Precision Cancer Medicine™ Oncology Company Developing Therapeutics that Target the Master

Regulator of Tumor Cell Division

NASDAQ: TROV

2

Forward-Looking Statements

Certain statements in this presentation are forward-looking within the meaning of the Private Securities Litigation Reform Act of 1995. These statements may be identified by the use of words such as "anticipate," "believe," "forecast," "estimated" and "intend," or other similar terms or expressions that concern Trovagene's expectations, strategy, plans or intentions.

These forward-looking statements are based on Trovagene's current expectations and actual results could differ materially. There are a number of factors that could cause actual events to differ materially from those indicated by such forward-looking statements. While the list of factors presented in the 10-K is considered representative, no such list should be considered to be a complete statement of all potential risks and uncertainties. Unlisted factors may present significant additional obstacles to the realization of forward-looking statements. Forward-looking statements included herein are made as of the date hereof, and Trovagene does not undertake any obligation to update publicly such statements to reflect subsequent events or circumstances.

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Company HighlightsDelivering on the Promise of Precision Cancer Medicine

► Single molecule, onvansertib, addressing multiple indications, each with significant medical need for new treatment options– Only 3rd-generation, oral Polo-like Kinase 1 (PLK1) inhibitor in clinical development– 3 active Investigational New Drug (INDs) for hematologic and solid tumor cancers– Rapid and efficient pipeline progress since licensing onvansertib in March 2017

► Large market opportunities of $3.4 billion with upside in additional cancers of +$7 billion

► Demonstrated synergy of onvansertib in combination with standard-of-care drugs suggests therapeutic potential and valuable partnership opportunities

► Biomarker strategy identifies patients most likely to respond to precision treatments, thereby containing treatment costs while maximizing therapeutic benefit

► Onvansertib has patent protection to 2032 and beyond

► Trovagene enjoys support from world-renowned clinical advisors and investigators

► Seasoned management team with proven track record of development and commercial success

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Exclusive Global Rights to OnvansertibLicensed from Nerviano Medical Sciences (NMS) in 2017

► Largest oncology research and development company in Italy; highly regarded throughout Europe and the U.S.

► Leader in protein kinase drug development (Polo-like Kinase Inhibitors)

► FDA-approved facility for manufacturing API and finished drug

Licensee Preclinical Phase 1 Phase 2 Phase 3 Registered

Encorafenib (B-RAF IP); Braf mutation in melanoma and colorectal cancer

Entrectinib (TRK, ROS, ALK); non-small cell lung cancer

Milciclib (CDK, other kinases); thymic cancer

MPS1 Inhibitor; solid tumors

Onvansertib (PLK1 inhibitor); AML, mCRPC, mCRC

ADC (PNU-652)

ADC (NMS-P945)

► Excellent track record licensing innovative drugs to pharma/biotech companies

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Onvansertib – Pipeline Within a MoleculeOpportunities in Leukemias/Lymphomas and Solid Tumors

Preclinical Phase 1 Phase 2

Metastatic Castration-Resistant Prostate (CRPC)

Phase 2 trial in combination with Zytiga® (abiraterone acetate)/prednisone - Ongoing

Colorectal (CRC)Phase 1b/2 trial in combination with FOLFIRI + Avastin ® - Ongoing

Acute Myeloid Leukemia – Orphan Drug Designation in the U.S. and EuropePhase 1b/2 trial in combination with low-dose cytarabine (LDAC) or Decitabine - Ongoing

► 3 Investigational New Drug (INDs) in place with the FDA

Myelodysplastic SyndromePhase 1b/2 Investigator Initiated Trial (commencing Q4’19 / Q1’20)

Leukemias and Lymphomas Solid Tumors

Ovarian, Breast, Pancreatic, Small-Cell LungPhase 1b/2 trial ready (Preclinical Data Available)

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PLK1Established Target for Cancer Therapy

► PLK1 belongs to a family of kinases (PLK1,2,3,4,5)

– Only with expression of PLK1 are cells able to pass-through the last checkpoint (G2Mitosis) and divide1-6

– PLK2-PLK5 have properties more consistent with tumor suppressor genes and are not essential for cell division7

– Over-expression of PLK1 is observed in numerous cancer types and associated with poor patient prognosis8

– Depletion of PLK1 induces cell death in tumor cells9

PLK1 is a Master Regulator of the Cell Cycle and Cell Division

Cell-cycle arrest

1Takai N, et al. Oncogene 2005;24:287–91; 2Rudolph D, et al. Clin Cancer Res 2009;15:3094–102; 3Chopra P, et al. Expert Opin Investig Drugs 2010;10:27–43; 4Strebhardt K. Nat Rev Drug Discov2010;9643–60; 5Zitouni S, et al. Nat Rev Mol Cell Biol 2014;15:433–52; 6Takaki T, et al. Curr Opin Cell Bio 2008;20:650–60; 7Bahasa EM. Polo-like kinases and DNA damage checkpoint: beyond the traditional mitotic functions. ExpBiol and Medicine 2011; 236: 648-657; 8Data derived from The Tumor Genome Atlas, http://togadata.nci.nih.gov/docs/publications/tcga;,9Liu et al., Mol. Cell. Biol. March 15, 2006; 26:6 2093-2108

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OnvansertibHighly-Selective Only for PLK1, Blocks Tumor Cell Division

► Tested against >260 kinases and PLK1 was the only active target (IC50 of 2nM)

► Selectivity driven by polar interaction with the carboxyl side chain of Glutamate 140 position of PLK11

1Data on File, Trovagene, Inc.

Highly-Selective, Oral PLK1 Inhibitor

Induces Cell Death by G2M Cell Cycle Arrest

► Blocks tumor cell division (mitosis)

PLK MemberOnvansertibIC50* (μM)

PLK1 0.002

PLK2 > 10

PLK3 > 10

Tumor Cell Division

Onvansertib Blocks Tumor Cell Division

Structural Formula

8

Onvansertib Profile

Profile CharacteristicsSmall Molecule • MW 648.60 Daltons

Formulation • 5mg and 20mg oral gelcaps

Plasma Protein Binding • 95% at 10μM and 91% at 50μM

Metabolic Studies • Moderate intrinsic clearance (9.3 mL/min/kg)1

• 2 metabolites identified in metabolic profiling; however, in low quantities (parent drug accounted for 93% of total drug-related material)1

• No Cytochrome P450 inhibition at therapeutic concentrations2

Pharmacokinetics3 • Systemic exposure of drug increased with dose, as shown by an increase in Cmax and AUC0-24

• Tmax is approximatively 3h• Half-life is approximately 24h

1Performed in human hepatocytes, 2Performed in human liver microsomes, 3Weiss et al.

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OnvansertibFirst-in-Class, 3rd-Generation PLK1 with Best-in-Class Attributes

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OnvansertibSynergy May Enhance Efficacy of Standard-of-Care Therapies1

Onvansertib Synergistic in

Combination with SOC

Therapies

Zytiga®

(abiraterone)

Avastin®

(bevacizumab)

Cytarabine

Doxorubicin

Cisplatin

Gemzar®

(gemcitabine)

Velcade®

(bortezomib)

Quizartinib

Beleodaq(belinostat)

Camptosar®

(Irinotecan)

Venclexta®

(venetoclax)

Taxol®

(paclitaxel)

Acute Myeloid LeukemiaChronic Lymphocytic Leukemia

Colorectal

T-Cell Lymphoma

ColorectalBreast

Non-Small Cell Lung

Acute Myeloid Leukemia

PancreaticBreast

OvarianNon-Small Cell Lung

Leukemias (Acute Myeloid Leukemia)

LeukemiasLymphomas

OvarianBreast

OvarianBladder

Non-Small Cell LungSmall Cell Lung

PancreaticBreast

OvarianNon-Small Cell Lung

Multiple Myeloma

Prostate

1Data on File, Trovagene, Inc. Onvansertib current clinical trials

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Predicting Response to OnvansertibBiomarker Strategy Utilizing a Simple Blood Test

► Biomarker assay uses a blood test to determine whether a patient has a greater likelihood to respond to onvansertib

► If patient is positive for biomarker assay, then drug is administered

► Blood test examines the extent to which onvansertib inhibits PLK1 enzymatic activity (called target engagement) [within circulating cancer cells]

pTCTP

TCTP

- +Onvansertib

pTCTP

TCTP

- +Onvansertib

Patient receivesa single dose of

onvansertibAssess target engagement

Pre-dose sample

3h post-dosesample

Obtain 2 vials of blood from

patientTreatment vial,Onvansertib

Control vial,Vehicle

Treat blood sample with onvansertib or vehicle control

Assess target engagement

Ex-vivo sampling (in development)

In-vivo sampling (current method) AML Example

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Summary of Active Programs

Indication Combination Therapy

TargetedBiomarker

Development Status Key 2019 Catalysts Market

Potential

Acute Myeloid Leukemia (AML)

Low-dose cytarabine or decitabine

pTCTP and TCTP

Phase 1b/2Orphan Drug Designation (US and EU)

- ESMO Phase 2 data (Sept)- ESH Phase 2 data (Oct)- ASH Phase 2 data (Dec)

$650 million

Metastatic Castration-Resistant Prostate Cancer (mCRPC)

Zytiga®

(abiraterone) and prednisone

PSA Phase 2 - Asian-Pacific Prostate Cancer (Aug)- ESMO Phase 2 data (Sept)- EMUC Phase 2 data (Nov)

$1.3 billion

Metastatic Colorectal Cancer (mCRC)

FOLFIRI and Avastin®

(bevacizumab)

KRAS Phase 1b/2 - Sites activated, recruiting & enrolling patients (Jun)

- Gastrointestinal Oncology Conference Phase 1b safety and preliminary efficacy data (Oct)

$1.5 billion

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Acute Myeloid LeukemiaSignificant Need for New Treatment Options

► Aggressive hematologic malignancy of immature blood cells

► 20,000 new cases annually

– 10,400 deaths annually

– 5-year survival rate of 25%

► Treatment options vary based on patient condition and age

– Chemotherapy / radiation / stem cell transplant

► Preliminary efficacy data demonstrated in preclinical in-vitro and in-vivo trials

– Onvansertib* as a single agent

– In combination with drugs used to treat AML

*Orphan Drug Designation granted for onvansertib by the FDA September, 2017 and by the EMA in July, 2018 ;1National Cancer Institute SEER 2016; 2Valsasina et al., Mol Cancer Ther; 11(4) April 2012

Acute Myeloid Leukemia

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Onvansertib Positioning in AMLPatient Selection Algorithm

AML Diagnosis 18,3761

cases/year

Eligible for Induction Treatment~11,000

Relapsed &

Refractory 30-50% 3,300-5,500

Onvansertib in combination with standard-of care chemotherapy and/or targeted therapeutics2

Responders 50-70%

Ineligible for

Induction Treatment

~7,400

Consolidation Treatment

1Visser et al. (2012), Eur J Cancer (48). Estimated cases in EU27 per year; 2e.g. Midostaurin for FLT3 mutation

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Phase 2: Assess safety and preliminary antitumor activity

► Efficacy Endpoints: Rate of complete response (CR + CRi) defined as morphologic leukemia-free state (MLF)

► Exploratory Endpoints: Evaluation of pharmacodynamic and correlative biomarkers

► Clinical Sites:

Ongoing Phase 1b/2 Clinical Trial in AMLOnvansertib in Combination with Low-Dose Cytarabine or Decitabine

Phase 1b: Dose escalation to assess safety and identify recommended Phase 2 dose

► Administered orally, once-daily on Days 1-5 of each cycle (21-28 days)

12 mg/m218 mg/m2

27 mg/m240 mg/m2

CompletedCompleted

CompletedCompleted

60 mg/m2

Enrolling

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Anti-Leukemic Activity

► Of the 26 patients evaluable for safety, 19 had an evaluable bone marrow biopsy to assess efficacy

► Preliminary efficacy in the evaluable population includes 3 patients achieving complete response (CR) and 1 patient achieving complete response with incomplete hematologic recovery (CRi)

Onvansertib + Decitabine Onvansertib + LDAC

-1 5 0

-1 0 0

-5 0

0

5 0

1 0 0

1 5 08 0 0

9 0 0

1 0 0 0

%c

ha

ng

e f

rom

ba

se

lin

e P ro g re s s iv e d is e a s e (P D )

S ta b le d is e a s e (S D )

M o rp h o lo g ic a l L e u k e m ic F re e S ta te (M L F S )

D a ta L a b e ls re p re s e n t o n v a n s e r t ib d o s e (m g /m 2 )

1 8

1 8

1 2 4 02 7 4 0 2 7

2 7 1 24 0

C o m p le te re s p o n s e (C R )

0 5 0 1 0 0 1 5 0 2 0 0 2 5 0 3 0 0 3 5 0

T r e a tm e n t d u r a t io n (d a y s )

*

*

12 m

g/m

218

mg/

m2

27 m

g/m

240

mg/

m2

* No BM data

PRSD

CRCRi

PD

Ongoing

MLFS

0 5 0 1 0 0 1 5 0 2 0 0 2 5 0 3 0 0 3 5 0

T r e a tm e n t d u r a t io n (d a y s )

*

*

12 m

g/m

218

mg/

m2

27 m

g/m

240

mg/

m2 * No BM data

PRSD

CRCRi

PD

Ongoing

MLFS

CR occurred at onvansertib 27mg/m2

- 1 5 0

- 1 0 0

- 5 0

0

5 0

1 0 0

1 5 0

%c

ha

ng

e f

rom

ba

se

lin

e

S ta b le d is e a s e (S D )

C o m p le te re s p o n s e (C R )1 8

1 82 7

1 8

1 2 4 0

2 7 2 7 4 0

D a ta L a b e ls re p re s e n t o n v a n s e rtib d o s e (m g /m 2 )

C o m p le te re s p o n s e w ith in c o m p le te h e m a to lo g ic a l re c o v e ry (C R i)

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PLK1 Inhibition by OnvansertibMonitored through pTCTP Status

► In the Phase 1b AML trial, 8 out of the 22 subjects (36%) tested showed a decrease in % pTCTP at 3h post-dose compared to pre-dose

1Cucchi et al., Anticancer Res., 2010

TCTP

PLK1

TCTP

P

P

Onvansertib

PLK1

TCTP

TCTP

Onvansertib

P

No Onvansertib

Target Engagement12 mg/m2

01-0020h 3h

pTCTP

TCTP

07-009

27 mg/m2

08-027 05-030

40 mg/m2

07-0360h 3h 0h 24h 0h 3h 0h 3h

► pTCTP as a marker of PLK1 activity:

– PLK1 phosphorylates the translational control tumor protein (TCTP) on serine 461

– pTCTP was identified as a specific marker for PLK1 activity in in-vivo preclinical models1

12 mg/m2

07-004

0h 3h

pTCTP

TCTP

07-013

27 mg/m2

01-024 07-033

No Target Engagement40 mg/m2

07-035

0h 3h 0h 3h 0h 3h 0h 3h

12 mg/m2

07-004

0h 3h

pTCTP

TCTP

07-013

27 mg/m2

01-024 07-033

No Target Engagement40 mg/m2

07-035

0h 3h 0h 3h 0h 3h 0h 3h

12 mg/m2

07-004

0h 3h

pTCTP

TCTP

07-013

27 mg/m2

01-024 07-033

No Target Engagement40 mg/m2

07-035

0h 3h 0h 3h 0h 3h 0h 3h

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PLK1 Inhibition by OnvansertibCorrelated with Higher Treatment Response

► Patients with target engagement had a significantly higher decrease in bone marrow blasts compared with patients with no-target engagement

► 4 of the 7 patients with target engagement had a decrease in bone marrow blasts of ≥50%

► Conversely, only 1 of the 9 patients with no-target engagement showed a decrease in bone marrow blasts upon treatment

T a rge t

E n g a g emen t

N o Ta rg

e t

E n g a g emen t

0

1 0 0

2 0 0

3 0 0

%b

last

s re

lativ

e t

o b

ase

line * *

% Bone Marrow Blast Change Relative to Baseline

p=0.009

% Bone Marrow Blast Reduction from Baseline

-1 5 0

-1 0 0

-5 0

0

5 0

1 0 0

1 5 08 0 0

9 0 0

1 0 0 0

%ch

an

ge

fro

m b

ase

line

T a rg e t E n g a g e m e n t

N o T a rg e t E n g a g e m e n t

*patient sample had low % circulation blasts (~1%) and showed a 40% reduction in pTCTP

*

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mCRPCOpportunity to Increase Duration of Response to Therapy

► 25,000 men die from metastatic prostate cancer annually and the 5-year survival rate is 37%2

► Treatments – Zytiga® (Johnson & Johnson)/prednisone

– Xtandi® (Astellas/Pfizer)

► Ongoing need to increase duration of response to treatment– Patients develop resistance within 9-15 months4 and do

not respond well to subsequent therapies

► Preclinical studies demonstrate synergy between onvansertib and Zytiga®

– PLK1 inhibition improves abiraterone efficacy by repressing the androgen signaling pathway3,4

12017 Annual Report on Prostate Disease – Harvard Health Publications; 2GlobalData. Prostate Cancer—Global Drug Forecast and Market Analysis to 2023. Apr, 2015; 3 National Cancer Institute Metastatic cancer. Mar, 2013. Available at: http://www.cancer.gov/about-cancer/what-is-cancer/metastatic-fact-sheet; 4GAntonarakis, Emmannel – Current Understanding of Resistance to Abiraterone and Enzalutamide in Advanced Prostate Cancer; Clinical Advances in Hematology & Oncology – May 2016 – Volume 14, Issue 5

Prostate Cancer

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Ongoing Phase 2 Clinical Trial in mCRPCOnvansertib in Combination with Zytiga® and Prednisone

Dosing Regimen Duration EvaluationDosing Regimen

Arm A

Dosing RegimenArm B

Onvansertib – 24 mg/m2

Days 1-5 (14-Day Cycle) + Abiraterone daily

6 Cycles = 12 Weeks

Onvansertib – 24 mg/m2

Days 1-5 (21-Day Cycle) + Abiraterone daily

4 Cycles = 12 Weeks Disease ControlPSA Stabilization or Decline

Disease ControlPSA Stabilization or Decline

► Efficacy Endpoints: Effect of onvansertib in combination with Zytiga®/prednisone on disease control assessed by prostate-specific antigen (PSA) decline or stabilization pre- and post-treatment

► Safety Endpoint: Safety of onvansertib in combination with Zytiga®/prednisone

► Exploratory Endpoints: Target inhibition of PLK1, evaluation of relevant biomarkers and correlation with patient response and genomic profile

► Clinical Sites:

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Early PSA Response ObservedAddition of Onvansertib to Daily Zytiga®

D a y -60

D a y -32

D a y -6

C 1D 1

C 1D 8

C 2D 1

C 2D 8

C 3D 1

C 4D 1

C 5D 10

1 0

2 0

3 0

4 0

5 0

T ro v 5 3 _ 0 3 -0 1 3 _ P S A le v e ls

PS

A (

ng

/mL

)

D a y 1 D a y 8 5

E ff ic a c y e n d p o in t

2 5 % o f b a s e lin e P S A (C 1 D 1 )

C T C s A R V 7 +

D a y -6 is th e s c re e n in g P S A v a lu e .

Abiraterone Abiraterone + Onvansertib

Efficacy evaluation at Day 85

► 6 patients have completed 4 cycles (3

months) of treatment with onvansertib +

abiraterone

► 2 of 6 patients had observed declines in

PSA levels after dosing with onvansertib

► To date, 1 patient has achieved the

efficacy endpoint of disease stabilization

based on PSA levels (primary endpoint)

► PSA trajectory in patient achieving primary efficacy endpoint changed from 100% increase

(16.05 ng/ml to 34.23 ng/ml) in the 60 days prior to adding onvansertib to only an 8.4% increase

during 84 days on treatment

► Tumor assessed at Cycle1 Day 1 as a variant known as AR-V7, considered an aggressive tumor

that is resistant to anti-androgen therapy

CT scan at end of 12 weeks

(efficacy endpoint) indicates

~30% tumor shrinkage

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Metastatic Colorectal CancerUnmet Need in mCRC

► 140,000 new cases of CRC in 2018 with 65% 5-year survival1

– ~51,000 deaths per year from mCRC1

► Tumor biomarkers drive therapy decisions for 1st-line mCRC therapy2

– ~50% mCRC is RAS mutant (Kras)– Targeted therapies exclude patients with RAS mutations

► Large unmet need in RAS mutant CRC2

– No targeted therapies are available for RAS mutant CRC– Standard-of-care is chemotherapy (FOLFOX/FOLFIRI)– 2nd-line therapies have ~5% response rate in mCRC

1https://seer.cancer.gov/statfacts/html/colorect.html; 2King et al, Frontline Strategies for Metastatic CRC, 2016, Amer J Hem/Onc; Loree&Kopetz, Recent Developments in treatment of mCRC, 2017, Ther Adv Med Onc;

Colorectal Cancer

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Synergy in Combination with IrinotecanPreclinical Data Demonstrates Reduced Tumor Growth

► Combination of onvansertib with irinotecan (FOLFIRI) significantly reduces tumor growth compared to either drug alone

► In 3 independent models tested, onvansertib induced maximal tumor regression of ~84% compared to vehicle

► Kras mutation is a biomarker for onvansertib sensitivity

► KRAS mutated NIH3T3 cells showed higher sensitivity to onvansertib compared with KRAS wild-type cells1

MutatedWild Type

1Investigator Brochure, Data-on-file, Trovagene

Vehicle

Onvansertib 45 mg/kg

Onvansertib 60 mg/kg

Irinotecan 45 mg/kg

Irinotecan 45 mg/kg + onvansertib 45 mg/kg

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Planned Phase 1b/2 Clinical Trial in mCRCWith FOLFIRI + Avastin for 2nd-Line Tx in Patients with a Kras Mutation

Phase 1b: Dose escalation to assess safety and identify recommended Phase 2 dose

► Administered orally, once-daily on Days 1-5 every 14-days (2 courses per 28-day cycle)

12 mg/m2

15 mg/m2

18 mg/m2

Phase 2: Assess safety and preliminary antitumor activity

► Efficacy Primary Endpoint: Objective response rate (ORR) in patients who receive at least 1 cycle (2 courses) of onvansertib in combination with FOLFIRI and bevacizumab

► Efficacy Secondary Endpoint: Preliminary efficacy defined as complete response (CR) plus partial response (PR) plus stable disease (SD)

► Clinical Sites:

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Clinical Advisors and Collaborators

Jorges Cortes, MD Filip Janku, MD, PhD

David Einstein, MD Glenn Bubley, MD Michael Yaffe, MD, PhD

Sandra Silberman, MD, PhD

Afsaneh Barzi, MD Heinz-Josef Lenz, MD, FACP Daniel Ahn, DO

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Key Inflection Points Q2’19 – Q1’20

Clinical Development Q2’19 Q3’19 Q4’19 Q1’20

Acute Myeloid Leukemia

Myelodysplastic SyndromeInvestigator Initiated

ü AACR Phase 1b data presentation (4/1)

ü Clinical Advisory Board Meeting

• ESMO Phase 2 data presentation (9/27)

• FDA meeting: Phase 2 AML and biomarker

plans

• ESH Phase 2 data presentation (10/24)

• ASH Phase 2 data presentation (12/7)

• Investigator-initiated trial activated

• Phase 2 AML trial data readout

• MDS initial safety and efficacy data readout

Metastatic Castration-Resistant Prostate Cancer

ü AACR data presentation (4/2)

ü Arm B – 14-day schedule enrolling

• Asian-Pacific Prostate Cancer Conference presentation (8/24)

• ESMO data

presentation (9/27)

• EMUC Conference data from 14-day dosing schedule (11/14-17)

• ASCO-GU Phase 1b safety and efficacy data (2/13)

Metastatic Colorectal Cancer

ü Sites activated, enrolling patients

ü Collaboration Agreement with

Nektar Therapeutics

• Preliminary safety data from Phase 1b

• Gastrointestinal Oncology Conference (10/10-11) Preliminary Phase 1b safety and efficacy data

• ASCO-GI Phase 2 efficacy data (1/23-25)

27

Financial Profile

Trovagene (Nasdaq: TROV)

Cash and Cash Equivalents as of

March 31, 2019

• $11.3 million

• PoC Capital funding mCRC clinical trial

Estimated 2019 quarterly cash burn • ~$4 million

Shares outstanding as of March 31, 2019 • 4.1 million

28

In Summary

Oncology Focus

► Single molecule addressing multiple indications, each with significant medical need– Onvansertib, only 3rd-generation oral Polo-like Kinase 1 (PLK1) inhibitor in clinical development– 3 active Investigational New Drug (IND) applications in hematologic cancers and solid tumors– Rapid and efficient pipeline progress since licensing onvansertib in March 2017

► Large market opportunities with upside in additional cancers

► Demonstrated synergy of onvansertib in combination with standard-of-care drugs suggests therapeutic potential and valuable partnership opportunities

► Biomarker strategy identifies patients most likely to respond to precision treatments, thereby containing treatment costs while maximizing therapeutic benefit

► Onvansertib has patent protection to 2032 and beyond

► Trovagene enjoys support from world-renowned clinical advisors and investigators

► Seasoned management team with proven track record of development and commercial success

2929

Thank You

For additional information please contact: ir@trovagene.com