Telomir (NASDAQ: TELO) details Telomir-1 dual epigenetic action

Rhea-AI Filing Summary

Telomir Pharmaceuticals filed an update on new laboratory data for its lead preclinical drug candidate, Telomir-1, which targets the biology of cancer, aging, and age-related diseases. In in vitro studies run by Eurofins Discovery, Telomir-1 potently inhibited the histone demethylase UTX (KDM6A), an enzyme tied to abnormal DNA methylation patterns that can silence tumor suppressors and activate disease-driving genes. By blocking UTX, the compound showed potential to help reset faulty gene regulation.

The company notes prior findings that Telomir-1 inhibits other epigenetic enzymes FBXL10, FBXL11, and JMJD3, and can reactivate silenced tumor suppressors such as STAT1 and TMS1 in prostate cancer models. The new data also highlight selectivity: Telomir-1 showed no activity against the broad acetyltransferase GCN5L2 (KAT2A), which is associated with toxicity when inhibited. It did show low-level inhibition of Tankyrases (PARP5A and PARP5B), suggesting modest interference with Wnt/β-catenin “fuel line” signaling that cancers use for growth. Overall, the results support Telomir-1’s profile as a potential first-in-class epigenetic therapy with a dual mechanism of resetting DNA methylation pathways and modestly impacting Wnt/Tankyrase signaling.

Insights

Biotech and drug development analyst

New in vitro data refine Telomir-1’s dual epigenetic and Wnt/Tankyrase profile but remain preclinical.

The disclosure centers on Telomir Pharmaceuticals updating mechanistic data for Telomir-1. Eurofins Discovery studies show potent inhibition of UTX (KDM6A), which is closely linked to DNA methylation control and gene on/off switching. This aligns with prior in vivo prostate cancer work where Telomir-1 reactivated tumor suppressors STAT1 and TMS1, reinforcing a consistent epigenetic mechanism.

Selectivity details matter: the compound showed no activity against broad acetyltransferase GCN5L2 (KAT2A), which the company associates with toxicity when inhibited, and only low-level inhibition of Tankyrases (PARP5A, PARP5B) that modulate the Wnt/β-catenin growth pathway. Earlier Werner Syndrome model results, where Telomir-1 elongated telomeres and reset DNA methylation and the epigenetic clock, are cited to suggest differentiated biology. All findings are still preclinical, so any eventual clinical or commercial significance would depend on future studies that are not described here.

8-K Event Classification

Item 8.01 — Other Events

1 item

Item 8.01 Other Events Other

Voluntary disclosure of events the company deems important to shareholders but not covered by other items.

FAQ

What did Telomir Pharmaceuticals (TELO) report about Telomir-1 in this 8-K?

Telomir Pharmaceuticals reported new in vitro data showing that its lead candidate Telomir-1 potently inhibits the epigenetic enzyme UTX (KDM6A) and has low-level activity against Tankyrases that regulate Wnt/β-catenin signaling, supporting a dual mechanism of action in gene regulation and cancer growth pathways.

How does Telomir-1 affect DNA methylation pathways according to Telomir (TELO)?

The company states that Telomir-1 inhibits UTX (KDM6A), a histone demethylase closely linked to DNA methylation. This inhibition is described as potentially resetting faulty DNA methylation patterns and restoring more normal gene regulation involved in cancer, aging, and age-related diseases.

What is the significance of Telomir-1’s activity on the Wnt/Tankyrase pathway for TELO?

New data showed Telomir-1 has low-level inhibitory activity against Tankyrases (PARP5A and PARP5B), which regulate the Wnt/β-catenin pathway that cancers often use as a growth “fuel line.” The company suggests this modest activity may interfere with cancer growth signaling while differing from potent Tankyrase inhibitors that can shorten telomeres.

Did Telomir (TELO) report any selectivity or safety-related findings for Telomir-1?

Yes. Telomir reports that Telomir-1 showed no activity against GCN5L2 (KAT2A), a broad acetyltransferase whose inhibition has been associated with widespread toxicity. This lack of activity is described as potentially giving Telomir-1 a cleaner safety margin compared with other epigenetic drugs.

How do prior in vivo results support Telomir-1’s mechanism for Telomir Pharmaceuticals (TELO)?

Prior prostate cancer in vivo studies cited in the filing showed that Telomir-1 reactivated silenced tumor suppressors STAT1 and TMS1 by reversing abnormal DNA methylation. In a Werner Syndrome accelerated-aging model, Telomir-1 reportedly elongated telomeres, reversed abnormal DNA methylation, restored youthful gene regulation, and reset the epigenetic clock.

Why does Telomir describe Telomir-1 as a potential first-in-class epigenetic therapy?

Based on the in vitro and in vivo data presented, the company describes Telomir-1 as a potential first-in-class epigenetic therapy because it combines two features: resetting DNA methylation across several gene-regulation pathways and modestly interfering with Wnt/Tankyrase signaling that cancers rely on for growth.

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Understanding 8-K Material Events →

Accepted by SEC EDGAR 08/27/2025 - 04:01 PM Learn about SEC filing dates

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UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

WASHINGTON, D.C. 20549

FORM 8-K

CURRENT REPORT

Pursuant to Section 13 or 15(d) of the
Securities Exchange Act of 1934

Date of Report (Date of earliest event reported): August 27, 2025

TELOMIR PHARMACEUTICALS, INC.

(Exact Name of Registrant as Specified in its Charter)

Florida		001-41952		87-2606031
(State or Other Jurisdiction of Incorporation)		(Commission File Number)		(IRS Employer Identification No.)

100 SE 2nd St, Suite 2000, #1009

Miami, Florida
(Address of Principal Executive Offices)

Registrant’s telephone number, including area code: (786) 396-6723

Not Applicable

(Former Name or Former Address, if Changed Since Last Report)

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:

Title of each class		Trading Symbol		Name of each exchange on which registered
Common Stock, no par value		TELO		The Nasdaq Stock Market LLC

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 8.01 Other Events

Telomir Pharmaceuticals Reports In Vitro Data Supporting the Potential of Telomir-1 as a First-in-Class Epigenetic Therapy Influencing DNA Methylation Pathways in Cancer, Aging, and Age-Related Diseases

In vitro findings reveal Telomir-1’s dual action: targeting DNA methylation switches and cutting into the Wnt “fuel line” that drives cancer growth.

Telomir Pharmaceuticals, Inc. (NASDAQ: TELO), a preclinical-stage biotechnology company developing therapies that target the root mechanisms of cancer, aging, and age-related diseases, today announced new in vitro results that expand understanding of its lead drug candidate, Telomir-1.

The studies, conducted by Eurofins Discovery, showed that Telomir-1 potently inhibits UTX (KDM6A), a histone demethylase that interacts closely with DNA methylation to control which genes are switched on or off. Abnormal UTX activity has been linked to silencing of tumor suppressors and inappropriate activation of disease-driving genes. This dysregulation is observed in cancer, autoimmune disease, aging, neurodegeneration, autism spectrum disorder, and metabolic dysfunction. By inhibiting UTX, Telomir-1 demonstrated the potential to reset faulty DNA methylation patterns and restore more normal gene regulation.

As previously reported, Telomir-1 also inhibited additional epigenetic enzymes — FBXL10, FBXL11, and JMJD3 — that are implicated in tumor progression, inflammation, metabolic dysfunction, and neurodevelopmental disorders. In prior prostate cancer studies in vivo, Telomir-1 reactivated silenced tumor suppressors STAT1 and TMS1 by reversing abnormal DNA methylation, providing functional evidence of its ability to reset gene programs that are often disabled in cancer.

Importantly, Telomir-1 showed no activity against GCN5L2 (KAT2A), a broad acetyltransferase enzyme whose inhibition has been associated with widespread toxicity. This selectivity may provide Telomir-1 with a cleaner safety margin compared to other epigenetic drugs.

The new in vitro data also showed that Telomir-1 had low-level inhibitory activity against Tankyrases (PARP5A and PARP5B). Tankyrases regulate the Wnt/β-catenin pathway, one of the body’s master growth-control circuits that cancers frequently hijack as a “fuel line” for unchecked proliferation and treatment resistance. Unlike potent Tankyrase inhibitors, which can shorten telomeres and pose systemic safety risks, Telomir-1’s modest activity may allow disruption of cancer’s fuel line without compromising telomere biology. Supporting this distinction, previously reported data from a validated Werner Syndrome accelerated-aging in vivo model showed that Telomir-1 significantly elongated telomeres beyond healthy levels while also reversing abnormal DNA methylation, restoring youthful gene regulation, and resetting the epigenetic clock.

Taken together, the results support Telomir-1’s emerging profile as a potential first-in-class epigenetic therapy with a dual mechanism of action:

	1.	Resetting DNA methylation across several pathways that regulate gene expression.
	2.	Modestly interfering with Wnt/Tankyrase signaling — the “fuel line” cancers rely on for growth.

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.

	TELOMIR PHARMACEUTICALS, INC.
Dated: August 27, 2025	By:	/s/ Erez Aminov
	Name:	Erez Aminov
	Title:	Chief Executive Officer