Aclerastide is an angiotensin receptor agonist. It can reduce fibrosis and scarring in the healing wounds. This action is more pronounced with longer administration of the peptide after injury. The action of this peptide is blocked by the AT receptor antagonist d-Ala7-angiotensin(1-7), which suggests that this receptor is involved in the healing responses to exogenous NorLeu3-A(1-7). Aclerastide has the potential in accelerating wound repair and reducing scar formation.
CAT No: 10-101-183
CAS No:227803-63-6
Synonyms/Alias:Norleu3-a(1-7); UNII-YYD6UT8T47; Asp-arg-nle-tyr-ile-his-pro; DSC127; DSC-127; USB-001;
Aclerastide, also known as PXL01, is a synthetic peptide derived from the human lactoferrin sequence and is recognized for its unique properties that modulate biological responses in tissue environments. Characterized by its potent anti-inflammatory and tissue-protective activities, Aclerastide has attracted significant research interest in the fields of wound healing, tissue engineering, and regenerative medicine. Its structure enables it to interact with various cellular targets, influencing pathways that are critical for cellular migration, extracellular matrix remodeling, and the attenuation of excessive inflammatory signaling. Due to these multifaceted actions, Aclerastide is regarded as a promising compound for advancing research in tissue repair and related biological processes.
Wound Healing Research: Aclerastide has been extensively investigated for its role in promoting the repair of damaged tissues. By modulating inflammatory responses and enhancing the migration and proliferation of key cell types such as keratinocytes and fibroblasts, it facilitates the restoration of skin integrity in a variety of experimental wound models. Researchers utilize this peptide to study mechanisms underlying improved re-epithelialization and to identify molecular mediators that can be targeted for optimizing wound closure. Its ability to reduce excessive inflammation while supporting tissue regeneration makes it an invaluable tool for elucidating the complex interplay between immune cells and the extracellular matrix during the healing process.
Tissue Engineering: In the context of tissue engineering, PXL01 is employed to enhance the integration and performance of bioengineered constructs. Its anti-adhesive and anti-fibrotic properties are particularly relevant for preventing the formation of unwanted scar tissue, which can compromise the function of implanted biomaterials. Scientists incorporate Aclerastide into scaffolds or surface coatings to investigate its capacity to modulate cell adhesion, guide tissue remodeling, and maintain the desired microenvironment for optimal tissue regeneration. These studies contribute to the development of next-generation materials and strategies for reconstructive surgery and organ repair.
Inflammation Modulation: The ability of Aclerastide to regulate key inflammatory mediators has made it a subject of interest in studies focused on chronic inflammation and fibrosis. By selectively inhibiting the activity of pro-inflammatory cytokines and enzymes, it helps to maintain a balanced immune response, thereby minimizing tissue damage and promoting resolution of inflammation. Researchers leverage its properties to dissect signaling pathways involved in chronic inflammatory diseases and to explore novel approaches for mitigating persistent tissue injury.
Nerve Repair Studies: The application of this peptide has expanded into the field of peripheral nerve repair, where its influence on axonal growth and inhibition of perineural adhesions are under investigation. By supporting a regenerative environment and reducing inhibitory scarring, Aclerastide is used to study mechanisms that enhance nerve regeneration and functional recovery following injury. Its integration into nerve conduits and repair protocols provides insights into optimizing outcomes in experimental models of nerve trauma.
Adhesion Prevention Research: Aclerastide's anti-adhesive effects are harnessed in research aimed at preventing post-surgical adhesions, a common complication that can lead to impaired tissue function and chronic pain. By interfering with the molecular events that drive excessive fibroblast activation and collagen deposition, it offers a means to study strategies for minimizing adhesion formation. Experimental applications include its use in models of tendon, peritoneal, and spinal surgery, where reducing scar tissue is critical for preserving mobility and function.
In summary, Aclerastide's versatile bioactivity positions it as a valuable compound for investigating wound healing, tissue engineering, inflammation modulation, nerve repair, and adhesion prevention. Its ability to modulate cellular and molecular processes across diverse tissue types supports a wide range of experimental designs in basic and translational research. As scientific understanding of its mechanisms continues to expand, Aclerastide is expected to play an increasingly prominent role in the advancement of regenerative medicine and tissue repair technologies.
Preclinical and clinical research shows that DSC127 is highly effective in the closure of diabetic wounds and is superior to Regranex in animal studies. Clinical development of DSC127 as a topical agent for the healing of DFU is underway. Further investigation into the mechanisms by which this product accelerates healing is warranted.
NorLeu3-Angiotensin (1-7) [DSC127] as a Therapy for the Healing of Diabetic Foot Ulcers
Derma Sciences, a tissue regeneration company focused on advanced wound and burn care, announced the termination of its Phase III clinical trials with aclerastide (DSC 127) for diabetic foot ulcer healing. This action is based on futility determinations conducted by the Data Monitoring Committee (DMC) for the planned, pre-specified interim analyses regarding the primary efficacy endpoint of confirmed complete wound closure of the target ulcer within 12 weeks of the start of treatment.
DSC 127 (aclerastide) fails diabetic foot ulcer healing trial and programme is cancelled- Derma Sciences Inc.
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