Leonhardt Ventures Announces Issuance of U.S. Patent for Bioelectric Modulation of SIRT6, a Protein Linked to Muscle Health and Healthy Aging

New issuance expands a bioelectric protein-expression portfolio spanning healing, healthspan and aesthetics. Commercialization and sales rights conditionally licensed to Lionheart Health, Inc. DBA Lionheart Longevity www.lionheartlongevity.com 

HUNTINGTON BEACH, Calif., October 17, 2026 — Leonhardt Ventures LLC and Lionheart Health, Inc. today announced the issuance of U.S. Patent No. 12,752,107 B2, “Modulation of SIRT,” on October 6, 2026. The patent names Howard J. Leonhardt and Jorge Genovese as inventors and is assigned to Leonhardt Ventures LLC. Commercialization and sales rights are conditionally licensed to Lionheart Health, Inc., subject to the applicable license terms.

The patent contains 16 claims. Its published first claim covers a method of treating muscle atrophy using a specified bioelectric stimulation signal applied to skeletal muscle tissue to increase expression of sirtuin 6, or SIRT6. The issuance represents an intellectual property milestone for the companies’ work on bioelectric regulation of proteins associated with tissue function and healthy aging. patentsgazette.uspto.gov

Why sirtuins matter to healthspan<

Healthspan refers to the years of life spent in good health, with physical function and independence preserved. Sirtuins are relevant to healthspan because they help regulate how cells respond to energy availability, damage and stress.

The seven mammalian sirtuins—SIRT1 through SIRT7—are NAD⁺-dependent enzymes with different functions and locations within cells. Their biological effects depend on the particular sirtuin, tissue, disease state and level of activity. Increasing protein expression does not automatically establish increased enzyme activity or a health benefit.

Experimental research connects sirtuins with processes central to maintaining healthy tissues, including DNA repair, mitochondrial function, metabolic regulation, inflammation control and cellular maintenance. These findings provide a scientific rationale for further investigation; they do not establish that bioelectric modulation of sirtuins extends human lifespan.

Potential ways appropriate sirtuin regulation may support health

The following summarizes major areas of scientific investigation across the sirtuin family. These are research findings and potential applications, primarily from cellular and animal studies—not demonstrated benefits of Lionheart products.

• Muscle energy metabolism: SIRT1-related pathways help regulate mitochondrial function and fatty acid oxidation in muscle, processes relevant to energy production and physical function. [1]
• DNA repair and genome stability: SIRT6 can promote repair of damaged DNA, including through activation of the DNA repair protein PARP1. [2]
• Healthspan and resistance to frailty: SIRT6 overexpression reduced frailty and extended lifespan in male and female mice in a published study. Human healthspan effects remain unestablished. [3]
• Metabolic resilience during aging: SIRT6 research has linked improved energy homeostasis with healthier aging in mice. [3]
• Regulation of inflammatory signaling: SIRT1 can suppress activity of NF-κB, a major regulator of inflammatory gene expression, in experimental systems. [4]
• Cellular cleanup and recycling: SIRT1 participates in regulation of autophagy, the process through which cells recycle components and remove damaged material. [5]
• Brain signaling and memory mechanisms: SIRT1 has been linked to synaptic plasticity and memory formation through pathways involving miR-134, CREB and BDNF in mice. [6]
• Blood vessel function and muscle circulation: Experimental research identifies endothelial SIRT1 as part of a signaling network involved in blood vessel maintenance and capillary responses in aging muscle. [7]
• Antioxidant defenses: SIRT3 supports mitochondrial antioxidant mechanisms that can reduce oxidative damage in experimental models. [8]
• Protection of hearing-related cells: SIRT3 was required for the protective effects of calorie restriction against age-related hearing loss in a mouse study. This does not establish a hearing treatment in humans. [8]
• Stem cell maintenance: SIRT7 helps regulate mitochondrial protein stress and the regenerative capacity of blood-forming stem cells in experimental research. [9]
• Preservation of cellular identity: Research in human mesenchymal stem cells links SIRT7 to maintenance of heterochromatin and resistance to cellular senescence. [10]

• Heart health and resistance to cardiac stress: SIRT3 may help protect heart muscle by strengthening antioxidant defenses and limiting harmful enlargement of heart muscle cells. These protective effects have been demonstrated in cellular and mouse studies. [11]
• Kidney cell protection: SIRT1 may support kidney health by preserving cellular stress defenses and reducing injury to kidney tubule cells. Kidney-specific SIRT1 overexpression protected against cisplatin-induced kidney injury in experimental studies. [12]
• Reduced kidney scarring: SIRT1 activation reduced kidney cell death and fibrosis in a mouse model of obstructive kidney injury, suggesting a potential role in preserving kidney tissue after damage. [13]
• Immune balance and healthier inflammatory responses: SIRT3 helps regulate the NLRP3 inflammasome, an immune signaling complex that drives inflammatory cytokine production. Experimental findings suggest that appropriate SIRT3 activity may limit excessive inflammation by protecting immune-cell mitochondria. [14]
• Age-related immune regulation: SIRT2-mediated regulation of the NLRP3 inflammasome reduced aging-associated inflammation and insulin resistance in cellular and mouse models, supporting investigation of sirtuins as targets for healthier immune aging. [15]

A broader platform for bioelectric protein expression

About Leonhardt Ventures LLC

About Lionheart Health, Inc.

Selected scientific references

1. Gerhart-Hines Z, et al. “Metabolic control of muscle mitochondrial function and fatty acid oxidation through SIRT1/PGC-1α.” The EMBO Journal. 2007;26:1913–1923. Full text.
2. Mao Z, et al. “SIRT6 promotes DNA repair under stress by activating PARP1.” Science. 2011;332:1443–1446. Full text.
3. Roichman A, et al. “Restoration of energy homeostasis by SIRT6 extends healthy lifespan.” Nature Communications. 2021;12:3208. Full text.
4. Yeung F, et al. “Modulation of NF-κB-dependent transcription and cell survival by the SIRT1 deacetylase.” The EMBO Journal. 2004;23:2369–2380. Full text.
5. Lee IH, et al. “A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy.” Proceedings of the National Academy of Sciences. 2008;105:3374–3379. Full text.
6. Gao J, et al. “A novel pathway regulates memory and plasticity via SIRT1 and miR-134.” Nature. 2010;466:1105–1109. Full text.
7. Das A, et al. “Impairment of an Endothelial NAD⁺-H₂S Signaling Network Is a Reversible Cause of Vascular Aging.” Cell. 2018;173:74–89.e20. Full text.
8. Someya S, et al. “Sirt3 mediates reduction of oxidative damage and prevention of age-related hearing loss under caloric restriction.” Cell. 2010;143:802–812. Full text.
9. Mohrin M, et al. “A mitochondrial UPR-mediated metabolic checkpoint regulates hematopoietic stem cell aging.” Science. 2015;347:1374–1377. Full text.
10. Bi S, et al. “SIRT7 antagonizes human stem cell aging as a heterochromatin stabilizer.” Protein & Cell. 2020;11:483–504. Full text.
11. Sundaresan NR, et al. “Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice.” Journal of Clinical Investigation. 2009;119:2758–2771. Full text.
12. Hasegawa K, et al. “Kidney-specific overexpression of Sirt1 protects against acute kidney injury by retaining peroxisome function.” Journal of Biological Chemistry. 2010. Full text.
13. He W, et al. “Sirt1 activation protects the mouse renal medulla from oxidative injury.” Journal of Clinical Investigation. 2010. Scientific abstract.
14. Traba J, et al. “Prolonged fasting suppresses mitochondrial NLRP3 inflammasome assembly and activation via SIRT3-mediated activation of superoxide dismutase 2.” Journal of Biological Chemistry. 2017. Full text.
15. He M, et al. “An Acetylation Switch of the NLRP3 Inflammasome Regulates Aging-Associated Chronic Inflammation and Insulin Resistance.” Cell Metabolism. 2020. Full text.

Patent reference: U.S. Patent No. 12,752,107 B2, “Modulation of SIRT,” issued October 6, 2026. USPTO issuance record.

Forward-Looking Statements: This release includes forward-looking statements concerning potential applications, research outcomes and commercialization. These statements involve scientific, clinical, regulatory, intellectual property and financing uncertainties. Actual results may differ materially. No assurance is given that investigational applications will demonstrate clinical benefit, obtain regulatory authorization or reach commercialization.