# EDGAR Filing Document

**Accession Number:** 0001822791
**File Stem:** 0001437749-26-001049
**Filing Date:** 2026-1
**Character Count:** 14529
**Document Hash:** fa8cdef4a7caf25098fe164ecaf36933
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001437749-26-001049.hdr.sgml**: 20260112

**ACCESSION NUMBER**: 0001437749-26-001049

**CONFORMED SUBMISSION TYPE**: 8-K

**PUBLIC DOCUMENT COUNT**: 14

**CONFORMED PERIOD OF REPORT**: 20260112

**ITEM INFORMATION**: Other Events

**ITEM INFORMATION**: Financial Statements and Exhibits

**FILED AS OF DATE**: 20260112

**DATE AS OF CHANGE**: 20260112

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** Clene Inc.
- **CENTRAL INDEX KEY:** 0001822791
- **STANDARD INDUSTRIAL CLASSIFICATION:** PHARMACEUTICAL PREPARATIONS [2834]
- **ORGANIZATION NAME:** 03 Life Sciences
- **EIN:** 852828339
- **STATE OF INCORPORATION:** DE
- **FISCAL YEAR END:** 1231

**FILING VALUES:**
- **FORM TYPE:** 8-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 001-39834
- **FILM NUMBER:** 26524812

**BUSINESS ADDRESS:**
- **STREET 1:** 6550 SOUTH MILLROCK DRIVE, SUITE G50
- **CITY:** SALT LAKE CITY
- **STATE:** UT
- **ZIP:** 84121
- **BUSINESS PHONE:** 801-676-9695

**MAIL ADDRESS:**
- **STREET 1:** 6550 SOUTH MILLROCK DRIVE, SUITE G50
- **CITY:** SALT LAKE CITY
- **STATE:** UT
- **ZIP:** 84121

**FORMER COMPANY:**
- **FORMER CONFORMED NAME:** Chelsea Worldwide Inc.
- **DATE OF NAME CHANGE:** 20200827

?xml version='1.0' encoding='ASCII'? clnn20260109_8k.htm

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**UNITED STATES**

**SECURITIES AND EXCHANGE COMMISSION**

**WASHINGTON, D.C. 20549**

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**FORM 8-K**

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**CURRENT REPORT**

**Pursuant to Section 13 OR 15(d)** 

**of The Securities Exchange Act of 1934**

**Date of Report (Date of earliest event reported): January 12, 2026**

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**CLENE INC.**

(Exact name of registrant as specified in its charter)

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| | | |
|:---|:---|:---|
| **Delaware** | **001-39834** | **85-2828339** |
| (State or other jurisdiction | (Commission File Number) | (IRS Employer |
| of incorporation) |  | Identification No.) |
| **6550 South Millrock Drive, Suite G50**<br> **Salt Lake City, Utah** |  | **84121** |
| (Address of principal executive offices) |  | (Zip Code) |

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**(801) 676-9695**

(Registrant's telephone number, including area code)

**N/A**

(Former name or former address, if changed since last report.)

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Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

**Securities registered pursuant to Section 12(b) of the Act:**

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| | |
|:---|:---|
| **Title of each class** | **Name of each exchange on which registered** |
| Common Stock, $0.0001 par value<br> CLNN | The Nasdaq Capital Market |

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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. ☐

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**Item 8.01 Other Events.**

On January 12, 2026, Clene Inc. issued a press release announcing additional CNM-Au8<sup>®</sup> biomarker data supporting a potential new drug application ("NDA") filing for an upcoming in-person meeting with the U.S. Food and Drug Administration ("FDA"). A copy of the press release is filed as Exhibit 99.1 to this Current Report on Form 8-K and is incorporated herein by reference.

**Item 9.01 Financial Statements and Exhibits.**

(d) Exhibits

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| | |
|:---|:---|
| **Exhibit Number** | **Exhibit Description** |
| 99.1 | [Press release, dated January 12, 2026, announcing additional CNM-Au8 biomarker data supporting potential NDA filing for upcoming in-person FDA meeting.](ex_905955.htm) |
| 104 | Cover Page Interactive Data File (formatted as Inline XBRL). |

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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. | CLENE INC. |
| Date: January 12, 2026 | By: | /s/ Robert Etherington |
|  |  | Robert Etherington |
|  |  | President and Chief Executive Officer |

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## Exhibit 99.1

**Exhibit 99.1**

**CLENE ANNOUNCES ADDITIONAL CNM-Au8 BIOMARKER DATA**

**SUPPORTING POTENTIAL NDA FILING FOR**

**UPCOMING IN-PERSON FDA MEETING**

● *The FDA has granted an in-person Type C meeting during the first quarter of 2026* 

● *New independent analyses across large observational ALS cohorts demonstrate that modest (~10%) NfL reductions are significantly associated with lower mortality risk, supporting NfL reduction as a candidate surrogate endpoint for accelerated approval* 

● *New exploratory findings demonstrate that in responders with IGFBP7 biomarker decline, CNM-Au8 30mg was strongly associated with 78% reduced mortality risk (HR 0.22, p=0.01) in the HEALEY ALS Platform Trial, consistent with emerging genetic evidence linking lower IGFBP7 to ALS reversals* 

**SALT LAKE CITY, Jan. 12, 2026** -- Clene Inc. (Nasdaq: CLNN) (along with its subsidiaries, "Clene" or the "Company") and its wholly owned subsidiary Clene Nanomedicine, Inc., a late clinical-stage biopharmaceutical company focused on revolutionizing the treatment of neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS), today announced that the U.S. Food and Drug Administration (FDA) has granted Clene an in-person Type C Meeting later this quarter.

**Evidence Supporting NfL Trajectory as a Candidate Biomarker for Accelerated Approval**

Clene has now submitted its pre-meeting briefing package to the FDA, which includes previously announced statistically significant reductions in neurofilament light chain (NfL) and glial fibrillary acidic protein (GFAP) from the HEALEY ALS Platform Trial and NIH-sponsored Expanded Access Program (EAP) with linked survival evidence (announced December 2025), and new analyses demonstrating that the NfL reductions observed with CNM-Au8 treatment may predict clinical benefit in patients with ALS.

These NfL biomarker-survival analyses were conducted according to a prespecified statistical analysis plan and applied across multiple independent ALS datasets. The analyses evaluated whether longitudinal changes in NfL were associated with survival outcomes, independent of baseline disease severity and other prognostic factors.

The briefing package answers the FDA's prior requests to **(1)** establish the clinical significance of the observed NfL declines, **(2)** confirm the NfL decline observed in the HEALEY ALS Platform Trial was reproducible and **(3)** link the NfL decline to clinical outcomes such as survival.

**Alignment with Potential FDA Accelerated Approval Framework for CNM-Au8**

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;1. <u>**NfL trajectory is independently associated with increased mortality risk in ALS**</u> Analyses across two large, independent ALS cohorts (APST, Answer ALS) demonstrated that longitudinal NfL increases were robustly and consistently associated with increased mortality risk (p<0.001), independent of baseline NfL and clinical covariates. Participants in the highest NfL slope categories experienced a significant 2.3-2.6-fold increased risk of death compared to patients with lower NfL slopes (p<0.001), with a clear NfL slope-dose response relationship observed across tertiles.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;2. <u>**CNM-Au8 treatment consistently reduces NfL levels, a critical biomarker in ALS**</u> Concordant evidence from the HEALEY ALS Platform Trial 24-week double-blind period and the externally controlled NIH-sponsored EAP study at Week 36 demonstrated statistically significant and reproducible NfL reductions following CNM-Au8 treatment (HEALEY Week 24 Plasma NfL GMR 0.905, p=0.0403; NIH EAP Plasma NfL Week 36 full analysis set AUC difference -0.090, p=0.0373). These findings demonstrate consistent pharmacodynamic effects of CNM-Au8 on a clinically relevant ALS biomarker across independent study designs.

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&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;3. <u>**NfL reduction is quantitatively associated with improved survival**</u> Analyses of large ALS patient datasets demonstrate that even modest reductions in NfL are associated with improved survival. Across cohorts, the NfL reduction observed with CNM-Au8 treatment (approximately 9–10%) was associated with an approximately 8–13% lower risk of death, while larger NfL reductions were associated with proportionally greater survival benefit—a clinically meaningful benefit in a rapidly progressive disease with median survival of 2–4 years.

These findings were robust across multiple complementary statistical methods, including parametric survival modeling, joint longitudinal–survival models, and Cox regression approaches designed to address missing biomarker data and survivorship bias. These analyses describe associations observed across ALS patient populations based on statistical models and do not directly represent estimates of treatment effect on survival. For example, from the HEALEY ALS Platform Trial long-term follow-up, CNM-Au8 30 mg treatment resulted in statistically significant survival improvement compared to concurrently randomized controls (HR: 0.272, 95% CI: 0.096 – 0.772, p=0.014) with 93% of participants alive at month 12, a pre-specified analysis timepoint.

Together, these results support the biological and clinical relevance of NfL trajectory as a prognostic biomarker in ALS and provide quantitative context for interpreting NfL changes observed in interventional clinical studies.

**New Exploratory Biomarker Findings: CNM-Au8 Induced IGFBP7 Decline was Strongly Associated with Improved Survival**

Clene has identified Insulin-like Growth Factor Binding Protein 7 (IGFBP7) as an additional pharmacodynamic biomarker of treatment response to CNM-Au8 30 mg from the double-blind period of the HEALEY ALS Platform Trial. IGFBP7 decline was strongly associated with improved survival with responders, defined as a cumulative AUC IGFBP7 reduction during the 24-week double-blind period, demonstrating 78% mortality risk reduction compared to concurrently randomized controls (n=38 of 56 evaluable; HR: 0.22, 95% CI: 0.07–0.71, p=0.012; 3 events in 38 responders vs 28% mortality in controls).

Notably, the decline in IGFBP7 levels has emerged as a plausible 'mechanistic hub' in a coordinated biomarker response. IGFBP7 showed strong, statistically significant correlations with concurrent declines in other disease-relevant biomarkers, including those associated with vascular integrity, synaptic function, protein clearance, and axonal integrity (AUC Week 0-24 change; r = 0.50–0.78; all p<0.001).

This correlation pattern, with IGFBP7 as the central node, supports a hypothesized mechanistic pathway linking CNM-Au8's mode of action to IGFBP7-mediated neuroprotection:

● CNM-Au8 catalyzes NAD+ regeneration → Improved cellular (neuronal) bioenergetics

● Reduced cellular stress → Decreased IGFBP7 secretion → Enhanced free IGF-1 bioavailability

● Downstream neuroprotection → Synaptic stabilization and reduced neuronal stress

These observations align with independent genetic evidence: a variant (rs4242007) associated with decreased IGFBP7 expression was significantly more common in patients with documented ALS reversals compared to typically progressive ALS (Crayle et al. Neurology 2024). Together, these data suggest that lower IGFBP7, whether achieved genetically or pharmacologically, may help protect against ALS progression. These findings are exploratory and hypothesis-generating and require prospective confirmation.

"ALS remains a devastating disease with limited therapeutic options, and the field urgently needs biomarkers that can meaningfully inform drug development," said Rob Etherington, Chief Executive Officer of Clene. "We appreciate the FDA's willingness to engage in a detailed discussion of our biomarker and survival data. Our goal in the upcoming Type C meeting is to review the totality of evidence supporting NfL and other emerging biomarkers and to seek FDA guidance on how these data may inform future regulatory pathways for CNM-Au8, including potential accelerated approval."

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**About Clene**

Clene Inc. (Nasdaq: CLNN), along with its subsidiaries, "Clene" and its wholly owned subsidiary Clene Nanomedicine, Inc., is a late clinical-stage biopharmaceutical company focused on improving mitochondrial health and protecting neuronal function to treat neurodegenerative diseases, including amyotrophic lateral sclerosis, Parkinson's disease, and multiple sclerosis. CNM-Au8<sup>®</sup> is an investigational first-in-class therapy that improves central nervous system cells' survival and function via a mechanism that targets mitochondrial function and the NAD pathway while reducing oxidative stress. CNM-Au8<sup>®</sup> is a federally registered trademark of Clene Nanomedicine, Inc. The company is based in Salt Lake City, Utah, with R&D and manufacturing operations in Maryland. For more information, please visit <u>www.clene.com</u> or follow us on <u>X</u> (formerly <u>Twitter</u>) and <u>LinkedIn</u>.

**About CNM-Au8<sup>®</sup>**

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<sup>®</sup> is a federally registered trademark of Clene Nanomedicine, Inc.

**Forward-Looking Statements**

**<u>Investor Contact</u>:** Kevin Gardner, LifeSci Advisors; <u>kgardner@lifesciadvisors.com</u>; 617-283-2856