Forward Looking Statements Non-Confidential Statements in this presentation that are not descriptions of historical facts are forward-looking statements that are based on management's current expectations and assumptions

Pieris Pharmaceuticals, Inc.

Nasdaq:PIRS Jefferies Conference - Investor Presentation June 2016 Exhibit 99.1

Forward Looking Statements

Non-Confidential Statements in this presentation that are not descriptions of historical facts are forward-looking statements that are based on management's current expectations and assumptions and are subject to risks and uncertainties. In

some cases, you can identify forward-looking statements by terminology including "anticipates," "believes," "can," "continue," "could," "estimates," "expects,"

"intends," "may," "plans," "potential," "predicts," "projects," "should," "will," "would" or the negative of these terms or other comparable

terminology. Factors that could cause actual results to differ materially from those currently anticipated include, without limitation, risks relating to the results of our research and development activities, including uncertainties relating to the

discovery of potential drug candidates and the preclinical and clinical testing of our drug candidates; the early stage of our drug candidates presently under development; our ability to obtain and, if obtained, maintain regulatory approval of our

current drug candidates and any of our other future drug candidates; our need for substantial additional funds in order to continue our operations and the uncertainty of whether we will be able to obtain the funding we need; our future financial

performance; our ability to retain or hire key scientific or management personnel; our ability to protect our intellectual property rights that are valuable to our business, including patent and other intellectual property rights; our dependence on

third-party manufacturers, suppliers, research organizations, testing laboratories and other potential collaborators; our ability to successfully market and sell our drug candidates in the future as needed; the size and growth of the potential

markets for any of our approved drug candidates, and the rate and degree of market acceptance of any of our approved drug candidates; developments and projections relating to our competitors and our industry; our ability to establish collaborations;

our expectations regarding the time which we will be an emerging growth company under the JOBS Act; our use of proceeds from this offering; regulatory developments in the U.S. and foreign countries; and other factors that are described more fully in

our Annual Report on form 10-K filed with the SEC on March 23, 2016. In light of these risks, uncertainties and assumptions, the forward-looking statements regarding future events and circumstances discussed in this report may not occur and actual

results could differ materially and adversely from those anticipated or implied in the forward-looking statements. You should not rely upon forward-looking statements as predictions of future events. The forward-looking statements included in this

presentation speak only as of the date hereof, and except as required by law, we undertake no obligation to update publicly any forward-looking statements for any reason after the date of this presentation to conform these statements to actual

results or to changes in our expectations.

Corporate Profile Multiple Paths to

Revenues & Risk Diversification High-value disease areas, including respiratory and IO Partnerships with leading pharmas: Roche, Sanofi, Daiichi: deal potential >$700M plus royalties Several emerging clinical value inflection points Multiple

Value Drivers Next-Gen IO Therapies Anticalins - Novel Therapeutic Proteins Superior drug-like properties; novel modes of action Potentially transformative multispecifics capabilities Track record of delivering to Big Pharma

specifications Unique Platform and Drug Class Novel Bispecifics & Complete Independence 4-1BB (CD137) / HER2 (PRS-343): targeted T cell agonist offers high differentiation over mAbs PD-1 based bispecific (PRS-332): synergistic dual checkpoint

blockade; future combination with PRS-343 Non-Confidential

Anticalins are a Novel Class of

Therapeutic Binding Proteins Anticalin in complex with a small molecule (Y-DTPA) Anticalin bound to the hepcidin peptide Anticalin bound to the CTLA4 protein Drug Class With Favorable Properties Anticalins are derived from lipocalins

- human extracellular binding proteins Small (18 kDa vs 150 kDa mAbs), high selectivity and potency, non-immunogenic Very stable Human lipocalin Red = key areas of target engagement High Hit RatesQuick to Development CandidateVersatile Use

Powered by Reliable Platform Highly diverse libraries (>1011) of potential drug candidates Automated high-throughput drug screening technology (phage display) Extensive protein engineering know-how Non-Confidential

Anticalins Share Several Features with

mAbs Yet are Highly Differentiated f Human-derived Natural binding molecule Non-immunogenic High affinity and specificity Systemic delivery Tunable pharmacokinetics -

PRS-080 ( ) Local delivery (e.g., inhalation) - PRS-060 Versatile multispecifics - PRS-343 Differentiating Features Antibody Anticalin Safety Related Efficacy Related Non-Confidential

Product Target(s) Indication Partner

Discovery Preclinical IND-enabling P1 P1b/2a PRS-080 Hepcidin Anemia PRS-060 IL4Ra Asthma PRS-332 PD-1 / X PRS-342 CD137/GPC3 PRS-300s n.d. Roche n.d. PRS-343 Daiichi PCSK9 Dyslipidemia Daiichi n.d n.d. Sanofi P. aeruginosa Infectious disease Zydus

cMet Oncology Inhalable Anticalin Half-life-optimized Anticalin - fastest drug to cPOC mAb-Anticalin Proprietary Non-IO IO Non-IO Partnered Programs Half-life optimized Anticalin (DS-9001) Tetraspecific Anticalin Ac-Ac (Fc) mAb-Anticalin

Anticalin Product Pipeline Immuno-Oncology Non-Confidential 4-1BB (CD137) / HER2 bispecific

Anticalins in Anemia and

PRS-080: Best-in-Class Hepcidin

Antagonist for Anemia of Chronic Disease Haematologica 2013 98:11 Hepcidin Elevation - a hallmark of anemia of chronic disease First Anticalin projected to achieve clinical Proof of Concept (increased hemoglobin) Addressing anemia patients

poorly responsive to ESAs and iron therapies Excellent Ph I results (ASH 2015) Safe and well tolerated in healthy subjects (36 drug + 12 placebo) Mode of action (iron mobilization) confirmed Statistically significant increase in serum iron

mobilization relative to placebo (p = 0.005) First-in-patient trial (ESRD) underway Single Ascending Dose trial completion expected H2 2016 in anemic pts undergoing hemodialysis Multi-dose completion expected mid 2017 Hemogloblin (Hb), reticulocyte

concentration of Hb as endpoints Target anemia population in U.S. ~ 90,000 patients Non-Confidential Hepcidin plays a significant role in the assimilation, mobilization and processing of iron for erythropoiesis

PRS-060: First-in-Class Inhaled IL4Ra

Antagonist For Uncontrolled Asthma First inhaled biologic to potently engage highly validated asthma target (IL4Ra) IL4Ra has emerged as a critical target in inflammation associated with uncontrolled asthma Target engagement on lung tissue via

pulmonary delivery is a key differentiator over s.c. mAbs Potential low-dose, low-COGs alternative to mAbs In vivo proof of concept for pulmonary delivery in preclinical disease models achieved Formulability for pulmonary delivery achieved

IND-enabling studies underway First-in-man study planned for 1H 2017 Clear line of sight to clinical POC in biomarker-focused trial Systemic exposure with s.c. mAbs targeting IL-4Ra Inhaled Anticalin for local IL4Ra blockade PRS-060 inhibits IL4Ra-

mediated inflammation in vivo Target asthma population WW ~ 20 Mio patients Non-Confidential

Anticalins in Immuno-Oncology

Differentiation Through Unique Multispecific Formats

Not Just Another Bispecifics

Platform Anticalin-Based Drug Candidates Can Be Tailored to Multiple Formats Pure Anticalins Multispecific mAb-Anticalins Multispecific Fc-Anticalins Potent Multi-target Engagement Novel MoA Excellent Drug-like Properties

Building blocks Mono' Bi' Tri' Tetra' Ac Fc mAb linker Non-Confidential

First IO Partnership with Roche

Validates Approach Scope: Independent from PRS-300 Series programs One-target but potentially multi-program Roche solely responsible from IND-enabling studies Economics: Pieris receives upfront payment of ~US$6.5 million Roche fully funds

collaborative research phase Total potential deal could exceed US$400 million Majority of agreed payments for development milestones Not including royalties, which are up to low double-digit Implications: Validation of Anticalins by industry leader

in cancer biologics Ability to sign additional partnerships Free cash flow to advance proprietary programs Non-Confidential

Lead IO Program (PRS-343) Addresses

Biology That's Been Intractable for mAbs T cell Tumor-targeting mAb or Ac Immune system- targeting Anticalin Tumor cell Pieris' tumor-targeted IO bispecifics or The Challenges of Agonistic mAb Approaches Inconsistent agonistic activity

in vivo (e.g. urelumab vs. utomilumab) Systemically agonizing mAbs have resulted in narrow therapeutic window due to cytokine storm (urelumab, TGN1412 ) Potential Benefits of Pieris' Approach Tumor-targeted drug clustering drives localized T

cell activation Reduced T cell-mediated systemic toxicity Increased therapeutic index in patients unresponsive to standard of care Non-Confidential

PRS-343: 4-1BB/HER2 Bispecific

Target Rationale for Lead IO Program 4-1BB (CD137) - Key Costimulatory Target Preclinically and clinically validated Marker for tumor-reactive T cells Activation leads to tumor elimination in vivo Pure mAb approaches are sub-optimal Systemic

immune system engagement Doses required for T cell activation have led to severe toxicity Her2 MHC-peptide Tumor Cell HER2 - Validated but not fully exploited Restricted expression on normal tissue favors immunotherapy approach Several HER2+

tumors nonresponsive to approved anti-HER2 therapies Bladder, Gastric, Endometrial, Breast, etc. Several non-responders have CD137+ TILs (T cells in tumor microenvironment) T cell receptor CD137 Clustering contributes to T Cell activation

Tumor-specific T Cell Non-Confidential CD137-targeting Ac HER2-targeting mAb

Bispecific Geometry Impacts

Activation of Human T Cells Cell activation = IL-2 response Construct A Construct B Construct C Construct D Constructs A to D exhibit different potency ex vivo, demonstrating the importance of bispecific geometry a-CD3 antibody Non-Confidential

T Cell Activation is HER2

Target-Dependent Construct A Construct B Construct C Construct D IL-2 response with Her2 blockade Addition of excess HER2-targeting trastuzumab prevents PRS-343 binding to HER2-positive cells and results in a loss of activity, as intended,

confirming mode of action a-CD3 antibody Excess trastuzumab Non-Confidential

PRS-343 Inhibits Tumor Growth and

Expands TILs in Cancer Model Isotype 100 g PRS-343 100 g no PBMC anti-CD137 benchmark 100 g Tumor growth (Median) TIL (hCD45-staining of tumors) PRS-343 shows best response PRS-343 leads to strong lymphocyte infiltration in tumors

Anti-CD137 benchmark mAb inferior insignificant response compared to isotype control no significant tumor infiltration of lymphocytes SK-OV-3 tumor model TIL (digital quantitation of IHC) Non-Confidential

High Mortality Rate With Anti-CD137

mAb, But Not PRS-343, Supports Enhanced Safety of Targeted T Cell Activation CD45+ of PBMC CD3+ of CD45+ CD3+CD8+ of CD45+ PBMC phenotyping at day 19 1 GvHD = graft vs host disease 2 Sanmamed et al., Cancer Res. 2015 Sep 1;75(17):3466-78 Mortality

on Day 20 Accelerated GvHD1 & significant mortality w/ benchmark CD137 mAb in line with literature2 Toxicity corresponds with expansion of CD8-positive T cells in PBMC for this group Non-Confidential

PRS-343 Target Indication Rationale

& Prioritized Indications Known Immune Component Existing tumor-infiltrating lymphocyte (TIL) repertoire Validated role of CD137 High Medical Need Populations where current HER2 therapies don't work HER2 = Attractive Marker Enriched in

target population; linked to poor prognosis Targeted Indication Characteristics Significant Commercial Potential Sizeable target population Clear Registration Path Manageable trial size and duration with clear endpoints Advanced Gastric Cancer

Muscle-invasive Bladder Cancer Resistant Metastatic HER2+Breast Cancer Non-Confidential

PRS-343 Phase 1 Initiation Planned

for 1H17 Lead drug candidate progressing through IND enabling studies Demonstrated ability to activate human T cells consistent with desired mode of action Potent, tumor-dependent activation Differentiation over anti-CD137 mAbs Desired drug-like

properties CMC / manufacturing: robust titers and long-term stability Low risk of immunogenicity observed ex vivo Antibody-like half-life in mouse and cynomolgus monkey First-in-Patient Clinical Trial planned for 1H17 HER2+ solid tumor patients

unresponsive to SOC PRS-343 CD137/HER2 IND-enabling Ph I mono 2016 2017 2018 combo w/ PD-1 mAb Non-Confidential

PRS-342: 4-1BB/GPC3 Bispecific

Repeating the Targeted Co-stim Paradigm Protease-resistant, non-immunogenic linkers Anti-CD137 Anticalin Anti-GPC3 Anticalin IgG4 Fc variant PRS-342 GPC3 Expression is pronounced in multiple cancers that are known to have CD137+ TILs Hepatocellular

Carcinoma (HCC): Overexpressed in 60-80% of lesions with no expression in healthy liver tissue; correlated with poor prognosis Merkel Cell Carcinoma: Overexpressed in 80% of tumors Melanoma: Overexpressed in 40-80% of melanoma lesions

PRS-342: 4-1BB/GPC3 Bispecific

Tumor-Dependent T Cell Activation IL-2 response to PRS-342 Without GPC3 blockade concentration [ g/mL] IL-2 response to PRS-342 with GPC3 blockade concentration [ g/mL] culture dish Signal 2 Signal 1 Activation Hep3B cell (GPC3-pos.)

PRS-342 construct T Cell a-CD3 antibody IL-2 +/- GPC3 blockade Expands therapeutic applications of key IO targets Wholly owned, internally generated Non-Confidential

Lead Dual Checkpoint Antagonist

(PRS-332): Aims to Enhance Clinical Activity of PD-1 Fully proprietary Anticalins Novel in-licensed PD-1 mAb sequences Several bispecifics with novel profiles under preclinical evaluation Objective of nominating PD-1 based bispecific development

candidate in 2H16 PD-1 mAb Undisclosed anti-c.p. Ac Peptide linker PRS-332: PD-1 based bispecifics Ac demonstrates competitive c.p. engagement, inhibiting binding to ligand Ac stable in PBS, hu & mu plasma after 1 week, 37 C aSEC Reference

1 week @37 Benchmark mAb Non-Confidential Anti-checkpoint Anticalin

Strategy For Clinical Development of

Innovative IO Approaches Engage immune costimulatory targets (e.g. 4-1BB) in highly novel, targeted manner with unique multispecifics Establish superior therapeutic window over mAbs Aim to safely improve on monotherapy activity Explore checkpoint

inhibitor combinations for maximum synergy, including PD-1 Create novel IO therapies built on key backbone components such as PD-1: next-generation multi-checkpoint antagonists Demonstrate superiority to existing PD-1 mAbs by leveraging flexibility

of Anticalins Fully proprietary PD-1 position; internally generated Demonstrate synergy between targeted costimulatory engagement and multi-checkpoint blockade within own pipeline 4-1BB (CD137) activation combined with PD-1 blockade results in

greater tumor growth inhibition than either monotherapy in preclinical studies1 1 Shindo, Y et al., Anticancer Res. 2015 Jan;35(1):129-36 Next-Generation IO Therapies: Novel multispecifics, novel combinations, wholly owned Non-Confidential

Financials - Accomplishments

Financial Highlights Cash & Cash

Equivalents $31.2M1 Total Debt $0.0M Revenue Since Inception $52.9M Grant Revenue Since Inception $14.1M 12 Months 2015 Cash Burn (includes $1.2M in debt repayment) $14.4M Common Shares Outstanding 39,833,023 Options Outstanding (as of 3-31-16)

3,761,210 (at W/A strike price of $1.91) June 8, 2016 Closed $16.5M PIPE Financing 8,188,804 units2 1 excludes $16.5M gross proceeds from June 8 PIPE financing 2 each unit includes 0.40 warrants with $2/share strike price and 0.20 warrants with