UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM
CURRENT REPORT
Pursuant to Section 13 OR 15(d)
of The Securities Exchange Act of 1934
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Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§240.12b-2 of this chapter).
Emerging growth company
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.
Item 7.01 Regulation FD Disclosure.
On March 14, 2022, Clene Inc. (the “Company”) issued a press release announcing four poster presentations, one of which was also selected as an oral presentation, of updated clinical data from the Phase 2 RESCUE-ALS and REPAIR clinical trials and preclinical ALS data at the 2022 MDA Clinical & Scientific Conference, taking place March 13-16, 2022. A copy of the press release, posters, and oral presentation are furnished as Exhibit 99.1, Exhibit 99.2, Exhibit 99.3, Exhibit 99.4, Exhibit 99.5, and Exhibit 99.6 to this Current Report on Form 8-K (the “Current Report”) and are incorporated herein by reference.
In connection with the March 14, 2022 press release, the Company released an updated corporate presentation (the “Corporate Presentation”) on its website, https://clene.com. A copy of the Corporate Presentation is furnished as Exhibit 99.7 to this Current Report and is incorporated herein by reference. The Company plans to use its website to disseminate future updates to the Corporate Presentation and may not file or furnish a Current Report on Form 8-K alerting investors if the Corporate Presentation is updated.
The information furnished in this Item 7.01, including Exhibit 99.1, Exhibit 99.2, Exhibit 99.3, Exhibit 99.4, Exhibit 99.5, Exhibit 99.6, and Exhibit 99.7, shall not be deemed to be “filed” for purposes of Section 18 of the Securities Exchange Act of 1934 (the “Exchange Act”), as amended, or otherwise subject to the liabilities of that section, and shall not be deemed to be incorporated by reference into any filing made by the Company under the Exchange Act or the Securities Act of 1933, as amended, regardless of any general incorporation language in any such filings, except as shall be expressly set forth by specific reference in such a filing.
Item 9.01 Financial Statements and Exhibits.
(d) Exhibits
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99.1 |
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SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned, hereunto duly authorized.
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CLENE INC. |
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Date: March 14, 2022 |
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/s/ Robert Etherington |
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Robert Etherington |
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President and Chief Executive Officer |
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Exhibit 99.1
Clene Nanomedicine Presents Updated Clinical Data from Phase 2 RESCUE-ALS and REPAIR trials and Preclinical ALS data at 2022 MDA Clinical & Scientific Conference
SALT LAKE CITY, March 14, 2022 – Clene Inc. (NASDAQ: CLNN) along with its subsidiaries “Clene” and its wholly owned subsidiary Clene Nanomedicine, Inc., a clinical-stage biopharmaceutical company focused on revolutionizing the treatment of neurodegenerative disease, today announced multiple presentations of updated clinical trial results from the Phase 2 RESCUE-ALS and REPAIR trials in addition to new mechanistic preclinical data in ALS at the 2022 MDA Clinical & Scientific Conference, taking place March 13-16 in Nashville.
The first poster, titled “RESCUE-ALS Trial Results: A Phase 2, Randomized, Double-Blind, Placebo-Controlled Study of CNM-Au8 to Slow Disease Progression in ALS,” selected as an oral presentation, and the second poster, “Evidence for a Potential Survival Benefit with CNM-Au8 Treatment from the RESCUE-ALS Trial Long-Term Open Label Extension,” further support Clene’s lead drug candidate CNM-Au8®, a catalytically active gold nanocrystal suspension, as a potential disease-modifying therapy for amyotrophic lateral sclerosis (ALS).
RESCUE-ALS, a Phase 2 multi-center, randomized, double-blind, parallel-group, placebo-controlled trial examined the efficacy, safety, pharmacokinetics, and pharmacodynamics of CNM-Au8 in 45 participants with early ALS over a 36-week treatment period. In the 36-week blinded period, there were significant benefits with CNM-Au8 treatment: slowing ALS disease progression (p=0.0125), decreasing the proportion of participants with a 6-point decline in the ALS Functional Rating Scale Revised (ALSFRS-R) (p=0.035), and improving quality of life as measured by the ALS Specific Quality of Life (ALSSQOL-SF) questionnaire (p=0.018).
The second poster presented updated evidence for survival benefit with CNM-Au8 treatment that was reported from the RESCUE-ALS trial long-term open label extension for both the active and placebo groups. Interim analyses of observed survival compared to estimated median survival derived from the validated ENCALS prediction model significantly favored CNM-Au8 treatment with a hazard ratio of 0.3 for participants who entered the open-label extension (HR 0.3; p=0.01, log-rank test). CNM-Au8 was shown to be well-tolerated with no safety signals identified over 96 weeks of treatment.
The third poster, titled “Evidence for Brain Energy Metabolic Support with CNM-Au8 Treatment: Results from Phase 2 REPAIR Clinical Trial With CNM-Au8,” demonstrated improved brain energy metabolism assessed by high-resolution magnetic resonance spectroscopy (31P-MRS). CNM-Au8 treatment resulted in improved brain NAD+/NADH ratio (primary endpoint, paired t-test, p=0.0371). This result was driven both by increase in NAD+ and a decrease in NADH (secondary endpoint, paired t-test, p=0.0264). CNM-Au8 treatment also resulted in homeostatic effects on brain energy-related phosphorous-containing metabolites, including ATP. Study participants with whole-brain ATP levels less than the population's baseline mean saw significantly increased ATP levels, while patients with baseline levels greater than the baseline mean decreased to the population mean (r2 = 0.711, p<0.0001). These data demonstrate CNS target engagement following treatment with CNM-Au8 and support its candidacy as a disease-modifying therapy for the treatment of neurodegenerative diseases associated with dysregulated neuronal energy metabolism.
The fourth poster accepted for presentation, “CNM-Au8 Gold Nanocatalysis Protects Neurons Against Degeneration and Death in Multiple in vitro models of ALS,” demonstrates CNM-Au8’s ability to promote neuronal survival and function in multiple independent in vitro models of ALS: (i) treatment of primary rat spinal motor neurons improved survival, preserves the neurite networks, and reduced cytoplasmic TDP-43 aggregate accumulation after either glutamate excitotoxic injury or exposure to beta-amyloid (Aβ 1-42) oligomers; (ii) treatment of spinal motor neurons from transgenic SOD1G93A rats protected motor neurons from death upon exposure to excitotoxic glutamate in a cAMP-dependent manner, and reduced SOD1 protein accumulation in a manner independent of cAMP; (iii) treatment of human induced pluripotent stem cell (iPSC)-derived neurons from C9ORF72 patients prevented neuronal death in response to stressors; and (iv) survival and neurite outgrowth of human iPSC-derived motor neurons in co-culture with toxic SOD1A4V ALS-patient derived astrocytes were significantly and dose-dependently improved with treatment of CNM-Au8.
“The preclinical and clinical data presented at MDA further support Clene’s lead drug candidate CNM-Au8 as a potential disease-modifying therapy for amyotrophic lateral sclerosis,” said Dr. Robert Glanzman, MD FAAN, Clene’s Chief Medical Officer. “We look forward to the continued advancement of the ALS clinical program with the top-line results from the HEALEY ALS Platform Trial expected in the second half of the year.”
Rob Etherington, Clene’s CEO, added, “This is an exciting time for Clene as we build a bigger body of scientific and clinical evidence in support of our CNM-Au8. Will continue to further the validation of our findings in neurological function and survival as we await results in larger clinical studies underway.”
About CNM-Au8®, a gold nanocrystal suspension
CNM-Au8 is an oral suspension of gold nanocrystals developed to restore neuronal health and function by increasing energy production and utilization. The catalytically active nanocrystals of CNM-Au8 drive critical cellular energy producing reactions that enable neuroprotection and remyelination by increasing neuronal and glial resilience to disease-relevant stressors. CNM-Au8® is a federally registered trademark of Clene Nanomedicine, Inc.
About Clene
Clene is a clinical-stage biopharmaceutical company focused on revolutionizing the treatment of neurodegenerative disease by targeting energetic failure, an underlying cause of many neurological diseases. The company is based in Salt Lake City, Utah, with R&D and manufacturing operations in Maryland. For more information, please visit https://clene.com or follow us on Twitter, LinkedIn and Facebook.
Forward-Looking Statements
This press release contains “forward-looking statements” which are intended to be covered by 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, you should not rely on these forward-looking statements as predictions of future events. Words such as “expect,” “estimate,” “project,” “budget,” “forecast,” “anticipate,” “intend,” “plan,” “may,” “will,” “could,” “should,” “believes,” “predicts,” “potential,” “might” and “continues,” and similar expressions are intended to identify such forward-looking statements. These forward-looking statements involve significant known and unknown risks and uncertainties, many of which are beyond Clene’s control and could cause actual results to differ materially and adversely from expected results. Factors that may cause such differences include Clene’s ability to demonstrate the efficacy and safety of its drug candidates; the clinical results for its drug candidates, which may not support further development or marketing approval; actions of regulatory agencies, which may affect the initiation, timing and progress of clinical trials and marketing approval; Clene’s ability to achieve commercial success for its marketed products and drug candidates, if approved; Clene’s ability to obtain and maintain protection of intellectual property for its technology and drugs; Clene’s reliance on third parties to conduct drug development, manufacturing and other services; Clene’s limited operating history and its ability to obtain additional funding for operations and to complete the licensing or development and commercialization of its drug candidates; the impact of the COVID-19 pandemic on Clene’s clinical development, commercial and other operations, as well as those risks more fully discussed in the section entitled “Risk Factors” in Clene’s Annual Report on Form 10-K, as well as discussions of potential risks, uncertainties, and other important factors in Clene’s subsequent filings with the U.S. Securities and Exchange Commission. Clene undertakes no obligation to release publicly any updates or revisions to any forward-looking statements to reflect any change in its expectations or any change in events, conditions or circumstances on which any such statement is based, subject to applicable law. All information in this press release is as of the date of this press release. The information contained in any website referenced herein is not, and shall not be deemed to be, part of or incorporated into this press release.
Investor Contact
John Woolford
Managing Director, Westwicke
clene@westwicke.com
+1-443-213-0506
Media Contact
Erica Fiorini, Ph.D., or David Schull
Russo Partners, LLC
Erica.fiorini@russopartnersllc.com
David.schull@russopartnersllc.com
+1-212-845-4253
RESCUE-ALS Trial Results: A Phase 2, Randomized, Double-Blind, Placebo-Controlled Study of CNM-Au8 to Slow Disease Progression in ALS Steve Vucic PhD, DSc, FRACP, FAHMS1, Parvathi Menon PhD, FRACP1, William Huynh PhD, FRACP2, Colin Mahoney, PhD, MB, MRCPI2, Karen S. Ho, PhD MSc3, Austin Rynders, RN3, Jacob Evan3, Jeremy Evan, PA-C3, Robert Glanzman, MD FAAN3, Michael T. Hotchkin3, Matthew C. Kiernan PhD, DSc, MBBS, FRACP, FAHMS 1Concord Repatriation General Hospital, University of Sydney, Australia; 2Brain and Mind Centre, University of Sydney, Australia; 3Clene Nanomedicine, Salt Lake City, UT, USA Baseline Value mean (sd) Age (yrs) Sex n, (%) Male | Female Onset Site n, (%) Limb | Bulbar Months from Onset FVC (% pred.) ALSFRS-R Score ENCALS Risk Profile1 MUNIX Sum All (n=45) 59.1 (12.3) M: 26 (58%) F: 19 (42%) L: 33 (73%) B: 12 (27%) 15.8 (9.3) 81.5 (16.7) 38.7 (6.0) -4.4 (1.8) 378.2 (175.3) CNM-Au8 30mg (n=23) 57.0 (13.3) M: 13 (57%) F: 10 (43%) L: 16 (70%) B: 7 (30%) 15.5 (7.6) 84.5 (18.3) 38.6 (6.6) -4.6 (1.7) 380.2 (198.0) Placebo (n=22) 61.3 (10.9) M: 13 (59%) F: 9 (41%) L: 17 (77%) B: 5 (23%) 16.1 (10.9) 78.2 (14.5) 38.8 (5.4) -4.2 (1.8) 376.2 (152.7) 36-Week Blinded Treatment Period with Long-Term Open-Label Extension Screening (4-weeks) Baseline Wk12 Wk36 Wk24 Wk48 Wk60 Wk72 Wk84 Wk96 Wk108+ Double-Blind Period Long-Term Open Label Extension Design Scheme Baseline Demographics 1° Endpoint | Summated MUNIX Change at Week 36 No CNM-Au8 related SAEs, drug discontinuations, or adverse event (AE) imbalance by system organ class. AEs predominantly mild-to-moderate & transient. The AEs most commonly associated with CNM-Au8 included aspiration pneumonia, n=3; nausea, n=2; abdominal discomfort, n=2. Early symptomatic ALS Randomized (1:1, CNM-Au8 30 mg or placebo) 36-week treatment period with open label extension 1st EP: MUNIX(4) summed %change of ADM, APB, BB, & TA 2nd EPs: absolute MUNIX change, % FVC Exploratory EPs: disease progression, 6-pt decline in ALSFRS-R, ALSSQOL-SF, & other neurophysiology endpoints Safety Summary Design Summary Clinical Endpoints | Exploratory CONCLUSION: RESCUE-ALS has established safety and suggested efficacy of CNM-Au8, a cellular energetic catalyst, for the treatment of ALS Acknowledgements: We thank the ALS study patients and their families for their support and willingness to engage in clinical research. We thank the site investigators for their research excellence and dedication to patients. We thank FightMND of Australia for substantially funding the RESCUE-ALS trial. 2° EP | FVC Change at Week 36 +45% Primary endpoint p-value is based on mixed model repeat measures with treatment, visit, treatment by visit interaction as fixed effects, and baseline value and ENCALS score as covariates. An unstructured covariance model was used. Exhibit 99.2
Evidence for an ALS Survival Benefit with CNM-Au8 Treatment: Interim Results from the RESCUE-ALS Trial Long-Term Open Label Extension All Randomized All OLE Participants (CNM-Au8 Treated) All CNM-Au8 Randomized All Placebo Randomized CNM-Au8 OLE ex-Placebo to CNM-Au8 OLE Survival by OLE Status Notes: All randomized subjects including study withdrawals. Data censored for all subjects of 1-February-2022. Vital status and date of death captured for all subjects withdrawn from the study through Dec 2021. Lost-to-follow-up (n=1) censored as of the last date of last study contact. ENCALS median survival estimate from baseline characteristics. Steve Vucic PhD, DSc, FRACP, FAHMS1, Parvathi Menon PhD, FRACP1, William Huynh PhD, FRACP2, Colin Mahoney, PhD, MB, MRCPI2, Karen S. Ho, PhD MSc3, Austin Rynders, RN3, Jacob Evan3, Jeremy Evan, PA-C3, Robert Glanzman, MD FAAN3, Michael T. Hotchkin3, Matthew C. Kiernan PhD, DSc, MBBS, FRACP, FAHMS 1Concord Repatriation General Hospital, University of Sydney, Australia; 2Brain and Mind Centre, University of Sydney, Australia; 3Clene Nanomedicine, Salt Lake City, UT, USA Acknowledgements: We thank the ALS study patients and their families for their support and willingness to engage in clinical research. We thank the site investigators for their research excellence and dedication to patients. We thank FightMND of Australia for substantially funding the RESCUE-ALS trial. Exhibit 99.3
Evidence for Brain Energy Metabolic Support with CNM-Au8 Treatment: Results from the REPAIR Phase 2 Clinical Trials Robert Glanzman1, MD FAAN, Chief Medical Officer, Jimin Ren2, PhD, Richard B. Dewey, III MD2, Austin Rynders1, RN, Senior Director, Clinical Operations, Karen S. Ho1 PhD MSc, Head, Translational Medicine Michael T. Hotchkin1, Chief Development Officer, Richard B. Dewey, Jr.2 MD, Benjamin Greenberg2 MD 1Clene Nanomedicine, Inc., 2University of Texas, Southwestern Design Scheme CONCLUSION: The REPAIR clinical trials demonstrate brain target engagement with CNM-Au8 treatment impacting brain energy metabolic support Clinic Visit Safety Clinic Visit Safety Clinic Visit Primary Endpoint 31P-MRS Scan Clinic Visit Follow-up 31P-MRS Scan Baseline Visit 31P-MRS Scan 4-6 weeks 1° Endpoint | NAD+/NADH Change at Week 121 2° Endpoint | NAD+ & NADH Fraction Objective Demonstration of CNS target engagement with 31P-magnetic resonance spectroscopy (31P-MRS) Design Open-label, dose blinded 12-week treatment (Enrolled: REPAIR-PD n=13, REPAIR-MS, n=13) Endpoints Primary: change of NAD+/NADH ratio based on pre-specified integrated analyses of PD & MS cohorts Secondary: change of NAD+ and NADH fractions of NAD pool Safety Well tolerated; 97% treatment compliance TEAEs were all mild-to-moderate severity and transient No SAEs Exploratory | Equilibration of Energetic Metabolites Acknowledgements: We are honored by the PD and MS study patients and their families for their support and willingness to engage in clinical research. We thank the site investigators for their research excellence and dedication to patients. We thank Jimin Ren, PhD and colleagues at the UTSW Advanced Imaging Research Center for development of the 31P-MRS imaging methodology. 1 NAD+/NADH ratio declines approximately 0.5% per decade in cross-sectional observational studies Exhibit 99.4
CNM-Au8 Gold Nanocatalysis Protects Neurons Against Degeneration and Death in Multiple in vitro Models of Amyotrophic Lateral Sclerosis Karen S. Ho1, Jean-Philippe Richard2,3, Arens Taga2, Michael Bekier4, Alexandre Henriques5, Noëlle Callizot5, Michael T Hotchkin1, Sami J Barmada4, and Nicholas J Maragakis2’. 1Clene Nanomedicine, Salt Lake City, UT; 2Johns Hopkins University, Baltimore MD; 3currently at Reprocell, USA, Inc., Beltsville, MD; 4University of Michigan, Ann Arbor, MI; 5NeuroSys, Gardanne, France. karen@clene.com Introduction – Nanocatalysis CNM-Au8® Catalytic mechanism of action enhances redox state in favor of energy production, while simultaneously lowering cellular oxidative stress Blood-brain barrier penetrant Suspension of 13 nm diameter, catalytically active, clean-surfaced, faceted gold nanocrystals Orally administered No-adverse effect level (NOAEL) nonclinical toxicology findings Well-tolerated; > 300 patient years of clinical exposure Results from Phase 2 Clinical trials presented at this meeting: Posters 034, 035, and 036. Oral P-presentation on RESCUE-ALS Clinical Trial results: Wed., Mar. 16, 11:10 AM Tennessee Ballroom. Acknowledgments We are very grateful to the individuals with ALS and healthy volunteers who donated fibroblasts, without whom the iPSC studies would not have been possible. The exceptional professional support of our colleagues at Clene has been invaluable. This study was funded by Clene Nanomedicine, Inc. (2) cAMP-Mediated CNM-Au8 Motor Neuron Neuroprotection of Wildtype and SOD1 (G93A) Rodent Motor Neurons CNM-Au8 Nanocrystal Mechanistic Effects Improved Energy Production and Utilization Neuroprotection, Remyelination (3) CNM-Au8 Neuroprotection of Human C9ORF72 iPSC-Derived Cortical Neurons Objective To determine whether CNM-Au8, a catalytic suspension of clean-surfaced, faceted gold nanocrystals, promotes neuronal survival and function in multiple independent in vitro models of ALS. Methods/Results CNM-Au8’s ability to promote neuronal survival and function in multiple independent in vitro models of ALS: (1) treatment of primary rat spinal motor neurons improves survival, preserves the neurite networks, and reduces cytoplasmic TDP-43 aggregate accumulation after either glutamate excitotoxic injury or exposure to beta-amyloid (Aβ 1-42) oligomers; (2) treatment of spinal motor neurons from transgenic SOD1G93A rats protects motor neurons from death upon exposure to excitotoxic glutamate in a cAMP-dependent manner, and reduces SOD1 protein accumulation in a manner independent of cAMP; (3) treatment of human induced pluripotent stem cell (iPSC)-derived neurons from C9ORF72 patients prevents their death in response to stress caused by mild neurotrophic factor withdrawal. Finally, we show (4) survival and neurite outgrowth of human iPSC-derived motor neurons in co-culture with toxic, SOD1A4V ALS-patient derived astrocytes are substantially and dose-dependently improved with treatment of CNM-Au8. Conclusion Addressing the deficits of ALS with the energetic catalyst CNM-Au8 appears to be a promising new therapeutic strategy for the treatment and disease-modification of ALS. Results (1) CNM-Au8 Neuroprotection of Rodent Spinal Motor Neurons from Glutamate Excitotoxicity and Amyloid-Beta (1-42) Oligomers (4) CNM-Au8 Neuroprotection of Human iPSC-derived Motor Neurons Co-Cultured with Toxic Patient iPSC-Derived Astrocytes Exhibit 99.5
RESCUE-ALS Phase 2 Trial Topline Results Phase 2 Results Exhibit 99.6
Disclosures & Acknowledgements Robert Glanzman, MD FAAN is an employee of Clene Nanomedicine, Inc. Funding support from FightMND Australia is gratefully acknowledged We thank ALS patients and their caregivers for participating in RESCUE-ALS Presenting on behalf of trial investigators
CNM-Au8 Nanocrystal Mechanistic Effects Improved Energy Production and Utilization Promotes Neuroprotection and Remyelination Oral CNM-Au8 | Improves Energy Production to Promote Neuroprotection and Remyelination
RESCUE-ALS | Design & Baseline Demographics Baseline Value mean (sd) Age (yrs) Sex n, (%) Male | Female Onset Site n, (%) Limb | Bulbar Months from Onset FVC (% pred.) ALSFRS-R Score ENCALS Risk Profile1 MUNIX Sum All (n=45) 59.1 (12.3) M: 26 (58%) F: 19 (42%) L: 33 (73%) B: 12 (27%) 15.8 (9.3) 81.5 (16.7) 38.7 (6.0) -4.4 (1.8) 378.2 (175.3) CNM-Au8 30mg (n=23) 57.0 (13.3) M: 13 (57%) F: 10 (43%) L: 16 (70%) B: 7 (30%) 15.5 (7.6) 84.5 (18.3) 38.6 (6.6) -4.6 (1.7) 380.2 (198.0) Placebo (n=22) 61.3 (10.9) M: 13 (59%) F: 9 (41%) L: 17 (77%) B: 5 (23%) 16.1 (10.9) 78.2 (14.5) 38.8 (5.4) -4.2 (1.8) 376.2 (152.7) 36-Week Blinded Treatment Period with Long-Term Open-Label Extension Screening (4-weeks) Baseline Wk12 Wk36 Wk24 Wk48 Wk60 Wk72 Wk84 Wk96 Wk108+ Double-Blind Period Long-Term Open Label Extension
Evidence for Motor Neuron Protection Primary Endpoint (MUNIX %, LS Mean Change) All Randomized All Placebo Limited Rate of MUNIX Decline in Bulbar Onset Insufficient Spinal Cord Lower Motor Neuron Progression in Early Bulbar Trial Participants RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc. +45%
Significant Impact on ALSFRS-R Decline Exploratory (ALSFRS-R Responder Analysis, < 6-point decline) All Randomized All Bulbar All Limb Sensitivity Analysis RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc.
Significant Quality of Life Improvement Exploratory (ALS Specific QOL-SF) All Randomized RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc.
Significant Impact on Disease Progression Exploratory Endpoint (Disease Progression) 1ALS Disease Progression defined as: Death, or Tracheostomy, or Non-invasive ventilation, or Gastrostomy tube All Bulbar All Limb Sensitivity RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc. All Randomized
Joint Rank Trend | Survival & ALSFRS-R Scoring Berry et al. Amyotroph Lateral Scler Frontotemporal Degener. 2013 Apr;14(3):162-8. ALSFRS-R Decline Survival CAFS All Randomized Exploratory Endpoint Pre-specified (Combined Assessment of Survival and Function [CAFS]) Score participants based on relative function or time of death
Impact on Long-Term Survival All Randomized All OLE Participants (CNM-Au8 Treated)
Impact on Long-Term Survival | by Randomization Group All CNM-Au8 Randomized All Placebo Randomized
Safety Summary | Well Tolerated & No Safety Signals Data on File, Clene Nanomedicine, Inc. No CNM-Au8 related serious adverse events (SAEs) No CNM-Au8 related drug discontinuations No imbalances in treatment emergent adverse event (TEAEs) by system organ classification TEAEs were predominantly mild-to-moderate and transient Most common TEAEs associated with CNM-Au8 (aspiration pneumonia, n=3; nausea, n=2; abdominal discomfort, n=2)
Conclusions Evidence of CNM-Au8 therapeutic efficacy Improved survival Significant slowing in disease progression Significant reduction in functional decline Significant improvement in quality of life Preservation of lower motor neurons CNM-Au8, well tolerated and safe in ALS Larger clinical trial underway
Exhibit 99.7
Forward Looking Statements 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, you should not rely on these forward-looking statements as predictions of future events. Words such as "expect," "estimate," "project," "budget," "forecast," "anticipate," "intend," "plan," "may," "will," "could," "should," "believes," "predicts," "potential," "might" and "continues," and similar expressions are intended to identify such forward-looking statements. These forward-looking statements involve significant known and unknown risks and uncertainties, many of which are beyond Clene’s control and could cause actual results to differ materially and adversely from expected results. Factors that may cause such differences include Clene’s ability to demonstrate the efficacy and safety of its drug candidates; the clinical results for its drug candidates, which may not support further development or marketing approval; actions of regulatory agencies, which may affect the initiation, timing and progress of clinical trials and marketing approval; Clene’s ability to achieve commercial success for its marketed products and drug candidates, if approved; Clene’s ability to obtain and maintain protection of intellectual property for its technology and drugs; Clene’s reliance on third parties to conduct drug development, manufacturing and other services; Clene’s limited operating history and its ability to obtain additional funding for operations and to complete the licensing or development and commercialization of its drug candidates; the impact of the COVID-19 pandemic on Clene’s clinical development, commercial and other operations, as well as those risks more fully discussed in the section the section entitled “Risk Factors” in Clene’s recently filed Annual Report on Form 10-K (filed March 11, 2022) as well as discussions of potential risks, uncertainties, and other important factors in Clene’s subsequent filings with the U.S. Securities and Exchange Commission. Clene undertakes no obligation to release publicly any updates or revisions to any forward-looking statements to reflect any change in its expectations or any change in events, conditions or circumstances on which any such statement is based, subject to applicable law. All information in this presentation is as of the date of presented or the date made publicly available. The information contained in any website referenced herein is not, and shall not be deemed to be, part of or incorporated into this presentation.
CLENE | Leadership Transforming the treatment of neurodegenerative disorders by restoring and protecting neurological function
CLENE | Overview December 31, 2021 Cash and restricted cash on hand (audited): $50.3M ALS Registration Trial Topline data in 2H 20222 >300 patient years of CNM-Au8 clinical exposure CNM-Au8® a gold nanocrystal suspension, in development as the first cellular energetic catalyst to remyelinate1 & protect neurological function Manufacturing expansion in progress, preparing for possible commercialization in 2023 Strong IP: 150+ patents on Clean-Surface- Nanocrystal technology (CSN®) platform Data on File, Clene Nanomedicine, Inc. 1Robinson et al. Sci Rep. 2020 Feb 11;10(1):1936.2https://clinicaltrials.gov/ct2/show/NCT04414345.
CLENE | Pipeline
Fu, H., et al; Nature Neuroscience (2018) 21: 1350-1358. Zhu et al. Proc Natl Acad Sci USA . 2015 Mar 3;112(9):2876-81. Rone et al. J Neurosci. 2016 Apr 27;36(17):4698-707. Neurons With High Energetic Demand Are At Increased Risk For Neurodegenerative Disease ~0.5% NAD+/NADH unit decline per decade (~0.13 mV units per year by 31P-MRS Imaging) Brain Energy Potential Declines With Normal Aging Closed squares = averaged data by age group: 21–26 yrs, 33–36 yrs, and 59–68 yrs old; Open squares= individual subject values PARKINSON’S DISEASE Dopaminergic Neurons AMYOTROPHIC LATERAL SCLEROSIS Motor Neurons HUNTINGTON’S DISEASE Medium Spiny Neurons FRONTOTEMPORAL DEMENTIA Spindle Neurons Specific Neuronal Populations Are Vulnerable to Energetic Failure MULTIPLE SCLEROSIS Axonal Degeneration
Vertices, Edges, & Facets Key to Catalytic Activity CNM-Au8 Catalytically Active Nanocrystal Suspension Clean Surfaced, Highly Faceted Shape Enhances Catalytic Activity CNM-Au8 Nanocrystal CNM-Au8® | Catalytically-Active Nanocrystals Intersection of Physics and Biology Electron Sharing Drives Catalytic Activity 60 mL per bottle (once daily)
CNM-Au8 Nanocrystal Mechanistic Effects Improved Energy Production and Utilization Promotes Neuroprotection and Remyelination CNM-Au8® | Improves Energy Production to Promote Neuroprotection and Remyelination
CNM-Au8® | Preclinical Evidence for Energetic Improvement Therapeutic Activity Across Remyelination + Neuroprotection Models Data on File, Clene Nanomedicine, Inc. Robinson et al. Sci Rep. 2020 Feb 11;10(1):1936. MN Neuroprotection ALS SOD1, In Vitro Forebrain Neuroprotection C9ORF72 In Vitro Alzheimer’s Disease Induced Neurons In Vitro
CNM-Au8® | Significant Global Opportunity Source: Lancet Neurol. 2018 Nov;17(11):939-953; ~6.1M patients globally, data as of 2016.. PARKINSON’S DISEASE ~6.1M pts globally; $6B projected by 20263 2ND most common neurodegenerative disorder; only symptomatic treatments Source: Lancet Neurol. 2018 Dec;17(12):1083-1097. MND includes amyotrophic lateral sclerosis, spinal muscular atrophy, hereditary spastic paraplegia, primary lateral sclerosis, progressive muscular atrophy, and pseudobulbar palsy MOTOR NEURON DISEASE (ALS, Other Orphan Disorders) ALS sales >$1B globally by 20291. Current drugs are largely ineffective, mostly generic Source: Lancet Neurol. 2019 Mar;18(3):269-285; ~2.2.M patients globally, data as of 2016 MULTIPLE SCLEROSIS ~2.2M pts globally; $23B market2 Only approved treatments are immunomodulators 1 Clarivate, DRG, ALS 2020. 2 Westad et al. 2017, doi:10.1038/nrd.2017.107;. 3 Parkinson’s Market Data Forecast, April 2021.
CNM-Au8® | Neuroprotection & Remyelination Data on File, Clene Nanomedicine, Inc. Phase 2 and Phase 3 Clinical Trials CNM-Au8 treatment effect on ALS disease progression Ongoing Established brain target engagement & safety Planned: Demonstrate Disease Modification Concluded enrollment due to COVID Established brain target engagement & safety Key Findings Disease Clinical Trials Q4 2021 Q3 2021 Q1 2022 Q2 2022 Q3 2022+ Establish target engagement & safety in non-active, progressive MS population
CNM-Au8® | Safety Summary Over 300 Years of Subject Exposure Without Identified Safety Signals Patient Exposure Across PD, MS, & ALS Long-term dosing experience up to 125 weeks All Animal Toxicology Studies Resulted in No-Adverse Effect Level (NOAEL) Findings Clean Toxicology Findings Multiple species up to 9-months treatment Up to maximum feasible dosing without any toxicology findings related to CNM-Au8 Assessed as Predominantly Mild-to-Moderate Severity and Transient Well Tolerated Adverse Event (AE) Profile No related CNM-Au8 AEs leading to discontinuation of treatment No SAEs related to CNM-Au8 considered severe, life-threatening, or resulting in death Data on File, Clene Nanomedicine, Inc.
Difference in brain NAD+ and NADH fraction at Week 12 (End of Treatment) Difference in bioenergetic metabolites (e.g., ATP, 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 2 CNM-Au8 Effects on Brain Energetic Metabolites A Phase 2, Open Label, Sequential Group, Investigator Blinded Study of Magnetic Resonance Spectroscopy (31P-MRS) to Assess the Effects of CNM-Au8 for the Bioenergetic Improvement of Impaired Neuronal Redox State (REPAIR) N = Up to 15 per dosing cohort (7.5, 15, 30, or 60 mg) Phase 2 Exploratory Stable Relapsing MS Early Parkinson’s Disease Clinic Visit Safety Clinic Visit Safety Clinic Visit Primary Endpoint 31P-MRS Scan Clinic Visit Follow-up 31P-MRS Scan Baseline Visit 31P-MRS Scan + 4-6 weeks Data on File, Clene Nanomedicine, Inc. Non-Active Progressive MS (Underway) Non-active, progressive MS patients is more severe than relapsing MS., and a high unmet need for disease modifying therapeutic options Day 0
CNM-Au8 Improves Brain Energy Metabolism Increases NAD+/NADH Ratio in MS & PD Phase 2 Results 1° Endpoint 2° Endpoint NAD is an essential molecule responsible for cellular energy production Exploratory (ATP Normalization) Glanzman et al. 2021. International Parkinson and Movement Disorder Society (MDS) Virtual Congress 2021. September 17 – 22, 2021 . Data on File, Clene Nanomedicine, Inc.
(January 2020); FPFV 16-Jan-2020; 45 of 42 enrolled (Nov-2020) Phase 2 1 Study was powered for MUNIX primary endpoint Neurophysiology MUNIX1 Pulmonary Function Forced Vital Capacity Function & QoL ALSFRS-R, ALSSQOL-SF Disease Progression & Survival Vucic et al. BMJ Open. 2021 Jan 11;11(1):e041479. Data on File, Clene Nanomedicine, Inc.
| Pioneered Use of MUNIX Biomarker Primary Endpoint: Spinal Cord Lower Motor Neuron Protection Muscle Fibers Spinal Cord Motor Neuron Bulbar Onset ALS (Brainstem) Limb Onset ALS (Spinal Cord) Primary Endpoint: Spinal Cord Lower Motor Neuron Motor Unit Index (MUNIX) Sum Biceps brachii Tibialis Anterior Abductor Pollicis Brevis Abductor Digiti Minimi + + + Motor Units MUNIX biomarker estimates the number of functioning lower motor neurons serving specific muscles Vucic et al. BMJ Open. 2021 Jan 11;11(1):e041479.
| Evidence for Motor Neuron Protection Primary Endpoint (MUNIX %, LS Mean Change) All Randomized All Placebo Limited Rate of MUNIX Decline in Bulbar Onset Insufficient Spinal Cord Lower Motor Neuron Progression in Early Bulbar Trial Participants RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc. +45%
| Significant Impact on ALSFRS-R Decline Exploratory (ALSFRS-R Responder Analysis, < 6-point decline) All Randomized All Bulbar All Limb Sensitivity RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc.
| Significant Quality of Life Improvement Exploratory (ALS Specific QOL-SF) All Randomized RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc.
| Significant Impact on ALS Disease Progression Exploratory Endpoint (Disease Progression) 1ALS Disease Progression defined as: Death, or Tracheostomy, or Non-invasive ventilation, or Gastrostomy tube All Bulbar All Limb Sensitivity RESCUE-ALS: A Phase 2, randomized, double-blind, placebo-controlled study of CNM-Au8 to slow disease progression in ALS. MNDA Virtual Symposium, 2021 Data on File, Clene Nanomedicine, Inc. All Randomized
| Joint Rank: Survival & ALSFRS-R Scoring Berry et al. Amyotroph Lateral Scler Frontotemporal Degener. 2013 Apr;14(3):162-8. ALSFRS-R Decline Survival CAFS All Randomized Exploratory Endpoint Pre-specified (Combined Assessment of Survival and Function [CAFS]) Score participants based on relative function or time of death
| Impact on Joint Rank Score to Wk36 Post Hoc (Combined Assessment of (i) Survival, (ii) King’s Clinical Stage 4, (iii) ALSFRS-R) Data on File, Clene Nanomedicine, Inc. ALSFRS-R Decline Survival Non-Invasive Ventilation Gastrostomy Tube King’s Clinical Stage 4 By Average of Summated Scores
All Randomized All OLE Participants (CNM-Au8 Treated) | Potential Impact on Long-Term Survival
| Potential Impact on Long-Term Survival All Placebo Randomized Survival Status by OLE Participation
| Well Tolerated & No Safety Signals Data on File, Clene Nanomedicine, Inc. No CNM-Au8 related serious adverse events (SAEs) No CNM-Au8 related drug discontinuations No imbalances in treatment emergent adverse event (TEAEs) by system organ class TEAEs were predominantly mild-to-moderate and transient Most common TEAEs associated with CNM-Au8 (aspiration pneumonia, n=3; nausea, n=2; abdominal discomfort, n=2) Safety Summary
Exploratory Endpoints Combined Joint Rank (Survival + ALSFRS-R) Voice pathology PRO (ALSAQ) Pharmacodynamic markers Slow Vital Capacity Hand-Held Dynamometry Survival Change in ALSFRS-R Registration Study: 24-Week Treatment Period (3:1 randomization, 120 active [30mg, 60mg]: 40 placebo) 1 2 Phase 3 Anticipated full unblinded data readout: 2H 2022
Exploratory Endpoints Treatment of Visual Pathway Deficits In Chronic Optic Neuropathy for Assessment of Remyelination 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, Placebo (n=73 of 150) Optical Coherence Tomography (OCT) Multi-focal VEP Amplitude & Latency Full field-VEP Amplitude & Latency MRI Endpoints Visual Function (High Contrast) QOL / EDSS 1 2 Change Composite Clinical Response 9HPT / SDMT / T25FW / LCLA Phase 2 -42 to -1 24-Week Blinded Fixed Treatment Period Up to 24-Week Blinded Extension Period (Until LPLV 24Wk Visit) LPLV *Subject to ongoing COVID-19 related site research restrictions generally implemented to protect MS patients taking standard-of-care immunosuppressive therapies Anticipated top-line unblinded data: 2H 2022 Insights to inform new Phase 2/3 MS trial
LCLA Phase 2 Primary: Functional Visual Improvement LCLA Correlates with clinically meaningful deficits in QOL, EDSS and MSFC, MRI, and OCT1 MS Functional Endpoints Phase 2 Exploratory: Neuroprotection/Remyelination Endpoints The Visual System is a Window into the Brain 9-Hole Peg Test Symbol Digit Modalities Timed 25-Ft Walk Measuring MS Functional Improvement 1Balcer et la. Mult Scler. 2017 Apr;23(5):734-747. doi: 10.1177/1352458517690822.
Significant Clinical Improvement Across Blinded Study Population Primary Endpoint: LCLA (Best-Corrected) & Secondary Endpoint: (m)MSFC Phase 2 2° | (m)MSFC 1° | LCLA Glanzman et al. VISIONARY-MS: Update to a Phase 2 Clinical Trial of CNM-Au8, Catalytically Active Gold Nanocrystals Suspension, for the Treatment of Chronic Optic Neuropathy ACTRIMS, February 2022.
Proportion of participants who require COVID-19 related hospitalization, or died at Day 28 Secondary Endpoint Exploratory Endpoints Primary Endpoint Time to substantial alleviation of COVID-19 symptoms through Day 28 Number of hospital free days through Day 28 Mean change in SARS-CoV-2 viral load Change in oxygen saturation slope Change in Global Impression (severity and change)
Trade Secrets Patent Status b Patent Description Issued & Allowed Patents 150+ Pending Applications ~20 Total Patents/ Applications >170 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/Pt; Antimicrobial) Plasma Conditioning Electrode Design & Cycling Trough Flow, Temp, Pressure Concentration & Filtration Strong Intellectual Property Extensive Patent Portfolio With Protection Through 2035 a & Proprietary Trade Secrets; Plus 7-year Orphan Drug Designation a With Patent Restoration Term (assuming 5-year extension). b As of 30-Sepbember-2021. CSN® Clean surface nanocrystal (CSN) therapeutics
Clene | Proprietary Nanocrystal Manufacturing In-House ISO8 Clean Room Clinical Production in Maryland Designed to be Scalable to Commercialization Validated CMC Processes Patented Hydro-electro- Crystallization Proprietary Trade Secrets
Anticipated Timeline & Upcoming Milestones 2020 - 2024 VISIONARY-MS
Nanotherapeutics Platform Potential first-in-class nanotherapeutic with high catalytic activity to drive energy production and utilization in stressed CNS cells Applications across neurology, infectious disease, and oncology Lead Asset: CNM-Au8 for Neurorepair CNM-Au8 improves cellular energy production and utilization to promote neuroprotection and remyelination Phase 2 ALS proof-of-concept evidence of clinical meaningful benefit Phase 3 Healey ALS platform trial results expected in 2H 2022 Phase 2 VISIONARY-MS trial results expected 2H 2022 Strong Execution Capabilities Proprietary electrochemical manufacturing process produces nanotherapeutics, scalable to commercialization Strong IP, including 150+ granted patents, and trade secrets CLENE | Company Highlights
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