstone in Oncology Treatment

Source: Company reports; 2011 Sep 15;71(18):6073-83. doi: 10.1158/0008-5472.CAN-11-1704. Epub 2011 Jul 29.

* IMBrave150 ph3 study

6

UNMET MEDICAL NEED

Anti-VEGF

mAbs

USD $7.6 B

Anti-Angiogenic

USD $18 B

Anti-VEGF therapy results in more

INVASIVE and METASTATIC

phenotypes

REGRESSION of VEGF-dependent

tumor blood vessels

FORMATION of normalized VEGF-

independent tumor blood vessels

VEGF ALONE CANNOT DESTROY ALL

TUMOR VESSELS

RESISTANCE TO ANTI-VEGF THERAPY

2018 Sales

USD $6.7 Billion

FDA APPROVED

Colon Cancer

Lung Cancer

Ovarian Cancer

Kidney Cancer

Brain Cancer (GBM)

POSITIVE PH3

Liver Cancer (+Tecentriq)*

2018 Sales

USD $821 Million

FDA APPROVED

Colon Cancer

Gastric Cancer

Lung Cancer

Liver Cancer

POSITIVE PH3

Bladder Cancer (PFS)

2018

FDA APPROVED

Colon Cancer

2018 Sales

USD $108 Million

Validated Target

The Problem

Bispecific Approach

DLL4-mediated NOTCH1 signaling represents an essential pathway for

vascular development of tumors and cancer stem cells, thus an

attractive target for angiogenesis-based cancer therapies

Historical cardiotoxicity attributed to DLL4-targeted monoclonal

antibodies raised serious safety concerns despite decent single agent

activity (Regereron/MedImmune/Celgene/Oncomed)

Efficacy: Dual blockade of VEGF/DLL4 shown to overcome VEGF

Resistance pre-clinically and now across 200 patients (TRIGR, ABBVIE,

OMED/MEREO)

Safety: Blocking both DLL4 and VEGF appears to limit the VEGF-

induced vascular sprouting (cardiox) which occurred with DLL4-mabs;

however, both ABBVIE and OMED/MREO had to significantly expand

their Phase 1a trials due to safety signals

Validated TargetDLL4-mediated NOTCH signaling represents an essential pathway for

vascular development of tumors and cancer stem cells, thus an

attractive target for angiogenesis-based cancer therapies

Historical cardiotoxicity attributed to anti-DLL4 monoclonal antibodies

raised serious safety concerns and curtailed their therapeutic

development despite single agent activity

(Regereron/MedImmune/Celgene/Oncomed)

Why Target DLL4/NOTCH As an Alternate Angiogenic

Mechanism To Overcome Primary VEGF-Resistance?

The Problem

7

3 Dual VEGF/DLL4 Bispecific Antibodies in the Clinic

8

PHASE 1A (MONOTHERAPY)Total Evaluable: 21 patients COLORECTAL/GASTRIC

Stable Disease: 14/21 (66%)

Partial Response: 1/21 (5%)

TETRAVALENT- BINDS TWO VEGF/DLL4

HTN (~50%); pulmonary HTN (1 case, 0.5% and Grade 1); NO DLT as of

12.5mg/kg dose

vs. ABT165: separation of binding sites, less steric hindrance (no cardiotxreported at any dose)

vs. navicixizumab: different DLL4 epitope, superior anti-tumor effect in pre-clinical head to head comparisons (no cardiotxreported at any dose)

PHASE 1A (MONOTHERAPY)Total Treated: 55 patients COLORECTAL/OVARIAN

Stable Disease: 30/55 (55%)Partial Response: 5/55 (11%)

TETRAVALENT- BINDS TWO VEGF/DLL4

HTN (55.6%), proteinuria (9.3%), pulmonary HTN (7.4%), GI perforation (3.7%) and STROKE

(1.9%)DLT/SAE reported as of 2.5mg/kg dose

PHASE 1B COLORECTAL (+FOLFIRI)

PHASE 2 COLORECTAL (+FOLFIRI)Vs AVASTIN+FOLFIRI N=100 pts

Initiated Q1’18 – ACTIVE NOT RECRUITING

Poster at EORTC-NCI-AACR, 2016 *ESMO 2018 Poster

** Historical RR in heavily pre-treated platinum resistant OC <15% Presented ASCO 2016

VEGF Dll4 VEGF

Dll4 Dll4

VEGFTR009

VEGF VEGF

Dll4 Dll4ABT-165

Navicixizumab

PHASE 1A (MONOTHERAPY)Total Treated: 66 patients COLORECTAL /OVARIAN

Stable Disease: 19/66 (29%)

Partial Response: 4/66 (6%)

BIVALENT – BINDS ONE VEGF/DLL4

HTN (58%),Pulmonary HTN (18%), BNP elevation, DLT/SAE concern as of 1mg/kg

PHASE 1B* (+PACLITAXEL) OVARIAN(Platinum resistant, prior Avastin & paclitaxel)

Unconfirmed ORR: 41%mPFS= 7.3 mosPulmonary HTN, peripheral edema, GRADE 1

HEART ATTACK

UNDER STRATEGIC REVIEW

PHASE 1B COMBINATION STUDY

(n=12-15)

▪ TR009 + Irinotecan (Gastric, Colorectal)

▪ TR0009 + Paclitaxel (Gastric, Ovarian)

▪ TR009 + PD-1/PD-L1 (partner

dependent)

Start: March 2020E (data H2’20)

9

Note: TR009 Monotx (single agent) is dosed Q2 weeks (28-day cycle)

*Assuming we finish all dose cohorts and launch combotx arm in Korea

Cohort 10.3mg/kg

Cohort 2(1mg/kg)

Cohort 3 (2.5 mg/kg)

Cohort 4

(5 mg/kg)

Cohort 5(7.5 mg/kg)

Cohort 6(10 mg/kg)

Cohort 7(12.5 mg/kg)

PHASE 1B MONOTHERAPY

EXPANSION STUDY (n=15)

▪ 3 cohorts: 7.5mg/kg – 12.5mg/kg

▪ PK/PD and RP2D

▪ DLL4 IHC at baseline

▪ Gastric, CRC, Other DLL4-driven

indications (Ovarian, HCC, Lung,

Pancreatic)

Start: December 2nd, 2019 (data H1’20)

Patient Population• Age > 19 years• Advanced metatstatic/non-resectable

solid tumors• Progressed on prior treatment• ECOG 0-2

Endpoints• Safety, tolerability, toxicity• MTD• PK/PD• Biomarkers; VEGF, soluble NOTCH 1,

soluble VEGFR-2, etc.

TR009 Phase 1A/1B Program Plan (N=54-60 patients)

Phase 1A Ongoing

Q4 2019E Completion

(n~21-27)

Cohort 8(15 mg/kg)

Cohort 9(17.5 mg/kg)

DOSE

ESCALATION

TR009 Phase 1 Dose Escalation: Clinical Benefit Rate of 71%

10*Unconfirmed

Dose Level Primary MalignancyBest Response /

Tumor Change (%)

Duration of Response

Days Months

0.3 mg/kg Gastric (PT 2) SD / -5% 127 4.2

Cholangiocarcinoma (PT 4) PD / 30% 42 1.4

Gastric (PT 5) PD / 75% 43 1.4

1.0 mg/kg Malignant melanoma (PT 7) PD / -13% 37 1.2

Colorectal (PT 10) SD / 4% 288 9.5

Ovarian (PT 11) SD / 3% 119 3.9

2.5 mg/kg Gastric (PT 12) SD / -17% 65 2.1

GIST (PT 13) SD / 7% 84 2.8

Colorectal (PT 14) PD / 23% 43 1.4

5 mg/kg Colorectal (PT 15) SD / 8% 214 7.0

Colorectal (PT 16) SD / 0% 289 9.5

Colorectal (PT 18) SD / -9% 92 3.0

7.5 mg/kg Colorectal (PT 19) PD / 9% 52 1.7

Gastric (PT 20) SD / -11% 138 4.5

Gastric (PT 21) SD / -20% 170 5.6

10.0 mg/kg Gastric (PT 23) SD / -26% 86 2.8

Colorectal (PT 24) PD / 7.7% 47 1.5

Gastric (PT 25) SD / -5% 169 5.6

12.5 mg/kg Colorectal (PT 26) SD / 15% 136 4.5 (RX ONGOING)

Gastric (PT 27) PR* / -40% 137 4.5 (RX ONGOING)

Colorectal (PT 28) SD / 4.3% 133 4.4 (RX ONGOING)

PR: POSITIVE DLL4 IHC (tumor and blood vessel)

Phase 1A Update

(Unaudited, as of

January 10th, 2020)

11

TR009 SINGLE AGENT ACTIVITY

Inherent Differences in Gastric Patient vs. Colorectal Patient

Response

-/-

NA

-/+

-/-

NA -/- NA -/-NA -/+ -/-

NA

-/- NA-/+

NA-/+

+/+-/-

-/-

+/+

-60.0%

-40.0%

-20.0%

0.0%

20.0%

40.0%

60.0%

80.0%

100.0%

0.3 0.3 2.5 12.5 7.5 5 10 2.5 12.5 1 1 5 10 0.3 5 7.5 1 2.5 7.5 10 12.5

% C

ha

ng

e in

Tu

mo

r S

ize

Waterfall Plot - All Evaluable Patients (N=21)

PR: 1

SD: 14

DLL4 Status (Tumor/Vessel)Negative –Positive +

Not applicable NA

Colorectal Cancer Gastric CancerOthers

Site of DLL4 Expression May Explain Differences in Clinical

Responses (Tumor Shrinkage vs. Long Disease Stabilization)

12DATA PRESENTED ARE PRELIMINARY & UNAUDITED

Patient Dose

(mg/kg)

MaxChange Tumor

Size (%)

DOR

(Months)

S002 0.3 -5% 127 days (4.2)

S012** 2.5 -17% 65 days (2.2)

S020 7.5 -11% 138 days (4.5)

S021** 7.5 -20% 170 days (5.6)

S023* 10 -26% 86 days (2.8)

S025* 10 -5% 169days (5.6)

S027* 12.5 -40% 137 days (4.5)(Rx Ongoing)

Patient Dose(mg/kg)

MaxChange

Tumor Size (%)DOR

(Months)

S010 1 4% 288 days (9.5)

S015 5 8% 214 days (7.0)

S016 5 0% 289 days (9.5)

S018 5 -9% 92 days (3.0)

S026 12.5 15% 136+days(4,5)(Rx Ongoing)

S028 12.5 4% 133+days(4.4)(Rx Ongoing)

Dll4 Expression48% Cells

22% Stroma

Dll4 Expression 71% Endothelial Cells

(Blood Vessels)

GASTRIC

Evaluable Patients = 8

Partial Response=1

Stable Disease=6

Clinical Benefit= 87.5%

COLORECTAL

Evaluable Patients = 9

Stable Disease=6

Clinical Benefit= 66.7%

Direct Tumor shrinkage may be due to DLL4-high expression

in on cancer cells and stroma

References: Clinical implications of DLL4 expression in gastric cancer. Ishigami, et al. Journal of Experimental & Clinical Cancer Research 201332:46

* PRIOR RAMUCIRUMAB **PRIOR RAMUCIRUMAB+NIVO/PEMRBOALL PATIENTS W PRIOR ANTI-VEGF (AVASTIN, REGORAFENIB, OR CETUXIMAB)

Tumor Growth Stops

Direct Tumor Killing

DLL4 expression contained in blood vessels seems to

halt tumor growth, with long term duration

13

Gastric Patients Prior Treatment Regimens and TR009 Tx DurationMean of Responders (PR + SD): 4.13 months

4.17

1.41

2.14

4.53

5.59

2.83

5.55

4.5

S-1, Cape+Cis,Tax, Irinotecan, FOLFOX, FOLFIRI

S-1, Cape+Cis, Ram+Pac, Irin

TS-1,FOLFIRI, VEGR-2+PAC, NIVO, NIVO+Pac

Cape+Oxaliplatin

HERCEPTIN+Cape+Cis; VEGF-R2 +PAC, Irinotecan, PD-1, Capox

Capox, VEGF-R2 +Paclitaxel

Paclitaxel, VEGF-R2 +Pacllitaxel, Irinotecan

Xelox, VEGF-R2 +Pac, Irinotecan, Oxali PR

SD

SD

SD

SD

SD

SD

PD

(Rx Ongoing)

MONTHS

0.3 MG/KG

0.3 MG/KG

2.5 MG/KG

7.5 MG/KG

7.5 MG/KG

10 MG/KG

10 MG/KG

12.5 MG/KG

0 1 2 3 4 5 6

PT 27, -40%

PT 25, -5%

PT 23, -26%

PT 21, -20%

PT 20, -11%

PT 12, -17%

PT 5, 75%

PT 2, -5%

Note: Mean treatment duration does not account for ongoing patients at higher doses

14

Colorectal Patients Prior Treatment Regimens and TR009 Tx DurationMean of Responders (SD): 7.25 months

9.5

1.4

7

9.5

3

1.7

1.5

4.47

4.37

1.0 MG/KG

2.5 MG/KG

5.0 MG/KG

5.0 MG/KG

5.0 MG/KG

7.5 MG/KG

10 MG/KG

12.5 MG/KG

12.5 MG/KG

AVASTIN+FOLFOX, AVASTIN+FOLFIRI, REGORAFENIB, XELODA

FOLFOX, AVASTIN+FOLFIRI, XELODA, REGORAFENIB, 5FU/LV

CAPE, CCRT+CAPE, XELODA, AVASTIN+FOLFIRI, AVASTIN+FOLFOX, REGORAFENIB, KEYTRUDA

5FU, CAPE, AVASTIN+FOLFIRI, CAPE, REGO

CETUXIMAB+FOLFIRI, AVASTIN+FOLFOX, CAPE, 5FU/LV

CETUXIMAB+FOLFIRI, AVASTIN+FOLFOX, CAPE, CKD516/IRI, SIROLIMUS

FOLFOX, AVASTIN+FOLFIRINOX, AVASTIN+FOLFOX

AVASTIN+FOLFIRI, AVASTIN+FOLFOX, AVELUMAB

AVASTIN+FOLFIRI, AVASTIN+FOLFOX,

SD

SD

SD

SD

SD

SD

PD

PD

PD

MONTHS

(Rx Ongoing)

(Rx Ongoing)

0 1 2 3 4 5 6 7 8 9 10

PT 28, 4%

PT 26, 15%

PT 24, 7%

PT 19, 9.4%

PT 18, -9%

PT 16, 0%

PT 15, 8%

PT 14, 23%

PT 10, 4%

Note: Mean treatment duration does not account for ongoing patients at higher doses

15

G1 G2 G3 G4 G5 Total

No. % No. % No. % No. % No. % No. %

Hypertension 4 16.7 4 16.7 4 16.7 12 50

Anemia 2 8.3 1 4.2 3 12.5

Epigastric Pain 1 4.2 2 8.3 3 12.5

General Weakness 2 8.3 1 4.2 3 12.5

Constipation 2 8.3 1 4.2 3 12.5

Abdominal Pain 2 8.3 2 8.3

Alkaline Phosphatase Elevated 2 8.3 2 8.3

Headache 2 8.3 2 8.3

Hypoalbuminemia 1 4.2 1 4.2 2 8.3

Insomnia 2 8.3 2 8.3

Malignant Neoplasm Progress 1 4.2 1 4.2 2 8.3

Upper Respiratory Infection 1 4.2 1 4.2 2 8.3

Pulmonary Hypertension 1 4.2 1 4.2

Other TEAE Occuring <5% 8 0.3 12 0.5 7 0.3 0 0 0 0 27 113

Treatment-Emergent AE by Grade

TR009 Mono Vs Approved 3+L Gastric Cancer Treatments

16

CYRAMZA®Ramucirumab

Eli Lilly (VEGF-R2 mab)

AITAN®Apatinib

Hengrui China (VEGF-R2 TKI)

TR009Anti-VEGF/DLL4

TRIGR

Clinical Trial Phase 3 REGARD 2:1 vs. placebo

Phase 3(2:1 vs Placebo)

Phase 1a (Single arm)

PatientsN=355 (238 Cyramza vs. 117

placebo); 2L/NO prior VEGFs

N=273 (176 Aptanib, 91 Placebo)

3L/NO prior VEGFs

N=84L+; 88% had Prior VEGF-

R2/Cyramza®, HER-2/Herceptin®, PD-1/PD-1

Treatment IV, MONO ORAL MONO IV MONO

RR 3% 2.8% 13%

SD /DCR 49% 42% 88%

mPFS 2.1 m 2.6mDuration of Tx: 4.13m

(mean)

mOS 5.2m 6.5m NA

GR3/4 Toxicity

16% Hypertension; other no diff from BSC

9% GR 3/4 Hand Foot Syndrome, HPN, Proteinuria,

Neutropenia

NO DLTGr2/3 HPN Gr3 Anemia

17

STIVARGA®Regorafenib

Bayer

LONSURF®Trifluridine/tipiracil

Taiho/Servier

ELUNATE®fruquintinib

Chi-Med

TR009Anti-VEGF/DLL4

TRIGR

Clinical Trial Phase 3(2:1 vs Placebo)

Phase 3(2:1 vs Placebo)

Phase 3(2:1 vs Placebo)

Phase 1a (Single arm)

PatientsN=505 (Stivarga); Multiple

prior tx including Avastin®, Erbitux®

N=534 (Lonsurf); Multiple prior txs

including Avastin®, Erbitux®

N=278 (Elunate)2L+; 60% NO prior anti-

VEGF (Avastin®/anti-EGFR

N=94L+; 100% had Prior Avastin®, Erbitux®,

Stivarga®, PD-1/PD-l1

Treatment Oral, MONO Oral, MONO Oral, MONO IV MONO

RR 1% (PR) 1.6% 5% (1CR) TRIAL ONGOING

SD /DCR 41% 44% 62% 67% (6/9)

mPFS 1.9 m 2m 3.7m SD mean 7.25m

mOS 6.4m 7.1m 9.3m NA

GR3/4 Toxicity

17% HFS, 10% fatigue, 7%HPN, diarrhea

50% Neutropenia GR3 21% HPN; 11% HFS

NO DLTGr2/3 HPN Gr3 Anemia

TR009 Mono Vs Approved 3+L MCRC Therapies

TR009 Key Points to Consider

Preliminary Clinical Activity Seen with TR009 MONOTHERAPY Indicates a Clinical Benefit Rate

(CBR) of 71%

o Blocks VEGF and DLL4/Notch1 pathways targeting tumor angiogenesis and cancer stem cells (CSCs)

o Gastric cancer- 88% CBR (SD + PR); mean treatment duration of 4 months

o Colorectal Cancer - 66% CBR (SD); mean treatment duration of 7.25 months

o Gastric PR patient had POSITIVE DLL4 IHC in both tumor cells and blood vessels

o CBR of 71% > both Abbvie (65%) and Oncomed (35%) reported Phase 1A

Tolerability Profile of TR009 Appears Superior to Both Navicixizumab and ABT-165

o Perhaps driven by unique DLL4 epitope of TR009; enables greater combineability with IO/chemoo No expansion of Phase 1A dose escalation required due to safety concerns

o No DLT or SAE reported as of 12.5mg/kg (No Stroke, Heart Attack, BNP elevation, and 1 case of grade 1

Pulmonary Hypertension)

Phase 1B Monotherapy Expansion Will Prioritize DLL4 Driven Tumors (Gastric, Colorectal,

Ovarian, HCC, Pancreatic, Lung) – open label study, data expected in H1’20

Phase 1B Combination Study Will Explore TR009 in Combination with Standard Chemotherapy

Backbones in Colorectal and Gastric Patients – open label study, data expected in H2’20

FDA pre-IND mtg planned in H2’20 for Phase 2 initiation as master protocol

18

TRIGR

IMMUNE ~ CELL ACTIVATORS

T R I A - 0 0 1

T R I A - 0 0 2

19

AGONISTIC STIMULATION OF 4-1BB CAUSES:

CD8+ T cells: Enhance proliferation, differentiation to memory cells, resistance to apoptosis, IL-2 and IFN-γ production

Dendritic cells (DC): Enhance tumor antigen presentation by upregulation of B7 co-stimulatory molecules (CD80, CD86)

Natural Killer (NK) cells: Enhance ADCC, IL-2 and IFN-γproduction

Regulatory T cells (Treg): Repress Treg function

20

4-1BB (CD137) Mediates Important

Immune Function Within the Tumor

Micro-Environment

4-1BB (CD137) is an inducible co-

stimulatory molecule on CD4+ T cells,

CD8+ T cells, regulatory T cells (Treg) and

NK cells, and DC

URELUMAB/BMS

Clinical Experience

Phase 1&2 (n=346)

o ORR=50% (n=46 Melanoma)

combination with Nivolumab

o Responses seen regardless of PDL1

status

o Significant hepatotoxicity at 1

mg/kg or above.

o Clinical development terminated

However, Significant Liver

Toxicity Was Seen with

Agonistic 4-1BB mAbs

PHASE 1

21

Urelumab

Utomilumab

Antigen Presenting Cell

4-1BBL

4-1BB

Activated T cell

TRIGR’s anti-41BB (1A10) Targets Different Epitope

BMS PFIZER

TRIA anti-41BB

1A10

o TRIGR’s anti-4-1BB antibody (1A10) binds to unique epitope (CRD4) and does not compete with 4-1BBL for binding to 4-1BB receptor

o TRIGR’s anti-41BB are engineered to activate upon cross-linking with target tumor antigens (TAA) within thetumor micro-environment

o Repeated doses of up to 75 mg/kg of 1A10 as anti-PD1/41BB have been administered to cynomolgus monkeys safely. No clinically relevant increases in liver chemistry

CRD: cysteine rich domain

✓ First in Class 4-1BB / BCMA BsAb

✓ 4-1BB selectively activates immune cells (T, NK

cells) in the tumor microenvironment

✓ IP: Proprietary 4-1BB clone targets different epitope

to urelimab or utomilumab

✓ Low cytokine release with high cell lysis; also,

shown to induce memory (CD-4) T cells in tumor

re-challenge in vivo experiment

✓ Repeated doses of up to 75 mg/kg of 1A10 as

BsAb have been safely administered to

cynomolgus monkeys. No clinically relevant

increases in liver chemistry

✓ TRIA-001 offers an off the shelf alternative to CAR-T

for MM

✓ IND Q1’2021E

T Cells NK Cells

4-1BB4-1BB

BCMA BCMA

22

TRIA-001(4-1BB/BCMA)

98% of Multiple Myeloma cells

express the BCMA protein or RNA1

1. Cancer cell (2017) 31,1-15

TRIA001 Treatment Resulted in Tumor Growth Inhibition and Expansion of TIL

Anti-Tumor Activity

0

10

20

30

40

CD45 staining

CD

45 H

PF

Tumor PeriTumor

Tumor PeriTumor

Tumor PeriTumor

Isotype 5D5 BiSP 5A6 BiSP

0

5

10

15

CD8 staining

CD

8 H

PF

Tumor PeriTumor

Tumor PeriTumor

Tumor PeriTumor

Isotype 5D5 BiSP 5A6 BiSP

hIgG

CD45

CD8

Tumor Peritumor

BCMAx4-1BB

(TRIA001)

hIgG

BCMAx4-1BB

hIgG BCMAx4-1BB

(TRIA001)

hIgG

BCMAx4-1BB

HPF : High-power field

TIL: Tumor infiltrated lymphocyte

Tumor removal and weighing

Tumor fix and IHC staining

(CD45, CD8)

Tumor injection

(5x106 S.C.) TRIA001 treatment (BIW, i.p, 7 doses)

BIW 7 doses

hIgG (10 mpk, No purified T cell)

BCMAx4-1BB (10 mpk, purified T cell)

hIgG (10 mpk, purified T cell)

NOG mice engrafted with BCMA+ H929 tumor and human T cells were used

Increased CD45+ and CD8+

cells in tumor

23

BCMA CAR-T vs. BCMA/CD3 BsAb

24

JNJ-4528/LCAR-B38M

(ph1b n=29)

ORR- 100%

(69% CR/sCR, 86%VGPR)

27/29 pts progression free at

6 mos

93% CRS

1 CRS death

86% triple refractory to PI, IMiD, and anti-CD38 antibody

CARTITUDE-1 STUDY Phase 1bASH 2019

BB21217

(ph2, N=140)

ORR- 83%

(33% sCR, 50%, VGPR)

mDOR 11.1 mos

66% CRS

1 GR5 CRS

*95% received prior PI, IMiD, and anti-CD38 antibody, 84% refractory to IMiD, PI, CD38.

ORR/PFS from high dose group cohort

KarMMa STUDY Ph2ASH 2019

CC-93269

(ph1, n=30)

ORR- 89%

(44% CR/sCR, 50%, VGPR)

No sign ds progression at 7 mo+

76% CRS

1 CRS death

*Nearly all pts received prior PI, IMiD, and anti-CD38 antibody, 67% refractory to IMiD, PI, CD38.

ORR/CR for 10 mg dose cohort

CC-93269 STUDY Phase 1ASH 2019

Anti-BCMA BsAB as Active as CAR-T Therapies in

Multiple Myeloma

Immune

Checkpoint

T Cells NK Cells

Immune

Checkpoint

4-1BB4-1BB

25

Immune Checkpoint / 4-1BB BsAb

First in Class – BIOMARKER DRIVEN

TAA mediated 4-1BB activation observed

in vitro and induce lysis of target TAA

expressing tumor cells

IND filing Q4’2021E

B7 Homolog Family

Down-regulates the body’s immune

system

Highly over-expressed in Breast,

Lung, Ovarian, and Endometrial

tumors

TRIA-002(4-1BB/Undisclosed Immune Checkpoint)

THANK YOU

George Uy

CEO & FOUNDER

guy@TrigrRx.com

001 949 648 0705

Miranda Toledano

COO & CFO

Miranda.toledano@TrigrRx.com

+972-58-55-88-470

26

APPENDIX

27

Founded in S Korea in 2016, 50+ employees

IPO KOSDAQ (KS 298380): $90M at $680M market cap (2018)

Bispecific Antibody (BsAb), Blood-Brain-Barrier (BBB) Penetrating BsAbs, and Antibody Drug Conjugates (ADC) core tech platforms

Global partnerships with TRIGR Rx, iMab Biopharma, LegoChem, Wuxi Biologics

Oncology and Neurodegenerative Disease Focus

Background on Our R&D Partner: ABL Bio

LICENSE & COLLABORATION FRAMEWORK

Discovery, In vitro/ In vivo, Process

Development

ABL Bio

IND-Enabling Activities

ABL Bio/TRIGR

Clinical and Commercialization TRIGR

28

Our symbiotic alliance with ABL BIO enables efficient, low capital-intensive

development of our pipeline