Sentynl Therapeutics Enters into Agreement with PRG S&T to License Molecule for Hutchinson-Gilford Progeria Syndrome

Sentynl Therapeutics Enters into Agreement with PRG S&T to License Molecule for Hutchinson-Gilford Progeria Syndrome

Sentynl Therapeutics Enters into Agreement with PRG S&T to License Molecule for Hutchinson-Gilford Progeria Syndrome

PR Newswire

AHMEDABAD, India and SOLANA BEACH, Calif., March 16, 2026

_Sentynl will acquire full rights to the investigational drug candidate, Progerinin (SLC-D011), _adding to its commercial portfolio of rare and ultra-rare disease products

AHMEDABAD, India and SOLANA BEACH, Calif., March 16, 2026 /PRNewswire/ – Sentynl Therapeutics Inc. (“Sentynl”), a U.S.-based biopharmaceutical company and wholly-owned subsidiary of Zydus Lifesciences Limited (“Zydus”), announced that it is entering into an agreement with PRG S&T, a Korean company specializing in the development of medicine for rare genetic diseases, to license its investigational molecule Progerinin (SLC-D011) for Hutchinson-Gilford Progeria Syndrome (HGPS or “progeria”).

The agreement will allow Sentynl to begin working with PRG S&T immediately to advance the clinical development of Progerinin (SLC-D011) for HGPS, which has been designated as an orphan drug by the United States Food and Drug Administration (FDA). Under the conditions that certain milestones are met, Sentynl will acquire full rights to the molecule for HGPS upon closing, making Progerinin the company’s second therapy intended for the treatment of HGPS. The program is currently finalizing a Phase 2A clinical trial and data are expected before the end of 1H 2026.

“This acquisition marks an important step in growing our portfolio of therapies for Hutchinson-Gilford Progeria Syndrome, which can have severe impacts on patient health if left untreated,” said Dr. Sharvil P. Patel, Managing Director, Zydus Lifesciences Limited. “Supporting patients in living healthy, fulfilled lives is core to what we do, and the agreement with PRG S&T directly furthers this mission by advancing orphan therapies for patients and families impacted by rare diseases.”

“Children with Hutchinson-Gilford Progeria Syndrome face an unforgiving disease. However, we are seeing real progress in progeria research, with new science changing what’s possible,” said Matt Heck, CEO, Sentynl. “This agreement, which will add Progerinin to our progeria portfolio, represents our commitment to translating that progress into another real therapy for children and families who need them.”

Progerinin is an investigational, orally active small-molecule drug being developed as a potential treatment for Hutchinson-Gilford Progeria Syndrome, a rare genetic disorder characterized by accelerated aging in children. The disease is caused by the accumulation of progerin, an abnormal form of the lamin A protein produced by mutations in the _LMNA _gene, which disrupts nuclear structure and leads to premature cellular aging. Progerinin is designed to inhibit the interaction and harmful effects of progerin within cells, thereby improving nuclear integrity and reducing cellular damage.  It is not currently approved by FDA or any other health authority.

“The Progeria Research Foundation (PRF) is proud to have funded the foundational research that led to the development of Progerinin, and we are happy to see this potential path moving forward,” said Leslie Gordon, MD, PhD, Medical Director at Progeria Research Foundation. “PRF’s mission is to find treatments and the cure for Progeria, and we are grateful for the efforts of PRG S&T and Sentynl to improve the lives of the children and young adults in our Progeria patient community.”

Early research and clinical trials aim to determine whether Progerinin can slow disease progression and improve survival in HGPS patients, potentially offering another therapeutic option. Currently, Zokinvy® (lonafarnib) is the only approved treatment for HGPS and certain processing-deficient Progeroid Laminopathies in the U.S., European Union, Great Britan, Israel, and Japan.

**About Progerinin

**Progerinin is a small-molecule drug candidate being developed to treat Hutchinson-Gilford Progeria Syndrome (HGPS), a rare genetic disorder that causes rapid aging in children. It works by targeting progerin, an abnormal protein produced from a mutation in the _LMNA _gene. In HGPS, this mutation causes cells to produce progerin instead of normal lamin A, which leads to defects in the cell nucleus and accelerates aging symptoms. In mouse models of HGPS, progerinin demonstrated encouraging outcomes. In mice with a severe form of the disease, treatment increased lifespan by 8–10 weeks and improved body weight. The untreated control group had a shorter lifespan (average = 16.8 weeks; maximum = 18 weeks), whereas the treated group exhibited a significantly extended lifespan (average = 25.2 weeks; maximum = 26 weeks; p < 0.001).

About Progeria
Collectively known as progeria, Hutchinson-Gilford Progeria Syndrome and progeroid laminopathies are ultra-rare, fatal, genetic premature aging diseases that accelerate mortality in young patients. HGPS is caused by an _LMNA _point mutation that produces the farnesylated lamin A variant, progerin, via aberrant splicing.  Progeroid laminopathies are genetic disorders of accelerated aging caused by mutations in LMNA and/or _ZMPSTE24 _that impair lamin A processing, resulting in the accumulation of farnesylated prelamin A proteins including progerin.2,3

Children with HGPS commonly die of atherosclerosis, the same heart disease that affects millions of normally aging adults by an average age of 14.5 years. Disease manifestations include severe failure to thrive, scleroderma-like skin, global lipodystrophy, alopecia, joint contractures, skeletal dysplasia, global accelerated atherosclerosis with cardiovascular decline, and debilitating strokes.1

**About Zydus Lifesciences Limited

**Zydus Lifesciences Limited is an innovation-led life-sciences company with leadership positions across pharmaceuticals and consumer wellness, supported by an emerging MedTech franchise and a global footprint across the United States, India and other international markets. As of September 30, 2025, the group employs 29,000 people worldwide including 1,500 scientists engaged in R&D and is driven by its mission to unlock new possibilities in life sciences through quality healthcare solutions that impact lives. The group aspires to transform lives through path-breaking discoveries. For more details visit

**About Sentynl Therapeutics Inc

**Sentynl Therapeutics Inc. (“Sentynl”) is a commercial stage U.S.-based biopharmaceutical company focused on bringing innovative therapies to patients living with rare diseases. Recognized for its commitment to the rare disease community, Sentynl leverages its global operations as well as its parent organization, Zydus Group, to advance the development, manufacturing, and delivery of treatments to patients who need them in numerous countries worldwide. Sentynl is dedicated to improving patient outcomes and access while upholding ethical standards and operating in compliance with applicable laws, regulations, and industry guidelines. For more information, visit

**About PRG S&T

**PRG S&T is a research & development company specializing in the treatment of rare genetic diseases. PRG S&T has been developing therapeutics for rare genetic diseases (laminopathies, neurodegenerative diseases, neuro-oncology etc.) with small molecules, which are derived from target sites on aberrant Protein-Protein Interactions (PPI). For more information, please visit www.eng.prgst.com.

Resources

1. Gordon LB, Brown WT, Collins FS. Hutchinson-Gilford Progeria Syndrome. 2003 Dec 12
[Updated 2019 Jan 17]. In: Adam MP, Ardinger HH, Pagon RA, et al., editors. GeneReviews® [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2020.
2. Gordon LB, Shappell H, Massaro J, et al. Association of lonafarnib treatment vs no treatment with mortality rate in patients with Hutchinson-Gilford progeria syndrome. JAMA. 2018;319(16):1687-1695. doi:10.1001/jama.2018.3264.
3. Marcelot A, Worman HJ, and Zinn-Justin S. Protein structural and mechanistic basis of progeroid laminopathies. FEBS Journal. 2021:288:2757-2772. Doi:10.111/febs.15526.

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