Slide 1: CLNN (NASDAQ)
CLNN (NASDAQ)
Slide 2: Forward Looking Statements
Forward Looking Statements 2 This presentation contains "forward - looking statements" within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995 . Clene's actual results may differ from its expectations, estimates, and projections and consequently, yo
Slide 3: Management Team
L a nx id e C o rp o r a ti on Dupont Lanxide Composites Lanxide Armor Company Lanxide Performance Materials Lanxide Electronic Components CDO CLENE | Management Team Ted Jeong , DM 3
Slide 4: Clene Nanomedicine
4 Clene Nanomedicine Cash on hand: $63M End of Q2 including PIPE & Venture debt of $24M Topline data from One Registrational Trial 1 by mid - 2022 and 3 Phase 2 Trials 2 by end of 2021 >200 patient years of CNM - Au8 clinical exposure CNM - Au8® a gold nanocrystal suspension, in development as the f
Slide 5: Platform & Pipeline
Novel electro - chemistry platform produces catalytic Clean Surface Nanocrystal drugs designed to avoid toxicities associated with synthetic chemistry 130+ G ra n ted Patents CLENE | Platform & Pipeline (Anticipated Launch in 2021) Brain Imaging Biomarker Study Brain Imaging Biomarker Study 2H 2022
Slide 6: Catalytically-Active Nanotherapeutic
CNM - Au8® | Catalytically - Active Nanotherapeutic Improved Cellular Energy Production & Utilization Energy Oral Suspension; Once Daily > 100 Trillion Nanocrystals per 60 mL Dose (At 30mg) 13 nm Median Diameter (Ribosome = 20 - 30 nm) Clean Surfaced Faceted Nanocrystal Novel mechanism of action to
Slide 7: Integrating Physics With Biology
CNM - Au8 | Integrating Physics With Biology Electron transfer (to - and - from) CNM - Au8 nanocrystals drives catalytic activity and cellular energy production Surface Based Catalytic Activity Electrons (e - ) Move Freely Across Nanocrystal Surface Vertices, Edges, & Faces Key to Catalytic Activity
Slide 8: Treating Energetic Failure
Treating Energetic Failure | Common Pathological Mechanism In Neurodegenerative Disorders (MS, ALS, PD) Respiratory Insuff ic ie n cy Dysphag i a/ Dysarthria Cognitive Impa irment Muscle Weakness/Atrophy ALS Neuronal Metabolic Failure MS Oligodendrocyte Remyelination Failure and Neuronal Die - Off V
Slide 9: Mechanism of Action
CNM - Au8 | MOA Therapeutic Effects a Nicotinamide Adenine Dinucleotide a 9
Slide 10: Significant Global Opportunity
1 0 CNM - Au8 | Significant Global Opportunity 707,158 103,903 828,703 596,407 256,455 1,407,7 0 1 0 400,000 800,000 1,200,000 1,600,000 U.S. Can ada W . E u ro pe Central/E. Europe J ap an China Est. Diagnosed PD Patients by Region Source: Lancet Neurol. 2018 Nov;17(11):939 - 953. ~7M pts PARKINSON
Slide 11: Evidence for Energetic Improvement
1 1 1 1 Robinson et al. Sci Rep. 2020, DOI: 10.1038/s41598 - 020 - 58709 - w. . 2 Ho et al. Society for Neuroscience Meeting, 2019. Ho et al. Motor Neuron Disease Associating Meeting, 2019. Data on File, Clene Nanomedicine, Inc. 2 CNM - Au8 | Evidence for Energetic Improvement Therapeutic Activity A
Slide 12: MOA & Remyelination Data Published
Robinson et al. Sci Rep. 2020 Feb 11;10(1):1936. doi: 10.1038/s41598 - 020 - 58709 - w Lysolecithin Re my e l i n atio n Data CNM - Au8 | MOA & Remyelination Data Published 12
Slide 13: Clinical Program Overview
Successful Phase 1 First - In Humans Safety Trial + Chronic Animal Toxicity Studies Phase 2 Brain Target Engagement 31 P - Magnetic Resonance Phase 2 MS Clinical Remyelination & Neurorepair CNM - Au8 | Clinical Program Overview Phase 3 Phase 2 & 3 ALS Clinical Neurorepair Phase 2 13
Slide 14: Clean Toxicology Findings
Genotoxicity In Vitro & In Vivo (Rodent) Safety Pharmacology CNS, CV, Renal Dose Range Finding Rodent, Minipig Single Dose Toxicokinetics Canine Multi - Dose To x icoki neti cs Canine (7 - Day) MTD Toxicokinetics Canine (4 - Wk) Max Feasible To x icoki neti cs Rodent (1 - Wk, SQ) Max Feasible To x i
Slide 15: Well Tolerated; No Dose-Limiting Safety Issues
• Single - ascending dose – 4 cohorts of 8 subjects plus one repeat (n=40) – 15, 30, 60, 90 mg – 3:1 randomized (active:control) – 1 dose; 17 - day follow - up • Most frequent TEAEs by System Organ Class: Nervous/GI - Nearly all of the TEAEs were Grade 1 severity (mild) • No serious TEAEs, TEAEs lea
Slide 16: Phase 2 REPAIR Study Design
• Difference in brain NAD+ and NADH fraction at Week 12 - 16 • Difference in bioenergetic metabolites (e.g., ATP, PCr, NAD) concentration at Week 12 – 16 • Difference in brain membrane markers (PE, PC, etc.) at Week 12 – 16 Change in Brain Bioenergetic Potential (NAD+/NADH) vs. Baseline 1 ι 2 ι CNM
Slide 17: Age Related Decline of Brain Energy Metabolism
NAD + /NADH | Age Related Decline of Brain Energy Metabolism (By 31 P - MRS Imaging) Closed squares = averaged data by age group: 21 – 26 yrs, 33 – 36 yrs, and 59 – 68 yrs old; Open squares= individual subject values ~0.5% NAD + /NADH unit decline per decade (~0.13 mV units per year) 17 Zhu et al. P
Slide 18: Improved Brain Energy Metabolism
CNM - Au8 | Improved Brain Energy Metabolism Increased NAD+/NADH Ratio in MS & PD Patients Phase 2 Results 18 1 ƒ Endpoint 2 ƒ Endpoints NAD is an essential molecule responsible for cellular energy production
Slide 19: Treatment Normalized Key Markers of Brain Metabolism in PD
β - ATP is used by the cell to maintain cellular metabolism and normal function Phosphorylation potential is the amount of available phosphorous that can be used to make ATP in times of stress or high metabolic activity CNM - Au8 | Treatment Normalized Key Markers of Brain Metabolism in PD Patients
Slide 20: Phase 2 ALS Study Design
(January 2020); FPFV 16 - Jan - 2020; 45 of 42 enrolled (Nov - 2020) Phase 2 Anticipated full unblinded data readout: 2H 2021 Exploratory Endpoints • Other Electromyography (SH i, NP i, MUSIX, MScan) • ALSFRS - R • Change in Rate of ALSFRS - R progression • QOL • Combined Joint - Rank (Survival + AL
Slide 21: Predictive Endpoints of Disease Progression
Predictive Endpoints of Disease Progression Clinical Endpo i nts • ALSFRS - R • Pulmonary Function (Vital Capacity) • Mortality • Loss of Motor Units Motor Unit Index (MUNIX) MUNIX Longitudinal Progression 21 Electromyography | Sensitive Biomarker Predictive of Clinical Progression
Slide 22: Emerging Evidence Predictive of Clinical Efficacy
Phase 2 Improv e m e nt Emerging Evidence Predictive of Clinical Efficacy | MUNIX(4) Sum Change Robert Glanzman MD FAAN, et al. “A Blinded Interim Update on RESCUE - ALS: A Randomized, Placebo - Controlled, Phase 2 Study to Determine the Effects of CNM - Au8 to Slow Disease Progression in Amyotrophi
Slide 23: Slower Rate of Vital Capacity Loss
SVC Avg. Slope Decline (% points/month) Slope Est. (9 - mon t h s) Empower (−2.73%) - 24.6% Benefit (−2.74%) - 24.7% PRO - ACT ( - 2.90%) - 26.1% − 10.5 − 19.6 − 6.7 Andrews et al. JAMA Neurol. 2018;75(1):58 - 64. Phase 2 Robert Glanzman MD FAAN, et al. “A Blinded Interim Update on RESCUE - ALS: A R
Slide 24: Phase 3 ALS Registration Study
Exploratory Endpoints • Combined Joint Rank (Survival + ALSFRS - R) • Voice pathology • PRO (ALSAQ) • Pharmacodynamic markers Slow Vital Capacity Hand Held Dynamometry Change in ALSFRS - R Registration Study: 24 - Week Treatment Period (3:1 randomization, 120 active [30mg, 60mg]: 40 placebo) (July 2
Slide 25: Phase 2 MS Study Design
2 5 Exploratory Endpoints Treatment of Vis ual Pathway Deficits I n Chronic O ptic N europathy for A ssessment of R em y elination in Non - Active Relapsing MS Change in Low Contrast Letter Acuity (LCLA) At Week 24 Up to 48 - Week Placebo - Control 2:1 Randomization (Active: Placebo ) 15mg, 30mg, Pl
Slide 26: Measuring MS Functional Improvement
LCLA Phase 2 Primary: Functional Visual Improvement LCLA Correlates with clinically meaningful deficits in QOL, EDSS and MSFC, MRI, and OCT MS Functional Endpoints Phase 2 Exploratory: Neuroprotection/Remyelination Endpoints The Visual System is a Window into the Brain 9 - Hole Peg Test 26 Symbol Di
Slide 27: Emerging Evidence of Clinical Improvement
Emerging Evidence of Clinical Improvement Glanzman, R., H. Beadnall, M. T. Hotchkin, A. Klistorner, M. Barnett, R. Sergott, A. Rynders, K. S. Ho, and Mark G. Mortenson. “Update to a Phase 2 clinical trial of catalytic gold nanocrystals, CNM - Au8, for the treatment of chronic optic neuropathy.” Pres
Slide 28: Strong Intellectual Property
CS N 28 ® Clean surface nanocrystal (CSN) therapeutics Issued & Allowed Patents 130+ Pending Applications >30 Total Patents/ Applications >160 Process And Method/Device (Clean Surface; Gold CSN) State of Matter (CNM - Au8) Method of Use (Prevent Demyelination & MoA) Method of Use (Bi - Metallic Au/P
Slide 29: Proprietary Nanocrystal Manufacturing
Clene | Proprietary Nanocrystal Manufacturing In - House ISO8 Clean Room Clinical Production in North East, MD Validated CMC Processes 29 Designed to be Scalable to Commercialization Patented Hydro - ele ctro - Crystallization Proprietary Trade Secrets
Slide 30: Anticipated Timeline & Investor Catalysts 2020-2023
Anticipated Timeline & Investor Catalysts 2020 - 2023 30
Slide 31: Investment Highlights
Unmet Medical Need & Market Opportunity Lead Asset: CNM - Au8 for Neuro Repair Clinical Development Pipeline Strong IP Portfolio Financials CNM - ZnAg for COVID - 19 CLENE | Investment Highlights • Energy enhancing nanotherapeutic • Robust Preclinical Remyelination & Neuroprotection Data Across Mult
Slide 32: Clene Inc. HQ & Clinical Development
Clene Inc. HQ & Clinical Development 6550 South Millrock Drive, Suite G50 Salt Lake City, UT 84121 R&D and Manufacturing 500 Principio Parkway, Suite 400 North East, MD 21901 © 2021 Clene Inc. Version: 16 - September - 2021