Exhibit 99.3
APPENDIX SLIDES — Third Quarter 2020 Financial Results and Business Update November 5, 2020 THERAVANCE BIOPHARMA ® , THERAVANCE ® , the Cross/Star logo and MEDICINES THAT MAKE A DIFFERENCE ® are registered trademarks of the Theravance Biopharma group of companies (in the U.S. and certain other countries). All third party trademarks used herein are the property of their respective owners. © 2020 Theravance Biopharma. All rights reserved.
Our science Organ - selective molecules designed to optimize therapeutic index
Theravance Biopharma difference: Targeting the right disease with the right molecular design TI, therapeutic index. 3 α STAT P STAT P STAT JAK β γ JAK N UCLEUS P STAT P STAT TI TI
Research and development portfolio of designed molecules: brain, lung, GI and eye 4 Molecular Design Biology Medicinal Chemistry DMPK Development and Commercial Symptomatic nOH (Neurogenic orthostatic hypotension) Asthma Lung Transplant Rejection IPF (idiopathic pulmonary fibrosis) COPD (chronic obstructive pulmonary disorder) — APPROVED COVID - 19 CD (Crohn’s disease) UC (ulcerative colitis) Celiac Disease DME (diabetic macular edema) DMPK, drug metabolism and pharmacokinetics; GI, gastrointestinal.
Program Indication Research Phase 1 Phase 2 Phase 3 Filed Marketed Collaborator Ampreloxetine (TD - 9855) NRI S ymptomatic nOH Wholly - owned Organ - Selective TD - 1473 GI JAKi UC CD TD - 5202 Irreversible JAK3i Inflammatory intestinal diseases YUPELRI ® (revefenacin) LAMA COPD TD - 0903 Inhaled JAKi COVID - 19 Wholly - owned TD - 8236 Inhaled JAKi Asthma Inhaled ALK5i Idiopathic pulmonary fibrosis Program Indication Research Phase 1 Phase 2 Phase 3 Filed Marketed Rights Economic Interests TRELEGY ELLIPTA 1 FF/UMEC/VI COPD GSK & Innoviva , Inc. Asthma Skin - selective JAKi Dermatological diseases Key programs supported by proven development and commercial expertise 1. TBPH holds 85% economic interest in upward - tiering royalty stream of 6.5% – 10% payable by GSK (net of TRC expenses paid and the amount of cash, if any, expected to be used by TRC pursuant to the TRC Agreement over the next four fiscal quarters). 75% of TRC income received is pledged to service outstanding notes, 25% of roy alt ies received retained by TBPH. All statements concerning TRELEGY ELLIPTA based on publicly available information. FF/UMEC/VI, fluticasone/umeclidinium/vilanterol; JAKi, Janus kinase inhibitor; LAMA, long act ing muscarinic receptor antagonist; NRI, norepinephrine reuptake inhibitor. 5 Phase 2 Phase 2 Phase 2b/3 Phase 1 Phase 3 Marketed Marketed Research Phase 2 Marketed Phase 1
TD - 0903 Program Nebulized lung - selective pan - JAK inhibitor to treat: ► Acute hyperinflammation of the lung in COVID - 19 ► Chronic inflammation for the prevention of lung transplant rejection
Leveraging respiratory expertise for potential acute treatment in response to a global pandemic 1. https://coronavirus.jhu.edu/map.html, number as of 9/10. 2. IHME. 7 US patients 1 >6M patients become hospitalized 2 ~2.4% No vaccine available Current treatment: Supportive therapy As of July 1, 2020: 439 drugs in 2327 trials worldwide S TRATEGIC O PPORTUNITY TD - 0903 Inhaled lung - specific therapeutic: potential to be used in combination with other treatment modalities (e.g., antivirals) to provide additional therapeutic benefit without risk of systemic immunosuppressive issues that may occur with systemic anti - inflammatories P ATIENT P OPULATION C URRENT T REATMENT L ANDSCAPE patients worldwide 1 >27.8M
S TRATEGIC O PPORTUNITY First - in - disease opportunity for the prevention of lung transplant rejection ‣ Calcineurin inhibitors (tacrolimus) ‣ Anti - proliferative agents (MMF) 1. http://www.transplant - observatory.org/data - charts - and - tables/ . 2. United Network for Organ Sharing (UNOS), https://unos.org/data/transplant - trends. 3. Chambers DC et al, JHLT 2018; 37(10): 1169 - 1183. 4. JHEOR. 2015. CA Jones https://pdfs.semanticscholar.org/108c/5cb16aaab19fa 9e9a1ccba64ae5869336f26.pdf CAGR, compound annual growth rate; CF, cystic fibrosis; CLAD, chronic lung allograft dysfunction; mAb, monoclonal antibody; M MF, mycophenolate mofetil. 8 lung transplants per year in US 2 2,714 TD - 0903 Potential first approved therapy specifically to prevent acute lung transplant rejection and development of CLAD Use following lung transplantation could improve patient morbidity and mortality risk, and reduce need for re - transplantation Lung transplants have the poorest prognosis of all solid organ transplants COPD, IPF, and CF top 3 diagnoses driving need for lung transplantation CAGR since 1988 15% mortality at 6 years post transplant 3 ~50% No FDA - approved therapies to prevent lung transplant rejection or CLAD Current standard of care: triple immunosuppression therapy medical/productivity costs (2015 – 2025) 4 $3.5B P ATIENT P OPULATION C URRENT T REATMENT L ANDSCAPE lung transplants worldwide, 2019 1 6,240 ‣ Corticosteroids ‣ IL - 2 mAb induction therapy ( basiliximab )
Month 6 0 5 10 15 20 F i r s t B P A R R a t e ( % ) Pan - JAK inhibitors can prevent transplant rejections Noninferiority trial of tofacitinib vs cyclosporine (CsA) in kidney transplant recipients 1 ‣ JAK inhibition was superior to cyclosporine in prevention of acute and chronic rejections ‣ Serious infections increased with systemic JAK inhibitors including CMV 1. Vincenti F, et al. Am J Transplant 2015;15:1644 - 53. *p<0.001 vs CsA . BPAR, biopsy - proven acute rejection; CMV, cytomegalovirus; SE, standard error; TWC2, time - weighted 2 - h post - dose concentrations . 9 Chronic Rejection Tofacitinib is superior to CsA in efficacy measures Acute Rejection Increased infection risk with tofacitinib over CsA CsA Tofacitinib 50 40 30 20 10 0 Month 12 * IF/TA % 24 5 53 25 0 20 40 60 Tofacitinib CsA CMV disease Serious infection 12 - month Kaplan - Meier estimates, % (SE)
Ampreloxetine (TD - 9855) Once - daily norepinephrine reuptake inhibitor to treat symptomatic neurogenic orthostatic hypotension
Reduced quality of life, significant care - giver burden and limited therapeutic options for symptomatic nOH patients 11 1. Mathias C, et al. J Neurol 1999;246:893 - 8. 2. Ha AD, et al. Parkinsonism Relat Disord 2011;17:625 - 8. 3. Not all patients are treated with prescription medication. P ATIENT P OPULATION US patients ~350K Current treatments (midodrine, fludrocortisone, droxidopa) have significant limitations Subset of patients do not respond None demonstrate durable effect Safety profiles that limit use Require multiple daily dosing nOH is a symptom of MSA, PAF and PD 70 – 80% of MSA patients 1 , and 30 – 50% of PD patients 2 have nOH 3 S TRATEGIC O PPORTUNITY Ampreloxetine Designed to reduce symptoms of nOH by prolonging the effect of endogenous norepinephrine with the potential to provide a meaningful and durable symptom improvement to underserved patients C URRENT T REATMENT L ANDSCAPE ~700K APAC patients ~700K EU patients
Untreated nOH NE Release at Neurovascular Junction Systolic Blood Pressure Designed to reduce symptoms of nOH by prolonging the effect of endogenous norepinephrine 1. Palma JA, Kaufmann H. Mov Disord Clin Pract 2017;4:298 - 308. NE, norepinephrine; NET, norepinephrine transporters. 12 Vasodilation Blood pressure Vasoconstriction Blood pressure Syncope Normal x Increased standing blood pressure x Increased brain perfusion x Reduce symptoms of symptomatic nOH 1 NE A XON TERMINAL D ENDRITE + Ampreloxetine Ampreloxetine Reduction in syncope Normal
Ampreloxetine: Potential to provide meaningful and durable symptom improvement to underserved patients Baseline OHSA #1 (Orthostatic Hypotension Symptom Assessment Question 1) >4 points. Negative change indicates improvement in symptoms; improvement of 1 point is defined as the MCID (minimal clinically importan t d ifference). ITT, intention - to - treat; SD, standard deviation. Mean (SD) change from baseline in OHSA #1 score n=17 n=13 n=7 n=6 Week Study 169: 4 weeks (N=188) Randomized, double - blind, placebo - controlled, parallel group Study 170: 22 weeks (N=254) Randomized 6 - week withdrawal phase Phase 3 registrational program ongoing; 4 - week efficacy data expected Q3 2021 13 Phase 3 Registrational Program Ampreloxetine Phase 2 data in nOH; 20 weeks of treatment Extension study: 3 years Completers: Considered clinically meaningful Withdrawal Durability Efficacy -7 -6 -5 -4 -3 -2 -1 0 1 2 3 0 4 8 12 16 20 24
Decentralized trials move activities from the clinic to home ‣ Site - centric operating model ‣ Burden on site resources ‣ Patient burden Source: Theravance Biopharma Clinical Operations. 14 Global clinical trials are being decentralized along a continuum Traditional Trial Operations Decentralized Trial ‣ Patient - centric model ‣ Leverage technology for remote visits, monitoring and data collection ‣ Established home health and distribution channels
TD - 1473 (JNJ - 8398) Oral gut - selective pan - JAK inhibitor to treat inflammatory bowel diseases
Need for new medicines to treat Inflammatory Bowel Disease 16 HRQoL, health - related quality of life; IBD, inflammatory bowel disease. 1. GBD 2017 Inflammatory Bowel Disease Collaborators. Lancet 2020;5:17 - 30. 2. https://www.crohnscolitisfoundation.org/sites/default/files/2019 - 02/Updated%20IBD%20Factbook.pdf . P ATIENT P OPULATION US disease burden 2 $31B Standard of care: Biologics have become the mainstay of treatment in moderate - to - severe patients global cases, 2017 1 6.8M global IBD treatment market, 2018 $16B Current US patients Steroids, immunosuppressants, and TNF inhibitors associated with side effects that further decrease HRQoL S TRATEGIC O PPORTUNITY TD - 1473 Gut - selective agent: if used earlier in the course of disease, has potential to be a new cost - effective therapy option that reduces associated disease management costs and improves patient HRQoL current US patients 2 1.6M C URRENT T REATMENT L ANDSCAPE 780K CD cases 907K UC cases
STAT - induced Inflammation α N UCLEUS STAT P STAT P STAT P STAT P STAT JAK β γ JAK JAK inhibitor JAK - STAT pathway: orchestrating signaling of multiple pro - inflammatory cytokines Clark JD, et al. J Med Chem 2014; 57:5023 - 5038. EPO, erythropoietin; GM - CSF, granulocyte - macrophage colony - stimulating factor; Tyk, tyrosine kinase. 17 γ c cytokines (IL - 2, IL - 4, IL - 7, IL - 9, IL - 15, IL - 21) Type 1 IFNs, IL - 10 family IL - 6, IL - 11, IL - 13, IL - 27, IL - 31, IL - 35 IFN γ IL - 12, IL - 23 EPO, TPO GM - CSF, IL - 3, IL - 5 α JAK1 β γ JAK3 α JAK1 β γ Tyk2 α JAK1 β γ JAK2 Tyk2 α JAK1 β γ JAK2 α JAK2 β γ Tyk2 α JAK2 β γ JAK2
TD - 1473 is an oral, gut - selective pan - JAK inhibitor Preclinical data package for TD - 1473 represents a potential breakthrough approach to the treatment of IBD Journal of Crohn’s & Colitis April 20, 2020. 18 Gut selectivity Potent inhibition of Tyk2 Anti - inflammatory activity in disease model x x Lumen Vehicle treated control TD - 1473 treatment x 7.5 8 8.5 9 9.5 10 Tofacitinib Izencitinib Inhibitory potency (pKi) Tyk2
Systemic exposures low; tissue concentrations at or above JAK inhibition levels *Tofacitinib concentrations extracted from J Pharmacol Exp Ther 348:165 – 173, January 2014. BID, twice daily; IC 50 , concentration to produce 50% maximal inhibition; PK, pharmacokinetics. 19 Tofacitinib 10 mg BID* TD - 1473 20 mg TD - 1473 80 mg TD - 1473 270 mg Colonic Tissue Concentrations of TD - 1473 TD - 1473 Dose 1 10 100 1000 10,000 20 mg 80 mg 270 mg Range of JAK IC 50 values TD - 1473 Total Concentration (nM) Plasma Concentrations in UC Patients Time (h) 100 200 300 0 0 1 2 3 4 Plasma Concentration (nM)
TD - 1473: Gut - selective pan - JAK inhibitor Late - stage studies in Crohn’s disease and ulcerative colitis Phase 2 Crohn’s and Phase 2b/3 ulcerative colitis studies ongoing Phase 2 Crohn’s and Phase 2b ulcerative colitis data expected Q3 2021 Global collaboration with Janssen leverages joint development expertise and provides significant economics to TBPH 2 1. Maintenance phase of the study will have induction responder patients re - randomized to active doses compared to placebo at 44 weeks. 2. Deal value up to $1B in payments to TBPH, including $100M upfront; profit - share in US (33% TBPH, 67% Janssen); double - digit r oyalties to TBPH ex - US. Crohn’s disease Ulcerative colitis Phase 2: 12 weeks (N=160) Dose - finding induction Active treatment extension: 48 weeks Phase 2b/3: 8 weeks (N=240) Dose - finding induction Maintenance phase 1 : 44 weeks Phase 3: 8 weeks (N=640) Dose - confirming induction Responders 20
TD - 5202 Organ - gut selective irreversible JAK3 inhibitor to treat inflammatory intestinal diseases
Celiac disease has no current treatments and serious health consequences 22 1. 1% prevalence, BeyondCeliac.org. 2. 2018 US population 327M Census.gov. 3. Theravance Market Research. S TRATEGIC O PPORTUNITY P ATIENT P OPULATION US patients 1,2 3.3M No approved treatment Only available intervention is strict life - long gluten - free diet 30% of diagnosed patients are poorly controlled despite best dietary efforts 3 TD - 5202 Organ - gut selective irreversible JAK3 inhibitor: potential to deliver significant value for both patients and payers increase in US over past 50 y 4 – 4.5x Global prevalence 1% higher healthcare costs than controls >2x C URRENT T REATMENT L ANDSCAPE Celiac Normal
JAK3 - dependent cytokines play central role in pathogenesis of celiac disease ‣ Proof - of - relevance from recent positive Phase 2 data with systemic JAK3 inhibitor in alopecia areata, another T - cell mediated disease ‣ Localized JAK3 inhibition important to avoid systemic immunosuppression (genetic JAK3 deficiency leads to severe immunodeficiency) Figure adapted from Jabri B and Sollid L. J Immunol 2017;198:3005 - 14. IE - CTL, intraepithelial cytotoxic lymphocyte; IEL, intraepithelial lymphocyte. 23 IL - 2, IL - 4, IL - 7, IL - 9, IL - 15, IL - 21 I MMUNE C ELL CD Pathogenesis α N UCLEUS STAT P STAT P STAT P STAT P STAT JAK1 β γ JAK3 P P P Gluten peptides G LUTEN - S PECIFIC T H 1 CELLS I NTESTINAL E PITHELIUM L AMINA P ROPIA I NTESTINAL L UMEN IFNγ IL - 2 IL - 21 IEL IE - CTL IL - 15
TD - 5202 First - in - Human Overall Results Summary ‣ No serious or severe AEs were reported ‣ All treatment - emergent AEs in TD - 5202 - treated subjects were mild in severity AE, adverse event; C max,ss , maximal steady - state concentration; NK, natural killer. 24 TD - 5202: generally well - tolerated (single dose ≤2000 mg, multiple doses ≤1000 mg BID) for 10 consecutive days in healthy subjects ‣ Systemic exposures were dose proportional from 100 to 1000 mg BID ‣ Low steady - state systemic exposures: mean C max,ss ~11 - fold below the protein - adjusted JAK IC 50 at the highest tested dose (1000 mg BID), consistent with a gut - selective approach ‣ No clinically significant changes from baseline in vital signs and ECG assessments ‣ No clinically significant changes in chemistry or hematology parameters – No changes in NK cell count
Inhaled ALK5i Potential best - in - disease therapy for the treatment of idiopathic pulmonary fibrosis (IPF)
Limited treatment options 2 currently approved therapies, with modest efficacy and poor tolerability S TRATEGIC O PPORTUNITY P ATIENT P OPULATION Inhaled ALK5i Potential first - in - class inhaled ALK5 inhibitor anti - fibrotic agent for IPF Despite treatment with the current SOC, IPF patients continue to experience disease progression and exacerbation C URRENT T REATMENT L ANDSCAPE Idiopathic pulmonary fibrosis (IPF) remains a fatal chronic lung disease with limited treatment options 1. Raghu G, et al. Lancet Resp. 2014: 2(7):566 - 572. 2. Raghu G, et al. Eur Respir J . 2016: 48(1):179 - 186. 3. National Heart Lung and Blood Institute (NIH), Public Domain, https://commons.wikimedia.org/w/index.php?curid=29590103. US prevalence; currently orphan diease 1,2 140,000 Lungs with IPF 3 26 Profound dyspnea, unrelenting cough, impairment of activities of daily living Mortality with IPF remains high
Significant opportunity remains for effective IPF treatments ‣ Mortality with IPF remains high – <50% alive 3 years after diagnosis 1 1. King TE, et al. Am J Respir Crit Care Med 2001;164:1171 - 81. 27 1.0 0.8 0.6 0.4 0.2 0.0 0 5 10 15 Years Probability of Survival Male Female To arrest disease progression with improved tolerability Goal
TGFβ, transforming growth factor β. 28 S CARRING TISSUES Collagen deposition Stimuli Genetic susceptibility Repetitive injury AEC damage TGF β A LVEOLAR E PITHELIAL C ELLS (AEC) T YPE 2 T YPE 1 Normal M YOFIBROBLASTS Fibrogenesis, proliferation Targeting the TGFβ pathway A core signaling pathway that drives fibrosis
a SMA , a - smooth muscle actin; ERK, extracellular signal - regulated kinase; JNK, c - Jun N - terminal kinase; PI3K, phosphatidylinositol - 4,5 - b isphosphate 3 - kinase; Smad2/3, mothers against decapentaplegic homolog 2/3; TGFR (ALK5), TGFβ receptor. Adapted from: Neuzillet C, et al. Oncotarget 2013;5:78 – 94. 29 F IBROBLASTS M YOFIBROBLASTS Fibroblast to Myofibroblast Transition (FMT) Increased extracellular matrix Increased a SMA Increased migration ERK Smad2/3 PI3K p38 JNK Rho IPF progression P P ALK5i Activation: Multiple an integrins Proteases Thrombospondin Free Radicals TGFR2 Latent TGFβ TGFR1 (ALK5) Selectively targeting the TGFβ pathway through ALK5 inhibition Inhibiting a core signaling pathway that drives fibrosis regardless of activation mechanism
ALK5 inhibition directly interrupts FMT 1 in IPF FTM, fibroblast to myofibroblast transition 30 Reference Standard ALK5i Log [M] % inhibition of α SMA - 9 - 8 - 7 - 6 - 5 0 50 100 150 FMT a SMA expressed a SMA reduced Negative control ALK5i treated
Current treatment options have no effect on FMT at clinically relevant concentrations FTM, fibroblast to myofibroblast transition; C max , maximal concentration; IC 50 , half maximal inhibitory concentration. 1. https://www.tga.gov.au/sites/default/files/auspar - nintedanib - esilate - 160208.pdf . 2. Ogura T, et al. Eur Respir J. 2015;45:1382 - 92. 31 -10 -9 -8 -7 -6 -5 -4 -3 -2 -1 0 Pirfenidone Nintedanib Log [M] Nintedanib IC 50 Pirfenidone IC 50 Clinical C max Unbound 1,2
Wound repair Bone healing Cardiovascular homeostasis Tumor suppression Endocrine function Lung selectivity avoids unwanted systemic side effects Minimizing systemic inhibition of a cytokine essential for homeostasis Modified from: Akhurst RJ, Hata A. Nat Rev Drug Discov 2012;11:790 - 811. 32 Maintaining key systemic regulatory roles of TGFβ Inhaled ALK5i
Ocular JAKi Potential best - in - disease, pan - JAK inhibitor with long - acting ocular anti - inflammatory activity
Diabetic macular edema causes blindness in diabetics 34 1. © 2016 DR/Decision Resources, LLC. All rights reserved. Reproduction, distribution, transmission or publication is prohibit ed. Reprinted with permission. 2. Romero - Aroca , World J Diabetes 2011;2(6): 98 - 104. 3. Lee et al Curr Med Res Opin 2008;24:1549 - 59. Images from Angiogenesis Foundation, www.scienceofdme.org. Vision with DME Normal vision US prevalence 1 2.7 million #1 anti - VEGF treatments Most patients have suboptimal response S TRATEGIC O PPORTUNITY P ATIENT P OPULATION Ocular JAKi C URRENT T REATMENT L ANDSCAPE Potential to offer an alternative treatment for DME patients who are not optimally responding to treatment with VEGFi 140% higher direct and indirect healthcare costs in patients with DME vs diabetics without ocular disease 3 cause of blindness in diabetes 2 1st Intraocular steroids Side effects limit utility 2nd Nonpharmacological treatments (e.g. laser coagulation) limited efficacy and significant adverse events
Inflammation, not just VEGF, is a key driver of DME Intraocular anti - VEGF agents 35 1. Gonzalez VH, et al. Am J Ophthalmol 2016;172:72 - 79. Current Pharmacological Treatments Intraocular steroids Hyperglycemia Disruption of blood - retinal barrier Vascular leakage DME VEGF Retinal capillary damage Inflammatory cytokines Need for broad, sustained release, anti - inflammatory with a safer side - effect profile ‣ High frequency of formation of cataracts and glaucoma ‣ One third do not respond to anti - VEGF while another third have a suboptimal response 1 ‣ Require frequent intravitreal injections
0.00 0.25 0.50 0.75 1.00 1.25 VEGF IL-6 IP-10 MCP-1 Unmet need for an anti - inflammatory drug: opportunity for eye - selective JAK inhibition Adapted from Sohn HJ, et. al. Am J Ophthalmol 2011; 152:686 - 694. 36 Effect of anti - VEGF Effect of Steroids 0.00 0.25 0.50 0.75 1.00 1.25 VEGF IL-6 IP-10 MCP-1 Untreated Treated Normalized Protein Level
Ocular pan - JAK inhibition has the potential to address key disease pathways in DME 37 TD - EyeJAKi inhibits key DME inflammatory pathways: JAK2 JAK1 IL - 6 Tyk2 JAK1 Interferons MCP - 1 IP - 10 TD - EyeJAKi ‣ IL - 6 and interferon signaling pathways in human primary cells ‣ IL - 6 induced pSTAT3 and interferon - induced IP - 10 in the back of the eye in vivo
0 1 2 3 0.000001 0.00001 0.0001 0.001 0.01 0.1 1 10 100 1000 Time (months) C o m p o u n d c o n c e n t r a t i o n ( g / m L o r g / g ) A potent pan - JAK inhibitor designed for eye selectivity with projected dosing interval of at least three months 38 Single intravitreal injection of TD - EyeJAKi in Rabbits Vitreous humor (depot) Retina Plasma α STAT P STAT P STAT JAK β γ JAK N UCLEUS P STAT P STAT JAKi
About YUPELRI ® (revefenacin) inhalation solution YUPELRI ® (revefenacin) inhalation solution is a once - daily nebulized LAMA approved for the maintenance treatment of COPD in the US . Market research by Theravance Biopharma indicates approximately 9 % of the treated COPD patients in the US use nebulizers for ongoing maintenance therapy . 1 LAMAs are a cornerstone of maintenance therapy for COPD and YUPELRI ® is positioned as the first once - daily single - agent bronchodilator product for COPD patients who require, or prefer, nebulized therapy . YUPELRI ® ’s stability in both metered dose inhaler and dry powder device formulations suggest that this LAMA could also serve as a foundation for novel handheld combination products . 1. TBPH market research (N=160 physicians); refers to US COPD patients. 39
YUPELRI ® (revefenacin) inhalation solution YUPELRI ® inhalation solution is indicated for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD) . Important Safety Information (US) YUPELRI is contraindicated in patients with hypersensitivity to revefenacin or any component of this product . YUPELRI should not be initiated in patients during acutely deteriorating or potentially life - threatening episodes of COPD, or for the relief of acute symptoms, i . e . , as rescue therapy for the treatment of acute episodes of bronchospasm . Acute symptoms should be treated with an inhaled short - acting beta 2 - agonist . As with other inhaled medicines, YUPELRI can produce paradoxical bronchospasm that may be life - threatening . If paradoxical bronchospasm occurs following dosing with YUPELRI, it should be treated immediately with an inhaled, short - acting bronchodilator . YUPELRI should be discontinued immediately and alternative therapy should be instituted . YUPELRI should be used with caution in patients with narrow - angle glaucoma . Patients should be instructed to immediately consult their healthcare provider if they develop any signs and symptoms of acute narrow - angle glaucoma, including eye pain or discomfort, blurred vision, visual halos or colored images in association with red eyes from conjunctival congestion and corneal edema . Worsening of urinary retention may occur . Use with caution in patients with prostatic hyperplasia or bladder - neck obstruction and instruct patients to contact a healthcare provider immediately if symptoms occur . Immediate hypersensitivity reactions may occur after administration of YUPELRI . If a reaction occurs, YUPELRI should be stopped at once and alternative treatments considered . The most common adverse reactions occurring in clinical trials at an incidence greater than or equal to 2 % in the YUPELRI group, and higher than placebo, included cough, nasopharyngitis, upper respiratory infection, headache and back pain . Coadministration of anticholinergic medicines or OATP 1 B 1 and OATP 1 B 3 inhibitors with YUPELRI is not recommended . YUPELRI is not recommended in patients with any degree of hepatic impairment . OATP, organic anion transporting polypeptide. 40