Disclosures The Impala trial was sponsored by Savara Pharmaceuticals I receive grant funding from the US National Institutes of Health I have consulted for: Boehringer Ingelheim, CSL Behring, Genzyme, Gilead, Grifols, GS

Safety and Efficacy of Inhaled GM-CSF

(Molgramostim) in Autoimmune Pulmonary Alveolar Proteinosis - The IMPALA Trial - Baseline Data and Blinded Treatment Period Results Bruce C. Trapnell, M.D. Translational Pulmonary Science Center Cincinnati Children's Hospital Medical Center

Professor of Medicine and Pediatrics Division of Pulmonary, Critical Care, and Sleep Medicine University of Cincinnati Medical Center Exhibit 99.1

Disclosures The Impala trial was

sponsored by Savara Pharmaceuticals I receive grant funding from the US National Institutes of Health I have consulted for: Boehringer Ingelheim, CSL Behring, Genzyme, Gilead, Grifols, GSK, Kiniksa, Medimmune, Merck, Savara, Sanofi,

Thick layer of surfactant PAP

sediment' Epithelial basement membrane Alveolar air space Endothelial basement membrane Red cell Fibroblast Normal oxygen uptake Displaced alveolar air Cellular debris Thin film of surfactant Alveolar macrophage Type II cell Interstitium Type

I cell Normal Alveolus M-CSF MCP-1 Endothelial cell Polycythemia B. Trapnell GM-CSF Reduced oxygen uptake Cholesterol crystals Lymphocytes GM-CSF autoantibody Foamy alveolar macrophage GM-CSF Alveolus in PAP Background: Autoimmune Pulmonary Alveolar

Proteinosis (aPAP) aPAP is characterized by: - Pulmonary surfactant accumulation - Progressive hypoxemic respiratory failure - Increased PAP biomarkers - Polycythemia (systemic response to lung disease) - Increased

infection risk (uncommon) - Pulmonary fibrosis (uncommon) GM-CSF is required to regulate alveolar macrophage - Differentiation - Functions - Population size GM-CSF autoantibodies cause aPAP by blocking stimulation of alveolar

macrophages, which reduces their ability to clear surfactant

Background: Inhaled GM-CSF Therapy of

aPAP 1996, Seymour: First patient treated with GM-CSF (SQ) 2000, Kavuru: 4 patients treated (SQ) 2001, Seymour: 14 patients treated (SQ) 2004, Aria: 1 patient treated (Inhaled) 2005, Tazawa: 3 patients treated (Inhaled) 2006, Wylam: 12 patients

treated (Inhaled) 2005, Venkateshiah: 25 patients treated (SQ) 2010, Tazawa: 39 Patients treated (inhaled) 2014, Papiris: 6 Patients treated (inhaled) 2019, Tazawa: 64 Patients treated (inhaled) IMPALA Trial, 138 patients treated (inhaled) After

Before Tazawa... 2010

Study Design of the IMPALA Trial

Screening Randomized, blinded Treatment (6 m) 0 24 Placebo Open-Label Treatment (6 or 12 m) 48 or 72 Time (weeks) Intermittent GM-CSF* Intermittent GM-CSF Continuous GM-CSF Continuous - Daily administration of inhaled GM-CSF (300 g)

(n=46) Intermittent - Daily administration of GM-CSF (300 g) every other week* (n=45) Placebo - Daily administration (n=47) Study Groups *Placebo administered on off' weeks

Study Design: Endpoints Safety: Number

of adverse events (AE) and serious adverse events (SAE) Efficacy: Change from baseline at 24 weeks in the following endpoints: Disease element Variable Pathology Chest CT ground glass opacification (GGO) score Serum PAP biomarkers Physiology

Alveolar-arterial difference in oxygen conc. (A-aDO2)* DLCO Health status & Function Saint Georges Respiratory Questionnaire (SGRQ) ** Six-minute walk test - Distance** Rescue therapy requirement (Whole lung lavage - WLL) Time to first WLL**

Number of patients with WLL, Number of WLL Systemic response to chronic lung disease (polycythemia) Hemoglobin concentration * = Primary end point, ** = Key Secondary end point

Baseline Characteristics: Demographics

Characteristic Continuous Intermittent Placebo Age, years 54.0 13.3 49.2 14.0 46.1 14.8 Gender (Male), % 60.9 57.8 53.2 Smoking history, % Never smoker 28.3 35.6 34.0 Ex smoker

58.7 44.4 42.6 Current smoker 13.0 20.0 23.4 Geographic region, % Europe 34.8 46.7 70.2 Japan 43.5 22.2 21.3 USA 4.3 4.4 0

Baseline Characteristics: Disease

Severity Characteristic Continuous Intermittent Placebo A-aDO2*, mm Hg (FAS) 40.5 19.6 40.9 20.2 40.2 14.3 DLCO, % predicted 52.1 18.6 46.1 14.5 49.6 14.3 Disease severity score (DSS), % DSS 1 (Mild) 8.7

11.1 6.4 DSS 2 26.1 31.1 34.0 DSS 3 37.0 28.9 29.8 DSS 4 10.9 20.0 21.3 DSS 5 (Severe) 17.4 6.7 8.5 SGRQ Total score** 47.2 20.4 44.4 21.4 44.1 21.7 6MWT-Distance**, m 412 144 447 117 447 125 Vital capacity,

% predicted 78.6 32.2 74.8 19.5 74.1 18.6 * = Primary end point, ** = Key Secondary end point

Baseline Characteristics: Previous

Therapies Characteristic Continuous Intermittent Placebo Supplemental oxygen use, % 32.6 26.7 23.4 Whole lung lavage Prior use of WLL (any), % 47.8 68.9 63.8 Total Number of WLLs 3.3 2.2 3.3 3.0 2.8 3.0 Time since last WLL, m

25.0 53.7 19.7 27.4 17.7 20. 7 GM-CSF therapy (any), % 13.0 15.6 12.8

Safety: AE, SAE, and Respiratory AE

Occurring in at least 5% of Patients No clinically significant changes in laboratory values No evidence of anti-drug antibody development Study completion: Continuous: 97.8%, Intermittent: 97.8%, Placebo: 91.5% AE (all) AE (Poss/prob related) SAE

(all) Worsening of aPAP 0 20 40 60 80 100 Continuous Intermittent Placebo All Cough Dyspnea Productive cough 0 20 40 60 80 100 Respiratory AE Event rate (% patients) Event rate (% patients)

Pathology: GM-CSF Improved Chest CT

GGO Score P=0.0002 P=0.1776 Continuous Intermittent Placebo *Comparison to Placebo * *

Pathology: GM-CSF Improved Serum

Biomarkers * Continuous Intermittent Placebo * = P<0.05, ns = P>0.05, comparison to Placebo * * * * ns * * ns ns ns ns SP-D LDH KL-6 SP-A Cyfra21-1 CEA

Physiology: GM-CSF Trended Towards

Improvement in the Primary End Point (A-aDO2) - Full Analysis Set (FAS) P=0.1688 Continuous Intermittent Placebo P=0.4444 * * *Comparison to Placebo

Correlation of PaO2 and A-aDO2

Identifies Patients Who Received Oxygen Therapy During Blood Collection as Outliers Patients that received supplemental oxygen via nasal canula during ABG specimen collection Patient A Patient B Patient C Patient D

Exclusion of Data for Patients On

Oxygen Therapy During Arterial Blood Collection Significantly Influenced the Primary Endpoint (A-aDO2 - Revised) P=0.0249 Continuous Intermittent Placebo P=0.2313 *Comparison to Placebo * *

Physiology: GM-CSF Improved DLCO

P=0.0074 Continuous Intermittent Placebo P=0.3097 *Comparison to Placebo * *

Health Status: GM-CSF Improved SGRQ

Total Score P=0.0103 Continuous Intermittent Placebo P=0.0173 + MCID is 4 Points in COPD patients *Comparison to Placebo * *

The Improvement in SGRQ was Robust

as Shown by Responder Analysis Favors Placebo | Favors GM-CSF Odds Ratio 8 points 6 points 4 points Threshold value used as cut off' for a positive response Placebo versus GM-CSF (Continuous)

A Pattern of Improvement was Seen

Across all SGRQ Domains Continuous Intermittent Placebo Activity Impact Symptoms P=0.0107 P=0.0223 P=0.4884

Function: GM-CSF Trended Towards

Improved 6MWT-Distance P=0.3159 Continuous Intermittent Placebo P=0.7809 *Comparison to Placebo * *

Rescue Therapy: GM-CSF Trended

Towards a Reduction in WLL WLL Therapy Requirement Group # patients # treatments Rate Ratio vs Placebo Continuous (n=46) 4 9 0.284 Intermediate (n=45) 4 7 0.367 Placebo (n=47) 6 17 - Favors Placebo | Favors GM-CSF Hazards Ratio Placebo

versus GM-CSF Time to WLL: Intermittent Time to WLL: Continuous

Systemic Response: GM-CSF Trended

Towards Reduced Hemoglobin Levels P=0.0506 Continuous Intermittent Placebo P=0.5886 *Comparison to Placebo * *

Totality of Outcome Data Favors

Continuous GM-CSF over Placebo Disease element Endpoint Units Treatment effect P-value Pathology Chest CT - GGO Score -2.4 0.0002 Serum LDH, KL-6, SP-D, CEA, Cyfra 21 1 IU/L pg/ml All favor GM-CSF <0.05 Physiology

A-aDO2* - FAS mm Hg -4.6 0.1688 A-aDO2* - Revised mm Hg -6.5 0.0249 DLCO % predicted 7.9 0.0074 Health status & Function SGRQ** total score -7.6 0.0103 6MWT-Distance** m 20.6 0.3159 Rescue therapy Time to WLL** WLL frequency Hazard

ratio Rate ratio 0.59 0.28 0.4204 0.1918 Systemic response Hemoglobin (g/dL) -0.5 0.0506 * = Primary end point, ** = Key Secondary end point

Conclusions Baseline clinical

features of aPAP A large, global cohort of adult aPAP patients was identified and carefully characterized Study groups were well-balanced for demographics and disease severity Clinical trial observations The Placebo group experienced an

unexpected degree of improvement in A-aDO2 Inhaled recombinant human GM-CSF therapy (molgramostim) of aPAP is: Safe and well-tolerated Effective as shown by changes in lung pathology, physiology, health status, function, and the systemic

response to chronic lung disease More effective when administered continuously than on alternating weeks

Acknowledgments We are grateful to

and thank: Our PAP patients whose collaboration made the IMPALA trial possible IMPALA Investigators - PAP care providers and staff - at 30 centers in 18 countries including: Australia Troy S (Sydney); Denmark Bendstrup E (Arhus); France

Jouneau S (Rennes); Israel Kremer M (Tikva); Italy Campo I (Pavia); Germany Bonella F (Essen), Kreuter M (Heidelberg), Behr J (Gauting), Bohnet S (L beck); Greece Papiris S (Athens); Japan Inoue Y (Osaka), Yamaguchi E, (Aichi), Nakata K

(Niigata), Baba T (Yokohama), Kobayashi M (Sendai); Portugal A Morais (Porto) Ferreira L (Lisboa); Russia Ilkovich M (St. Petersburg); Slovakia Slivka R, Hagy V; South Korea Pyo Chung P, Woo Song J, Mi Choi S (Seoul); Spain Molina M (Barcelona);

Switzerland Lazor R (Lausanne); The Netherlands Veltkamp M (Nieuwegein); Turkey Cetinkaya E (Istanbul); United Kingdom Morgan C (London); United States Wang T (Los Angeles), Ataya A (Gainesville), Trapnell B (Cincinnati) IMPALA Protocol Committee:

Denmark Bendstrup E; Germany Costabel U, Bonella F; Italy Campo I; Japan Inoue Y; France Jouneau S; UK Morgan C; Greece Papiris S; USA Trapnell B Waterer G (Perth, Australia) who provided clinical and analytical expertise Savara Pharmaceuticals who

sponsored the IMPALA trial