Taking a Precision Cancer Medicine™ Approach to Develop Targeted Drugs for Cancer Indications with Significant Need for New Treatment Options NASDAQ: TROV

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.

Trovagene Oncology Developing First-in-Class, Third-Generation, Oral PLK1 Inhibitor Robust, diversified pipeline with single molecule, onvansertib, addressing multiple cancer indications, each with significant medical need for new treatment options Preclinical data demonstrating efficacy of onvansertib in combination with standard-of-care drugs, expanding therapeutic and partnership opportunities Precision Cancer Medicine approach and integration of biomarkers to target treatment for patients most likely to respond Encouraging initial efficacy data from ongoing clinical trials with additional data readouts in 2019-2020 Experienced team with proven oncology drug development experience

Experienced Management Team Drug Development Expertise + Biomarker Technology Thomas Adams, PhD Chief Executive Officer and Chairman Mark Erlander, PhD Chief Scientific Officer Vicki Kelemen Vice President Clinical Development

Our Vision Rapidly Advancing Clinical Development Programs 2H 2019 3 clinical-stage programs Safety and efficacy data readouts Clinical data readouts from all 3 programs Phase 2 trials completed Registrational trials initiated Commercialization partner(s) FDA approval of onvansertib in at least 1 indication Second compound licensed and in the clinic 1H/2H 2020 Vision 2022

Demonstrated Operational Stability Cost-Effective and Efficient Model Raised Capital & Clinical Research Commitment Q1-2, 2019 $8.0 million Cash and Cash Equivalents as of March 31, 2019 $11.3 million Estimated Quarterly Cash Burn $4.0 million Projected Cash Ending Q2, 2019 $10.8 million

Exclusive Global Rights to Onvansertib Licensed from Nerviano Medical Sciences (NMS) in 2017 Largest oncology research and development company in Italy; highly regarded throughout Europe and the U.S. Completed Phase 1 Solid Tumor Trial and IND Excellent R&D Reputation and Track Record Experts in Protein Kinase Drug Development Established CMC (chemistry, manufacturing, controls) GMP / FDA Validated Manufacturing Completed Preclinical Data, Including Synergy PLK1 Proven Effective Cancer Therapeutic Target Licensed Drugs to Genentech, Array/Pfizer, Ignyta/Roche

Optimized Operations and Clinical Development Leveraging Internal Expertise and External Resources 3 INDs in place (1 in each oncology division of the FDA); Orphan Drug Designation in AML Licensed drug with established safety and recommended Phase 2 dose Extensive in-vitro and in-vivo data package providing rationale for combination therapy across multiple cancers Outsourced clinical trial management to CRO, including regulatory, medical/safety monitoring, data management Readily available supply of API and finished drug for clinical trials

We Have the Perfect Target Onvansertib – Polo Like Kinase 1 (PLK1) Inhibitor PLK1 Inhibitor Over-expressed in most cancers Only oral, first-in-class, third-generation PLK1 in clinical trials Preclinical data to support clinical development across multiple tumor types Proven target for cancer therapeutics

Onvansertib Targets the PLK1 Enzyme A Proven Drug Target and Overexpressed in Most Cancers High selectivity for PLK1, only Tested against >260 kinases; PLK1 only active target (IC50 of 2nM) PLK Member Onvansertib IC50* (M) PLK1 0.002 PLK2 > 10 PLK3 > 10 Small molecule (MW 648.60 Daltons) Selectivity driven by stable interaction with carboxyl side chain of amino acid glutamate of PLK1 within PLK1’s ATP binding pocket Onvansertib blocks cells from dividing by arresting them before they divide Tumor Cell Division Onvansertib Blocks Tumor Cell Division P L K 1 p o c k e t O n v a n s e r t i b b i n d s w i t h i n P L K 1 p o c k e t

Onvansertib Benefiting from Class Experience 1st and 2nd generation PLK inhibitors demonstrated clinical activity, but were non-specific for PLK1 and had toxicity issues Product Attributes 1st and 2nd Generation PLK Inhibitors 3rd Generation Onvansertib Selectivity for PLK1 panPLK inhibition of PLK1,2,3* Highly-selective only for PLK1 Antileukemic Activity Phase 2 & 3 trial results indicate activity Improved response rates Clinical response in patients Biomarker strategy identifies patients most likely to respond Administration Intravenous (IV) Oral Half-Life ~135 hours (5.5 days) ~24 hours Dosing and Schedule Fixed treatment schedule Fixed dose for all patients Treatment schedule flexibility Dose determined based on BSA Tolerability Insufficient time between treatment cycles negatively impacted tolerability/survival Time allotted between cycles for patient recovery from on-target hematologic toxicities Infection Prophylaxis Increased rate of fatal infections Antibiotics to proactively mitigate infections

Onvansertib First-in-Class, Third-Generation PLK1 with Best-in-Class Attributes

Diversified Pipeline with 3 Clinical-Stage Programs Opportunities 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 Europe Phase 1b/2 trial in combination with low-dose cytarabine (LDAC) or Decitabine - Ongoing 3 Investigational New Drug (INDs) in place with the FDA Myelodysplastic Syndrome Phase 1b/2 Investigator Initiated Trial (commencing Q4’19 / Q1’20) Leukemias and Lymphomas Solid Tumors Ovarian, Breast, Pancreatic, Small-Cell Lung Phase 1b/2 trial ready (Preclinical Data Available)

Encouraging Initial Data and Near-Term Readouts TROV-052 AML Phase 1b/2 Completion of 6 dose escalation cohorts with no dose-limiting toxicities Initial data demonstrating efficacy – complete response (CR) Determine recommended Phase 2 dose (Q4 2019) Enroll patients in Phase 2 (Q1-2 2020) TROV-053 mCRPC Phase 2 Initial safety and efficacy data Enroll 3 patients in Arm B safety lead-in Identify patients with ARv7 and correlate with treatment response (Q2-3 2019) Provide data from patients completing 3-months of treatment (Q4 2019) TROV-054 mCRC Phase 1b/2 Activate clinical trial sites Enroll 3 patients in initial dose level cohort Provide data on biomarker assessment of tumor burden change (Q3 2019) Provide initial data from first cohort of 3 patients in dose escalation study (Q4 2019) Initiate second dose level cohort to enroll 3 patients (Q4 2019) mCRPC = metastatic castration-resistant prostate cancer; mCRC = metastatic colorectal cancer; AML = acute myeloid leukemia

Combination Therapy for Cancer Treatment Two Drugs are Better Than One (1+1 = 5) Onvansertib is uniquely synergistic (1 +1 = 5) with many FDA-approved drugs; it selectively targets the enzymatic activity of PLK1 that is fundamental for tumor growth Increases efficacy of the therapeutic effect, particularly when the two drugs differ in their mechanism of action and both deliver anti-tumor activity Decreases required dose of each drug and associated toxicity, potentially reducing side effects Minimizes the development of drug resistance because the two drugs block different tumor-promoting pathways for cancer growth Combination Therapy The Cornerstone of Precision Cancer Medicine™

Onvansertib Synergy May Enhance Efficacy of Standard-of-Care Therapies1 Acute Myeloid Leukemia Chronic Lymphocytic Leukemia Colorectal T-Cell Lymphoma Colorectal Breast Non-Small Cell Lung Acute Myeloid Leukemia Pancreatic Breast Ovarian Non-Small Cell Lung Leukemias (Acute Myeloid Leukemia) Leukemias Lymphomas Ovarian Breast Ovarian Bladder Non-Small Cell Lung Small Cell Lung Pancreatic Breast Ovarian Non-Small Cell Lung Multiple Myeloma Prostate 1Data on File, Trovagene, Inc. Onvansertib current clinical trials 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)

Phase 2 Trial: metastatic Castration-Resistant Prostate Cancer

Onvansertib Market Opportunity in mCRPC Significant Disease Burden - Need for More Effective Treatment Options Disease Burden Treatment Opportunity 1 of 6 men will be diagnosed with prostate cancer2 25,000 men die from metastatic prostate cancer annually2 5-year survival rate is 37%2 Standard-of-care is Zytiga® and Xtandi®; resistance develops within 9-15 months4 Tumors re-engineer androgen receptor (AR), variant 7 (ARv7); tumor growth without need for androgens4 Up to 40% ARv7 resistance; very aggressive with no viable treatment options5 PLK1 inhibition improves Zytiga® efficacy, repressing androgen signaling pathway3,4 PLK1 inhibition destabilizes AR and ARv76 Inhibiting PLK1 blocks expression of ARv7; stopping this resistance pathway6 $7.9 billion global market; $12.0 billion by 20257 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; 5Armstrong et al., 2019, JCO 37: 1120- 6Zhang et al., 2015, Cell Cycle 14:13, 2142—2148; 7https://www.grandviewresearch.com/industry-analysis/prostate-cancer-therapeutics-market

Phase 2 Clinical Trial in mCRPC Disease Control Assessed by PSA Stabilization or Decline Dosing Schedule Duration Efficacy Endpoint 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 and tolerability 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 D o s i n g R e g i m e n A r m A D o s i n g R e g i m e n A r m B O n v a n s e r t i b – 2 4 m g / m 2 D a y s 1 - 5 ( 1 4 - D a y C y c l e ) + A b i r a t e r o n e d a i l y 6 C y c l e s = 1 2 W e e k s O n v a n s e r t i b – 2 4 m g / m 2 D a y s 1 - 5 ( 2 1 - D a y C y c l e ) + A b i r a t e r o n e d a i l y 4 C y c l e s = 1 2 W e e k s D i s e a s e C o n t r o l P S A S t a b i l i z a t i o n o r D e c l i n e D i s e a s e C o n t r o l P S A S t a b i l i z a t i o n o r D e c l i n e

Early PSA Response Observed Addition of Onvansertib to Daily Zytiga® 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 in Arm A 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 A b i r a t e r o n e A b i r a t e r o n e + O n v a n s e r t i b E f f i c a c y e v a l u a t i o n a t D a y 8 5

Phase 1b/2 Trial: metastatic Colorectal Cancer

Onvansertib Market Opportunity in mCRC Only 5% Response to Current Second-Line Therapies Disease Burden Treatment Opportunity 140,000 new cases of CRC in 20181 65% 5-year survival1 ~51,000 deaths per year from mCRC1 Tumor biomarkers drive therapy decisions for 1st-line mCRC therapy2 ~50% mCRC has RAS (KRAS) mutation2 Standard-of-care is chemotherapy (FOLFOX/FOLFIRI)2 2nd-line therapies have ~5% response rate in mCRC2 Onvansertib + irinotecan (FOLFIRI) significantly reduces tumor growth3 KRAS mutation is biomarker for onvansertib sensitivity Research partnership with Nektar Therapeutics $9.0 billion global market, expected to grow to $11.0 billion by 20254 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; 3Investigator Brochure, Data-on-file, Trovagene; 4https://www.globaldata.com/store/report/gdhc141pidr--pharmapoint-colorectal-cancer-global-drug-forecast-and-market

Synergy in Combination with Irinotecan Preclinical 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 Mutated Wild 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

Phase 1b/2 Clinical Trial in mCRC Objective Response Rate (ORR) in Second-Line Treatment 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)

Phase 1b/2 Trial: Acute Myeloid Leukemia

Onvansertib Market Opportunity in AML Providing a New Treatment for Relapsed/Refractory Patients Disease Burden Treatment Opportunity 20,000 new cases annually 5-year survival rate of only 25%1 Aggressive blood cancer that usually occurs in the elderly1 Today’s standard-of-care for elderly AML patients is Venclexta® plus azacytidine or decitabine Patients develop resistance to Venclexta® in ~11 months with no viable treatment options2 Onvansertib + chemotherapy has significant activity in AML models3 Onvansertib induces cell death in AML model insensitive to Venclexta® 4 Onvansertib + decitabine will be evaluated as treatment in Venclexta® resistant patients $1.0 billion global market by 20235 1National Cancer Institute SEER 2016; 2DiNardo et al, Blood, 2019 2Valsasina et al., Mol Cancer Ther; 11(4) April 2012; 4Trovagene, data on file; 5https://www.medgadget.com/2019/04/global-acute-myeloid-leukemia-treatment-market-is-expected-to-reach-usd-1-billion-with-cagr-of-5-3

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 Phase 1b/2 Clinical Trial in AML Onvansertib + 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/m2 18 mg/m2 27 mg/m2 40 mg/m2 Completed Completed Completed Completed 60 mg/m2 Completed

Patients Achieving Complete Response Onvansertib is Safe and Well Tolerated 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 0 8 0 0 9 0 0 1 0 0 0 % c h a n g e f r o m b a s e l i n e P r o g r e s s i v e d i s e a s e ( P D ) S t a b l e d i s e a s e ( S D ) M o r p h o l o g i c a l L e u k e m i c F r e e S t a t e ( M L F S ) D a t a L a b e l s r e p r e s e n t o n v a n s e r t i b d o s e ( m g / m 2 ) 1 8 1 8 1 2 4 0 2 7 4 0 2 7 2 7 1 2 4 0 C o m p l e t e r e s p o n s e ( C R ) - 1 5 0 - 1 0 0 - 5 0 0 5 0 1 0 0 1 5 0 % c h a n g e f r o m b a s e l i n e S t a b l e d i s e a s e ( S D ) C o m p l e t e r e s p o n s e ( C R ) 1 8 1 8 2 7 1 8 1 2 4 0 2 7 2 7 4 0 D a t a L a b e l s r e p r e s e n t o n v a n s e r t i b d o s e ( m g / m 2 ) C o m p l e t e r e s p o n s e w i t h i n c o m p l e t e h e m a t o l o g i c a l r e c o v e r y ( C R i ) - 1 5 0 - 1 0 0 - 5 0 0 5 0 1 0 0 1 5 0 % c h a n g e f r o m b a s e l i n e S t a b l e d i s e a s e ( S D ) C o m p l e t e r e s p o n s e ( C R ) 1 8 1 8 2 7 1 8 1 2 4 0 2 7 2 7 4 0 D a t a L a b e l s r e p r e s e n t o n v a n s e r t i b d o s e ( m g / m 2 ) C o m p l e t e r e s p o n s e w i t h i n c o m p l e t e h e m a t o l o g i c a l r e c o v e r y ( C R i ) - 1 5 0 - 1 0 0 - 5 0 0 5 0 1 0 0 1 5 0 8 0 0 9 0 0 1 0 0 0 % c h a n g e f r o m b a s e l i n e P r o g r e s s i v e d i s e a s e ( P D ) S t a b l e d i s e a s e ( S D ) M o r p h o l o g i c a l L e u k e m i c F r e e S t a t e ( M L F S ) D a t a L a b e l s r e p r e s e n t o n v a n s e r t i b d o s e ( m g / m 2 ) 1 8 1 8 1 2 4 0 2 7 4 0 2 7 2 7 1 2 4 0 C o m p l e t e r e s p o n s e ( C R )

Biomarker Evaluates Inhibition of PLK1 Identifies Patients Most Likely to Respond to Treatment Blood test examines the extent that onvansertib inhibits PLK1 enzymatic activity (target engagement) by assessing the phosphorylated status of TCTP within circulating leukemic blast cells TCTP antibody (capture) pTCTP antibody (reporter) pTCTP ANTIGEN pTCTP TCTP - + Onvansertib pTCTP TCTP - + Onvansertib Current method: Western-Blot No Target Engagement Target Engagement Method in development: immuno-PCR based technology P a t i e n t r e c e i v e s a s i n g l e d o s e o f o n v a n s e r t i b A s s e s s t a r g e t e n g a g e m e n t P r e - d o s e s a m p l e 3 h p o s t - d o s e s a m p l e O b t a i n 2 v i a l s o f b l o o d f r o m p a t i e n t T r e a t m e n t v i a l , O n v a n s e r t i b C o n t r o l v i a l , V e h i c l e T r e a t b l o o d s a m p l e w i t h o n v a n s e r t i b o r v e h i c l e c o n t r o l A s s e s s t a r g e t e n g a g e m e n t E x - v i v o s a m p l i n g ( i n d e v e l o p m e n t ) I n - v i v o s a m p l i n g ( c u r r e n t m e t h o d )

Biomarker to Assess Inhibition of PLK1 Correlation of Biomarker+ Patients with Treatment Response PLK1 inhibition can be monitored in patients through pTCTP status to determine target engagement of onvansertib with PLK1 pTCTP as a marker of PLK1 activity: PLK1 phosphorylates the translational control tumor protein (TCTP) on serine 46 pTCTP was identified as a specific marker for PLK1 activity in vivo in preclinical models The comparative change in pTCTP status between pre-dose and 3 hours post-dose is being assessed TCTP PLK1 TCTP P P Onvansertib PLK1 TCTP TCTP Onvansertib P No Onvansertib

Biomarker-Positive Patients Significantly Correlated with Treatment Response PLK1 inhibition by onvansertib (target engagement) is correlated with higher response to treatment Patients with target-engagement had a significantly greater decrease in BM blasts compared to patients with no target-engagement 6 out of the 9 patients with target-engagement had a decrease in BM blasts > 50% Among the 4 patients with objective responses, 3 had target engagement (> 50% decrease in pTCTP) and 1 had a 40% decrease in pTCTP % Bone marrow blast change relative to baseline % Bone Marrow Blast Reduction from Baseline * CR’s * Patient sample showed a 40% reduction in pTCTP -150 -100 -50 0 50 100 150 800 900 1000 % c h a n g e f r o m b a s e l i n e Target Engagement No Target Engagement T a r g e t E n g a g e m e n t N o T a r g e t E n g a g e m e n t 0 100 200 300 400 500 %BM blasts relative to baseline % B M b l a s t s r e l a t i v e t o b a s e l i n e p= ** 0.0033

Trovagene Oncology Developing First-in-Class, Third-Generation, Oral PLK1 Inhibitor Robust, diversified pipeline with single molecule, onvansertib, addressing multiple cancer indications, each with significant medical need for new treatment options Preclinical data demonstrating efficacy of onvansertib in combination with standard-of-care drugs, expanding therapeutic and partnership opportunities Precision Cancer Medicine approach and integration of biomarkers to target treatment for patients most likely to respond Encouraging initial efficacy data from ongoing clinical trials with additional data readouts in 2019-2020 Experienced team with proven oncology drug development experience

Thank You For additional information please contact: ir@trovagene.com