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Scarless Laboratories Announces Positive Results from its Phase 1/2a Clinical Study in Scar Reduction

Los Angeles, California–Scarless Laboratories, Inc., a biotechnology company with a platform technology in scar reduction and wound healing, announced today that it has completed its First-in-Human Phase 1/2a clinical study for improvement in scar appearance and wound healing in patients undergoing elective abdominoplasty.

Scarless’ platform technology is based on its lead candidate SLI-F06, a novel peptide that had previously demonstrated safety and preliminary effectiveness in large animal models, has now been shown to be safe in humans and to improve the appearance of acute scars in patients undergoing elective abdominoplasty when compared to vehicle control.

In a 22-patient clinical study conducted at 3 Investigative sites in the United States, SLI-F06 treated study arm showed significant improvement in scar appearance when compared to vehicle (placebo). With proof of concept and safety complete Scarless’ clinical plans include further study including dose optimization in abdominoplasty and in scar revision and treatment of Diabetic Foot Ulcers.

“Completion of our first Phase 1/2a clinical study is a major milestone for Scarless” said Dr. Soo “and we look forward to continued development and expansion with our SLI-F06 platform technology to help the millions of people who are burdened with untreated or inadequately treated scars and wounds.”

The economic and physiological burden of scaring is staggering. There are an estimated 12 million traumatic lacerations treated in the U.S. emergency rooms each year, 250 million surgical incisions created worldwide every year, and 11 million burns severe enough to warrant medical treatment worldwide.  In the U.S alone, over $20 billion per year are spent on the treatment and management of scars.  Scars can be associated with severe psychological, physical, and functional complications that erode an individual’s quality of life. Currently  there are no approved drugs or biologics that can adequately address the existing unmet need for effective therapies in the multi-billion-dollar scar and wound healing markets.

About Scarless Laboratories, Inc.

Scarless Laboratories is a clinical stage biotechnology company focused on revolutionizing tissue repair and disrupting the billion-dollar scar prevention, scar reduction, and chronic wound healing industries. Scarless was founded by UCLA Professors Drs. Chia Soo, Ting Kang and Zheng Zhong  and is located in Los Angeles, California. It is supported by private investors and National Institute of Health (NIH) grants. For more information, please visit www.scarlessLabs.com.

Researchers may have found a way to mitigate or eliminate excessive scarring during wound healing

FINDINGS
A study published April 12 in Nature Communications identifies a protein that helps prevent excessive scarring. The protein, called fibromodulin (FMOD) forms a complex of molecules with interleukin 1β that stops myofibroblasts from forming excessive scar tissue. IMPACT
The findings could lead to a new way to reduce or prevent excessive scarring, which could benefit patients recovering from surgery, injuries, or burns. BACKGROUND
In previous studies, the researchers had described the critical role of FMOD in enabling scarless fetal-type repair as well as preventing excessive scarring during adult-type repair. For this new study, the researchers investigated the effects of FMOD on myofibroblasts, a key cell in healing and scar formation. Myofibroblasts should die off after a wound heals, but they can continue forming tissue long afterwards, leading to excessive scarring.  The fibromodulin-based complex promotes the death of myofibroblasts.

COMMENT
“Dr. Eric Kang Ting and I have been studying how to reduce skin scarring for the past two decades at UCLA,” said Dr. Chia Soo, professor of surgery and vice chair for research for the UCLA Division of Plastic and Reconstructive Surgery.  “This publication explores the crucial role of naturally occurring fibromodulin in regulating a key scar-forming cell, the myofibroblast. This, combined with our team’s FDA-approved clinical study led by Dr. Zhong Zheng using a fibromodulin-derived peptide in 54 patients for scar reduction, demonstrates a significant leap in potential treatments for patients with excessive scarring.”

AUTHORS
Study co-authors :

• Wenlu Jiang
• Xiaoxiao Pang
• Pin Ha
• Chenshuang Li
• Grace Xinlian Chang
• Yuxin Zhang
• Lawrence A. Bossong
• Eric Kang Ting
• Zhong Zheng.

FUNDING
National Institute of Dental and Craniofacial Research, National Institute of Arthritis and Musculoskeletal and Skin Diseases, UCLA CTSI grant (UL1TR000124), UCLA Operation Mend, UCLA Orthopaedic Hospital, UCLA Orthopaedic Hospital Research Center, the International Orthodontics Foundation, China Postdoctoral Science Foundation, Natural Science Foundation of Chongqing, China, and Chongqing Medical University Program for Youth Innovation in Future Medicine. DISCLOSURES
Eric Kang Ting, Chia Soo, and Zhong Zheng are inventors of fibromodulin-related patents assigned to UCLA; founded Scarless Laboratories Inc. and Saint Therapeutics Inc., which sublicense fibromodulin-related patents from the UC Regents, who also hold equity in the company, and are also past or present officers of Scarless Laboratories, Inc. and Saint Therapeutics Inc.

Novel therapeutic approach could eliminate excessive scarring following orofacial cleft repair

Somerville, Mass., 05/07/2025 – Cleft lip and/or cleft palate are among the most common craniofacial birth defects in the United States. These conditions, collectively referred to as orofacial clefts, occur when a baby’s lip or mouth do not form properly during pregnancy.

When an orofacial cleft is closed surgically, it commonly produces a raised, thick scar known as a hypertrophic scar, which can be disfiguring and affect function, with huge social and economic impacts to the patient.

A recent study from scientists at ADA Forsyth Institute (AFI) and University of California-Los Angeles (UCLA) suggests a new cutting-edge therapeutic approach may mitigate or even prevent excessive scarring, significantly advancing the field of wound healing and regeneration.

Scars are an important part of the body’s natural response to injury to wall off the injured site from normal tissues. During healing, scars are replaced gradually with healthy tissues. However, in abnormal healing, excessive myofibroblasts – cells that produce and organize collagen and play a key role in wound healing – and other abnormal activities can lead to excess scarring that does not heal normally.

A research team including AFI adjunct faculty Eric Kang Ting, D.M.D., D.Med.Sc., and UCLA researchers Chia Soo, M.D., Pin Ha, D.D.S., M.D., and Zhong Zheng, Ph.D. identified a molecule – fibromodulin (FMOD) protein – which works to maintain a balanced level of myofibroblasts, resulting in minimal scarring at the surgical site. The scientists detail this mechanism in a new paper published in Nature Communications.

“Our team has been exploring ways to improve scarring from cleft lip repair,” said Dr. Ting. “We have identified a new peptide drug derived from fibromodulin that may help reduce scarring. This publication demonstrates the broader role of fibromodulin in regulating a key cell involved in scarring: the myofibroblast.”

FMOD can prevent excessive scarring when included in surgical procedures that close tissue such as suturing of cleft lip. This method may also be successful in preventing keloid scars, a form of scarring that results in excess tissue growth beyond the boundaries of an original wound.

“By targeting the biology of scarring at the molecular level, this breakthrough has the potential to transform outcomes for patients undergoing cleft repair and other surgical procedures,” said AFI chief science officer and chief operating officer Ben Wu, D.D.S., Ph.D. “This powerful translational science brings fundamental biological insights to clinical care and would not have been possible without critical funding support by NIH.”

“Dr. Ting and I have been studying how to reduce skin scarring for the past two decades,” Dr. Soo said. “This recent breakthrough describing how fibromodulin may reduce excessive scarring through controlled cell death demonstrates a significant leap in potential treatments for patients with excessive scarring.”

The research offers a shift in perspective toward minimizing scarring and improving clinical outcomes in cutaneous wound repair. Dr. Zheng said, “in this study, we demonstrate that fibromodulin, a matricellular proteoglycan, accelerates the clearance of myofibroblasts without disrupting initial wound repair, providing a new mechanism to minimize scarring.” Dr. Zheng leads an FDA-approved clinical study currently in Phase 1/2A using a fibromodulin-derived peptide.

Additional collaborators on the project included Wenlu Jiang (UCLA), Xiaoxiao Pang (Chongqing Medical University), Chenshuang Li (University of Pennsylvania), Grace Xinlian Chang (UCLA), Yuxin Zhang (Chongqing Medical University), and Lawrence A. Bossong (Princeton University).

This work was funded by :

• NIH NIDCR R44DE024692 (to C.S. and Z.Z.)

• SB1DE026972 (to K.T., C.S., and Z.Z.)

• NIH NIAMS R44AR064126 (to C.S. and Z.Z.)

• UCLA CTSI grant UL1TR000124 (to C.S.)

• UCLA Operation Mend (to C.S.)

• UCLA Orthopaedic Hospital (to C.S.)

• UCLA Orthopaedic Hospital Research Center (to C.S.)

• International Orthodontics Foundation.

“Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling,” Nature Communications. DOI#1038/s41467-025-58906-z

The ADA Forsyth Institute was founded in 1910 as the Forsyth Dental Infirmary for Children (later, the Forsyth Institute), to provide dental care to the disadvantaged children of Boston. While continuing to serve children in need, yet recognizing the ultimate goal is to prevent dental disease, the Institute in 1915 began to focus on scientific research and is today the world’s leader in oral health research. In October of 2023, the Institute joined with the American Dental Association to form the ADA Forsyth Institute, a 501(c)(3) entity dedicated to improving people’s oral and overall health and powering the profession of dentistry through cutting-edge basic research, creative translational science, innovative clinical technologies, and global public health outreach. Consistent with the Institute’s founding mission, the ADA ForsythKids mobile dental program continues to serve children in need.

Newly identified protein could mitigate or eliminate excessive scarring during wound healing

Fibromodulin (FMOD) accelerates myofibroblast clearance in rat and pig models with reduced scar formation. Credit: Nature Communications (2025). DOI:10.1038/s41467-025-58906-z

A study published April 12 in Nature Communications identifies a protein that helps prevent excessive scarring. The protein, called fibromodulin (FMOD) forms a complex of molecules with interleukin 1β that stops myofibroblasts from forming excessive scar tissue.

The findings could lead to a new way to reduce or prevent excessive scarring, which could benefit patients recovering from surgery, injuries, or burns. In previous studies, the researchers had described the critical role of FMOD in enabling scarless fetal-type repair as well as preventing excessive scarring during adult-type repair.

For this new study, the researchers investigated the effects of FMOD on myofibroblasts, a key cell in healing and scar formation. Myofibroblasts should die off after a wound heals, but they can continue forming tissue long afterwards, leading to excessive scarring. The fibromodulin-based complex promotes the death of myofibroblasts.

“Dr. Eric Kang Ting and I have been studying how to reduce skin scarring for the past two decades at UCLA,” said Dr. Chia Soo, professor of surgery and vice chair for research for the UCLA Division of Plastic and Reconstructive Surgery.

“This publication explores the crucial role of naturally occurring fibromodulin in regulating a key scar-forming cell, the myofibroblast. This, combined with our team’s FDA-approved clinical study led by Dr. Zhong Zheng using a fibromodulin-derived peptide in 54 patients for scar reduction, demonstrates a significant leap in potential treatments forpatients with excessive scarring.”

Study co-authors are :Wenlu Jiang, Xiaoxiao Pang, Pin Ha, Chenshuang Li, Grace Xinlian Chang, Yuxin Zhang, and Lawrence A. Bossong, Eric Kang Ting, and Zhong Zheng.

More information: Wenlu Jiang et al, Fibromodulin selectively accelerates myofibroblast apoptosis in cutaneous wounds by enhancing interleukin 1β signaling, Nature Communications (2025).

DOI: 10.1038/s41467-025-58906-z Provided by University of California, Los Angeles

Citation: Newly identified protein could mitigate or eliminate excessive scarring during wound healing (2025, May 6) retrieved 29 January 2026 from https://medicalxpress.com/news/2025-05-newly-protein-mitigate-excessive-scarring.html

Parternership in Wound healing-related grants

NIH  R21DE015118                        Role of Fibromodulin in Scarless Repair

NIH  R43AR064126                        A novel anti-scar peptide for cutaneous wound repair

NIH  R43AR063558                        Safety and efficacy testing of novel anti-scar peptide vs corticosteroid for scar

NIH  R44DE024692                        Anti-scar peptide for cleft lip repair

NIH  R44AR064126                        A novel anti-scar peptide for cutaneous wound repair

NIH  R44DE026080                        Novel peptide-coated suture for cleft lip and palate repair

NIH  SB1DE026972                       Anti-scar peptide for cleft lip repair

NIH  U24DE026914                       Center for Dental, Oral, & Craniofacial Tissue & Organ Regeneration (C-DOCTOR) 2017 Spring ITP Team Award

Peptide-impregnated hydrogel system for improving cleft lip and palate wound healing.

Plastic Surgery Foundation   Translational Research Grant (#571906)       A peptide-impregnated gel for accelerating wound tensile strength reestablishment.

NIH  R44DE026080                        Novel-peptide-impregnated hydrogel as a wound healing device

NIH  R44DK131648                       Novel peptide for enhancing diabetic wound healing