8-K

UNITED STATES
SECURITIES AND EXCHANGE COMMISSION

Washington, DC 20549

FORM 8-K

CURRENT REPORT
Pursuant to Section 13 or 15(d) of the Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): August 21, 2017

Trovagene, Inc.

(Exact name of registrant as specified in its charter)

Delaware	001-35558	27-2004382
(State or other jurisdiction	(Commission File	IRS Employer
of incorporation or organization)	Number)	Identification No.)

11055 Flintkote Avenue

San Diego, CA 92121

(Address of principal executive offices)

Registrant’s telephone number, including area code: (858) 952-7570

(Former name or former address, if changed since last report)

Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

o            Written communication pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

o            Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

o            Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

o            Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Indicate by check mark whether the registrant is an emerging growth company as defined in as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).  Emerging growth company o

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.  o

Item 8.01Other Events.

On August 21, 2017, Trovagene, Inc.  (the “Company”) issued a press release announcing compelling results of preclinical research of PCM-075 with a Histone deacetylase (HDAC) inhibitor in Non-Hodgkin Lymphoma (NHL) cell lines.  A copy of the press release is furnished as Exhibit 99.1 to this Form 8-K.

The Company intends to conduct meetings with third parties in which its corporate slide presentation will be presented.  A copy of the presentation materials is attached as Exhibit 99.2 to this Current Report on Form 8-K and is incorporated herein by reference.

Item 9.01. Financial Statements and Exhibits

(d) Exhibits.

99.1	Press Release of Trovagene, Inc. dated August 21, 2017
99.2	Corporate Presentation of Trovagene, Inc.

SIGNATURE

Pursuant to the requirements of the Securities Exchange Act of 1934, the Registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.

Dated:         August 21, 2017

TROVAGENE, INC.
By:	/s/ William J. Welch
	William J. Welch
	President and Chief Executive Officer

2

EX-99.1

Exhibit 99.1

Trovagene’s PLK1 Inhibitor PCM-075 Demonstrates Synergy with a HDAC Inhibitor in Non-Hodgkin Lymphoma Cell Lines

Additionally, Trovagene announces PCM-075 synergy in combination with more than ten chemo and targeted therapeutics across a broad range of solid tumor and hematologic malignancies

SAN DIEGO, CA — August 21, 2017 — Trovagene, Inc. (NASDAQ: TROV), a precision medicine biotechnology company, today announced compelling results of preclinical research of PCM-075 with a Histone deacetylase (HDAC) inhibitor in Non-Hodgkin Lymphoma (NHL) cell lines.  This synergy assessment study was conducted by Dr. Steven Grant, Associate Director for Translational Research and co-Leader, Developmental Therapeutics Program, Massey Cancer Center.

PCM-075, Trovagene’s investigational Polo-like kinase 1 (PLK1) inhibitor, showed significant synergy in combination with a HDAC inhibitor of up to 80% in aggressive double-hit B-cell lymphoma (DLBCL) and mantle-cell lymphoma cell lines.  DLBCL and mantle cell lymphomas within NHL represent challenging malignancies without a standard-of-care treatment and confer a poor prognosis for patients.

Additionally, PCM-075 synergy has been evaluated in combination with more than ten different chemotherapeutics, including cisplatin, cytarabine, doxorubicin, gemcitabine and paclitaxel, and targeted therapies, such as HDAC inhibitors, FLT3 inhibitors, and bortezomib. These therapeutics are used clinically for treatment of many solid and hematologic cancers, including Acute Myeloid Leukemia (AML), Acute Lymphocytic Leukemia (ALL), Non-Hodgkin Lymphoma (NHL), Multiple Myeloma, Adrenocortical Carcinoma (ACC), Triple-Negative Breast Cancer (TNBC), Small-Cell Lung Cancer (SCLC), and Ovarian Cancer.

“We are excited to see the synergistic benefits with PCM-075 in combination with a HDAC inhibitor in the most difficult cell lines in NHL,” said Bill Welch, CEO of Trovagene. “This data complements our recent announcement of an in-vivo study demonstrating synergy of PCM-075 with a leading investigational FLT3 inhibitor, as well as PCM-075 synergy with many chemotherapeutics. We have an active Investigational New Drug (IND) in place with the FDA for each of solid tumors and hematologic malignancies, which could facilitate the development of PCM-075 across a number of cancer types.”

The consistent and significant synergistic effects observed in preclinical research on tumor cell death indicates that PCM-075 could be effective in combination therapies to address a broad range of tumor types, as well as the emergence of drug-resistant tumors.

About PCM-075

PCM-075 is a highly-selective adenosine triphosphate (ATP) competitive inhibitor of the serine/threonine polo-like-kinase 1 (PLK 1) enzyme, which is over-expressed in multiple

Trovagene Inc.  |  11055 Flintkote Avenue  |  San Diego  |  CA 92121  |  Tel.: USA [+1] 888-391-7992

hematologic malignancies, as well as solid tumors such as adrenocortical, breast, prostate, ovarian, lung, gastric and colon cancers. PCM-075 is orally bioavailable and has been explored in an initial Phase 1, open-label, dose-escalation safety study in patients with advanced metastatic solid tumor cancers. Trovagene plans to initiate clinical trials of PCM-075 in AML, since it has significant advantages over prior PLK1 inhibitors evaluated in this indication, including a higher selectivity, greater potency, oral bioavailability and shorter half-life.

About Trovagene, Inc.

Trovagene is a precision medicine biotechnology company developing oncology therapeutics for improved cancer care by leveraging its proprietary Precision Cancer Monitoring® (PCM) technology in tumor genomics.  Trovagene has broad intellectual property and proprietary technology to measure circulating tumor DNA (ctDNA) in urine and blood to identify and quantify clinically actionable markers for predicting response to cancer therapies.  Trovagene offers its PCM technology at its CLIA/CAP — accredited laboratory and plans to continue to vertically integrate its PCM technology with precision cancer therapeutics.  For more information, please visit https://www.trovagene.com.

Forward-Looking Statements

Certain statements in this press release 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.  These factors include, but are not limited to, our need for additional financing; our ability to continue as a going concern; clinical trials involve a lengthy and expensive process with an uncertain outcome, and results of earlier studies and trials may not be predictive of future trial results; our clinical trials may be suspended or discontinued due to unexpected side effects or other safety risks that could preclude approval of our product candidates; uncertainties of government or third party payer reimbursement; dependence on key personnel; limited experience in marketing and sales; substantial competition; uncertainties of patent protection and litigation; dependence upon third parties; our ability to develop tests, kits and systems and the success of those products; regulatory, financial and business risks related to our international expansion and risks related to failure to obtain FDA clearances or approvals and noncompliance with FDA regulations.  There are no guarantees that any of our technology or products will be utilized or prove to be commercially successful, or that Trovagene’s strategy to design its liquid biopsy tests to report on clinically actionable cancer genes will ultimately be successful or result in better reimbursement outcomes.  Additionally, there are no guarantees that future clinical trials will be completed or successful or that any precision medicine therapeutics will receive regulatory approval for any indication or prove to be commercially successful.  Investors should read the risk factors set forth in Trovagene’s Form 10-K for the

year ended December 31, 2016, and other periodic reports filed with the Securities and Exchange Commission.  While the list of factors presented here 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 Contact:

Vicki Kelemen

VP, Corporate Communications

858-952-7652

vkelemen@trovagene.com

EX-99.2

Exhibit 99.2

Transforming Oncology With Precision Cancer Therapeutics Company Overview August 2017 Company Overview January 2017

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.

Company Overview Precision Cancer Therapeutics Clinical stage biotechnology company developing treatments for hematological and solid tumor cancers Core DNA/RNA Technology Expertise Proprietary technology in tumor genomics and CLIA/CAP-accredited laboratory for drug development programs Broad Intellectual Property Identify and quantify clinically-actionable biomarkers for predicting patient response to cancer therapeutics NASDAQ: TROV Headquarters: San Diego, CA Shares (07/31/17): 37.3M outstanding

Significant Market Opportunities Investment Highlights FDA approved PCM-075 IND and protocol to conduct Phase 1b/2 clinical trial in acute myeloid leukemia (AML) Phase 1 trial completed in solid tumor cancers; published in Investigational New Drugs Additional phase 2 protocol under development in ACC Progressing Pipeline First-in-class Polo-like kinase (PLK) 1 inhibitor for broad clinical applications Acute myeloid leukemia, Non-Hodgkin Lymphoma Adrenocortical Carcinoma, Castrate-Resistant Prostate, Small-Cell Lung Strong IP Protection Technology Platform 125 issued patents and 56 pending patent applications, globally Patent holder of NPM1 for diagnosis and monitoring therapy response in AML Proprietary biomarker technology to optimize drug development Partnerships with pharma and research institutions to purchase NextCollect™ urine collection and DNA preservation device

PCM-075 Expanding Pipeline Indication (Target) Preclinical Phase 1 Phase 2 Non-Hodgkin Lymphoma Acute Myeloid Leukemia - Phase 1b/2 combination FDA approved IND / protocol – active Indication (Target) Preclinical Phase 1 Phase 2 Phase 1 Advanced Solid Tumors Completed and published Castrate-Resistant Prostate Small-Cell Lung Adrenocortical Carcinoma Phase 2a protocol in development Liquid Tumors Solid Tumors

Phase 1 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 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 One patient experienced grade 3 constipation, which was likely due to concomitant opiate therapy Phase 1 dose escalation study in patients with advanced or metastatic solid tumors * "Phase 1 Dose-Escalation Study of NMS-1286937, an Orally Available Polo-Like Kinase 1 Inhibitor, in Patients with Advanced or Metastatic Solid Tumors," Investigational New Drugs.

PLK1: Target for Cancer Therapy PLK1, PLK2, PLK3 are members of a family of serine/threonine kinases that are important regulators of cell-cycle progression1–6 PLK1 is a master regulator of mitotic progression and is the only family member expressed exclusively in dividing cells1-6 Other members of polo-like kinase family have other cellular functions roles, including tumor suppression and neuron expression1–6 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. PLK1 Anaphase Checkpoint Cytokinesis G1/S Phase Checkpoint G2/M Phase Checkpoint

PLK1 As a Cancer Target Higher Expression of PLK1 is Associated with Shorter Overall Survival2 Overexpression of PLK1 Observed in Numerous Cancer Types1 Adrenocortical Carcinoma 1Data derived from The Tumor Genome Atlas, https://tcga-data.nci.nih.gov/docs/publications/tcga; 2Bussey et al. Clin Trans Med, 2016, 5:1 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

PCM-075: A PLK1 Inhibitor Highly-selective, oral, polo-like kinase 1 (PLK1) inhibitor with demonstrated activity in hematologic and solid tumor cancers Licensed exclusive global development and commercialization rights from Nerviano Medical Sciences, S.r.l. Upfront payment of $2.0 million Milestones (Development: Phase 3; Regulatory: NDA submission; Commercial Launch) Tiered royalty payments up to and over $1.0 billion Trovagene has all rights to manufacturing of bulk and finished goods NerPharMa (subsidiary of Nerviano) FDA approved contract manufacturer for clinical trials Almac drug depot and distribution for execution to clinical trial sites

PCM-075 Attributes

PCM-075 Biochemical Profile Selective, adenosine triphosphate (ATP) competitive PLK1 inhibitor Selectivity driven by polar interaction with the carboxyl side chain of Glutamate 140 position of PLK1 Polo-like kinase 1 (PLK1) inhibitor PLK Member PCM-075 IC50 (nM)1 PLK1 2 PLK2 > 10,000 PLK3 > 10,000 1Data on File, Trovagene, Inc.

PCM-075 Mechanism of Action Induces a cellular phenotype of G2/M, leading to cell death Clear evidence of in-vitro pathway modulation in AML Mitotic inhibitor demonstrating anti-proliferative activity* AML-NS8 Patient-Derived Cells Treated with 200 nM PCM-075 for 24 Hrs1 * In numerous human cel lines; 1Casolaro et al (2013) PLOS One PCM-075 PLK1 blocking

AML 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: AML is known to be genetically diverse and PLK1 selectivity presents opportunity to work across patient sub-populations *Opportunity to pursue ODD designation. 1National Cancer Institute SEER 2016

PCM-075 In-Vivo Activity Response observed in various xenograft models as a single agent and in combination1 Compound Median Survival Time (days) %TGI Placebo 28 Cytarabine 38 128.6 PCM-075 62 221.4 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

PLK Inhibition in AML Pan-PLK inhibitor demonstrated increased response rates, improvements in event-free survival, and overall survival benefit in combination with low-dose cytarabine (LDAC)1 Adverse events observed in Phase 3 study, potentially due to drug accumulation and pan-PLK inhibitor activity2 Opportunity for a more selective PLK inhibitor with less drug accumulation paired with a precision medicine diagnostic Clinical activity published on PLK inhibitors Compound Selectivity Half-Life (hrs) Dosing Clinical Activity in AML Volasertib pan-PLK 135 iv 25-30% CR+CRi (+LDAC)* PCM-075 PLK1 24 oral P1b/2 Trial *higher incidence of severe adverse events with volasertib plus LDAC in phase 3 study. 1Dohner et al. Randomized, Phase 2 Trial of Cytarabine with or without Volasertib in AML Patients Not Suitable for Induction Therapy. 2Phase 3 POLO-AML-2 Study of Volasertib – June 11, 2016 Press Release

PCM-075 Phase 1b/2 AML Clinical Trial PCM-075 in Combination with Standard-of-Care (SOC) in Subjects with Acute Myeloid Leukemia Open-label trial to evaluate safety and anti-leukemic activity Phase 1b: dose escalation in combination with SOC to assess safety, tolerability, dose and scheduling, and determine recommended dose for Phase 2 continuation trial Phase 2: administration of recommended clinical dose in combination with SOC to further assess safety, tolerability and anti-leukemic activity Enrollment and Dosing Schedule Phase 1b – up to 42 subjects; Phase 2 – up to 32 subjects Starting dose in Phase 1b: 12 mg/m2, administered orally, in combination with SOC, for 5 consecutive days on Day 1 – Day 5, every 28-days Dose escalation by 50% increments until reaching the maximum tolerated dose (MTD), which will be considered the Phase 2 recommended clinical dose Trial Endpoints Safety: Characterization of safety, pharmacokinetics and correlative pharmacodynamic biomarkers Efficacy: Rate of complete response in Phase 2 defined as morphologic leukemia-free state

Phase 1b/2 Biomarker Assessment1 Biomarkers will be measured and correlated with pharmacokinetic drug levels to assess: Inhibition of PLK1 enzymatic activity Blockage of cell division (G2M arrest) Tumor cell death Blood sample (baseline) AML Patient + PCM-075 Blood sample (post PCM-075) Pre- and Post-Dose Blood Sampling 1TruSight Myeloid Sequencing Panel; Illumina

ACC Market Opportunity Adrenocortical carcinoma (ACC) is a rare cancer with significant unmet clinical needs Incidence: 0.7 to 2 cases per 1 million population per year1,2 Prognosis: 5-year survival in patients with metastatic disease is <15%3-7 40-70% of patients present with advanced or metastatic disease Patients with resectable tumors have 40% 5-year survival Treatment is mitotane, a highly toxic adrenolytic chemotherapy, approved in 1960 and remains the only approved therapy There is no treatment standard for advanced disease8,9 1Golden et al., J Clin Endocrinol Metab 2009;94:1853-78; 2Kebebew et al., World J Surg 2006;30:872-8; 3Icard et al, World J Surg 2001;25:891-7; 4Abiven et al., J Clin Endocrinol Metab 2006;91:2650-5; 5Assié G et al., J Clin Endocrinol Metab 2007;92:148-54; 6Fassnacht et al., Cancer 2009;115:243-50; 7Lughezzani et al., Eur J Cancer 2010;46:713-9; 8Fay et al., Crit Rev Oncol Hematol. 2014; 92: 123–132; 9Fassnacht et al, NEJM, 2012; 366:2189-2197 Malignant cells form in the outer layer of the adrenal gland

PLK1 inhibition in ACC: Therapeutic Opportunity 1Demeure et al.; ASCO-2016 Tumor Prior to Treatment Tumor Necrosis Following Treatment High PLK1 expression in ACC is associated with decreased patient survival Super-responder observed had high phospho-PLK1 expression prior to therapy Post-therapy biopsy indicated complete tumor necrosis Phase 1/2 study of PLK1 agent in patients with ACC1 Tumor Tumor Necrosis

Combination Therapy Opportunities High PLK1 expression is associated with the most aggressive forms of hematologic malignancies and solid tumor cancers PCM-075 may be synergistic and enhance the efficacy of current and future standard-of-care therapies 1Alphabetical order. 2Preclinical data on file with PCM-075 and these combined therapeutics Synergistic Drugs1 Cisplatin Cytarabine Doxorubicin Gemcitabine HDAC Inhibitors Pacitaxel Quizartinib (FLT3) Bortezomib Associated Cancers2 Liquid Tumors: Acute Myeloid Leukemia Acute Lymphocytic Leukemia Non-Hodgkin Leukemia Multiple Myeloma Solid Tumors Adrenocortical Carcinoma Triple-Negative Breast Small-Cell Lung Ovarian Sarcomas

PCM-075 is Synergistic in Combination PCM-075 is synergistic with both targeted drugs and chemotherapeutics CI > 1.0 Antagonistic CI < 1.0 Synergy CI = 1.0 Additive *Data on File at Trovagene, Inc..

Acute Myeloid Leukemia (AML): Combination of PCM-075 with FLT3 Inhibitor Evaluation of the 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 Available FLT3 inhibitors provide opportunity for combination with PCM-075 Midostaurin recently FDA approved; 3 additional FLT3 inhibitors are currently in Phase 3 clinical development2 The combination of PCM-075 and Quizartinib demonstrated 96% tumor growth inhibition and regression in FLT3 AML xenograft model3 Vehicle PCM-075 Quizartinib PCM-075 + Quizartinib

Non-Hodgkin Lymphoma (NHL): Combination of PCM-075 with histone deacetylase (HDAC) inhibitor Aggressive NHL progresses rapidly and accounts for 60% of cases in the U.S. Target population is relapse and refractory patients; there is no standard-of-care regimen and prognosis is poor Subtypes: Diffuse large B-cell lymphoma (DLBCL), including double-hit Mantle cell lymphoma Peripheral T-cell lymphoma (PTCL) PCM-075 demonstrates synergy with HDAC inhibitor of up to 80% in aggressive double-hit B-cell lymphoma cell lines1 1 Steven Grant, MD, Virginia Commonwealth University, Massey Cancer Center. Unpublished Research Data PCM-075 combined with HDACIs reduces survival of double-hit DLBCL and mantle-cell lymphoma cell lines1 Cell line Double-hit Cell line Mantle Cell Control PCM-075 HDAC PCM-075 / HDAC

Sensitivity to PCM-075 in Breast Cancer Driven by Triple-Negative Cell Lines Triple negative breast cancer (TNBC) represents a significant challenge due to: aggressive clinical course resistance to chemotherapy lack of effective targeted therapies Polo-like kinase 1 (PLK1) is significantly overexpressed (p < 0.0001) in TNBC compared with the other breast cancer subtypes TNBC cell lines are significantly more sensitive to PCM-075 than in other breast cancer cell lines In TNBC patient-derived mouse xenografts (PDX), significant tumor growth inhibition was observed TNBC Cell Lines are Highly Sensitive to PCM-0751 PCM-075 Demonstrated Efficacy in Patient-Derived TNBC Xenografts2 High Low Median Sensitivity ER+ = 1000 nM Median Sensitivity TBNC = 49 nM 1Data on File at Trovagene, Inc. 2Data Presented at AACR - 2016

PCM-075 Summary PCM-075 is an oral, highly-selective PLK1 inhibitor with clinical development opportunities in hematological and solid tumor cancers Strong key opinion leader support for PCM-075 across numerous indications Highly synergistic with >10 chemo and targeted therapeutics, with broad clinical opportunities Phase 1 trial in solid tumors established safety of PCM-075 and identified a recommended Phase 2 dose of 24 mg/m2/day Phase 1b/2 trial in AML initiated: Dr. Cortes (MD Anderson) as lead investigator, ten trial sites identified, site-activation in process Phase 2a protocol for Adrenocortical Carcinoma (ACC) in development with leading key opinion leaders Ongoing preclinical evaluation in Small-Cell Lung Cancer (SCLC), Non-Hodgkin Lymphoma (NHL), Triple-Negative Breast Cancer (TNBC) and Castrate-Resistant Prostate Cancer (CRPC)

Value Inflection Points PCM-075 AML Phase 1b/2 Clinical Trial Activation and execution Open-label: interim data throughout Completion of Phase 1b dose escalation Pharmacokinetic and Pharmacodynamic analysis Commencement of Phase 2 PCM-075 Clinical Development in Other Cancer Types Development and submission of ACC Phase 2 protocol to FDA Expansion of clinical studies in hematologic malignancies and solid tumors: NHL, SCLC, CRPC, TNBC Commercialization Precision Diagnostics royalties and business development Precision Therapeutics business development Presentations and publications

Thank you for more information, please email ir@trovagene.com