Monopar Therapeutics Inc. · NASDAQ:MNPR
Monopar Therapeutics — Investor Presentation (May 2026)
37 slides from Monopar Therapeutics's investor presentation, May 2026
Slide 1: Monopar Therapeutics Inc.
Monopar Therapeutics Inc. Nasdaq: MNPR May 2026 1
Slide 2: Disclaimer, Forward-Looking Statements
Disclaimer, Forward-Looking Statements This presentation does not and shall not constitute an offer to sell or the solicitation of an offer to buy the securities, nor shall there be any offer, solicitation or sale of the securities in any state or jurisdiction in which such offer, solicitation or sa
Slide 3: Overview of Monopar Therapeutics
Overview of Monopar Therapeutics ▪ Clinical-stage biopharmaceutical company developing ALXN1840 for Wilson Disease and MNPR-101 for oncology ▪ ALXN1840 is a first-in-class albumin tripartite complex (ATC) activator that has completed a Phase 3 trial meeting its primary endpoint and with a mechanisti
Slide 4: Experienced Team
Experienced Team STRONG MANAGEMENT TEAM WITH A HISTORY OF SUCCESS IN DRUG DEVELOPMENT Christopher Starr, PhD – Co-Founder, Exec Chairman Chandler Robinson, MD, MBA, MSc – Co-Founder, CEO ▪ Co-Founder & Former CEO, Raptor Pharma (Nasdaq: ▪ Co-Founder, Tactic Pharma and Wilson Tx; lead drug RPTP), acq
Slide 5: Pipeline
Indications ALXN1840 4 Wilson Disease (Rare Disease) Cancers Trial Active and (Oncology) (Imaging) Recruiting Phase 1a Clinical Trial Active and Recruiting MNPR-101-Lu Advanced Solid (Oncology) Cancers MNPR-101-Ac Advanced Solid Late Preclinical (Oncology) Cancers e inical (oncology) — —/?> wate A .
Slide 6: ALXN1840
ALXN1840 A . ah Monopar Therapeutics
Slide 7: Wilson Disease Background
Wilson Disease Background Copper (Cu) balance is normally maintained in the body by hepatic ▪ Rare genetic disorder of impaired copper (Cu) transport with devastating excretion of excessive copper in bile. In Wilson disease there is: hepatic and neurological consequences that require life-long thera
Slide 8: Wilson Disease – A High Clinical Unmet Need Therapeutic Area
Wilson Disease – A High Clinical Unmet Need Therapeutic Area Landscape has had limited innovation There is a significant need for novel mechanistic approaches Current Standard of Care (SOC) treatments that: introduced more than 40 years ago ▪ Effectively and safely reduce accumulated copper SOC chel
Slide 9: Overview of ALXN1840 for Wilson Disease
Overview of ALXN1840 for Wilson Disease ▪ ALXN1840 (tiomolibdate choline) is an investigational, novel mechanism, first in class albumin tripartite complex ( ATC) activator With TMC, copper is sequestered in a ▪ ALXN1840 mobilizes copper and sequesters it as a tripartite tripartite complex complex w
Slide 10: ALXN1840 Dataset Characterizing Novel Mechanism, Safety, and Effectiveness Is Comprehensive
ALXN1840 Dataset Characterizing Novel Mechanism, Safety, and Effectiveness Is Comprehensive ▪ Characterized protein-centered mechanism of Cu mobilization and sequestration1 In vitro and In Vivo Mechanistic ▪ Confirmed high Cu affinity (~10,000x greater than penicillamine/trientine)2 Studies ▪ Demons
Slide 11: ALXN1840 Dataset Characterizing Novel Mechanism, Safety, and Effectiveness Is Comprehensive
ALXN1840 Dataset Characterizing Novel Mechanism, Safety, and Effectiveness Is Comprehensive Phase 3 Pivotal Study ▪ Met primary endpoint (~3x greater Cu mobilization compared to penicillamine, trientine, and/or zinc)1 (NCT03403205) ▪ Cu mobilization was rapid and sustained over 48 weeks1 ALXN1840: N
Slide 12: Wilson Disease Market Dynamics Point to Significant Opportunity for ALXN1840
Wilson Disease Market Dynamics Point to Significant Opportunity for ALXN1840 MARKET DYNAMIC ALXN1840 OPPORTUNITY High awareness of limitations of SOC Market is ripe for disruption from a novel MOA therapies innovation Opportunity for Monopar to establish a leading Limited branded players promotional
Slide 13: ALXN1840 Go-To-Market Strategy Centers on Disruptive Innovation
ALXN1840 Go-To-Market Strategy Centers on Disruptive Innovation to Usher in a New Era in the Treatment of Wilson Disease Positioning focus on novel protein-centered mechanism of action with demonstrated efficacy and safety across largest clinical development program ever conducted in Wilson disease
Slide 14: ALXN1840 Phase 2 and Phase 3 Study Results
ALXN 1840 Phase 2 and Phase 3 Study Results 14
Slide 15: Phase 3 Clinical Trial: ALXN1840 Met Primary Endpoint
Phase 3 Clinical Trial: ALXN1840 Met Primary Endpoint ALXN1840 demonstrated superior More patients had neurologic improvement copper mobilization versus SoC (n=207) while fewer worsened on ALXN1840 vs SoC* Primary Endpoint Daily mean area under the effect-time curve (AUEC) MCID Status Standard of AL
Slide 16: Phase 2 Absorption/Excretion Clinical Trial (1 of 4)
Phase 2 Absorption/Excretion Clinical Trial (1 of 4) Kirk et al, Journal of Hepatology 2024. vol. 80, 586–595 16
Slide 17: Phase 2 Absorption/Excretion Clinical Trial (2 of 4) – ALXN1840 Blocks Absorption
Phase 2 Absorption/Excretion Clinical Trial (2 of 4) – ALXN1840 Blocks Absorption PET/CT 15 hours post oral 64Cu ingestion Trientine Penicillamine ALXN1840 No Treatment Kirk et al., J Hep 2024 Sandhal et al, Aarhus University Hospital, 2022 17
Slide 18: Phase 2 Absorption/Excretion Clinical Trial (3 of 4)
Phase 2 Absorption/Excretion Clinical Trial (3 of 4) In Wilson Disease patients, ALXN1840 treatment reduces copper accumulation in the liver and brain Kirk et al, Journal of Hepatology 2024. vol. 80, 586–595 18
Slide 19: Phase 2 Absorption/Excretion Clinical Trial (4 of 4)
Phase 2 Absorption/Excretion Clinical Trial (4 of 4) PET/MRI imaging 6 hours post Copper-64 administration to Wilson Disease patients before (left) and after (right) ALXN1840 treatment showing less copper accumulation in the liver Kirk et al, Journal of Hepatology 2024. vol. 80, 586–595 19
Slide 20: Rapidly Improved Copper Balance with ALXN1840
Rapidly Improved Copper Balance with ALXN1840 Recent Publication Key Findings Oral Bis-choline Tetrathiomolybdate Rapidly Improves Copper Balance in ▪ The authors clarified that the prior analysis of copper balance only accounted for certain routes of copper loss Patients with Wilson Disease ▪ By co
Slide 21: Sustained Long-term Clinical Improvement over 6-Years
Sustained Long-term Clinical Improvement over 6-Years 21
Slide 22: Sustained Long-term Neurologic and Psychiatric Benefit
Sustained Long-term Neurologic and Psychiatric Benefit Long-term sustained improvement of neurological symptoms in Wilson disease patients on tiomolybdate choline Neurologic benefit reproduced across independent trials Patients who switch from SoC to ALXN1840 further improve UWDRS Minimum Clinically
Slide 23: ALXN-1840 Mechanistic Data
ALXN-1840 Mechanistic Data 23
Slide 24: ALXN1840 Decreases Total Body Copper in WD Mice
ALXN1840 Decreases Total Body Copper in WD Mice 800 * p < 0.05 vs control 700 600 Mean Total Body Cu (μg) 500 Total body Cu is significantly lower after 8 weeks in WD mice treated with ALXN1840 400 (n = 5 mice per group) 300 200 100 Water ALXN1840 ALXN1840 ALXN1840 D-penicillamine (control) 5 mg/kg
Slide 25: ALXN1840 Induces 1:1 Biliary Excretion with Cu in WD Rats
ALXN1840 Induces 1:1 Biliary Excretion with Cu in WD Rats Cu and Mo in Bile1 Fecal Cu (ng/g)1 400 50,000 Cu concentration (nmol/ml) Cu concentration (ng/g) 40,000 300 30,000 200 20,000 100 10,000 0 100 200 300 400 Mo concentration (nmol/ml) Study Day Once bound, Cu-ALXN1840 is excreted intact Fecal
Slide 26: Cu Transits Through Sites of Albumin Processing – Does Not Accumulate
Cu Transits Through Sites of Albumin Processing – Does Not Accumulate Total Body Cu at Week 81 Sites of albumin 700 processing 600 500 Mean Cu (μg) Cu transits with albumin (as ALXN1840-Cu-albumin complex) 400 through sites of albumin processing before excretion in WD mice 300 200 100 Albumin proces
Slide 27: Mo Transits Thru Sites of Albumin Processing – Does Not Accumulate
Mo Transits Thru Sites of Albumin Processing – Does Not Accumulate Sites of albumin Total Body Cu Total Body Mo processing 600 600 500 500 400 400 Mean Mo (μg) Mean Cu (μg) 300 300 < 2 daily doses of ALXN1840 200 200 100 100 2 wks 2 wks 8 wks 16 wks 2 wks 2 wks 8 wks 16 wks Control ALXN1840 (15 mg/k
Slide 28: Transits Thru Sites of Albumin Processing – Does Not Accumulate
Transits Thru Sites of Albumin Processing – Does Not Accumulate Kidney Cu Kidney Mo 20 15 Total (μg) After a 2-week withdrawal period 10 in WD mice, kidney Cu and Mo levels decrease in parallel 5 2 wks on 2 wks on, 2 wks on 2 wks on, 2 wks off 2 wks off ALXN1840 (15 mg/kg) treatment ALXN1840 (15 mg/
Slide 29: Clinical Data Corroborate Nonclinical Findings; TPC Transit Appears Safe
Clinical Data Corroborate Nonclinical Findings; TPC Transit Appears Safe Before ALXN1840 After ALXN1840 Hepatic Kidney ↓ Hepatic ↑ Kidney Cu Cu Cu Cu ALXN1840 blocks Cu uptake in liver1; transits through the kidney in a manner that appears safe Drug-related Adverse Events2 Number of patients 266 Pat
Slide 30: No Impact on Kidney Function in Humans Across 6 Years of Treatment
No Impact on Kidney Function in Humans Across 6 Years of Treatment Serum Creatinine Mean serum creatinine (top) and mean 24-hour urine creatinine (bottom) were within normal limits across 6 years on ALXN1840 24-hr Urine Creatinine Source: Pooled Phase 2/3 Safety Analysis 30
Slide 31: Clean SAE Profile at Sites of Albumin Processing
Clean SAE Profile at Sites of Albumin Processing SAEs from Phase 3 Clinical Trial (48-weeks) All SAEs Related only ALXN1840 SoC ALXN1840 SoC System Organ Class (n=137) (n=70) (n=137) (n=70) Gastrointestinal disorders 1 (0.7%) 2 (2.9%) 0 0 Musculoskeletal and connective tissue disorders 1 (0.7%) 2 (2
Slide 32: MNPR-101
MNPR-101 A . ah Monopar Therapeutics
Slide 33: MNPR-101 is a Radiolabeled Antibody Targeting uPAR
MNPR-101 is a Radiolabeled Antibody Targeting uPAR Leading Cancer Deaths % Patients Cancer 2024 with uPAR Type Expression 20% Breast1 97% 9% Bladder2 89% uPAR 55% 8% Ovarian3 88% 7% Pancreatic4 87% Colorectal5 85% Lung and Bronchus Colon and Rectum Pancreas Breast Urothelial cell carcinoma showing O
Slide 34: Biodistribution Supports Strong Preclinical Efficacy
Biodistribution Supports Strong Preclinical Efficacy Pancreatic Cancer Triple Negative Breast Cancer MIA-PaCa2 xenograft mouse model MDA-MB-231 xenograft mouse model 2500 3000 Control Group(No treatment) * Control Group (No treatment) 100 µCi MNPR-101-Lu Group * 2500 100 nCi MNPR-101-Ac Group % of I
Slide 35: Human Clinical Data Confirms MNPR-101’s Tumor Targeting Ability
Human Clinical Data Confirms MNPR-101’s Tumor Targeting Ability MNPR-101-Zr Phase 1 – imaging, dosimetry, tumor uptake, biodistribution, & safety 10 MNPR-101-Lu Phase 1a – therapeutic (efficacy), safety, & dose-escalation Next Milestone: Ongoing data readouts from these 72-year-old female open-label
Slide 36: MNPR-101-Zr Comparison with FDG
MNPR-101-Zr Comparison with FDG ¹⁸F-fluorodeoxyglucose (FDG) MNPR-101-Zr (72h) 10 0 SUV FDG image acquired 14 days prior to MNPR-101-Zr administration on the same Siemens Biograph Vision Quadra PET/CT System. Presented at European Association of Nuclear Medicine 2024 36
Slide 37: Thank You
Thank You May 2026 A Monopar Therapeutics
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