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 su

Using Our Precision Medicine Strategy

to Develop Oncology Drugs That Target Mitosis July 2018 Exhibit 99.1

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.

Strategy for Oncology Drug Development

Taking a precision medicine approach to developing PCM-075 by integrating a highly-selective antimitotic drug with a biomarker strategy Leveraging a proven cancer target, PLK1, that is highly expressed in tumor cells and integral to cell division

(mitosis) Developing a first-in-class, 3rd generation PLK1 inhibitor, benefiting from prior drug class clinical experience, including efficacy, safety and single vs combination therapy trial design Combining PCM-075 with already approved drugs that

have demonstrated synergy in combination: Phase 1b/2 trial of PCM-075 + cytarabine or decitabine in Acute Myeloid Leukemia (AML) Phase 2 trial of PCM-075 + abiraterone acetate (Zytiga ) in metastatic Castration-Resistant Prostate Cancer (mCRPC)

Pursuing partnership opportunities with Japanese companies to expand development of PCM-075

Our PCM-075 Oncology Pipeline

Opportunities in Solid Tumors and Leukemias/Lymphomas Preclinical Phase 1 Phase 2 Solid Tumor Cancers Leukemias & Lymphomas Metastatic Castration-Resistant Prostate Phase 2 trial in combination with with abiraterone acetate

(Zytiga )/prednisone Lung Colon Ovarian Others (adrenocortical, sarcomas, head and neck, skin, liver, pancreatic, ampullary) Triple Negative Breast Acute Myeloid Leukemia - Orphan Drug Designation in the U.S. Phase 1b/2 trial in

combination with low-dose cytarabine (LDAC) or decitabine Non-Hodgkin Lymphoma

Trovagene's Management Team

Proven Leadership in Oncology Tom Adams, PhD Chairman of the Board Interim CEO Mark Erlander, PhD Chief Scientific Officer George Samuel, Esq. VP, General Counsel Vicki Kelemen VP, Corporate Communications Sandra Silberman, MD, PhD Chief Medical

Scientific Advisors Principal

Investigators and Collaborators Jorge Cortes, MD - MD Anderson Deputy Chair, Professor of Medicine, Department of Leukemia and Director of CML and AML programs Glenn Bubley, MD - Beth Israel Deaconess Medical Center Director,

Multidisciplinary Genitourinary Cancer Program David Einstein, MD - Beth Israel Deaconess Medical Center Principal Investigator, mCRPC Phase 2 Trial Filip Janku, MD, PhD - MD Anderson Associate Professor, Investigational Cancer

Therapeutics (Phase 1 Clinical Trials Program) Michael Yaffe, MD, PhD - MIT Director, MIT Center for Precision Cancer Medicine, Professor of Biology and Biological Engineering Amer Zeidan, MBBS, MHS - Yale Assistant Professor of Medicine

Licensed Drug Candidate from NMS

PCM-075 - Polo-like Kinase 1 (PLK1) Inhibitor Largest oncology research and development company in Italy Developed anthracycline class of drugs (doxorubicin) Leader in protein kinase drug development (Polo-like Kinase Inhibitors)

Identification and validation of molecular targets focused on driver oncogenes, cell-cycle regulation and DNA repair, cancer metabolic pathways and immune oncology Excellent track record licensing innovative drugs to pharma/biotech companies

including: Genentech (Roche), Ignyta (Roche), Novartis Oncology Drug Discovery Developing Oncology Drugs That Target Mitosis Licensed global development and commercialization rights for PCM-075 Nerviano will continue manufacturing GMP API and

finished drug Two active INDs in place with the FDA (solid tumor and hematologic cancers) Partnering discussions ongoing with several Japanese companies to expand development of PCM-075 Financing in place to advance clinical trial program into

mid-2019 IND = Investigational New Drug

Leveraging Proven Cancer Target

PLK1: Established Target for Cancer

Therapy PLK1 Plays a Critical Role in Initiation, Maintenance and Completion of Mitosis PLK1 belongs to a family of kinases (PLK1, 2,4,4 and 5) Dysfunction of PLK1 promotes cancerous formation and drives cancer progression PLK1 is over-expressed in

dividing cells in numerous cancers and is associated with poor patient prognosis1 Inhibition of PLK1 interferes with multiple stages of mitosis and leads to cancer cell death 1Liu et al- PLK1, A Potential Target for Cancer Therapy; Translational

Oncology - Vol. 10 - pp. 22-32; February 2017 Cell-cycle arrest Mitosis PLK1 Expression Cell Cycle

PLK1 is Over-Expressed in Multiple

Cancers "In our view, combined therapies targeting other relevant pathways together with Plk1 may be vital to combat issues observed with monotherapy, especially resistance." July 2016 PLK1 Inhibitors in Cancer Therapy: From

Laboratory to Clinics Randomized, Phase 2 Trial of Low-Dose Cytarabine with or without Volasertib in AML patients not suitable for Induction Therapy "By adding volasertib to LDAC, the overall response was more than doubled, with 31% vs 13% for

LDAC alone." August 2014 PLK1 Inhibition Enhances the Efficacy of Androgen Signaling Blockade in Castration-Resistant Prostate Cancer "Our results offer a strong mechanistic rationale to evaluate PLK1 inhibitors in combination drug

trials to enhance the efficacy of Androgen Signaling Inhibitors in mCRPC." September 2014 Overexpression of PLK1 Observed in Numerous Cancers Tumor Type PLK1 Fold Change Over-Expression AML 13.0 B-cell Lymphoma 56.3 Prostate 3.3 Adrenocortical

4.5 Lung Adeno 9.7 Lung Squamous 20.8 Breast 11.3 Esophageal 10.2 Stomach 4.8 Colon 2.5 Head & Neck 4.2 Pancreatic 2.2 Ovarian 31.7 Glioblastoma 12.4 Kidney 4.7 Liver 11.7 Uterine 21.3 Bladder 9.1 1Liu et al- PLK1, A Potential Target for Cancer

Therapy; Translational Oncology - Vol. 10 - pp. 22-32; February 2017

Developing First-in-Class 3rd

Generation PLK1 Inhibitor

PLK Inhibitor Landscape 1st

Generation PLK inhibitors: BI-2536, TAK-960, GW843682 Pan inhibitors: No selectivity between PLK1, 2, & 31 TAK-960, GW843682 (toxicity issues) Phase 1 & 2 results (BI-2536) Tolerable and reversible hematological toxicities2-4 Limited

efficacy as single agent in AML3, lymphoma2, and solid tumors4 2nd Generation PLK inhibitor: BI-6727 Pan inhibitor for PLK 1, 2 & 3 Long half-life (~5 days) and I.V. (intravenous) formulation Phase 2 results Significant efficacy demonstrated in

AML for the combination BI-6727 + cytarabine5 Limited efficacy as single agent observed in ovarian cancer6 1https://www.medchemexpress.com; 2Vose et al., Leukemia & Lymphoma 2013 54:4, 708-713;3M ller-Tidow et al., Br J Haematol. 2013

Oct;163(2):214-22; 4Awad et al., Lung Cancer. 2017 Feb;104:126-130;5Dohner et al., Blood, 2014 124:9, 1426-1433; 6Pujade-Lauraine, E et al., J Clin Oncol. 2016 Mar 1;34(7):706-13

PCM-075: 3rd Generation PLK1

Best-in-Class Attributes Highly Selective Favorable Safety and Tolerability Orally Available Synergistic in Combination Ideal Pharmacokinetics

PCM-075: Characteristics PCM-075 is

a small molecule, selective PLK1 inhibitor (MW 650 Daltons)1 Half-life of ~24 hours Formulated as 5 mg and 20 mg hard gelatin capsules 4-year shelf-life when stored at 5 C 3 C (36 F to 46 F) Nerviano manufacturer for GMP

API and finished goods ADME Profile2 Highly stable in human hepatocytes Plasma protein binding ranging from 83% to 93% in the different species No Cytochrome P450 inhibition observed at therapeutic concentrations Good oral bioavailability,

low-medium clearance and high-volume of distribution in all tested species in single and repeated pharmacokinetic studies 1Data on File, Trovagene, Inc.; 2ADME = Absorption, Distribution, Metabolism, Excretion

PCM-075 Intellectual Property Four

worldwide patent families Genus, Compound, Combinations, Salt Mature portfolio Granted in most major jurisdictions Patent term 2030 plus up to 5 years extension

PCM-075: Selective 3rd Generation

PLK1 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. Selective PLK1 Inhibitor

Induces tumor cell death by G2M cell cycle arrest AML-NS8 Patient-Derived Cells Treated with 200 nM PCM-075 for 24 Hrs1 PCM-075 DMSO PCM-075 Control Treatment of cells with PCM-075 resulted in a clear mitotic block accompanied by an increase of the

G2/M population (4N DNA content) PLK Member PCM-075 IC50* ( M) PLK1 0.002 PLK2 > 10 PLK3 > 10

Phase 1 Safety Trial in Solid

Tumors1 Favorable First-in-Human Data Phase 1 Trial Design PCM-075 Trial Results Included: colorectal, pancreatic, lung, sarcomas, hepatocellular, ampullary, prostate, ovarian, skin Established safety of PCM-075 and identified a recommended Phase 2

dose of 24 mg/m2/day 16 of the 19 patients (84.2%) treated with PCM-075, were evaluable for efficacy, with stable disease at any dose observed in 5 (31.2%) of the patients Reversible, on-target thrombocytopenia and neutropenia, consistent with the

expected mechanism of action, were the primary adverse events No GI disorders, mucositis, or alopecia was observed, confirming that bone marrow cells are the most sensitive to PCM-075 inhibition with the applied dosing schedule Phase 1 Dose

Escalation Trial in Patients with Advanced or Metastatic Solid Tumors Open-label dose escalation trial in patients with solid tumor malignancies 19 of 21 patients enrolled administered PCM-075 orally, once daily for 5 consecutive days, every 3 weeks

1Weiss G et al., Phase I dose escalation study of NMS-1286937, an orally available Polo-like Kinase 1 inhibitor, in patients with advanced or metastatic solid tumors - Invest. New Drugs DOI 10.1007/s10637-017-0491-7

Benefiting From Drug Class

2nd Generation PLK Inhibitor

(BI-6727) Randomized Phase 2 Clinical Trial in AML LDAC 2 x 20 mg/day sc, Days 1-10 Every 28 days Adults with previously untreated AML Ineligible for intensive therapy LDAC 2x20 mg/day sc, Days 1-10 + BI 6727 50 mg Days 1 + 15 Every 28

days n=45 n=42 4-week cycles until progression, relapse, intolerance, patient/ or investigator requested Randomized Phase 2 Trial of BI-6727 + LDAC vs LDAC Alone in Acute Myeloid Leukemia Survival distribution function (%) 0 40 100 Time (months) 0 4

20 28 80 60 20 36 8 12 16 24 32 LDAC LDAC + BI-6727 LDAC + BI-6727 (n=42) LDAC (n=45) Median OS, months 8.0 5.2 (95% CI) (3.2-14.5) (3.2-9.1) HR (95% CI) 0.63 (0.40-1.00) p=0.047 2 6 10 14 18 22 26 30 34 Results Increased response

rate with BI-6727 + LDAC (31.0%) vs LDAC alone (13.3%) Significant survival benefit in elderly patients ineligible for induction therapy Response across all AML genetic subgroups Clinically manageable safety profile

2nd Generation PLK Inhibitor

(BI-6727) Randomized Phase 3 Clinical Trial in AML Primary analysis for efficacy included 371 of a total 666 patients randomized Results: BI-6727 + LDAC vs placebo + LDAC Increase in remission rate (CR + CRi): 25.2% vs 16.8% (central assessment)

- Overall Response 1.659; p=0.071 29.7% vs 19.2% (investigator assessment) - Overall Response 1.757; p=0.034 Negative overall survival trend (HR: 1.26; p=0.1129) Increased frequency of fatal AEs (fatal infections being the major

contributor) Trial was unblinded after the primary analysis Patients remaining on treatment were allowed to continue based on individual benefit-risk evaluations HR = Hazard Ratio.

PCM-075 Clinical Development

Benefiting From Class Experience Product Attributes 1st and 2nd Generation PLK Inhibitors 3rd Generation PCM-075 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 Early data from Phase 1b/2 trial indicates activity Biomarker strategy to identify patients most likely to respond Dosing and Schedule Fixed treatment schedule Fixed dose for all patients Treatment schedule

flexibility Dose determined based by BSA Tolerability Insufficient time between treatment cycles negatively impacted tolerability/survival Time allotted between cycles for patient recovery from drug-induced neutropenia Infection Prophylaxis

Increased rate of fatal infections in patients not given prophylactic antibiotics Protocols require mandatory prophylactic antibiotics *PLK2-PLK5 have properties more consistent with tumor suppressor genes and are not essential for cell division;

BSA = Body Surface Area.

Combination Therapy Approach

PCM-075: Combination Therapy

Strategy Combination therapy is considered the cornerstone of precision cancer medicine Demonstrated synergy in combination with chemotherapies and targeted therapeutics Enhances efficacy compared to monotherapy approach because it targets key

pathways in a characteristically synergistic or additive manner Approach potentially reduces drug resistance, while simultaneously providing therapeutic benefits, including: Reducing tumor growth and metastatic potential Arresting mitotically active

cells Inducing apoptosis (programmed cell death) 1Mokhtari, R et al - Combination Therapy in Combatting Cancer - Oncotarget, 2017, Vol. 8 (No. 23), pp: 38022-38043

PCM-075: Synergistic in Combination

High PLK1 expression is associated with the most aggressive forms of solid tumor cancers, leukemias and lymphomas Synergistic activity of PCM-075 may enhance efficacy of standard-of-care therapies 1Alphabetical order. 2Preclinical data on file with

PCM-075 and these combined therapeutics Potentially Synergistic Drugs1,2 Abiraterone acetate Bevacizumab Bortezomib Cisplatin Cytarabine Doxorubicin FLT3 Inhibitors (Quizartinib) Gemcitabine HDAC Inhibitors (Belinostat) Paclitaxel Associated

Cancers2 Leukemias/Lymphomas: Acute Myeloid Leukemia Acute Lymphocytic Leukemia Non-Hodgkin Leukemia Multiple Myeloma Solid Tumor Cancers Castration-Resistant Prostate Adrenocortical Carcinoma Triple Negative Breast Sarcomas Small Cell Lung Colon

PCM-075: Rationale for Combination

with DNA Damaging Agents1,2 Active PLK1 PLK1 Inhibited 1van Vugt & Yaffe, Cell Cycle 2010 9:2097-2101; 2van Vugt et al., 2010, PLoS 8:1-19 DNA Damaging Agents Cytarabine Doxorubicin Cisplatin DNA Damage Response (DDR) arrests cells at G2/M

checkpoint G2/M Arrest Mitosis Checkpoint adaptation PLK1 inhibits DDR, induces mitotic entry for tumor cells & cell division Cell Death Keeps tumor cells in G2/M arrest leading to apoptosis For cells that escape, mitosis is blocked, also

leading to apoptosis

Synergy: PCM-075 + Cytarabine Acute

Myeloid Leukemia (AML) Cell Line (HL-60) 1 10 100 1000 Concentration [nM] Combination Index (CI) 0.67 PCM-075 IC50 60.40 nM Cytarabine IC50 37.40 nM Combination IC50 30.09 nM Expected Combination IC50 46.40 nM Data: Nerviano Medical Sciences

Greatest Synergy Observed with Highest % Cell Death

Synergy: PCM-075 + FLT3 Inhibitor

Acute Myeloid Leukemia (AML) 1Kindler et al, Blood 2010; 116:5089-10. 2Stone et al, N Engl J Med 2017; 377:454-64. 3Data on File at Trovagene, Inc. 30% of AML patients harbor a FLT3 mutation1 Midostaurin (FDA approved); 3 additional FLT3 inhibitors,