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 Corporate Presentation January 2017 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.

Expanding the Playing Field for

Therapeutic Proteins Non-Confidential Novel Modes of Action Validation and Growth Capital Fully proprietary and unique Excellent drug-like properties and clinical validation Potentially transformative immuno-oncology (IO) multispecifics TME-targeted

T cell agonists / Multi-checkpoint blockade Inhalation - a topical approach to asthma may bring enormous benefits Transformative IO partnership with Servier brings significant upfront payment, fully retained US rights on several novel

multispecific drug candidates $2.5 B in biodollar potential across Large Pharma partnerships + royalties $60+ million in cash on hand after Servier upfront provides runway into 2019 through key value inflection points on fully proprietary pipeline

PRS-343 (IO): first-in-patient trial initiation 1H17; PRS-060 (asthma): first-in-man trial initiation mid '17; PRS-080 (anemia): multi-dose trial read-out (hemoglobin) 2H17 Anticalins - A Novel Therapeutic Protein Drug Class

Multiple Paths for Success & Risk Diversification Partnerships and Capital to Pursue Clinical-based Inflection Points Novel Drug Class

Servier Immuno-Oncology Partnership is

a Transformative Strategic Alliance Non-Confidential Strategic Alliance Highlights IO co-development alliance with ~$30M upfront, up to $1.8B in potential milestones and low double-digit royalties 5 committed IO bispecifics, including PRS-332

(PD-1-based bispecific) Potential to expand to 3 additional bispecific programs Retained co-development and full US commercial rights on PRS-332 and up to 3 additional programs A "True Partnership" - equal voice with a collaborator

having a shared strategic vision and resources to develop several novel IO bispecifics Strategic Implications of Partnership Underscores the value of Pieris' powerful multispecifics platform in IO Strengthens cash position to fund development

of proprietary product pipeline, while extending financial runway into 2019, through several clinical-stage value inflection points Fully retained rights on lead IO bispecific, PRS-343 (4-1BB/HER2), and ability to enter into additional

Diversified Immuno-Oncology (IO) and

Non-IO Product Pipeline Non-Confidential

Entering an Acceleration Phase Drug

Class Validation Growing Disease Focus Acceleration Phase The Early Years 2001 - 2007 2008 - 2013 2014 - 2016 2017+ 2001 Founded in Munich, Germany Platform Improvements Initial drug discovery efforts 2008 $25M Series B led by

OrbiMed 2010-2011 Multiple Large Pharma Collaborations 2010 First Anticalin enters clinic 2014 Focus on IO Multispecifics and Inhaled Biologics for Respiratory Disease 2015 First IO Partnership 2014-2015 Go Public Set up Boston HQ 2015-2016

Lead IO and Respiratory Programs IND-enabling Studies 2017 Strategic, Multi-program Co-development IO Alliance Retaining US rights on 4 programs 2017 Clinical entry of inhaled respiratory program, PRS-060 2017 Clinical entry of fully proprietary IO

program, PRS-343 2017 Key data readout (Hb) for anemia program, PRS-080 2017 Continued exploration of additional partnerships Projected events Non-Confidential

Overlay of several lipocalin X-ray

structures 3 of 12 human lipocalins and endogenous ligands Anticalins are recombinantly engineered human lipocalins Lipocalins are non-immunogenic, extra-cellular binding proteins Lipocalins have very low sequence identity, yet structural

conservation among the 12 known human members is the foundation of the scaffold Monomeric, stable, low molecular weight (~18 kDa) Phage display-based drug discovery platform Anticalin Drug Class Origins Non-Confidential

Differentiating Features Human-derived

Natural binding molecule Non-immunogenic High affinity and specificity Systemic delivery Tunable pharmacokinetics ( ) Valent- and geometry-versatile

multispecifics Inhalable Protein class exclusivity Positive freedom to operate landscape Anticalins Share Several Features with mAbs yet are Highly Differentiated Monoclonal Antibodies (mAbs) are highly

successful drugs Anticalins share many of the beneficial properties of mAbs yet are highly differentiated Antibody Anticalin Safety Related Efficacy Related IP Related Non-Confidential

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 Valent- and Geometry-Versatile

Multi-specifics to Achieve Optimal Biology Non-Confidential

Anticalins in Immuno-Oncology

Differentiation Through Unique Multispecific Formats

Next-Generation I-O Therapy Strategy

Engage immune costimulatory targets in highly novel, targeted manner with unique multispecifics, led by PRS-343 (wholly owned by Pieris) Establish superior therapeutic window over mAbs Improve on benefits of leading checkpoint antagonists and other

therapies Simultaneously block multiple immune checkpoints in one drug built on key backbone components (e.g. PD-1), led by PRS-332 (partnered with Servier) Demonstrate superiority to existing PD-1 mAbs Exploit independent and fully proprietary PD-1

position Demonstrate intra-pipeline synergy between targeted costimulatory engagement and multi-checkpoint blockade within own pipeline 4-1BB (CD137) activation combined with PD-1 blockade expected to result 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

Lead IO Program (PRS-343) Addresses

Biology Challenging for Antibodies Alone 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 (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 Localized T cell activation Reduced T cell-mediated systemic

toxicity Increased therapeutic index in patients unresponsive to standard of care Non-Confidential

PRS-343 is a First-in-Class

TME-activated Co-stim Agonist 4-1BB (CD137) - Key Costimulatory Target Marker for tumor-specific T cells in TME Ameliorates T cell exhaustion Critical for T cell expansion Induces anti-tumor cytolytic activity Drives central memory T cell

differentiation for sustained response Her2 MHC-peptide Tumor Cell TCR 4-1BB (CD137) Clustering contributes to T Cell activation Tumor-specific T Cell Non-Confidential 4-1BB-targeting Ac HER2-targeting mAb PRS-343 HER2 - Strongly Validated

Tumor Target Restricted expression on normal tissue Multiple HER2+ tumors with high-unmet need Breast, Gastric, Esophageal, Colorectal, Biliary, Pancreas, Bladder, Ovarian, Endometrial, Lung (AdenoCa), Salivary Duct, Head/Neck Mediates drug

mobilization and immune receptor activation within the tumor bed

PRS-343 Demonstrates Targeted T Cell

Activation Ex Vivo Cell activation = IL-2 response PRS-343 in presence of HER2-positive tumor cells (step 1) (Step 1) PRS-343 potently activates T cells mediated by 4-1BB cross-linking upon binding to HER2-positive tumor cells (SKBR3)

Non-Confidential (Step 2) 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 PRS-343 in solution, following addition of excess

trastuzumab (step 2) IL-2 response with HER2 blockade a-CD3 antibody step 1 step 2

PRS-343 Shows Bifunctional Activity

- Dose-dependent Tumor Growth Inhibition & CD8(+)TIL Expansion in SK-OV-3 Model Tumor growth (Median) PRS-343 shows dose-dependent tumor growth inhibition, which is dominated by anti-HER2 activity PRS-343 leads to strong and dose-dependent

lymphocyte infiltration in tumors; monospecific anti-HER2 mAb (IgG4 backbone) lacks this activity Monospecific anti-4-1BB benchmark mAb shows insignificant response compared to isotype control and no significant tumor infiltration of lymphocytes

Non-Confidential TIL frequency (hCD45) SK-OV-3 tumor model Incomplete group due to mortality 100 g Isotype Ctrl 100 g PRS-343 100 g Anti-4-1BB CD3 CD45 CD4 CD8 CD3 CD45 CD4 CD8 CD3 CD45 CD4 CD8 hCD4 hCD3 hCD8 Plot TIL phenotyping by

IHC PRS-343 100 g IHC Tras-IgG4 80 g IHC

PRS-343 Repeatedly Demonstrates

Differentiation Over anti-HER2 and 4-1BB mAbs Non-Confidential Anti-CD137 benchmark mAb shows accelerated GvHD with significant mortality at day 20 in line with literature data2 Toxicity corresponds with expansion of CD8-positive T cells in PBMC for

this group PBMC phenotyping at day 19 Mortality at study end (Day 20) 1 GvHD = graft vs host disease 2 Sanmamed et al., Cancer Res. 2015 Sep 1;75(17):3466-78. % CD45+ of PBMC % CD8+ of CD45+

PRS-343: IND Enabling Activities on

Track to Support a FIM in H1 2017 PRS-343 4-1BB/HER2 IND-enabling Ph I mono 2016 2017 2018 combo w/ PD-1 mAb Known Immune Component Existing tumor-infiltrating lymphocyte (TIL) repertoire Validated role of CD137 High Medical Need HER2 Patient

Populations unresponsive to or relapsed from standard of care Targeted Indication Characteristics Straightforward Registration Path Manageable trial size and duration with clear endpoints Advanced Gastric Cancer Muscle-invasive Bladder Cancer

Resistant Metastatic HER2+Breast Cancer Priority Patient Populations Non-Confidential

PRS-343: Summary and Milestones

Differentiated profile vs HER2- and 4-1BB-directed benchmark mAbs PRS-343 has dual functionality based on monospecific HER2-targeting and bispecific, tumor-localized costimulation of 4-1BB. Potential for synergistic anti-tumor activity Anti-HER2

mediated tumor growth inhibition 4-1BB-mediated anti-tumor T cell activation Potential to avoid undesirable peripheral T cell activation (reduced systemic side effects) Excellent drug-like properties Antibody-like half-life in mice and cynomolgus

monkey Low immunogenicity risk (ex vivo Lonza Epibase test) High titers at GMP stage (1000L) and excellent stability Near-term clinical-stage milestones First-in-patient clinical trial initiation planned for 1H17 HER2+ solid tumor patients

unresponsive to SOC Data-driven focus on high unmet need tumors, e.g. gastric, bladder and breast Combination trial with PD-1 mAb planned for 2018 Non-Confidential

PRS-332: Novel PD-1-based IO

Bispecific - Co-Developed by Pieris & Servier Bispecific protein comprising proprietary Anticalin & novel in-licensed PD-1 mAb Several bispecific permutations under preclinical evaluation Future combination with PRS-343 PD-1 mAb

Undisclosed anti-c.p. Ac Peptide linker PRS-332: PD-1-based bispecifics Anti-checkpoint Anticalin is a potent, competitive antagonist Non-Confidential Checkpoint Target inhibition Benchmark mAb Anti-checkpoint Anticalin

Anticalins in Anemia and Asthma

PRS-080 Potently Neutralizes

Hepcidin, The Master Regulator of Iron Metabolism Hepcidin is a peptide hormone that serves as a key regulator of iron metabolism by regulating iron entry into plasma from the three main sources of iron: Dietary absorption in the duodenum Release of

recycled iron from macrophages Release of stored iron from hepatocytes Chronic inflammation drives increased hepcidin production Prevents transferrin-mediated transport to the bone marrow for erythropoiesis Causes anemia of chronic disease

"functional" iron deficiency (FID) vs absolute iron deficient anemia PRS-080 is a pegylated Anticalin that binds with high affinity and neutralizes Hepcidin Haematologica 2013 98:11 Non-Confidential

PRS-080 Drives Iron Mobilization in

Healthy Subjects; Ongoing Development in FID ESRD Patients Excellent Ph I results (ASH 2015) Safe, well tolerated in HV (36 drug + 12 placebo) Mode of action (iron mobilization) confirmed Increase in serum iron mobilization (p = 0.005)

First-in-patient trial (ESRD) ongoing Single Ascending Dosing completion expected end of Jan 2017 Drug well tolerated - Encouraging activity Disclosing unblinded data by end of Q2 17 Multi-dose trial initiation expected April 2017 Hemoglobin

(Hb), reticulocyte concentration of Hb as endpoints Disclosing data in 2H 17 Non-Confidential Serum Iron [ M] Mean Iron Concentrations [ M] Subjects achieving iron response > 34.5 M Time after start of infusion [hours] First

Anticalin projected to achieve clinical Proof of Concept (increased hemoglobin) Will address FID anemia patients poorly responsive to ESAs and iron therapies Within ESRD, among highest economic burden patient population Est. 90k patients in the US

and 80k patients in JP Significant Commercial opportunity Ph Ib (SAD) Ph 2 2016 2017 (Hemoglobin e.p.) = report data

PRS-060: First-in-Class Inhaled

IL4Ra Antagonist For Uncontrolled Asthma First inhaled biologic to potently engage highly validated asthma target (IL4Ra) IL4Ra is a critical target in uncontrolled asthma Target engagement on lung tissue is a key differentiator over SQ injected

mAbs Potential low-dose, low-COGs alternative to mAbs Preclinical In-vivo POC for pulmonary delivery Formulability for pulmonary delivery Systemic exposure with s.c. mAbs targeting IL-4Ra Inhaled Anticalin for local IL4Ra blockade PRS-060 inhibits

IL4Ra- mediated inflammation in vivo Non-Confidential Vs.