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

Transforming Patient Care with Targeted

Cancer Therapeutics Company Overview | january, 2018 Company Overview January 2017 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.

Lead Asset: PCM-075 PCM-075 is an oral,

highly-selective Polo-like Kinase 1 (PLK1) inhibitor Trovagene licensed exclusive global development and commercialization rights from Nerviano Medical Sciences in 2017 Nerviano is the current manufacturer and has bulk material and finished product

available for clinical trials Nerviano Medical Sciences: largest oncology-focused R&D company in Italy, highly regarded in Europe Other licensees include: Genentech (Roche), Pfizer, Array Pharmaceuticals, Servier, and Ignyta

Trovagene Snapshot NASDAQ: TROV 2017

Year-End Cash: $8.2M Shares Outstanding: 52.8M Oncology Focus PCM-075, the only oral, selective PLK1 inhibitor to enter clinical trials 2 active INDs: Hematologic and Solid Tumor Cancers Completed and published Phase 1 safety study in solid tumor

cancers Orphan Drug Designation in AML Proprietary tumor profiling technology Results from Phase 1b segment of Acute Myeloid Leukemia (AML) study with recommended Phase 2 dose Initiation of AML Phase 2 continuation study Initiation of Phase 2 trial

in metastatic Castration-Resistant Prostate Cancer (mCRPC) Both Phase 2 trials are open-label studies with potential for early data results Investment Case Significant Milestones Oncology Focus

PCM-075: A Best in Class PLK1 Inhibitor

Targeting Hematologic and Solid Tumor Cancers Acute Myeloid Leukemia (AML) Metastatic Castration-Resistant Prostate Cancer (mCRPC) Phase 1b/2 Phase 2 Combination of PCM-075 with standard-of-care chemotherapy to extend response to treatment in AML

patients ineligible for intensive induction therapy or who have refractory or relapsed disease Combination of PCM-075 with abiraterone (Zytiga ) to extend response to anti-androgen therapy in patients showing early disease progression

Hematologic Tumors Solid Tumors

Pipeline Assets Indication (Target)

Preclinical Phase 1 Phase 2 Non-Hodgkin Lymphoma Acute Myeloid Leukemia - Orphan Drug Designation TROV-052 Phase 1b/2 open-label clinical trial in combination with standard-of-care ongoing Indication (Target) Preclinical Phase 1 Phase 2 Phase

1 Advanced Solid Tumors Completed and published in Investigational New Drugs Castration-Resistant Prostate TROV-053 Phase 2 protocol submitted to FDA solid tumor IND Adrenocortical Carcinoma Triple Negative Breast Hematologic Tumors Solid

PLK1 - Cancer Therapeutic Target

Key Regulator of Cell Division PLK1 is the master regulator of the cell- cycle and the last checkpoint prior to cell division (G2/Mitosis phase)1-6 Inhibition of PLK causes mitotic arrest in prometaphase (polo arrest) and subsequent cell death

(apoptosis)1-4 Over-expression of PLK1 is observed in numerous cancer types and associated with poor patient prognosis7 Depletion of PLK1 induces cell death in tumor cells8 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 Discov 2010;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; 7Data derived from The Tumor Genome Atlas, https://tcga-data.nci.nih.gov/docs/publications/tcga; 8Liu et al., Mol. Cell. Biol. March 15, 2006; 26:6 2093-2108 PLK1 - Cancer Therapeutic Target

PLK1 Overexpressed in Numerous Cancers

Publications Illustrate Broad Application "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 Randomizes, 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 Over-Expression AML 13.0 B-cell Lymphoma

56.3 Adrenocortical 4.5 Lung Adeno 10.5 Lung Squamous 20.9 Breast 14.4 Esophageal 7.8 Stomach 2.2 Colon 2.5 Head & Neck 3.1 Skin Melanoma 18.3 Ovarian 31.7

PLK Inhibitor Landscape Drug/Company

Drug Target(s) Development Stage Cancer Types Studied Status Volasertib1 Boehringer Ingelheim Non-specific (Pan) PLK1,2,3 Inhibitor Phase 3 (AML) AML Solid Tumors Failed Phase 3 trial due to infections, most likely the result of not administering

prophylactic anti-infectives or dosing schedule Rigosertib2 Onconova Non-targeted, broad spectrum multi-kinase inhibitor (RAF, PI3K, PLK) Phase 3 (MDS) Pancreatic Myeloid Dysplastic Syndrome (MDS) Failed Phase 3 trial; currently testing IV drug in

high-risk MDS patients CY1405 Cyclacel PLK1,2,3 Preclinical Esophageal Cancer Ongoing 1https://trials.boehringer-ingelheim.com/public/trial_results_documents/1216/1216.11_121611U935541DRCOpdf.pdf et al; 2Expert Rev Anticancer Ther. 2016

Aug;16(8):805-10; 3Clin Cancer Res. 2011 May 15;17(10):3420-30;

Clinical Efficacy PLK Inhibitor Drug

Class Experience Increased response rate and improved survival in AML patients ineligible for intensive induction therapy Demonstrated response across all AML genetic subgroups and had a clinically manageable safety profile PLK Inhibition Increased

Overall Survival in Phase 2 AML Study1 Volasertib, an investigational pan PLK inhibitor (PLKi) IV formulation with half-life of ~135 hours 1Dohner et al; Randomized, Phase 2 Trial of Low-Dose Cytarabine with or without Volasertib in AML Patients not

Suitable for Induction Therapy - Blood, 28 August 2014 - Vol 124, Number 9 - 1426-1433; 2 Results reported by Boehringer Ingelheim, June 2016 Percentage of patients with an objective response was higher with volasertib plus LDAC,

compared to placebo plus LDAC; however, the difference was not statistically significant Data showed an unfavorable overall survival trend, the result of an increase in infection rate associated with the volasertib plus LDAC dosing regimen

Volasertib Plus LDAC Phase 3 AML Study2

PCM-075 - Highly-Selective for

PLK1 Highly Selective Short Half-Life Acceptable Safety Profile Broad Applicability Orally Available

PCM-075 - Selective PLK1

Inhibitor Tested against >260 kinases and PLK1 was the only active target with 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 G2/M cell cycle arrest AML-NS8 Patient-Derived Cells Treated with 200 nM PCM-075 for 24 Hrs1 Molecular Weight : 648.60 Daltons PCM-075 DMSO PCM-075 Control

PCM 075 - Synergistic in

Combination High PLK1 expression is associated with the most aggressive forms of hematologic malignancies and solid tumor cancers PCM-075's synergistic activity potentially enhances the efficacy of numerous standard-of-care therapies

1Alphabetical order. 2Preclinical data on file with PCM-075 and these combined therapeutics Potentially Synergistic Drugs1,2 Abiraterone Bortezomib Cisplatin Cytarabine Doxorubicin Gemcitabine HDAC Inhibitors Pacitaxel Quizartinib (FLT3) Associated

Cancers2 Liquid Tumors: Acute Myeloid Leukemia Acute Lymphocytic Leukemia Non-Hodgkin Leukemia Multiple Myeloma Solid Tumors Castration-Resistant Prostate Adrenocortical Carcinoma Triple Negative Breast Sarcomas Small Cell Lung

Acute Myeloid Leukemia (AML)

Combination of PCM-075 with FLT3 Inhibitor Evaluation of Efficacy of PCM-075 for MV-4-11 Human Acute Myeloid Leukemia (AML) Xenograft Model in NOD.SCID Mice 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 recently FDA approved; 3 additional FLT3 inhibitors, including quizartinib, are currently in Phase 3 clinical development2 The combination of PCM-075 and quizartinib

demonstrated 97% tumor growth inhibition and regression in FLT3 AML xenograft model3

Why PCM-075 Characteristic Benefit

PCM-075 Oral; 24-Hour Half-Life Enables sustaining drug levels without compromising safety Selective for PLK1 Provides highly-targeted therapy for G2/M cell-cycle division checkpoint Reversible, on-target side effects, consistent with the

expected mechanism of action3 Synergistic in Combination1 Combination therapies potentially yielding "1+1=3" clinical activity Demonstrated synergy with (e.g., cytarabine, paclitaxel and abiraterone) Enhances mechanism of action

without increasing on-target toxicities Tumor Cell Sensitivity Normal cells are 10-fold less sensitive than tumor cells to induced cell death2 No GI disorders, mucositis, or alopecia observed in Phase 1 solid tumor study Resistance

Mechanism Ability to induce cell death in tumor cells that express transporters (e.g. MDR1)3 1Preclinical data on file with PCM-075 in combination with chemo and targeted therapeutics; 2Valsasina et al., Molecular Cancer Therapeutics; 11(4)

April 2012; 3Investigator Brochure for PCM-075, 22 June 2017 Trovagene data on file

PCM-075 - AML Enhancing

standard-of-care in patients ineligible for intensive induction therapy

Acute Myeloid Leukemia Market

Opportunity1 AML: aggressive hematologic malignancy Incidence: 20,000* new cases and 10,400 deaths annually in the U.S. Prognosis: 5 year survival rate is 25% Treatment options vary based on patient condition / age, but can include: Chemotherapy

Radiation Stem cell transplant Genetically diverse landscape: PLK1 selectivity presents opportunity across patient sub-populations *Orphan Drug Designation granted by the FDA September 28, 2017; 1National Cancer Institute SEER 2016

How PCM-075 Fits Within Treatment

Pathway for Acute Myeloid Leukemia AML Diagnosis 20,0001 cases/year Eligible for Induction Treatment 12,000 Relapse & Refractory 30-50% 4,000 to 6,000 TROV-052 Phase 1b/2 AML Study: to assess the safety and efficacy of PCM-075 in combination

with standard-of-care Responders 50-70% Ineligible for Induction Treatment ~8,000 Consolidation Treatment 1National Cancer Institute SEER 2016

Compelling Pre-Clinical Data

Supports Phase 1b/2 Study Response observed in various xenograft models as a single agent and in combination1 Compound Median Survival Time (days) Placebo 28 Cytarabine 36 PCM-075 62* In Vivo Disseminated Leukemia Model (AML-NS8 Cells) Treatment

with PCM-075 Started 20 Days Post-Inoculation 60 mg/kg BID (Days 1 and 2, 3 Cycles) 1Casolaro et al (2013) PLOS One Vehicle PCM-075 60 mg/kg BID Cytarabine 75 mg/kg Vehicle PCM-075 60 mg/kg BID Cytarabine 75 mg/kg *p = 0.001

Phase 1b/2 Study in Acute Myeloid

Leukemia TROV-052 dose escalation; safety and efficacy in combination with standard-of care (n=74): NCT03303339 SCREENING DOSING (DAYS/CYCLE) PCM-075 Chemotherapy 1 11 - 28 Study Design Dose escalation (starting at 12 mg/m2) in Phase 1b with

expansion cohort at maximum tolerated dose (MTD) for Phase 2 continuation Safety Assess side effects and tolerability to identify the MTD for use in the Phase 2 Determine the most beneficial combination regimen, dose and scheduling for Phase 2

Efficacy Endpoints Rate of complete response (CR + CRi) in Phase 2, defined as morphologic leukemia-free state (MLF) plus: For CR: Patient is independent of transfusions Absolute neutrophil count (ANC) of >1000/mm3 Platelets of

100,000/mm3 For CRi: Meets all criteria for CR except for either neutropenia (ANC <1000/mm3) or thrombocytopenia (<100,000/mm3) Exploratory Endpoints Pharmacodynamic correlative biomarker evaluation FOLLOW-UP (DAYS/CYCLE) BONE

MARROW ASSESSMENT 2 3 4 5 6 7 8 9 10

Biomarker Assessment to Measure Drug

Activity and Effect on Tumors Biomarkers will be measured and correlated with pharmacokinetic drug levels to assess: Inhibition of PLK1 enzymatic activity by assessing inhibition of TCTP phosphorylation Blockage of cell division (G2/M arrest) Tumor

DNA biomarkers Blood sample (baseline) AML Patient + PCM-075 Blood sample (post PCM-075) Pre- and Post-Dose Blood Sampling 1TruSight Myeloid Sequencing Panel; Illumina

PLK1 Enzymatic Activity Biomarker

for PCM-075 inhibition1 PCM-075 ( M): 0 .01 .032 .1 .32 1 3 10 pTCTP Total TCTP 1Trovagene, data on file PLK1 activity: as measured by pTCTP (Translationally Controlled Tumor Protein) which is activated by PLK1 1Trovagene Data on file Vehicle

(DMSO) PCM-075 Positive Control (Nocodazole) Blockage of Cell Division by PCM-075 G2/M Arrest by Analysis of DNA Content PLK1 Enzymatic Activity Inhibited by PCM-075 PLK1 activity: as measured by G2/M arrest of cell division

Molecular Profiling and Patient

Response1 AML Genomic Subgroup Frequency of Patients Most Frequently Mutated Genes (%) DNA Panel RNA Panel NPM1 mutation 27% NPM1(100), DNMT3A(54), FLT3(39), NRAS(19), TET2(16), PTPN11(15) Mutated chromatin, RNA-splicing genes, or both 18%

RUNX1(39), MLLPTD(25), SRSF2(22), DNMT3A(20), ASXL1(17), STAG2(16), NRAS(16),TET2(15),FLT3ITD(15) TP53mutations, chromosomal aneuploidy, or both 13% Complex karyotope(68), -5/5q(47), -7/7q(44), TP53(44), -17/17p(31), +8/8q(16)

inv(16)(p13.1q22) or t(16;16)(p13.1;q22);CBFB-MYH11 5% inv(16) (100), NRAS(53), +8/8q(16), KIT(15), FLT3TKD(15) biallelic CEBPA mutations 4% CEBPAbiallelic(100), NRAS(30), WT1(21), GATA2(20) t(15;17)(q22;q12);

PML-RARA 4% t(15;17) (100), FLT3 ITD(35), WT1(17) t(8;21)(q22;q22); RUNX1-RUNX1T1 4% t(8;21) (100), KIT(38), -Y(33), -9q(18) MLL fusion genes; t(x;11)(x;q23) 3% t(x;11q23) (100), NRAS(23)

inv(3)(q21q26.2) or t(3;3)(q21;q26.2); GATA2,MECOM(EVI1) 1% inv(3) (100), -7(85), KRAS(30), NRAS(30), PTPN11(30), ETV6(15), PHF6(15), SF3B1(15) IDH2R172 mutations and no other class-defining lesions 1% IDH2R172(100), DNMT3A(67),

+8/8q(17) t(6;9)(p23;q34); DEK-NUP214 1% t(6;9) (100), FLT3ITD(80), KRAS(20) 1Papaemmanuil et al. Genomic classification and prognosis in acute myeloid leukemia; NEJM 2016;374:2209-2221

PCM-075 - Solid Tumors

Combination therapy with chemo and targeted therapies to extend treatment response and overall survival

Successful Phase 1 Safety Study

Completed in Solid Tumors* Phase 1 Study Design 19 of 21 patients enrolled administered PCM-075 orally, once daily for 5 consecutive days, every 3 weeks PCM-075 Study Results Included: colorectal, pancreatic, lung, sarcomas, hepatocellular,

ampullary, prostate, ovarian, skin Open-label dose escalation trial in patients with solid tumor malignancies 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 study in patients with advanced or metastatic solid tumors *