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“A New Molecule That Restores Youth” ...

2026-03-25

“A New Molecule That Restores Youth” — Scientists Turn Off the Aging Switch in Stem Cells [Unboxing the Lab]

Konkuk University Team Develops Novel DDR1 Inhibitor
Doubles Wound-Healing and Regenerative Capacity, Opening New Possibilities for Anti-Aging Therapies

Remember the excitement of opening a package you’ve been waiting for? In university laboratories, remarkable discoveries that could change our lives are being made every day—they’re just wrapped in the thick packaging of academic papers.

In “Unboxing the Lab,” we cut through the complex equations and theories to bring you the key findings that matter most.

So, shall we open the box? Today’s research spotlight is this one.
 

건국대 조쌍구 교수팀이 개발한 신물질 'AC-4067'이 줄기세포의 '노화 스위치(DDR1)'를 꺼서 젊음을 되찾는 모습을 시각화했다. 늙은 피부(왼쪽)가 분자 열쇠로 스위치를 'OFF'로 전환하자 생기 넘치는 피부

Novel DDR1 Inhibitor AC-4067 Shows Potential to Rejuvenate Aged Stem Cells

Konkuk University-led research demonstrates enhanced wound healing and regenerative capacity, opening new possibilities for anti-aging and regenerative therapies

A research team led by Prof. Ssang-Goo Cho of Konkuk University has developed a novel compound, AC-4067, that targets DDR1, a protein associated with stem cell aging.

The study found that inhibiting DDR1 can restore key functions of aged stem cells, significantly improving their regenerative and wound-healing capabilities. The findings suggest a promising new approach for regenerative medicine, anti-aging therapeutics, and advanced stem cell applications.

Targeting the “Aging Switch” in Stem Cells

As stem cells age, their ability to regenerate damaged tissue gradually declines. The research team identified DDR1 as a key protein closely linked to this loss of regenerative capacity.

Using computational drug-design approaches, the researchers developed AC-4067 to selectively inhibit DDR1 activity. The compound showed approximately 18-fold greater selectivity for DDR1 than for DDR2, a closely related protein, demonstrating its ability to precisely target the intended pathway.

Restoring Regenerative Capacity

Treatment with AC-4067 produced measurable improvements in aged stem cells.

The proportion of cells showing senescence-associated markers decreased significantly, while levels of γ-H2AX, a marker of DNA damage, were also reduced.

In wound-healing assays, AC-4067 demonstrated activity at a concentration as low as 30.9 nM. Treated cells showed more than a twofold increase in migration capacity compared with untreated aged cells, along with faster wound closure.

These findings indicate that DDR1 inhibition may not only slow cellular aging but also help restore regenerative functions that have already declined.

Potential Applications in Regenerative Medicine

The research could help address one of the major challenges in stem cell therapy: the gradual loss of cellular quality during large-scale expansion.

By preserving or restoring the regenerative capacity of stem cells, the technology may contribute to the production of more consistent and high-quality stem cell therapeutics.

The findings also have potential applications in the development of treatments for degenerative diseases, tissue injuries, wound healing, skin regeneration, and anti-aging therapies.

International Collaborative Research

The study was led by Prof. Ssang-Goo Cho’s research team at Konkuk University, in collaboration with Prof. Kyung Lee’s team at Dongguk University College of Pharmacy and researchers from Weill Cornell Medicine in the United States.

By combining advanced drug-design technologies with regenerative medicine research, the international team developed a new strategy for restoring the function of aged stem cells.

The research was published in Biomedicine & Pharmacotherapy, an internationally recognized journal in pharmacology and biomedical research.

This study represents an important step toward developing next-generation regenerative therapies that go beyond delaying cellular aging and instead aim to restore lost cellular function.

김만기 기자 (monarch@fnnews.com)