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

TR009 (DLL4/VEGF BsAb) Stabilized or Shrank 71% of tumors in 4th Line+ Metastatic Gastric and Colorectal patients

o Shown to overcome VEGF, multi-VEGF, EGFR, PD-1/PD-L1 resistance o 38% gastric cancer patients had =>20% tumor shrinkage; PR patient (tx ongoing)o Unique DLL4 epitope binding vs. 2 other agents in class establishes differentiated safety profileo 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; Phase 1B +Paclitaxel/+Irinotecan (+PD-1 / L-1 under discussion)o Prioritizing DLL4-expressing tumors with exploratory biomarker work (IHC expression)o Plan for FDA Phase 2 Master Protocol Filing(2020E); NMPA Greater China 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 (ABL Bio)o Efficient corporate leadership and advisory structure

TRIGR Therapeutics SummaryOur 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: • Conserves stability attributes of 1st generation mAb structure (IgG, Fc for PK/PD, symmetric tetravalent binding)• Proprietary clones designed to enhance specificity / overcome toxicities known to other drugs in the class

Immune Cell Engaging BsAb (TRIA001 and TRIA002): • 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

• We plan to explore the combination of our 4-1BB IO engagers with TR009 (IO + dual-angiogenic backbone)

Pipeline Target Indication Phase 1A Phase 1B/2A

TR009VEGF/DLL4

(Dual Angiogenic Blocker)

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

12/2/2019

TRIA001* 4-1BB/BCMA(Immunotherapy)

Multiple MyelomaFirst in Class Q1, 2021E

TRIA002 4-1BB/+IO CheckPoint(Immunotherapy)

Solid TumorsFirst in Class Q4, 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 LEADERSHIPGeorge Uy (CEO, Founder), 35 yrs biopharma commercial leadership experienceMiranda Toledano (COO, CFO), 20 yrs biopharma / Wall St leadership experience

ACADEMIAProfessor Edward Chu MD, M.M.S. UPMC Hillman Cancer Center, University of PittsburghProfessor Yung-Jue Bang, MD, Seoul National University College of Medicine and HospitalProfessor Eric Van Cutsem, MD, PhD University of LeuvenProfessor Howard Hochster, MD, Rutgers Robert Wood Johnson Medical SchoolProfessor Jin Li, MD, Tongji University Shanghai East HospitalProfessor Patricia M. LoRusso, DO, Yale Cancer Center

PHARMA EXPERIENCEDr. Jean-Pierre Bizzari, MD former EVP and Global Head of Oncology at Celgene, Sanofi-Aventis, ServierDr. Joanna Horobin M.B., Ch.B., former CEO Syndax, CMO (Verastem/ Idera), SanofiDr. Ye Hua, MD, MPH, CEO Bionova, former Clinical Head at Hutchison MediPharm

4

5

TR009

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 BAnti-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 SalesUSD $6.7 Billion

FDA APPROVED Colon CancerLung Cancer

Ovarian CancerKidney Cancer

Brain Cancer (GBM)POSITIVE PH3

Liver Cancer (+Tecentriq)*

2018 SalesUSD $821 Million

FDA APPROVED Colon CancerGastric CancerLung CancerLiver Cancer

POSITIVE PH3 Bladder Cancer (PFS)

2018

FDA APPROVED Colon Cancer

2018 SalesUSD $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 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 anti-DLL4 monoclonal antibodies raised serious safety concerns and curtailed their therapeutic development despite single agent activity (Regereron/MedImmune/Celgene/Oncomed)

Why Target DLL4 As an Alternate Angiogenic Mechanism To Overcome Primary VEGF-Resistance?

The Problem

7

RP2D/MTD DLTs Most Frequent AEs SAEs

Enoticumab

(REGENERON)DISCONTINUED

4mpk Q3W and 3mpk Q2W;No MTD reached.

DLT:G3 nausea (0.5 mpk Q3W);G3 abdominal pain (1 mpk

Q2W)

Fatigue, nausea, vomiting,HBP, headache, anorexia

G1 BNP ↑ (0.25 mpg Q3W), G3 troponin I ↑(4 mpk Q3W),

G3 right ventricular dysfunction and G3 pulmonary hypertension (1.5 mpk Q2W),

G3 left ventricular dysfunction and G3 pulmonary hypertension (3 mg/kg Q2W)

Demcizumab

(ONCOMED)DISCONTINUED

G3 anemia and dyspnea (2.5mpk weekly), G3 colitis

with bleeding (2.5mpk Q2W), G4 HBP with G5 brain

metastases with bleeding leading to death (10mpk Q2W)

HBP or bloodpressure increased (47%),

fatigue (31%), anemia (22%), headache (20%),

nausea (13%), hypoalbuminemia,

dizziness, and dyspnea

Prolonged administration was associated with an increased risk of congestive heart failure

Navicixizumab

(ONCOMED)

RP2D 5mpk Q3W.G3 large intestine perforation

(2.5mpk)

HBP (57.6%), headache (28.8%), fatigue (25.8%), pulmonary hypertension

(18.2%)

Pulmonary hypertension was similar across the dose levels, its severity appeared to be dose dependent, incidence:

0.5- 5mpk: 7/36 (19.4%), 6 G1 and 1 G2;7.5-12.5mpk: 5/30 (16.6%), 1 G1, 3 G2 and 1 G3

ABT-165

(ABBVIE)

RP2D 3.75mpk Q2W, Combo with chemo 2.5mpk

Q2WG3 headache

G3 HBP

HBP (67.3%, G3 29.1%), fatigue (47.3%), headache

(43.6%), nausea (38.2%), decrease appetite (34.5%),

diarrhea (30.9%)

Pulmonary hypertension (10.9%), Gastro-intestinal Perforation (3.6%), Ischemic stroke (1.8%)

TR009

(TRIGR Rx)MTD not reached/no DLT

HPN (50%), anemia (16%), epigastric pain (13%)

No DLT in phase 1A study; 1 case pulmonary hypertension G1; no GI perforation or other cardiotox

Anti-DLL4 Toxicity Profile: TR009 Compares Favorably to Failed and Current Agents in the Class

8

Anti-DLL4 mAb

Anti-DLL4/VEGF

3 Dual VEGF/DLL4 Bispecific Antibodies in the Clinic

9

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

Stable Disease: 14/21 (66%)Partial Response: 1 (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 cardiotx reported 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 (COMPLETED) COLORECTAL/OVARIAN

Stable Disease: 30/55 (55%)Partial Response: 5 (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 (2.5mg/kg+FOLFIRI)

PHASE 2 COLORECTAL (ABT165 +FOLFIRI)Vs AVASTIN+FOLFIRI N=100 ptsInitiated 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 Dll4VEGF

Dll4 Dll4

VEGFTR009

VEGF VEGF

Dll4 Dll4ABT-165

Navicixizumab

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

Stable Disease: 19/66 (29%)Partial Response: 4 (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 ATTACKUNDER STRATEGIC REVIEW

o Gastrico Colorectalo Ovariano Intrahepatic biliary tracto NSCLCo Triple Negative Breast o 1st/2nd line GBM o Pancreatic Cancer

Boosting clinical benefit of existing standards of care

o 3rd/4th line Gastrico 3rd/ 4th line Colorectal o Other DLL4 Driven

Tumors

Basket trial designPotential biomarker

driven label

Safety, tolerability, toxicityExtend survival

TR009: Positioned as Dual-Angiogenic Flagship MoleculeMultiple Targeted Indications, Global Clinical Strategy

DLL4-High IndicationsM O N O T H E R A P Y

DLL4-High Indications+ C H E M O T H E R A P Y

o Gastric Cancer*o Colorectal Cancer*o HCC**o NSCLCo Bladder Cancero Pancreatic Cancer

*Regorafenib+Nivolumab shown to improved ORR/mPFS in 3L+ GC/CRC in

ph1b (ASCO19 abstract#2522)

**TECENTRIQ+AVASTIN shown to improved OS in 1L HCC in ph3(vs sorafenib)

IMBrave150 study

Overcome Checkpoint Resistance; Synergy with IO to improve ORR, PFS,

or OS

DLL4-High Indications+ A N T I - P D 1 / P D L - 1

10

11

TR009Phase 1A

UPDATE OF CLINICAL TRIAL RESULTS(Unaudited, as of November 27th, 2019)

TR009: Phase 1 Dose Escalation Trial, Summary of Clinical Benefit

Patients Colorectal Gastric Other AllPartial Response* 0 1 0 1 PR Rate 13% 5%Stable Disease 6 6 2 14 SD Rate 67% 75% 50% 67%Progressed Disease 3 1 2 6Total 9 8 4 21 Clinical Benefit (PR + SD) 67% 88% 50% 71% Tumor Reduction =>20% 0% 38% 0% 14%

• All patients enrolled in our Phase 1A trial were heavily pre-treated (4L+) and had progressed on all available therapies, including chemotx and targeted biologicals such as Avastin®/Erbitux®/Cyramza®, PD-1/PD-L1 (Opdivo®/Bavencia®) and small molecules such as multi-VEGF Stivarga®/Sutent®

• Single agent TR009 stabilized or shrank tumors in 15/21 of our evaluable patients treated (CBR = 71%) and a mean treatment duration on therapy of 4.90 months (ongoing)

13

TR009 Phase 1A: Dose Escalation Scheme

1 Unconfirmed PR (12.5mg/dose); 14 SD; 5 PD (sub 2.5mg/kg dose) – Clinical Benefit Rate of 71.4%TR009 is dosed Q2W as a single agent (monotx). 1 cycle = 2 doses = 1 month.

Cohort No.

ABL001 Dose Level

(mg/kg)

No. of Patients

No. of Drop-out/

Withdrawn Patient

No. of Dose (Cycle) No. of Patients w/DLT

(cycle 1)Median Range

1 0.3 4 1 3 (2) 3-9 (2-5) 02 1 4 1 6 (4) 3-20 (2-11) 03 2.5 3 0 4 (3) 3-6 (2-4) 04 5 4 1 15 (8) 6-19 (4-10) 05 7.5 3 0 9 (5) 4-10 (3-5) 06 10 3 0 On-going 07 12.5 3 0 On-going 0

14

TR009 Phase 1A: Patient Demographics & Clinical Characteristics

Demographic or Clinical Characteristics

No. of Patients (N=24)

Age, years 54 (35-81)ECOG performance Status

0 21 22

Sex

Male 15Female 9

Primary malignancy

Colorectal 11Gastric (or Gastric Esophageal)

9

Ovary 1GIST (small intestine) 1Cholangiocarcinoma 1

Malignant Melanoma 1

Demographic or Clinical Characteristics

No. of Patients (N=24)

Prior surgery of primary tumor 19

Prior radiotherapy 11

Stage IV 24

Measurable site/rgan

Liver 10

Lung 9

Lymph node 7

Peritoneum 3

Ovary 2

Abdomen 1

Bone 1

Rectum 1

Stomach 1

Demographic or Clinical Characteristics No. of Patients (N=24)

Previous therapy

Chemotherapy 24

Radiotherapy 11

VEGF-targeting agents (including prior Avastin®, Cyramza®, Stivarga®, Sutent®)

19

Immunotherapy (Opdivo®, Bavencio®) 8

Investigational agent 5

No. of Line of Previous Chemotherapy

All (N=24) Median: 4.0 (1-7)

Colorectal Cancer (N=11) Median: 4.0 (2-5)

Gastric Cancer (N=9 Median: 3.0 (1-5)

Others (CholangioCa, GIST, Melanoma, Ovarian) (N=4)

Median: 4.5 (2-7)

15

TR009 Phase 1A: Patient Demographics & Clinical Characteristics

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

16

Dose Level Primary Malignancy Best 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% 174 (RX ONGOING) 5.72 (RX ONGOING)

12.5 mg/kg Colorectal (PT 26) SD / 15% 97 (RX ONGOING) 3.19 (RX ONGOING)

Gastric (PT 27) PR* / -31% 98 (RX ONGOING) 3.22 (RX ONGOING)

Colorectal (PT 28) SD / 4.3% 94 (RX ONGOING) 3.09 (RX ONGOING)

*Unconfirmed

PR: POSITIVE DLL4 IHC(tumor and

blood vessel)

Site of DLL4 Expression May Explain Differences in Clinical Responses (Tumor Shrinkage vs. Long Disease Stabilization)

17DATA 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% 174 days (5.7+)(Rx Ongoing)

S027* 12.5 -31% 98 days (3.22+)(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% 97+days(3.2+)(Rx Ongoing)

S028 12.5 4% 94+days(3.1+)(Rx Ongoing)

Dll4 Expression48% Cells

22% Stroma

Dll4 Expression 71% Endothelial Cells

(Blood Vessels)

GASTRICEvaluable Patients = 8

Partial Response=1Stable Disease=6

Clinical Benefit= 87.5%

COLORECTALEvaluable Patients = 9

Stable Disease=6Clinical 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

18

Gastric Patients Prior Treatment Regimens and TR009 Tx DurationMean of Responders (PR + SD): 3.85 months

4.17

1.41

2.14

4.53

5.59

2.83

5.72

3.22

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)

(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 7

PT 27, -31%

PT 25, -5%

PT 25, -5%

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

19

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

3.2

3.1

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, REGORAFENIB

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 20, 15%

PT 24, 7%

PT 19, 9.4%

PT 18, -9%

PT 18, -9%

PT 15, 8%

PT 14, 23%

PT 10, 4%

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

TR009 Monotx Compares Favorably With Approved 3+L Gastric Cancer Treatments

20

CYRAMZA®Ramucirumab

EliLilly(VEGF-R2mab)

AITAN®Apatinib

Hengrui China(VEGF-R2TKI)

TR009Anti-VEGF/DLL4

TRIGR

ClinicalTrial Phase3REGARD2:1vs.placebo

Phase3(2:1vsPlacebo)

Phase1a(Singlearm)

PatientsN=355(238Cyramza vs.117

placebo);2L/NOpriorVEGFs

N=273(176Aptanib,91Placebo)

3L/NOpriorVEGFs

N=84L+;88%hadPriorVEGF-

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

Treatment IV,MONO ORAL IVMONO

RR 3% 2.8% 13%

SD/DCR 49% 42% 88%

mPFS 2.1m 2.6m DurationofTx:3.85m(mean,ongoing)

mOS 5.2m 6.5m NA

GR3/4Toxicity

16%Hypertension;othernodifffromBSC

9%GR3/4HandFootSyndrome,HPN,Proteinuria,

Neutropenia

NODLTGr2/3HPNGr3Anemia

TR009 Monotx Clinical Activity Compares Favorably With Approved 3+L Colorectal Cancer Treatments

21

STIVARGA®Regorafenib

Bayer

LONSURF®Trifluridine/tipiracil

Taiho/Servier

ELUNATE®fruquintinibChi-Med

TR009Anti-VEGF/DLL4

TRIGR

ClinicalTrial Phase3(2:1vsPlacebo)

Phase3(2:1vsPlacebo)

Phase3(2:1vsPlacebo)

Phase1a(Singlearm)

PatientsN=505(Stivarga);Multiple

priortx includingAvastin®,Erbitux®

N=534(Lonsurf);MultiplepriortxsincludingAvastin®,

Erbitux®

N=278(Elunate)2L+;60%NO prioranti-VEGF(Avastin®/anti-

EGFR

N=94L+;100%hadPriorAvastin®,Erbitux®,

Stivarga®,PD-1/PD-l1Treatment Oral,MONO Oral,MONO Oral,MONO IVMONO

RR 1%(PR) 1.6% 5%(1CR) TRIALONGOING

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

mPFS 1.9m 2m 3.7m SDmean7.25m

mOS 6.4m 7.1m 9.3m NA

GR3/4Toxicity

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

50%NeutropeniaGR3 21%HPN;11%HFS

NODLTGr2/3HPNGr3Anemia

22

1.22

1.38

1.41

1.41

1.54

1.71

2.14

2.76

2.83*

2.92

3.09*

3.02

3.19*

3.22*

4.17

4.53

5.59

5.72*

7.03

9.46

9.49

0.00 1.00 2.00 3.00 4.00 5.00 6.00 7.00 8.00 9.00 10.00

C2C1C1C3C6C5C3C3C6C2C7C4C7C7C1C5C5C6C4C2C4

Mean Treatment Duration: 3.68 months(Excluding ongoing patients)

Mean Treatment Duration of Responders (PR = SD) 4.9 months (Excluding ongoing patients)*Ongoing Patient

PDPDPDPDPD

TR009 Treatment Duration All Evaluable Patients By Indication

23

Treatment-Emergent AE by Grade

No. % No. % No. % No. % No. % No. %Hypertension 4 17 4 17 4 17 0 0 12 50Anemia 0 3 13 1 4 0 0 4 17Epigastric Pain 1 4 2 8 0 0 0 3 13Hypoalbuminemia 1 4 1 4 0 0 0 2 8Abdominal Pain 0 2 8 0 0 0 2 8ALT Increased 0 1 4 1 4 0 0 2 8ALP Increased 0 0 1 4 0 0 1 4Anorexia 1 4 1 4 0 0 0 2 8General Weakness 0 1 4 1 4 0 0 2 8Insomnia 0 2 8 0 0 0 2 8Upper Respiratory Infection 1 4 1 4 0 0 0 2 8

Malignant Neoplasm Progress 0 1 4 0 0 1 4 2 8

(Progression Disease)Allergic Rhinitis 0 1 4 0 0 0 1 4Anal Mucositis 0 1 4 0 0 0 1 4Ascites 0 1 4 0 0 0 1 4AST increased 0 0 1 4 0 0 1 4Cancer Bleeding 0 0 1 4 0 0 1 4Chronic Paranasal Sinusitis 0 1 4 0 0 0 1 4

Constipation 0 1 4 0 0 0 1 4

AllAdverse Event Grade 1 Grade 2 Grade 3 Grade 4 Grade 5

24

Treatment-Emergent AE By Grade Cont’d

No. % No. % No. % No. % No. % No. %Cough 1 4 0 0 0 0 1 4Delirium 0 0 1 4 0 0 1 4Diarrhea 1 4 0 0 0 0 1 4Dyspnea 1 4 0 0 0 0 1 4E.Coli Bacteremia 0 1 4 0 0 0 1 4Enteritis 0 1 4 0 0 0 1 4Fatigue 0 1 4 0 0 0 1 4Headache 0 1 4 0 0 0 1 4Ileus 0 1 4 0 0 0 1 4Nausea 1 4 0 0 0 0 1 4Pancreatitis 0 0 1 4 0 0 1 4Peripheral Neuropathy 0 1 4 0 0 0 1 4

Pleural Effusion 0 0 1 4 0 0 1 4Proteinuria 1 4 0 0 0 0 1 4Pulmonary Hypertension 1 4 0 0 0 0 1 4

Rt.Inguinal Area Discomfort 1 4 0 0 0 0 1 4

Thromboembolism 0 0 1 4 0 0 1 4Vomiting 1 4 0 0 0 0 1 4

Adverse event Grade 1 Grade 2 Grade 3 Grade 4 Grade 5 All

25

Treatment-Emergent AE Per CohortCohort 1 Cohort 2 Cohort 3 Cohort 4 Cohort 5 Cohort 6 Cohort 7

0.3 mg/kg (4 pts) 1 mg/kg (4 pts) 2.5mg/kg (3 pts) 5 mg/kg (4 pts) 7.5 mg/kg (3 pts) 10 mg/kg (3 pts) 12.5 mg/kg (3 pts)

Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt)Hypertension 3 (2) 3 (3) 0 9 (3) 1 (1) 2 (2) 3 (1)Pulmonary Hypertension (G1)

1(1)

Anemia 8 (3) 0 0 0 0 0 0Epigastric Pain 2 (2) 0 0 0 1 (1) 0 0Hypoalbuminemia 3 (2) 0 0 0 0 0 0Abdominal Pain 0 1 (1) 0 0 0 0 0ALP Increased 0 0 0 1 (1) 0 1 (1) 0Anorexia 0 1 (1) 1 (1) 0 0 0 0AST increased 0 0 0 0 0 3 (1) 0General Weakness 1 (1) 1 (1) 0 0 0 0 0Insomnia 0 0 0 2 (2) 0 0 0Upper Respiratory Infection

0 0 1 (1) 1 (1) 0 0 0

Malignant Neoplasm Progress

2 (2) 0 0 0 0 0 0

Ascites 1 (1) 0 0 0 0 0 0Allergic Rhinitis 0 1 (1) 0 0 0 0 0ALT Increased 0 0 0 0 0 2 (1) 0Anal Mucositis 0 0 0 1 (1) 0 0 0Cancer Bleeding 0 0 0 1 (1) 0 0 0Chronic Paranasal Sinusitis 0 1 (1) 0 0 0 0 0

Constipation 1 (1) 0 0 0 0 0 0

26

Treatment-Emergent AE Per Cohort

Cohort 1 Cohort 2 Cohort 3 Cohort 4 Cohort 5 Cohort 6 Cohort 7

0.3 mg/kg (4 pts) 1 mg/kg (4 pts) 2.5mg/kg (3 pts) 5 mg/kg (4 pts) 7.5 mg/kg (3 pts) 10 mg/kg (3 pts) 12.5 mg/kg (3 pts)

Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt) Episode# (pt)Cough 0 0 0 0 1 (1) 0 0Delirium 1 (1) 0 0 0 0 0 0Diarrhea 0 0 0 0 0 1 (1) 0Dyspnea 0 0 0 1 (1) 0 0 0E.Coli Bacteremia 1 (1) 0 0 0 0 0 0Enteritis 0 1 (1) 0 0 0 0 0Fatigue 0 0 0 0 1 (1) 0 0Headache 0 1 (1) 0 0 0 0 0Ileus 0 0 1 (1) 0 0 0 0Nausea 0 0 1 (1) 0 0 0 0Pancreatitis 1 (1) 0 0 0 0 0 0Peripheral Neuropathy

1 (1) 0 0 0 0 0 0

0 1 (1) 0 0 0 0 00 0 0 0 1 (1) 0 00 0 0 1 (1) 0 0

Rt.Inguinal Area Discomfort

0 1 (1) 0 0 0 0 0

Thromboembolism 1 (1) 0 0 0 0 0 0Vomiting 0 0 1 (1) 0 0 0 0

Pleural Effusion

PHASE 1B COMBINATION STUDY (n=12-15)

§ TR009 + Irinotecan (Gastric, Colorectal)§ TR0009 + Paclitaxel (Gastric, Ovarian)§ TR009 + PD-1/PD-L1 (partner dependent)

Start: January 10th, 2020 (data H2’20)

27

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 OngoingQ4 2019E Completion

(n~21-27)

Cohort 8(15 mg/kg)

Cohort 9(17.5 mg/kg)

Dose Escalation

TR009 Key Points to Consider

Preliminary Clinical Activity Seen with TR009 Indicates a Clinical Benefit Rate (CBR) of 71%o Gastric cancer- 88% CBR (SD + PR); mean treatment duration of 4 monthso Colorectal Cancer - 66% CBR (SD); mean treatment duration of 7.25 monthso Gastric PR patient had POSITIVE DLL4 IHC in both tumor cells and blood vesselso 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 H1’20 for Phase 2 initiation as master protocol

28

TRIGRIMMUNE ~ CELL ACTIVATORS

T R I A - 0 0 1T R I A - 0 0 2

29

AGONISTIC STIMULATION OF 4-1BB CAUSES:CD8+ T cells: Enhance proliferation, differentiation to memory

cells, resistance to apoptosis, IL-2 and IFN-γ productionDendritic 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

30

4-1BB (CD137) Mediates Important Immune Function Within the Tumor

Micro-Environment4-1BB (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

31

5T4/4-1BB

ANTI-FAP (4B9)/4-1BB

TAA/4-1BB

HER2/4-1BB

PDL1/4-1BB

PDL1/4-1BB

HER2/4-1BB

BIOLOGICAL TESTING

PHASE 1

Companies Develop Strategies to Address Liver Tox Issues Using Bispecific Antibodies Constructs

TAA

T Cells NK Cells

4-1BB4-1BB

TAA

TRIGR IMMUNE-CELL ACTIVATORS (TRIA)BINDS TO 4-1BB & TUMOR ANTIGEN

ü TRIA are engineered to activate T and NK cells only at the tumor micro-environment

(TME) where clustering occurs

ü Designed to reduce liver toxicity

TRIAs Are Engineered to Minimize Liver Toxicity

32

IN THE CIRCULATION TUMOR MICRO-ENVIRONMENT

Activation at TME can potentially reduce off-target toxicities such as hepatotoxicity associated with anti-4-1BB monoclonal antibodies

TRIA are engineered to activate T-cells only at the tumor micro-environment (TME) where

clustering occurs

0

100

200

300

400

500

600

700

0 5 10 15 20 25

Tum

or V

olum

e (m

m3 )

Days After Tumor InJection

Control

4-1BBmAb

0

20

40

60

80

100

120

Control 4-1BB mAb 4-1BB BsAb

Seru

m A

LT (u

nit/

L)

Anti-tumor Effect with TRIGR 4-1BB BsAb (TRIA)

No Liver Toxicity with TRIA 4-1BB BsAb

No Liver Tox

Severe Liver Tox

with 4-1BB mAb e.g.

Urelumab/BMS

TRIA

32

First in Class 4-1BB / BCMA BsAb

4-1BB selectively activates immune cells (T, NK cells) in the tumor microenvironment (Safety)

Proprietary BCMA clone targets different epitope to urelimab (Safety)

Pre-clinical data: low cytokine release but high cell lysis; also, shown to induce memory (CD-4) T cells

TRIA-001 offers an off the shelf alternative to CAR-T for MM;

BsAb retains Fc region facilitating PK advantage (No continuous dosing required)

IND Q1’2021E

T Cells NK Cells

4-1BB4-1BB

BCMA BCMA

33

TRIA-001(4-1BB/BCMA)

98% of Multiple Myeloma cells express the BCMA protein or RNA1

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

BCMA CAR-T vs. BCMA/CD3 BsAb

34

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% CRS1 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% CRS1 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

Recent Data Bode Well for Bispecific Approach

T Cells NK Cells

Immune Checkpoint

4-1BB4-1BB

35

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

Immune Checkpoint

B7 Homolog Family

Down-regulates the body’s immune system

Highly over-expressed in Breast, Liver, Ovarian, and Endometrial tumors

TRIA-002(4-1BB/Undisclosed Immune

Checkpoint)

THANK YOU

George UyCEO & FOUNDERguy@TrigrRx.com001 949 648 0705

Miranda ToledanoCOO & CFO

Miranda.toledano@TrigrRx.com+972-58-55-88-470

36

Corporate Leadership Team

37

GEORGE UY, Founder and Chief Executive Officer

MIRANDA TOLEDANO, Chief Operating Officer & Chief Financial Officer20 years of biotech related Wall Street principal investment, capital market and strategic leadership experienceEVP Strategy/Corporate Development at Sorrento Therapeutics (SRNE) (ICD-38 CAR-T/RTX; oncolytic virus/Ztlido®)MD & Head of Healthcare Investment Banking at MLV & Co. (acquired by B. Riley FBR & Co.)VP Investment Team at Royalty Pharma (focus on oncology/hematology/auto-immune, mAb investments)BA in Economics from Tufts University and an MBA in Finance and Entrepreneurship from the NYU Stern School of Business

35 years of pharmaceutical and biotech commercial leadership experience20 year career with ROCHE (Manila, Basel, China, US) led strategic marketing /commercial initiatives (launched Xeloda®) Chief Commercial Officer: Abraxis Biosciences, Sorrento Therapeutics (SRNE), Spectrum Pharmaceuticals, Inc. (SPPM)Bachelor of Science in Medical Technology from the Cebu Institute of Medicine, Philippines

37

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

38

Our symbiotic alliance with ABL BIO enables efficient, low capital-intensive development of our pipeline

39

Clinical Implications of High DLL4

OVARIANo DLL4 was overexpressed in 72% of tumors examined where it was an independent

predictor of poor survival.o Patients with tumors responding to anti-VEGF therapy had lower levels of DLL4 than

patients with stable or progressive disease.

GASTRICo Cancerous and stromal DLL4 expression was found in 48% and 22% in gastric cancer,

and significantly affected postoperative clinical outcomeso Cancerous and stromal DLL4 expression may be an effective target of anti-DLL4

treatment in gastric cancer

PANCREATICo High IHC DLL4 expression in cancer cells was associated with worse overall survival

(OS) and disease-free survival (DFS) than low DLL4 expression (median OS: 12.9 vs 30.4 months, P=0.004; median DFS: 8.8 vs 17.4 months, P=0.02).

o Low DLL4 abundance was associated with a longer OS–only for patients who received an adjuvant gemcitabine-based chemotherapy (P<0.001) but not for patients who did not receive gemcitabine (P=0.72).

48% Cells22% Stroma

72% Cancer cells &

endothelial cells

References: J Exp Clin Cancer Res. 2013 Jul 30;32:46Clinical implications of DLL4 expression in gastric cancer. Ishigami, et al. Journal of Experimental & Clinical Cancer Research 201332:46DLL4 expression is a prognostic marker and may predict gemcitabine benefit in resected pancreatic cancer. Drouillard, et al: British Journal of Cancer volume 115, pages 1245–1252 (08 November 2016)Biological roles of the Delta family notch ligand Dll4 in tumor and endothelial cells in ovarian cancer. Hu, et al: Cancer Res; 71(18); 6030–9

40

Clinical Implications of High DLL4 GLIOBLASTOMAo DLL4 expression was correlated positively with the degree of edema

(r = 0.845 and p < 0.001)o DLL4 was an independent predictor of prognosis in patients with

HGGs (p = 0.001).

30%-80%Endothelial Cells (Depending on

grade)

BREAST CANCERo Surgical removal of high- grade breast cancer resulted in significant reduction in

DLL4 plasma levels (p = 0.003). The ratio of DLL4+/ CD31+ vascular density (VD) ranged from 23 to 88 % (median 49 %).

o High DLL4 cancer cell expression and high DLL4+ VD were significantly linked with nodal involvement (p = 0.004 and 0.01, respectively)

Dll4Tumor Cells

&Vasculature

NSCLCo Notch1 and Notch3 expression positively associated with NSCLC progressiono Greater possibility of lymph node metastasis (LNM) and higher tumor stages were

linked with Notch1 expression.o Notch3 associated with overall survival rate of lung adenocarcinoma patients

(pooled HR=1.33).References: Correlation of high delta-like ligand 4 expression with peritumoral brain edema and its prediction of poor prognosis in patients with primary high-grade gliomas: Qiu, et al. J Neurosurg Vol 123 2015Delta-like ligand 4 (DLL4) in the plasma and neoplastic tissues from breast cancer patients: Correlation with metastasis Emmanuel Kontomanolis, Marianthi Panteliadou, Alexandra Giatromanolaki, Stamatia Pouliliou, Eleni Efremidou, Vassilios Limberis, Georgios Galazios, Efthimios Sivridis, Michael I. Koukourakis .Med Oncol (2014) 31:945Scientific Reports 5, article number: 10338(2015). X Yuan, et al.

70%-80%Depending on histology

41

DLL4-positive gastric cancer patients have worst survival

Both cancer and stromal DLL4 expression significantly correlated with more advanced tumor depth, nodal involvement, lymphatic and venous invasion in patients with gastric cancer

TR009 Efficacy Appear to Correlate with High Expression DLL4 in gastric xeno models

Predictive Biomarker Approach in Gastric Cancer

Clinical implications of DLL4 expression in gastric cancerSumiya Ishigami, et al.

42

q SPON2 and DTX1 genes dose-dependently and consistently decreased at 21 days after 1st

dosing.

q Consistent results with OncoMedand AbbVie’s PK analysis

q DTX1: positive regulator of the notch signaling pathway

PD Analysis Shows Down Regulation of Key NOTCH Signaling Pathways Consistent with anti-Dll4 Activity

TR009 Ph1A

§ Cell line: AGS SQ-Luc§ TR009/ ABL001: 3.25 mg/kg, twice a week, i.p§ Irinotecan: 10 mg/kg, twice a week, i.p

§ Cell line: MKN45-Luc§ TR009/ ABL001: 3.25 mg/kg, twice a week, i.p§ Irinotecan: 10 mg/kg, twice a week, i.p

§ Cell line: SW620§ TR009/ ABL001: 2 mg/kg, twice a week, i.p§ Irinotecan: 20 mg/kg, weekly, i.p

SW620 Xenograft

0 5 10 15 20 25 300

500

1000

1500

2000Control(10)mABL001(10)Irinotecan(10)Combo(10)

Days

Tum

or v

olum

e (m

m^3

)

SW48 Xenograft

0 5 10 15 20 250

1000

2000

3000Control(10)mABL001(10)Irinotecan(10)Combo(10)

DaysTu

mor

vol

ume

(mm

^3)

§ Cell line: SW48§ TR009/ ABL001: 1.25 mg/kg, twice a week, i.p§ Irinotecan: 40 mg/kg, weekly, i.p

43

TROO9 (ABL001) TROO9 (ABL001)

TROO9 (ABL001) TROO9 (ABL001)

GASTRIC

COLORECTAL

TR009 + Irinotecan in Gastric Cancer/CRC Xenograft

TR009 + Paclitaxel in Gastric Cancer PDX

44

Tumor Growth(GAPF006-FP1+3)

0 5 10 15 20 25 300

500

1000

1500

2000

2500

Days post administration

Tum

or V

olum

e (m

m3 ) Vehicle control

hABL001 (3 .25 m g/kg , Q 3D)Paclitaxe l (15 m g/kg, Q W )Com bo

***

Vehic

le co

ntrol

hABL0

01 (3

.25 m

g/kg,

Q3D)

Pacli

taxel

(15 m

g/kg,

QW)

Combo

0

1

2

3

4

5

Tumor volume measured at last day (3.25 combo)

GroupsTu

mor

Wei

ght (

g)

Vehicle controlhABL001 (3 .25 m g/kg , Q 3D)Paclitaxe l (15 m g/kg, Q W )Com bo

Fisher’s LSD test:*, p<0.05; **, p<0.01, compared with Vehicle group

CRO: LIDE

Vehic

le co

ntrol

hABL0

01 (3

.25 m

g/kg,

Q3D)

Pacli

taxel

(15 m

g/kg,

QW)

Combo

0

1000

2000

3000

4000

5000

Tumor volume measured at last day (3.25 combo)

Groups

Tum

or V

olum

e (m

m3 ) Vehicle control

hABL001 (3 .25 m g/kg , Q 3D)Paclitaxe l (15 m g/kg, Q W )Com bo

Model ID PatientGender

PatientAge Description Lauren

ClassificationScoring

DLL4 Notch1 NICD

GAPF006 Male --

Poorly-Moderately

differentiated adenocarcinoma

Intestinal type 2.3 (+) 4.0 (+++) 5.0 (++)

***

TR009 Combinational effect with PD-1 BlockadeIn HSC-humanized Model (MKN45) GASTRIC CANCER: In-house Data from ABL Bio

Resultso Anti-PD-1 Ab (Keytruda) not effective in

HSC (hematopoietic stem cell, 2 donor) humanized MKN45 xenograft model using NSG mouse

o Combination ABL001 + Keytruda showed synergistic effect

Group Treatment Dose Dosing schedule Route No. of donor #5650

No. of donor #5655

G1 Human IgG 10 mg/kg Twice a week IP 5 5

G2 Keytruda 7.5 mg/kg Twice a week IP 5 5

G3 ABL001/TR009 2 mg/kg Twice a week IP 5 5

G4 Combo 7.5 + 2.0 Twice a week IP 5 5

TR009/ABL001

Combo

HuIgG

Keytruda

Tum

or v

olum

e (m

m3 )

1 5 8 13 16 20 22

Days

45

Abbvie: ABT-165 Phase 1A Experience (n=55)

Phase 1A Summary:

2 DOSE ESCALATION PROTOCOLS

IMPLEMENTEDDUE TO

TOXICITY as of 2.5 mg/kg

dose (stroke, hypertension)

46

References: Invest New Drugs (2019) 37:461-472

Cohort 10.5mg/kg

N=3

Cohort 2(1mg/kg)

N=3

Cohort 3-4(2.5 mg/kg)

N=6

Cohort 5-6(3.5 mg/kg)

N=12

Cohort 7(5 mg/kg)

N=6

Cohort 8(7.5 mg/kg)

N=6

Cohort 9(10 mg/kg)

N=10

Cohort 10(12.5 mg/kg)

N=5

EXPANSION(7.5 mg/kg)

N=13

Oncomed/MREO: Navicixizumab Phase 1A Experience

1 Gr3 Large Intestine

Perforation (5 days after 1st

dose). Expanded to 6 pts, 4 pts

discontinued due to HPN

1 elevated BNP(outside DLT

window)

Enrollment terminated after 5 pts due to chronic

pulmonary HPN

N= 66

Ovarian, 12

Colorectal, 11

Breast, 4Pancreatic, 4

Uterine, 4

Endometrial , 4

Other, 11

Clinical Benefit Rate = 29% (19/66)Partial Responseo Ovarian= 3/11(27%)o Uterine= 1/4 (25%)Stable Diseaseo CRC= 4/7 (56%)o Ovarian= 7/11 (64%)

Treatment Related Adverse Eventso HPN= 58%o Headache=29%o Fatigue=26%o Pulmonary HPN=18%

(Asymptomatic at < 5mg/kg4 Gr2, 1 Gr3 at >5mg/kg)

o Tox Withdrawal =30%(GI perforation, pulmonary HPN,BNP elevation, infusion rxn)

66 patients treatedMedian age=60

ECOG PS 0 (48%), 1 (52%)

Toxicity during dose escalation led to patient expansion to 53 patients

47