Gain Therapeutics Files 8-K

TL;DR

Gain Therapeutics filed an 8-K on Oct 8th covering events from Oct 7th. Standard disclosure.

AI Summary

Gain Therapeutics, Inc. filed an 8-K on October 8, 2024, reporting on events that occurred on October 7, 2024. The filing includes information related to Regulation FD disclosure, other events, and financial statements and exhibits. The company is incorporated in Delaware and headquartered in Bethesda, Maryland.

Why It Matters

This 8-K filing provides an update on material events and disclosures for Gain Therapeutics, Inc., which could impact investor understanding of the company's current status and future outlook.

Risk Assessment

Risk Level: low — This filing is a routine 8-K report and does not appear to contain any specific negative or positive material events that would inherently increase risk.

Key Players & Entities

• Gain Therapeutics, Inc. (company) — Registrant
• October 7, 2024 (date) — Earliest event reported
• October 8, 2024 (date) — Filing date
• Delaware (jurisdiction) — State of Incorporation
• Bethesda, Maryland (location) — Principal executive offices

FAQ

Key Financial Figures

• $0.0001 — nge on which registered Common Stock, $0.0001 par value GANX The NASDAQ Stock Marke

Filing Documents

• tm2425756d1_8k.htm (8-K) — 32KB
• tm2425756d1_ex99-1.htm (EX-99.1) — 19KB
• tm2425756d1_ex99-1img001.jpg (GRAPHIC) — 3KB
• 0001104659-24-107052.txt ( ) — 235KB
• ganx-20241007.xsd (EX-101.SCH) — 3KB
• ganx-20241007_lab.xml (EX-101.LAB) — 33KB
• ganx-20241007_pre.xml (EX-101.PRE) — 22KB
• tm2425756d1_8k_htm.xml (XML) — 4KB

01

Item 7.01. Regulation FD Disclosure. On October 7, 2024, Gain Therapeutics, Inc. (the "Company") issued a press release announcing preclinical data of its product candidate GT-02287. A copy of the press release is attached hereto as Exhibit 99.1. The information in this Current Report on Form 8-K under Item 7.01, including the information contained in Exhibit 99.1, is being furnished to the Securities and Exchange Commission, and shall not be deemed to be "filed" for the purposes of Section 18 of the Securities Exchange Act of 1934, as amended (the "Exchange Act"), or otherwise subject to the liabilities of that section, and shall not be deemed to be incorporated by reference into any filing under the Securities Act of 1933, as amended, or the Exchange Act, except as shall be expressly set forth by a specific reference in such filing.

01

Item 8.01. Other Events. On October 7, 2024, the Company announced the presentation of preclinical data for the Company's product candidate, GT-02287, in preclinical animal models of both GBA-1 and idiopathic Parkinson's disease. In animal models of GBA-1 and idiopathic Parkinson's disease (PD), rescue of motor and cognitive function associated with administration of GT-02287 was observed to be persistent upon wash out of GT-02287 without significant effect in performance for more than a week following discontinuation when compared to the animals in which treatment was continued. Another presentation for GT-02287 described its association with improved mitochondrial function and neuroprotection in GBA1-Parkinson's disease models. A second presentation described the reduction in Tau accumulation associated with GT-02287 in both GBA-1 mutation and wild type cell lines. In animal models of both GBA1 and idiopathic Parkinson's disease, GT-02287 was administered after a clinical phenotype was established and then withdrawn from half the animals for more than one week prior to conclusion of the study. Neuromuscular function, motor coordination, and activities of daily living/cognition were measured in wire hang, beam walk, and nest building tests, respectively, throughout the study. GT-02287 was shown to rescue deficits in neuromuscular function and motor coordination in both models as well as to prevent the development of deficits in cognition and activities of daily living. Notably, withdrawal of GT-02287 for more than one week did not significantly affect performance in any of the tests. In an in vitro model - in which cultured rat mesencephalic dopaminergic neurons were treated with conduritol beta epoxide (CBE) to cause partial knockdown of GCase activity comparable to that seen in PD patients carrying heterozygous GBA1 mutations (GBA1 is the gene encoding GCase)- treatment with GT-02287 reduced the level of mitochondrial reactive oxygen species (ROS) as well as

Financial Statements and Exhibits

Financial Statements and Exhibits. (d) The following Exhibit 99.1 is furnished with this report: Exhibit No. Description 99.1 Gain Therapeutics, Inc. Press Release dated October 7, 2024. 104 Cover Page Interactive Data File (embedded within the Inline XBRL document). SIGNATURE 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. GAIN THERAPEUTICS, INC. Date: October 8, 2024 By: /s/ Gene Mack Name: Gene Mack Title: Chief Financial Officer

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View this 8-K filing on SEC EDGAR